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Ventricular action potential |This article does not cite any references or sources. (December 2009)| In electrocardiography, the ventricular myocyte membrane potential is about −90 mV at rest, which is close to the potassium reversal potential. When an action potential is generated, the membrane potential rises above this level in four distinct phases. The beginning of the action potential, phase 0, specialized membrane proteins (voltage-gated sodium channels) in the cell membrane selectively allow sodium ions to enter the cell. This causes the membrane potential to rise at a rate of about 300 V/s. As the membrane voltage rises (to about 40 mV) sodium channels close due to a process called inactivation. The Na+ channel opening is followed by inactivation. Na+ inactivation comes with slowly activating Ca2+ channels at the same time as a few fast K+ channels open. There is a balance between the outward flow of K+ and the inward flow of Ca2+ causing a plateau of length in variables. The delayed opening of more Ca2+-activated K+ channels, which are activated by build-up of Ca2+ in the sarcoplasm, while the Ca2+ channels close, ends the plateau. This leads to repolarisation. The depolarization of the membrane allows calcium channels to open as well. As sodium channels close calcium provides current to maintain the potential around 20 mV. The plateau lasts on the order of 100 ms. At the time that calcium channels are getting activated, channels that mediate the transient outward potassium current open as well. This outward potassium current causes a small dip in membrane potential shortly after depolarization. This current is observed in human and dog action potentials, but not in guinea pig action potentials. Repolarization is accomplished by channels that open slowly and are mostly activated at the end of the action potential (slow delayed-rectifier channels), and channels that open quickly but are inactivated until the end of the action potential (rapid delayed rectifier channels). Fast delayed rectifier channels open quickly but are shut by inactivation at high membrane potentials. As the membrane voltage begins to drop the channels recover from inactivation and carry current.

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Disease-causing pathogens are among the most intriguing forces shaping human evolution, as they have a tremendous impact on our genome and themselves evolve over time. Through natural selection, genetic variants that confer resistance to infectious diseases can spread through human populations over time, leaving distinctive patterns in the human genome. The classic example of such an effect is the evolution of human genetic resistance to malaria across Africa. In the era of genomics, we can now probe information buried in the millions of sequence variations that have occurred and persisted in the human genomes in search of signatures of recent evolution. We have developed computational methods, such as CMS, LRH and XP-EHH tests, to detect genetic variants under positive selection. These methods identify variants that have recently emerged and spread through populations, relying on the breakdown of recombination as a clock for estimating the ages of alleles. We have applied these methods to large datasets of human genetic variation finding many novel candidates for selection. We are developing methods to further refine the signals from large candidate regions to localize the underlying selected polymorphism. We have also developed software to make detection of selection, by these and other methods, possible for the rapidly expanding empirical data on genetic variation in humans and other species. The Sabeti lab continues to refine existing, and develop novel, methods and tools to detect and localize signals of selection in humans and other organisms. We are using approaches that take advantage of rapidly expanding datasets of genetic variation and larger population sampling, increasingly affordable full-genome sequencing, and new insights into the structure of genetic variation in the genome. We will apply our methods to look for instances of natural selection, using our own data and data collected from humans in two international efforts: The International Haplotype Map Consortium (1000 individuals genotyped for 1 million polymorphisms) and the 1000 Genomes Consortium (full genome sequences from 1000 individuals). Through our search for positively selected genes in the human genome, we discovered a novel target of selection in a Nigerian study population - the LARGE gene, a protein that is critical for infection with Lassa virus. We continue to carry out studies of genetic susceptibility to Lassa hemorrhagic fever, investigate the genetic properties of resistance alleles, and seek to develop genetic association methods that utilize signals of natural selection. Figure 1. The strongest signal of natural selection in the Yoruba of Nigeria is a 300 kb genomic region that lies entirely within the gene LARGE. (A) The signal, based on the LRH test, on Chromosome 22. (B) A visual display of an allele at 39% prevalence with long-range associations (haplotype) across the region to either side, suggesting it is a common allele of young age. The bottom diagram, for comparison, shows another common allele, not believed to be under selection, with much greater decay of long-range associations, suggesting an older age.

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From Other Journals Frequent Amblyopia Screening Improves Children's Vision Am Fam Physician. 2002 Nov 1;66(9):1765. The long-established practices of early childhood screening for amblyopia and patching of the dominant eye are not supported by evidence of good clinical outcome. Williams and colleagues used a large longitudinal study of child development in southwest England to analyze the outcomes of screening and early intervention in children with amblyopia. All children who were born in the region during a six-month period were eligible for the study. The 3,490 participating children received the usual early screening administered by family physicians and nurse practitioners and, later, screening for visual acuity by school nurses. Participants in the study were randomly allocated to normal amblyopia surveillance or intensive screening and intervention. Children in the intensive-screening group received age-appropriate visual testing and assessment by an orthoptist at eight, 12, 18, 25, 31, and 37 months of age. Children in the control group were assessed by an orthoptist at 37 months of age. All children who failed acuity or cover testing were referred to a hospital-based eye service. At 7.5 years, data were available for 1,088 (54 percent) of the intensive-screening group and 826 (55 percent) of the control group. The prevalence of amblyopia in the intensive-screening group was 0.6 percent, significantly less than the 1.8 percent prevalence in the control group. Mean visual acuity in the amblyopic eye was significantly better in children treated in the intensive-screening group than in children in the control group who also had been treated for amblyopia. The proportion of children appropriately referred for hospital treatment before three years of age was significantly higher (48 percent) in the intensive-screening group than in the control group (13 percent). In multivariate analysis, maternal education was the only variable that was significantly associated with outcome. The authors conclude that children who required treatment for amblyopia were four times more likely to remain amblyopic if they were screened only at 37 months of age. In addition, early treatment for amblyopia was more effective than later interventions. Williams C, et al. Amblyopia treatment outcomes after screening before or at age 3 years: follow up from randomised trial. BMJ. June 29, 2002;324:1549–51. editor's note: The “inverse care law” strikes again! Families with more resources and comfort with the health care system benefited most from the services, even when treatment was free. Despite problems with follow-up, this study provides evidence that early detection and intervention for amblyopia improves vision in young children. The implications for their academic and social development are obvious. Our challenge is to find ways to ensure that all children are screened and treated, especially those from the most vulnerable families.—a.d.w. Copyright © 2002 by the American Academy of Family Physicians. This content is owned by the AAFP. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP. Contact firstname.lastname@example.org for copyright questions and/or permission requests. Want to use this article elsewhere? Get Permissions

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Diet and substance abuse recovery Substance abuse recovery and diet; Nutrition and substance abuse Substance abuse harms the body in two ways: - The substance itself affects the body - It causes negative lifestyle changes, such as irregular eating and poor diet For example, infants who were exposed to alcohol while in the womb often have physical and mental problems. The alcohol affects the growing baby by crossing the placenta. After birth, the baby may have withdrawal symptoms. The mother's poor nutrition while she is drinking can harm the baby's growth and development while still in the womb. Recovery from substance abuse also affects the body in other ways, including metabolism (processing energy), organ function, and mental well-being. Proper nutrition may help the healing process. Nutrients supply the body with energy. They provide substances to build and maintain healthy organs and fight off infection. The impact of different drugs on nutrition is described below. Opiates (including codeine, oxycontin, heroin, and morphine) affect the gastrointestinal system. Constipation is a very common symptom of abuse. Symptoms that are common during withdrawal include: These symptoms may lead to a lack of enough nutrients and an imbalance of electrolytes (such as sodium, potassium, and chloride). Eating balanced meals may make these symptoms less severe (however, eating can be difficult due to nausea). A high-fiber diet with plenty of complex carbohydrates (such as whole grains, vegetables, peas, and beans) is recommended. Alcoholism is one of the major causes of nutritional deficiency in the United States. The most common deficiencies are of pyridoxine (vitamin B6), thiamine, and folic acid. A lack of these nutrients causes anemia and nervous system (neurologic) problems. Korsakoff's syndrome ("wet brain") occurs when heavy alcohol use causes a lack of enough thiamine. Alcohol intoxication also damages two major organs involved in metabolism and nutrition: the liver and the pancreas. The liver removes toxins from harmful substances. The pancreas regulates blood sugar and the absorption of fat. Damage to these two organs results in an imbalance of fluids, calories, protein, and electrolytes. Other complications include: - High blood pressure - Permanent liver damage (or cirrhosis) - Severe malnutrition - Shortened life expectancy Laboratory tests for protein, iron, and electrolytes may be needed to determine if there is liver disease in addition to the alcohol problem. Women who drink heavily are at high risk of osteoporosis and need to take calcium supplements. Stimulant use (such as crack, cocaine, and methamphetamine) reduces appetite, and leads to weight loss and poor nutrition. Abusers of these drugs may stay up for days at a time. They may be dehydrated and have electrolyte imbalances during these episodes. Returning to a normal diet can be hard if a person has lost a lot of weight. Memory problems, which may be permanent, are a complication of long-term stimulant use. Marijuana can increase appetite. Some long-term users may be overweight and need to cut back on fat, sugar, and total calories. Nutrition and psychological aspects of substance abuse When people feel better, they are less likely to start using alcohol and drugs again. Because balanced nutrition helps improve mood and health, it is important to encourage a healthy diet in people recovering from alcohol and other drug problems. However, people who have just given up an important source of pleasure may not be ready to make other drastic lifestyle changes. It is more important that people avoid returning to substance abuse than that they stick to a strict diet. - Stick to regular mealtimes - Eat a low-fat diet - Get more protein, complex carbohydrates, and dietary fiber - Vitamin and mineral supplements may be helpful during recovery (this may include B-complex, zinc, and vitamins A and C) People with substance abuse are more likely to relapse when they have poor eating habits. This is why regular meals are so important. People who are addicted to drugs and alcohol often forget what it's like to be hungry and instead think of this feeling as a drug craving. They should be encouraged to consider that they may be hungry when cravings become strong. During recovery from substance abuse, dehydration is common. It is important to get enough fluids during and in between meals. Appetite usually returns during recovery. People in recovery are often more likely to overeat, particularly if they were taking stimulants. Eat healthy meals and snacks and avoid high-calorie foods with low nutrition (such as sweets), if possible. The following tips can help improve the odds of a lasting and healthy recovery: - Eat nutritious meals and snacks. - Get physical activity and enough rest. - Reduce caffeine and stop smoking, if possible. - Seek help from counselors or support groups on a regular basis. - Take vitamin and mineral supplements. O'Connor PG. Alcohol abuse and dependence. In: Goldman L, Schafer AI. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 32. Reviewed By: Fred K. Berger, MD, Addiction and Forensic Psychiatrist, Scripps Memorial Hospital, La Jolla, California. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M. Health Solutions, Ebix, Inc.

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Hot Literature: Lyme borreliosis in man and his best friend As pet owner awareness of zoonotic diseases increases, so does collaborative research between veterinarians and physicians. A workshop at the Centers for Disease Control and Prevention (CDC) brought together specialists in veterinary parasitology and human internal medicine and vector-borne infectious disease to address Lyme borreliosis. These experts summarized some recent study findings and the similarities and differences between the disease in people and dogs in the United States. Transmission and clinical signs Symptoms in people usually develop shortly after infection, often before seroconversion. About 70% to 80% of infected people develop a characteristic rash, called erythema migrans, at the site of the tick bite. This rash can be followed by flu-like symptoms and, chronically, by arthritis, carditis, and neurologic disease. Infected dogs do not develop erythema migrans, and most infected dogs do not develop any clinical signs of Lyme borreliosis. Dogs that do develop clinical signs typically do so weeks or months after infection. Common signs include polyarthritis, anorexia, and lymphadenopathy. Dogs may also develop a glomerulonephritis syndrome. The prognosis for dogs that develop this Lyme nephropathy is poor. Diagnosis, treatment, and prevention Since most dogs have seroconverted by the time clinical signs are seen, a patient-side assay specific for the C6 peptide of the infectious organism is reliable for diagnosis and for evaluating response to treatment, but it cannot distinguish between dogs with active infection and those that have been exposed but have not developed clinical disease. The recommended treatment for Lyme borreliosis in dogs and people is doxycycline. Beta-lactam antibiotics are also effective against B. burgdorferi. However, antibiotics in the penicillin family are not effective against other rickettsial pathogens that are common coinfections in dogs and people with Lyme borreliosis. One course of antibiotic treatment is adequate and is most effective when initiated early in the course of the disease. Dogs and people are susceptible to reinfection with subsequent exposure to B. burgdorferi. No vaccine is available for people, but dogs may obtain an effective level of protection by a program of vaccination in endemic areas. The mainstay of prevention for people and dogs is still considered to be limiting exposure to infected ticks. Environmental and tick habitat management, prompt tick removal, and the use of repellents for people and acaricides for dogs are primary control and prevention recommendations. Man's best friend In general, wide-spread testing has shown that exposure in dogs correlates to the geographical distribution of exposure in people. The experts at the CDC workshop thought that monitoring antibody responses in dogs may help identify when B. burgdorferi begins to populate nonendemic locations. In this way, they thought that dogs could serve as sentry animals, further helping to protect human health. For a link to the abstract, click here.

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Background: In the United States in the 1990s, the incidence of reported pertussis in adults, adolescents and infants increased; infants younger than 1 year of age had the highest reported incidence. Methods: In 4 states with Enhanced Pertussis Surveillance, we examined the epidemiology of reported pertussis cases to determine the source of pertussis among infants. A source was defined as a person with an acute cough illness who had contact with the case-infant 7-20 days before the infant's onset of cough. Results: The average annual pertussis incidence per 100,000 infants younger than 1 year of age varied by state: 22.9 in Georgia; 42.1 in Illinois; 93.0 in Minnesota; and 35.8 in Massachusetts. Family members of 616 (80%) of 774 reported case-infants were interviewed; a source was identified for 264 (43%) of the 616 case-infants. Among the 264 case-infants, mothers were the source for 84 (32%) and another family member was the source for 113 (43%). Of the 219 source-persons with known age, 38 (17%) were age 0-4 years, 16 (7%) were age 5-9 years, 43 (20%) were age 10-19 years, 45 (21%) were age 20-29 years and 77 (35%) were age ≥30 years. Conclusions: The variation in reported pertussis incidence in the 4 states might have resulted from differences in awareness of pertussis among health care providers, diagnostic capacity and case classification. Among case-infants with an identifiable source, family members (at any age) were the main source of pertussis. Understanding the source of pertussis transmission to infants may provide new approaches to prevent pertussis in the most vulnerable infants.

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The risks were lower for total stroke, clot-related (ischemic) stroke and bleeding (hemorrhagic) stroke, researchers said. Compared to women who didn't walk, those who usually walked at a brisk pace had a 37 percent lower risk of any type of stroke, and those who walked two or more hours a week had a 30 percent lower risk of any type of stroke. Women who typically walked at a brisk pace had a 68 percent lower risk of hemorrhagic stroke and those who walked two or more hours a week had a 57 percent lower risk of hemorrhagic stroke. Women who usually walked at a brisk pace had a 25 percent lower risk of ischemic stroke and those who usually walked more than two hours a week had a 21 percent lower risk of ischemic stroke, both "borderline significant," according to researchers. Physical activity is essential to promoting cardiovascular health and reducing risk of cardiovascular disease, and walking is one way of achieving physical activity. More physically active people generally have a lower risk of stroke than the least active, with more-active persons having a 25 percent to 30 percent lower risk for all strokes, according to previous studies. Researchers followed 39,315 U.S. female health professionals (average age 54, predominantly white) participating in the Women's Health Study. Every two to three years, participants reported their leisure-time physical activity during the past year, specifically time spent walking or hiking, jogging, running, biking, doing aerobic exercise/aerobic dance, using exercise machines, playing tennis/squash/racquetball, swimming, doing yoga and stretching/toning. No household, occupational activity or sedentary behaviors were assessed. The women who were most active in their leisure-time activities were 17 percent less likely to have any type of stroke compared to the least-active women.

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Volume 16, Number 2—February 2010 Avian Influenza (H5N1) Outbreak among Wild Birds, Russia, 2009 To the Editor: Highly pathogenic avian influenza (HPAI) virus (H5N1) has been endemic in poultry in Southeast Asia since 2003 (1). In April 2005, an outbreak of influenza virus (H5N1) infection was detected in wild birds on Qinghai Lake in western China (2). Subsequently, the Qinghai-like (clade 2.2) HPAI virus (H5N1) lineage was detected in wild birds and poultry in many countries (1,3,4). The source of these introductions, although still debated, is likely through bird migration (5). In June 2006, an influenza (H5N1) outbreak was detected in wild birds on Uvs-Nuur Lake in western Siberia, Russia. We showed that A/duck/Tuva/01/2006, isolated during the outbreak, was highly pathogenic for chickens and mice and belonged to the Qinghai-like group (2.2 clade) (6). The first case of Fujian subclade 2.3.2 influenza virus (H5N1) lineage in the Russian Far East was recorded in April 2008 (7). Before this case, no HPAI (H5N1) outbreaks of the Fujian lineage had been reported in Russia. In June 2009, an outbreak of HPAI in wild birds was recorded in Mongolia (4) and on Uvs-Nuur Lake in Russia. RNA extracted from organs (liver, spleen, intestine) of 10 dead birds belonging to 4 species (great crested grebe [Podiceps cristatus], little grebe [Tachybaptus ruficollis], black-headed gull [Larus ridibundus], and spoonbill [Platalea leucorodia]) was positive for type A influenza RNA and for the H5 subtype by real-time reverse transcription–PCR (8). We isolated 2 viruses from embryonated specific antibody–negative fowl eggs. Hemagglutination (HA) and neuraminidase (NA) inhibition assays with monospecific antiserum confirmed the H5N1 subtype. Viruses were designated as A/black-headed gull/Tyva/115/2009 and A/great crested grebe/Tyva/120/2009, and sequences of their HA and NA segments were defined. No HPAI virus (H5N1) was found in cloacal swabs obtained from 36 live birds (of the 4 species listed above) from Uvs-Nuur Lake. Phylogenetic analysis (9) of the HA gene (Figure) showed that viruses belong to clade 2.3.2. These viruses are clearly distinguishable from the HPAI viruses previously isolated in this Russian region in 2006, A/duck/Tuva/01/2006 (clade 2.2) but are more related to A/whooper swan/Mongolia/8/2009 and A/whooper swan/Mongolia/2/2009. For the NA gene, isolated viruses were most closely related to viruses found in Mongolia. Analysis of NA protein determined that the viruses found are sensitive to NA inhibitors. Both viruses were shown to be highly pathogenic for chickens (intravenous pathogenicity index 3). This finding is consistent with the results of the sequence analysis of the HA gene. The HA protein possesses a series of basic amino acids (PQRERRRKR) at the cleavage site. Several amino acid changes were found between HA of investigated viruses and viruses from clade 2.3.2 that were isolated in Russia in 2008. However, the receptor-binding site of HA (positions 222–224) was not changed. The spread of HPAI (H5N1) west across the globe has caused serious debates on the roles of migratory birds in virus circulation (2,5,7). In the 2009 outbreak we describe, we doubt that wild birds were infected from local poultry because domestic poultry are not present in the Uvs-Nuur Lake region and there have been no reports of HPAI among poultry in Russia since early 2008. We suggest that wild birds brought the virus to Uvs-Nuur Lake from outside the country. Because prior to June 2009 the only case of new Fujian sub-clade 2.3.2 influenza virus (H5N1) lineage was in the Russian Far East, we believe that the virus isolated in 2009 from Uvs-Nuur Lake was probably introduced by wild birds that wintered in Southeast Asia. Many different bird species stop at Uvs-Nuur Lake during the spring and fall migrations. Qinghai-like viruses were introduced to the region from central China by wild birds in 2006 (6). The introduction of the H5N1 Fujian-lineage to the lake 3 years later shows further evidence that Uvs-Nuur Lake is an major area for wild bird migration and breeding and hence an environment that could potentially support the introduction of influenza virus variants from migrating wild birds. Bodies of water such as Qinghai Lake and Uvs-Nuur Lake may play a major role in the circulation of avian influenza. Therefore, we continue to study new outbreaks thoroughly and take into account the ecology and pathobiology of the species involved. Areas where large numbers of birds congregate should be closely monitored because these areas could serve as the breeding ground for avian influenza virus variants that might spread globally. Additionally, we must keep in mind that wild bird species can vary greatly in their response to HPAI and that naturally resistant waterfowl could serve as vectors for the introduction of HPAI into new locations (1,2,5,7). Because wild birds can be involved in virus introduction, continuing surveillance is warranted. Detection of any influenza A (H5N1) virus in wild birds in a new region should be immediately followed up with efforts to characterize the virus and to control the spread of new HPAI viruses. We thank George Happ for assistance. This work was supported by the Bio Industry Initiative–International Science and Technology Center (3436). - Alexander DJ, Brown IH. History of highly pathogenic avian influenza. Rev Sci Tech. 2009;28:19–38. - Chen H, Smith GJ, Zhang SY, Qin K, Wang J, Li KS, H5N1 virus outbreak in migratory waterfowl. Nature. 2005;436:191–2. - Lipatov AS, Evseenko VA, Yen HL, Zaykovskaya AV, Durimanov AG, Zolotykh SI, Influenza (H5N1) viruses in poultry, Russian Federation, 2005–2006. Emerg Infect Dis. 2007;13:539–46. - World Organisation for Animal Health. Avian influenza [cited 2009 Jun 1]. http://www.oie.int/eng/info_ev/en_AI_factoids_H5N1_Timeline.htm - Keawcharoen J, van Riel D, van Amerongen G, Bestebroer T, Beyer WE, van Lavieren R, Wild ducks as long-distance vectors of highly pathogenic avian influenza virus (H5N1). Emerg Infect Dis. 2008;14:600–7. - Evseenko VA, Bukin EK, Zaykovskaya AV, Sharshov KA, Ternovoi VA, Ignatyev GM, Experimental infection of H5N1 HPAI in BALB/c mice. Virol J. 2007;4:77. - L’vov DK, Zhchelkanov MIu, Vlasov NA, Prilipov AG, Deriabin PG, Fediakina IT et al. The first break-through of the genotype 2.3.2 of high-virulence influenza A virus A/HSN1, which is new for Russia, in the Far East [in Russian]. Vopr Virusol. 2008;53:4–8. - Spackman E, Senne DA, Myers TJ, Bulaga LL, Garber LP, Perdue ML, Development of a real-time reverse transcriptase PCR assay for type A influenza virus and the avian H5 and H7 hemagglutinin subtypes. J Clin Microbiol. 2002;40:3256–60. - Tamura K, Dudley J, Nei M, Kumar S. MEGA4: Molecular Evolutionary Genetics Analysis (MEGA) software version 4.0. Mol Biol Evol. 2007;24:1596–9. Suggested citation for this article: Sharshov K, Silko N, Sousloparov I, Zaykovskaya A, Shestopalov A, Drozdov I. Avian influenza (H5N1) outbreak among wild birds, Russia, 2009 [letter]. Emerg Infect Dis [serial on the Internet] 2010 Feb [date cited]. Available from http://wwwnc.cdc.gov/eid/article/16/2/09-0974 - Page created: December 13, 2010 - Page last updated: December 13, 2010 - Page last reviewed: December 13, 2010 - Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Office of the Director (OD)

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Chronic Pancreatitis Diet Plan, Restrictions Pancreatitis is a condition wherein the patient’s pancreas is inflamed. The various enzymes released by this organ are responsible for digestion of food. When the release of these enzymes is restricted, the patient experiences severe or constant pain in the abdomen as well as nausea, fever, and vomiting. Some other symptoms include oily stool, rapid breathing, low blood pressure, dehydration, rapid pulse, and internal bleeding. Chronic pancreatitis causes include alcohol abuse, diseases such as lupus, hereditary pancreatitis, cystic mutations or fibrosis, and blockage of your pancreatic duct from stones, tumor and trauma. A chronic pancreatitis diet plan to manage the disease constitutes consuming nothing but healthy and natural ingredients. It is important to follow a chronic pancreatitis diet menu and change your lifestyle, because if not treated in time, pancreatitis can turn into a long-lasting illness. As part of the chronic pancreatitis therapy diet, most dieticians recommend vegetables and fruits. You could eat fresh vegetable or have vegetable juice instead. Vegetables have a high content of enzymes, minerals, and vitamins that help cure pancreatitis. Spinach, for example, has high levels of iron that is good for pancreatitis. If you want to benefit from the chronic pancreatitis therapy diet, make sure you include rice in your daily meals. Salads are also good for inflamed pancreas. You can also eat oatmeal, cereals, and bread at breakfast or while snacking in between meals. Soy based foods are a great antioxidant source, which help prevent further damage to your pancreas. To avoid pancreatitis from a high-protein diet plan make sure you add probiotics in your daily meals. This could include foods such as yoghurt that help regulate digestion, reduce inflammation, and boost your immunity. Chronic pancreatitis diet restrictions include spicy foods, carbonated drinks, and drinks that contain caffeine such as coffee and tea. It is also advisable that you reduce your consumption of foods with high fat content. This is because the pancreas has to work harder to break down the fat molecules. If you are suffering acute pancreatitis, your diet plan should not be high in carbohydrates, fat and protein, instead eat large helpings of vegetables and fruits for the optimal health of your pancreas. Chronic Pancreatitis Foods Here are some foods you should include in you chronic pancreatitis food list. For those suffering from chronic pancreatitis, foods to avoid include: - Yogurt is an important food for chronic pancreatitis. The live bacteria present in the yoghurt help keep your digestive system well-balanced and also helps maintain the immunity levels of your body. - Vegetable soup is also another great option. A tomato-based soup is recommended as it is high in antioxidants. - Spinach makes for an excellent choice as it contains high iron levels. You could either have it as a side dish or a salad base. - Blueberries contain antioxidants that help your body fight the free radicals, which worsen your condition. - Red wine or red grapes contain an antioxidant called resveratrol and are good for pancreatitis. - Eat foods that are high in antioxidants, such as cherries, blueberries, tomatoes, bell peppers, and squash. - Include foods high in B-vitamins such as whole grains, sea vegetables, and dark leafy greens. - If you need to have meat, opt for lean cuts. Tofu is a good substitute for meat. - Increase your intake of fluids. Drink plenty of water and juices. Drink vegetable soup or light chicken soup regularly. - Avoid refined foods such as pastas, sugar, and white bread. - Avoid red meats, if possible. - Make sure you avoid margarine and also cut out foods that contain trans fats, such as commercially made cakes, cookies, and doughnuts. - There is a connection between chronic pancreatitis and drinking alcohol as well. If you are susceptible to pancreatitis avoid alcohol. - Avoid stimulants such as tea and coffee. - Other foods that you should avoid are pizza, beans, cheeses, fried foods, butter, and eggs. - You should also avoid stimulants such as cigarettes. - In addition to eating the right food for chronic pancreatitis, drink lots of water and have a number of small meals during the day instead of three large meals. If you are suffering from pancreatitis, it is advisable to talk to your health care provider or nutritionist and draw a chronic pancreatitis diet plan. Chronic Pancreatitis Nutrition A proper chronic pancreatitis nutrition therapy plan needs to be followed if you want to get relief from pancreatitis. Here are a few chronic pancreatitis nutrition guidelines that you can keep in mind. - Eliminate suspected food allergens such as wheat (gluten), dairy (cheese, ice cream, and eggs), soy, corn, chemical food additives, and preservatives. - Use healthy oils such as vegetable oil or olive oil for cooking. - Reduce significantly or totally cut out foods that contain trans-fatty acids such as crackers, cakes, French fries, doughnuts and onion rings. - Check with your day care provider and add multivitamins containing vitamins C, A, E, and B-complex and trace minerals such as calcium, magnesium, zinc and selenium in your diet. - You could also consume omega-3 fatty acids to help improve immunity and decrease inflammation. - After doing a chronic pancreatitis nutritional assessment, you can also take vitamin C, 1 to 6 gm daily. You can also take a probiotic and alpha-lipoic supplement. - If you have a problem with digestion, try using a vegetable juice extractor and drink vegetable juice instead. Juices are easier to digest than whole vegetables and also allow you to get the required vitamins and nutrients in liquid form. - To sum up, people suffering from pancreatitis should (1) abstain from alcohol, cigarettes, and refined and fatty products including red meat, (2) consume a low fat diet that is replete with vegetables and fruits, and (3) avoid abdominal trauma. Those who have high levels of triglyceride should exercise, lose weight, and avoid medications that increase the levels of triglyceride in the body. Check with your health care provider and take some antioxidant supplementation that is extremely beneficial for patients suffering from pancreatitis. If the pain is continuous and extreme, it is best that you go and see your doctor.

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Your child is having an EGD (Esophagogastroduodenoscopy), also know as Upper Endoscopy. Most children receive a light anesthesia for this test. Others are given medicine which makes them very relaxed and drowsy ("moderate sedation"). During this test the doctor will pass a special tube with a light on the end of it into the throat and beyond. The doctor usually looks at the esophagus (food tube), stomach and the first part of the small bowel (duodenum). The doctor looks for signs of irritation and may take tissue samples (biopsies). The tissue samples help to identify causes of esophagus, stomach or small bowel irritation. Biopsies can also detect the stomach bacteria Helicobacter pylori. After the test: - Your child may begin his/her normal play/activity after the medicine or anesthesia given for the test has worn off. He/she may return to school the next day. The doctor will tell you what type of diet your child can have. - Most children are fussy for the first few hours after the test. Parents are invited to the Post Anesthesia Care Unit (PACU) when your child wakes up. - Your child may get a red, flushed look to his/her face and chest 1-2 hours after the test. This blotchy red color is a normal response to medicine given for anesthesia. - Your child may complain of a sore throat, gagging or a stomachache. This is normal and should be gone in a few days. Your child might vomit small amounts of blood. This may be normal, especially if biopsies (small tissue samples) were taken. When to call your child's doctor: - Your child has problems with swallowing or bleeding. - Your child's temperature is greater than 101.5F rectally or by mouth. Slight fevers after surgery are normal. You should take your child's temperature once before bedtime tonight. - Your child has vomiting that lasts more than six hours or vomiting is severe. Your child can become dehydrated when he/she has prolonged or severe vomiting and is not able to drink enough fluid to keep up with the loss. The signs of dehydration are: Your child's nurse will discuss this with you before your child goes home. - Dry mouth - Sunken look around eyes - No tears when crying - Decreased amount of urine, which means fewer wet diapers than usual in an infant/toddler REMEMBER: Please call if you have any questions. Use the phone number your nurse gives you. Disclaimer: This information is not intended to substitute or replace the professional medical advice you receive from your child's physician. The content provided on this page is for informational purposes only, and was not designed to diagnose or treat a health problem or disease. Please consult your child's physician with any questions or concerns you may have regarding a medical condition.

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Low Apgar Scores At Birth Linked To Cerebral Palsy A recent study conducted by the Norwegian Institute of Public Health found that individuals with low Apgar scores at birth were more likely to be later diagnosed with cerebral palsy. The study suggests that the link between low Apgar scores and cerebral palsy is related to the damage caused to the motor control centers of the brain. This damage can occur during pregnancy, during childbirth, or even after birth. To determine a baby’s Apgar score, the baby's muscle tone, heart rate, muscle reflex, skin coloration, and respiration are evaluated. Each factor is scored on a scale of 0 to 2, with 2 being the best score. The scores are added together and the resulting Apgar score ranges from zero to 10. This test is generally done at one and five minutes after birth, and may be repeated later if the score is and remains low. Scores 3 and below are generally regarded as critically low, 4 to 6 fairly low, and 7 to 10 generally normal. Cerebral palsy is caused by an injury to the infant’s brain that can occur before, during or shortly after birth. Exposures to radiation and infection during pregnancy have lead to cerebral palsy. Examples of these infections include rubella, cytomegalovirus, herpes, and toxoplasmosis. Asphyxia (lack of oxygen) before birth, hypoxia of the brain, and birth trauma during labor and delivery also cause injury to the infant’s brain, which can lead to cerebral palsy. According to the Centers for Disease Control and Prevention, about 2 to 3 children in 1,000 are affected by brain injuries leading to cerebral palsy. The National Institute of Neurological Disorders and Stroke has estimated that about 800,000 individuals in the United States have cerebral palsy. Babies with cerebral palsy often have an irregular posture and may be born with other birth defects, such as spinal curvature, a small jawbone, or a small head. However, some babies born with cerebral palsy do not show obvious signs and symptoms right after birth. Our Chicago birth injury lawyers at Levin & Perconti have decades of experience fighting for victims whose children have suffered severe damage following complications from childbirth. All doctors need to be aware that every necessary step should be taken to ensure that the child has the best chance possible of being born healthy. Too often medical professionals make preventable childbirth mistakes—from not acting quickly enough to failing to take appropriate actions at all. In any case, the innocent children and their families have legal rights to help in those situations. If you know of a victim, be sure to contact a birth injury attorney to begin the process of redress and reform.

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Volume 19, Number 7—July 2013 Babesia microti Infection, Eastern Pennsylvania, USA Infection with Babesia microti has not been well-described in eastern Pennsylvania, USA, despite the vector of this organism being prevalent. We report 3 cases of babesiosis in eastern Pennsylvania in persons without recent travel outside the region or history of blood transfusions, suggesting emergence of this infection. Babesiosis is an intraerythrocytic infection caused by protozoan parasites of the genus Babesia. In the United States, Babesia microti is the most common species that causes human babesiosis. Disease-endemic areas include specific regions in the northeast and upper Midwest United States. Infection with this organism can be asymptomatic to life-threatening. Signs and symptoms include high fever, diaphoresis, chills, headaches, and anorexia. Patients can also have hemolytic anemia and thrombocytopenia (1). B. microti is transmitted by the Ixodes scapularis tick, which is also the vector of Borrelia burgdorferi and Anaplasma phagocytophilum (2). Although B. burgdorferi is endemic to Pennsylvania (3), B. microti is not considered endemic to this region (4,5). We report 3 cases of human babesiosis in patients from Northampton County in eastern Pennsylvania, USA, who had not recently traveled outside the region or had blood transfusions. None of the patients had risk factors for severe babesiosis, such as asplenia. Patient 1 was a 68-year-old man who was hospitalized on August 18, 2011, because of 6 days of fever, arthralgias, generalized weakness, and confusion. He was given doxycycline for treatment of presumptive Lyme disease but showed no improvement. He had not traveled outside eastern Pennsylvania for >3 years. He had never received any blood transfusions. Although he did not recall any tick attachments, he enjoyed gardening and other outdoor activities. Pertinent clinical and laboratory data are shown in the Table. During testing for thrombocytopenia, a peripheral blood smear was obtained on hospital day 1 and showed ring forms with tetrads (Figure) and a parasitemia level of 10%. A PCR result for the blood sample was positive for B. microti. Despite treatment for 5 days with clindamycin and quinine, the treatment of choice for severe babesiosis, the fever persisted. Antimicrobial drug therapy was changed to atovaquone and azithromycin. The patient completed 10 days of treatment and showed resolution of symptoms and normalization of platelet count and total bilirubin level. Parasitemia level at the time of discharge was 1.2%. Laboratory data after discharge were not available. Patient 2 was an 84-year-old woman with microcytic anemia who was hospitalized on June 8, 2012, because of 2 weeks of fever, diaphoresis, myalgias, progressive dyspnea, and fatigue. Originally from New Hampshire, she had been living in Northampton County, Pennsylvania, for >4 years. She had not traveled outside the region in the past 4 years. She received a blood transfusion for chronic anemia 1 year before onset of this illness. She recalled multiple tick bites in the recent past. Because of pancytopenia (Table), a bone marrow biopsy was performed and showed intraerythrocytic ring forms with tetrads. Parasitemia level for a peripheral blood smear was 1.4%. A PCR result for B. microti was positive. The patient was given atovaquone and azithromycin for 10 days and showed resolution of symptoms and improvement in abnormal laboratory values. A repeat blood smear on June 18 showed a parasitemia level of 0.1%, and a blood smear 1 month later showed no parasites. Patient 3 was a 71-year-old man who was hospitalized on June 26, 2012, because of 2 weeks of fever and gradually worsening malaise and weakness. He had not traveled outside eastern Pennsylvania in the past 2 years and never received a blood transfusion. Two weeks before admission, he had an insect bite that developed into a larger, oval rash. Initial testing for thrombocytopenia included a peripheral blood smear, which showed intraerythrocytic ring forms and tetrads and a parasitemia level of 0.4%. A PCR result was positive for B. microti. He was given atovaquone and azithromycin for 10 days. Because results of enzyme immunoassay and Western blot for B. burgdorferi were positive, he was also given doxycycline. Symptoms resolved, and the laboratory values improved. A repeat blood smear 1 week after starting antimicrobial drug therapy showed no parasites. This report supports the hypothesis that babesiosis caused by B. microti is emerging in eastern Pennsylvania. As B. microti is spread by I. scapularis ticks, this infection might emerge in the range of the vector. Babesiosis is considered endemic to some states in which I. scapularis ticks are prevalent (6,7), but not in Pennsylvania. All of these cases were confirmed by using robust laboratory methods. The 3 cases showed intraerythrocytic tetrad forms, an uncommon finding that is considered pathognomonic for Babesia infection (1). The strength of the diagnoses was further enhanced by PCR testing. Although PCR will amplify all Babesia species that are pathogenic in humans, the peak melting point temperature of amplicons for the 3 samples was nearly identical (difference ≤0.2°C) to that of the control B. microti amplicon, supporting B. microti as the causative agent (C.P. Cartwright, ViroMed Laboratories, Minnetonka, MN, USA, pers. comm.). Two other persons with babesiosis have been treated at our institution since 2011. These case-patients were not included in this report because of inadequate laboratory confirmation for 1 patient and lack of a strict travel limitation for the other patient. One of these patients was given a diagnosis of babesiosis on the basis of serologic data obtained 2 months after the initial illness without blood smear confirmation. The second patient had traveled to western New Jersey, a babesiosis-endemic region, over a brief period before his illness. The Pennsylvania Department of Health has received 39 voluntary reports of smear-positive babesiosis during 2005–2012 (K. Waller, Pennsylvania Department of Health, Harrisburg, PA, USA, pers. comm.). More than 60% of those reports were made after babesiosis became nationally reportable in 2011. Although many of these cases lacked detailed historical information to confirm that the cases were acquired in Pennsylvania, they further support the notion that B. microti is emerging in Pennsylvania. Data on the prevalence of B. microti in I. scapularis ticks in eastern Pennsylvania are limited. However, 0.7% (3/443) of ticks collected from animals and humans in Monroe County in eastern Pennsylvania during 2004–2006 were infected with B. microti (3), supporting the plausibility of zoonotic transmission in the state. Before these patients were identified, no cases of babesiosis had been diagnosed at our tertiary care center over the previous 10 years. Cases could have been missed because of the nonspecific nature of symptoms. However, this increase in the number of documented cases in 1 hospital is unlikely to be entirely explained by missed diagnoses. Furthermore, no other cases of babesiosis have been described at other institutions in this region. This study had a few limitations. Recall bias could have played a role in obtaining a travel history. However, for each of these patients, family members were able to confirm the travel history, making recall bias unlikely. One of the patients had a blood transfusion 1 year before onset of systemic symptoms, making a transfusion-related infection unlikely. However, because this same patient was originally from New Hampshire, she might have been a chronic carrier. These cases support the premise that babesiosis caused by B. microti infection is emerging in eastern Pennsylvania. Knowledge of the geographic distribution of B. microti is essential. Diagnosis requires strong clinical suspicion and supportive laboratory data. Timely diagnosis and treatment for patients and testing of blood donors in areas in which B. microti is found might further prevent transfusion-related infection (8–10). Having this infection reportable in Pennsylvania and other states to which I. scapularis ticks are endemic might help identify the geographic region of this parasite. Dr Perez Acosta is a second-year internal medicine resident at St. Luke’s University Hospital and Health Network in Bethlehem, Pennsylvania. Her research interests include vector-borne diseases and infectious diseases of the skin. - Vannier E, Krause PJ. Human babesiosis. N Engl J Med. 2012;366:2397–407 and. - Cherepko J, Berry GJ, Keeler SP, Huffman JE. Prevalence of Borrelia burgdorferi, Bartonella spp., Bartonella henselae, Babesia microti and Anaplasma phagocytophila in Ixodes scapularis ticks collected in Monroe County, Pennsylvania, show a risk for co- and tri- infections. J Pa Acad Sci. 2010;84:74–8. - Centers for Disease Control and Prevention. Reported cases of Lyme disease by state or locality, 2002–2011 [cited 2013 Mar 3]. http://www.cdc.gov/lyme/stats/chartstables/reportedcases_statelocality.html - Centers for Disease Control and Prevention (CDC). Babesiosis surveillance—18 states, 2011. MMWR Morb Mortal Wkly Rep. 2012;61:505–9 . - Babesiosis. Pennsylvania Epi Notes, 2011;1:4–5 [cited 2013 Jan 5]. http://www.portal.state.pa.us/portal/server.pt/gat eway/PTARGS_0_2_1206780_0_0_18/EpiNotes%20Fall%202 011.pdf - Herwaldt BL, McGovern PC, Gerwel MP, Easton RM, MacGregor RR. Endemic babesiosis in another eastern state: New Jersey. Emerg Infect Dis. 2003;9:184–8. - Rodgers SE, Mather TN. Human Babesia microti incidence and Ixodes scapularis distribution, Rhode Island, 1998–2004. Emerg Infect Dis. 2007;13:633–5. - Herwaldt BL, Linden JV, Bosserman E, Young C, Olkowska D, Wilson M. Transfusion-associated babesiosis in the United States: a description of cases. Ann Intern Med. 2011;155:509–19 . - Johnson ST, Cable RG, Tonnetti L, Spencer B, Rios J, Leiby DA. Seroprevalence of Babesia microti in blood donors from Babesia-endemic areas of the northeastern United States: 2000 through 2007. Transfusion. 2009;49:2574–82. - Young C, Chawla A, Berardi V, Padbury J, Skowron G, Krause PJ; Babesia Testing Investigational Containment Study Group. Preventing transfusion-transmitted babesiosis: preliminary experience of the first laboratory-based blood donor screening program. Transfusion. 2012;52:1523–9 . Suggested citation for this article: Perez Acosta ME, Ender PT, Smith EM, Jahre JA. Babesia microti infection, eastern Pennsylvania, USA. Emerg Infect Dis [Internet]. 2013 Jul [date cited]. http://dx.doi.org/10.3201/eid1907.121593

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Amniocentesis is a test used to determine whether your unborn baby has any genetic abnormalities (genetic amniocentesis) or whether its lungs are developed enough for birth (maturity amniocentesis). Your doctor will use a long, thin needle to collect a small amount of amniotic fluid. This fluid surrounds and protects the baby while it is in your womb. It is then tested for certain genetic conditions, including Down syndrome, spina bifida, and cystic fibrosis. The test results can help you determine whether to continue with your pregnancy. The test can also tell you whether or not your baby is mature enough to be born. It is also helpful for determining whether you need to deliver early to prevent complications from your pregnancy. You might consider genetic amniocentesis if the results of your prenatal screening test are abnormal. Amniocentesis can confirm or rule out a diagnosis made during the initial screening test. If you have already had a child with a birth defect or neural tube defect (a serious abnormality of the brain or spinal cord), you can use amniocentesis to check whether your unborn child also has such a condition. If you are 35 or older, your baby is at a higher risk for chromosomal abnormalities, such as Down syndrome. Amniocentesis can identify these abnormalities. If you or your partner is a known carrier of a genetic disorder, such as cystic fibrosis, amniocentesis can detect whether your unborn child will be affected. You might consider maturity amniocentesis if you need to deliver your baby early due to complications from your pregnancy. This test can determine whether your baby’s lungs are developed enough to allow the child to survive outside the womb. Amniocentesis may also be performed if your doctor suspects that your unborn child may have an infection or anemia. Your doctor may also order amniocentesis if he or she thinks that you have a uterine infection. The procedure can also decrease the amount of amniotic fluid in your womb, if necessary. This test is performed on an outpatient basis, so you won’t need to stay in the hospital. Your doctor will first perform an ultrasound to determine the exact location of your baby in the uterus. An ultrasound is a non-invasive procedure that uses high-frequency sound waves to create an image of your unborn baby. Your bladder must be full during the ultrasound, so drink plenty of fluids beforehand. After the ultrasound, your doctor may apply numbing medication onto a section of your belly. Then, they’ll insert a needle through your belly and into your womb, withdrawing a small amount of amniotic fluid. This portion of the procedure usually takes about two minutes. The results of genetic tests on your amniotic fluid are usually available within a few days. The results of tests to determine the maturity of your baby’s lungs are usually available within a few hours. Amniocentesis is usually performed during your second trimester. There is a slight risk of miscarriage (between one in 300 and one in 500) if the test is performed after 16 weeks of pregnancy. The risk is slightly higher if the test is done before 15 weeks of pregnancy. Some women experience cramping or a small amount of vaginal bleeding after the procedure. Rarely, amniocentesis may cause amniotic fluid to leak out of your body or it may trigger a uterine infection. In rare cases, this test may cause some of your baby’s blood cells to enter your bloodstream. If you have a type of protein called the Rh factor on the surface of your red blood cells, you are considered Rh positive. If you do not, then you are Rh negative. It is possible for you to have Rh negative blood and your baby to have Rh positive blood. In this case, when your blood cells mix, your body may react as if it were allergic to your baby. If this happens, your doctor will give you a drug called RhoGAM. This medication will prevent your body from making antibodies that will attack your baby’s blood cells. If you have an infection, such as hepatitis C or HIV, amniocentesis could cause your infection to be transmitted to your unborn baby. If the results of your amniocentesis are normal, your baby most likely does not have genetic or chromosomal abnormalities. In the case of maturity amniocentesis, normal test results will assure you that your baby is ready to be born. Abnormal results may mean that your baby has a genetic problem or serious birth defect. Discuss all test results with your doctor and your partner so that you can make an informed decision about whether or not to continue your pregnancy.

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The transition from adolescence to adulthood is especially challenging for youths with mental illness, who have lower rates of education and employment than their peers without mental illness and higher rates of poverty, unplanned pregnancy, sexually transmitted disease, substance use disorders, homelessness, and involvement in the criminal justice system (1–3). The challenges inherent in the transition to adulthood among transition-age youths (generally, youths age 16 to 25) are often complicated by emancipation among foster care youths, a lack of mentors, and a need for services related to life transitions that is not adequately met by the mental health service system (4–6). As a result, transition-age youths are more likely than adults to drop out of mental health treatment; predictors of dropout include practical barriers to accessing care, the perceived relevance of treatment, and the quality of the therapeutic relationship (7–12). This disconnect between service needs and service provision for youths with mental illness has been conceptualized as a discordance between developmental and institutional transitions (3,13). The developmental transition includes natural cognitive, moral, social, and sexual development and the formation of identity. The developmental transition is mediated by cultural norms and celebrated by rites of passage. In contrast, the institutional transition is governed by bureaucratic and legal guidelines and is in part determined by a bifurcated mental health system that is geared toward either children or adults but not necessarily toward individuals transitioning between developmental periods. Common themes related to barriers encountered in the institutional transition include deficits in continuity of care and transition planning and a lack of age-specific institutional supports (3,13). Mentorship has been identified as both a predictor of success and a potential target of intervention among transition-age youths with serious mental illness (14). Mentoring relationships have been defined as connections built on mutuality, empathy, and trust that have an impact on youths through social, emotional, cognitive, and modeling processes (6). Quantitative studies of nonkin or nonparental natural mentors have found that mentorship is associated with improved self-reported health status; reduced symptoms of depression, suicidal ideation, and perceived stress; less fighting; and fewer sexually transmitted infections (5,15). Qualitative studies have identified the importance of similarities in life experiences between mentors and youths; trust, consistency, empathy, and authenticity are key qualities of the mentoring relationship (16). Interventions to improve mentorship of youths with mental illness focus on supporting natural mentors or employing professional mentors who work in youth-specific programs. The Transition to Independence Process model employs mentors in the form of transitional facilitators (also described as life coaches) who use specific core processes (for example, social problem solving, in-vivo teaching, and planning to prevent high-risk behaviors) to help youths to make better decisions and to improve their progress and outcomes (17). California's Mental Health Services Act (MHSA) provided new sources of funding for services for transition-age youths. The California Council on Youth Relations concurrently issued a set of policy recommendations that include promoting involvement of youths in decision making, identifying the family as the unit of service, providing age-appropriate clinical services, improving communication about medication, preparing adults to support and respect youths, providing a safe environment and sense of purpose, and reducing stigma (4). However, there has been little effort to determine whether youths receiving services in these programs perceive barriers to accessing mental health services and other services. In the general population, common perceived barriers to mental health service use include financial costs, the inconvenience of receiving services, stigma, and the belief that mental health problems will resolve themselves (18). Studies of special populations, such as veterans, immigrants, and older adults, have emphasized the need for age-appropriate and culturally appropriate services and providers with specific training or expertise (19–21). This study assessed the needs of transition-age youths receiving services in youth-specific programs in San Diego County, California, to learn about their perceived needs for services and barriers to receiving services as a way to inform strategies to reduce these barriers. This qualitative study is based on 13 focus groups, conducted between June 2008 and January 2009. The study purposefully sampled transition-age youths age 18 to 24 who were receiving services in youth-specific programs (75 youths in eight groups), along with parents (14 parents in two groups) and providers (14 providers in three groups). Youths were sampled from geographically diverse programs to obtain a broad range of perspectives from San Diego County. All focus groups were conducted on site at youth-specific programs. Four groups were gender specific (two were for males and two for females). Gender-specific focus groups were conducted in order to elicit responses that might not be provided in a mixed-gender group. Participants were recruited by program staff and by flyers posted in communal areas. Two focus groups were conducted with parents of transition-age youths. Participants were recruited through two organizations focused on parents of children with mental illness. One parent group consisted primarily of well-educated, middle-class professionals. A second group consisted of parents whose children had been legally removed from their homes. Three focus groups were conducted with providers of services to youths. Most were clinical therapists and social workers; child and adolescent psychiatrists declined to participate because of their busy schedules. Participants were recruited by word of mouth by a provider who assumed responsibility for recruitment at each site. All participants provided written informed consent before participating in the groups. Participants were compensated for their time with refreshments and $25 gift cards. This study was approved by the Human Research Protections Program of the University of California, San Diego. Focus groups were conducted with semistructured questionnaires that were designed to elicit information about needs for mental health services, including mental health, general medical health, and substance abuse services, and the need for services promoting independent living, including housing, education, employment, and transportation services and social and financial support. Examples of questions posed included: Are mental health services easy or difficult to get? Do you think that the mental health system does a good job of meeting your needs (are your needs being met)? Do you have any suggestions about how those needs could be met? Before the start of the focus groups, the facilitators were trained by the authors in conducting such groups, including training on using the interview guide, establishing rapport with participants, collecting sensitive data, and maintaining confidentiality (22). Focus group discussions were recorded, transcribed, and analyzed with a methodology of “coding consensus, co-occurrence, and comparison” outlined by Willms and colleagues (23) and rooted in grounded theory (24). The qualitative data analysis software Atlas.ti was used (25). An initial coding scheme of key concepts and categories was created after review of several cross-sections of transcripts (26,27). These codes were then independently applied to five interviews in order to refine and create more nuanced coding. To ensure intercoder reliability of the coding scheme, multiple sections of five additional interviews were coded, and discrepancies in coding between the multiple coders were discussed and resolved among all members of the research team (28,29). If new codes emerged, the coding scheme was changed and the transcripts were reread and recoded according to the new structure. The qualitative analysis followed an inductive approach in which investigators focused on generating themes and identifying relationships between themes (30). Through the process of repeatedly comparing these categories with each other, the categories were further condensed into broad themes illustrating the needs of transition-age youths (23,24). The focus group discussions yielded several themes. The themes are organized below by whether they are related to clinical services or to services that promote independence. [A table presenting sample quotes from group participants by theme is available online as a data supplement to this article.] Mental health and substance abuse services Youths identified several barriers to their use of mental health and substance abuse services, including needs for improved scheduling of services and reduced wait times, stronger patient-provider relationships, and more relevant content for group therapy. Parents and providers described a need for increased access to community-based services. Among youths' more frequently mentioned concerns were the inconvenient scheduling of services and substantial wait times. Early morning meetings were considered difficult to attend by youths who had to rely on time-consuming public transportation and by those with medication-related side effects that affected morning wakefulness. Once youths arrived at their providers' offices, wait times proved to be a concern, particularly for working youths who might be penalized or lose their job because of a delay. Youths' comments indicated that expectations and standards of conduct vis-á-vis appointment timeliness differed for providers and clients, resulting in a double standard of punctuality: “To some degree I find it funny that if we show up late, we get chewed out, but if the doctor's an hour late, it's like, deal with it.” Weak patient-provider relationships also emerged as a significant concern. Both the duration and frequency of appointments were deemed insufficient for providers to review their cases, reestablish rapport, and discuss progress made or challenges experienced by clients. Youths demonstrated awareness that program funding was limited and that providers were under pressure as a result of large caseloads and related time constraints. Youths recognized the resulting frustrations among both providers and clients and even offered suggestions for increasing the efficiency of the office visits—for example, by having nurses prepare providers by eliciting information from clients in advance and by improving health literacy among clients. Provider turnover was viewed as having a negative impact on continuity of care. Youths also voiced dissatisfaction with the content of group therapy. Suggested topics of interest for group therapy included coping with effects of violence against family members and with intimate partner violence, addressing the aftermath of sexual abuse, grieving, acquiring skills for establishing and maintaining healthy relationships, problem solving related to couples issues, and parenting skills. One youth commented, “They have music appreciation, they have yoga, they have fitness training, three days a week they have [dual disorders] recovery. And stuff like that. And they have cooking classes, and they have car washes, they have stuff like that. But they don't have the groups that will actually help us along the way. Say like someone lost someone they really love? They don't have a group where we'll be able to talk about our feelings about it and help us like, you know, help us through the feelings we're feeling about that loss.” Some youths mentioned that services were unavailable at an appropriate level of intensity: “We can talk about anything but [the fact is that] you need more support. But me, I need a lot more support for what happened in my past.” Another youth in the focus group responded to this statement by saying, “Watching your mom get beat to death, it's not a good thing for a ten-year-old.” Parents and providers identified a need for additional community-based services. Parents expressed a need for services that were closer to home and for peer services: “I would like to see rehabilitation services in the communities again, you know, for my son to go to that are peer to peer.” Some providers emphasized delivering services in the community, outside traditional clinics—essentially mobile services. One said, “Our most effective services are services that … get pushed out into the community and [are] flexible in how they engage.” Services that foster a transition to independence Youths, parents, and providers identified needs for additional services to help them succeed in living independently in the community, and all agreed on the need for housing and mentorship. Parents and providers also identified a need for employment support. Several youths expressed a desire for affordable, age-specific housing: “It would be really cool if they had a place like this that was … a transitional living program just for people in a certain age group.” Parents and providers also felt strongly that more age-specific housing was needed; the current lack of housing was thought to increase youths' vulnerability. Emergency housing was deemed critical, particularly for youths transitioning from inpatient care and for those who may need additional medication management support. It was suggested that housing combined with an independent living skills program would help facilitate youths' transitions to adulthood while encouraging socialization. Provision of mental health services at housing sites was also suggested; it was felt that such on-site services would be attractive to youths and might be less stigmatizing because they would not be situated in a mental health facility. Youths also identified a need for mentorship, either from within the service system or by someone familiar with it (for example, a peer). As one youth stated, “It would be nice to have like a CASA [Court Appointed Special Advocate, an advocacy and support service offered to children who are abused or neglected] again, just so you know that somebody who is familiar with the systems [and who works] with the systems can help you with what you need, that they're willing to be a friend if you need, you know in the middle of the night to call and say, I'm freaking out.” Youths expressed a need for mentorship, which was related to their having limited social support from family or friends. They also expressed a desire for help in multiple domains, including assistance with maintaining finances, pursuing academic goals, and obtaining employment. Several youths reported needing assistance opening bank accounts and establishing and staying within a budget. Another participant who was interested in attending junior college felt that a mentor could help facilitate her transition to higher education, including preparing for classes, since she perceived that the activities required to continue schooling were overwhelming. Parents and providers also remarked upon the need for mentorship services, noting that peer mentors who had experienced mental illness are potentially best suited for this role. They believed that relationships with peer mentors would increase youths' receptivity to and engagement in services and assist in the development of their independent living skills. Parents in particular believed that it was important for youths to have support from nonparental mentors with similar life experiences: “If they had somebody that they could talk to that's their own age that is going through some of the issues that they're going through, you know, I think that'd be really powerful.” Parents and providers raised concerns regarding a lack of employment opportunities. They felt that additional services, such as vocational interest tests and educational and vocational training, would enable youths to define a work path. Programs that provide employment support were viewed as critically important. Such programs would help participants develop resumes and complete applications, teach them how to perform well in a job interview, and place them in jobs. As one provider stated, “[It would be good to have] job developers, who could develop relationships with employers willing to hire these kids. [It would be good for kids to know] that they have a job coach who will work through the issues with them. It would be kind of a two-part thing—people to develop jobs specifically that will help kids work toward their goals and also a job coach to help them along.” This study sought to determine the service needs of transition-age youths who were receiving age-specific services in San Diego County. Results showed that even in these specialized programs, youths expressed needs for mental health services, housing, employment, and mentorship. This study provides new findings with respect to the content of group therapy and insights into the importance of having mentoring relationships—a need that youths described differently compared with parents and providers. Youths expressed needs for better scheduling of services, shorter wait times, and stronger patient-provider relationships. These elements are not unique to the experience of transition-age youths. For example, high provider turnover is common in public mental health systems (31). However, these common concerns are particularly problematic for transition-age youths, who have high rates of dropout from mental health treatment (8). The barriers of long wait times and provider turnover may have an outsized impact on transition-age youths. Directing more resources toward improving these common deficiencies may lead to better retention of youths in treatment. Youths also expressed a need for more relevant group therapies. They indicated that existing wellness-focused groups, and even dual-diagnosis groups, were not meeting their needs. Suggested topics included building healthy relationships and dealing with current and past experiences of violence and sexual abuse. The lack of concordance between current offerings and service needs highlights the importance of including the input of youths in the development and provision of services. Youths, parents, and providers all expressed needs for increased housing options and for mentors who could serve as role models, information brokers, and sources of social support for youths pursuing education and employment goals. We found it interesting that the recovery-oriented goals of education and employment were raised in this context, suggesting that mentors may be crucial in facilitating recovery and independence (17). We also found it interesting that although parents emphasized peer mentoring, youths emphasized professional mentoring by adult personnel in youth-specific programs. Youths indicated that they would like someone whom they could trust and who would help them negotiate the challenges of the mental health system and their lives; parents and providers suggested that these mentors should be peers. The limited literature on mentoring of youths with mental illness and the broader literature on various vulnerable youth populations provide little guidance about effective approaches. Additional research in the field of mentoring is greatly needed, particularly research to specify models of mentoring and to discover which types of mentoring are best for which populations. The supported employment model, in which specialists help clients obtain competitive employment and provide ongoing support when the client is employed, speaks directly to the need raised by parents and providers for increased employment opportunities among transition-age youths (32). Recent research has shown that individual placement and support programs are effective in helping clients obtain and maintain long-term employment (33). The study had several limitations. This study purposefully sampled transition-age youths receiving mental health services in youth-specific outpatient programs. We were interested in hearing the voices of youths who were receiving services in programs that were explicitly designed for this population and in identifying unmet needs. We did not provide specific instructions to program staff other than to recruit youths who would be willing to share their experiences with the program. However, we found that youths who participated described a wide range of mental health service needs and experiences. Although both mixed-gender and single-gender groups participated in the study, the analysis did not find obvious themes related to group composition. Another limitation is that the parents of transition-age youths who participated in the focus groups were not necessarily parents of the youths who were enrolled in the youth-specific programs. Thus the comments of these parents were not necessarily informed by their experiences with the youth-specific programs. Also, the provider focus groups did not include psychiatrists, who might have provided additional insight into issues related to pharmacotherapy and medication adherence. Findings from this study suggest that there is room for improvement in the provision of services that are relevant to the current needs and life experiences of transition-age youths. The findings illustrate the challenges that youths face in accessing and benefitting from mental health services while simultaneously transitioning to independence. This study received financial support from Adult and Older Adult Mental Health Services, County of San Diego Health and Human Services Agency. Dr. Ojeda is funded by grant K01DA025504 from the National Institute on Drug Abuse. The authors are grateful to the focus group participants for sharing their insights and experiences. The authors thank Eliza Robillos, Yiase Brunette, and David Thomas for research support. The authors report no competing interests.

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Oedematous malnutrition, represented by its most severe form kwashiorkor, is rampant in many parts of the world and is associated with a high case fatality rate. Despite being first described more than a century ago, the pathogenesis of kwashiorkor is still not clear. The traditional thinking is that it results from a deficiency of dietary protein and is usually associated with an infection. This has now been challenged by the finding that there is no difference in diets of children developing marasmus or kwashiorkor. Nutritional oedema is associated with an increased secretion of anti-diuretic substance (probably antidiuretic hormone) which prevents the normal excretory response to water administration. Experimental studies have shown that feeding low-protein, low-calorie diets results in delayed and incomplete response to a water load, and that the livers of the animals show a reduced capacity for inactivating anti-diuretic hormone. There is now evidence that links generation of free radicals and depletion of anti-oxidants with the development of oedema in kwashiorkor. Key words Antidiuretic hormone--kwashiorkor--malnutrition--nutritional odema--oxidative changes Dropsy (Care and treatment) Edema (Risk factors) Edema (Care and treatment) Pituitary hormones (Health aspects) Malnutrition (Health aspects) Antioxidants (Health aspects) |Publication:||Name: Indian Journal of Medical Research Publisher: Indian Council of Medical Research Audience: Academic Format: Magazine/Journal Subject: Biological sciences; Health Copyright: COPYRIGHT 2009 Indian Council of Medical Research ISSN: 0971-5916| |Issue:||Date: Nov, 2009 Source Volume: 130 Source Issue: 5| |Geographic:||Geographic Scope: India Geographic Code: 9INDI India| Kwashiorkor, the classical example of severe acute malnutrition, is characterised by the presence of oedema. In addition to oedema, the hallmarks of the condition include dermatosis, diarrhoea, and fatty liver (1). Typically there are skin lesions (pigmented or depigmented areas with or without ulceration), scanty lustreless hair, an enlarged fatty liver, loss of interest in the surroundings, and loss of appetite. Oedema may even progress to generalised swelling or anasarca. Fluid homeostasis in the body is altered resulting in excess accumulation of fluid in the extracellular space. Cicely Willliams first introduced the name kwashiorkor in 1935, which in the Ga language of West Africa means "the disease of the deposed child" (2). This literally refers to the child who develops oedema after being weaned with starchy gruels following the birth of a sibling who is breastfed. Kwashiorkor, which occurs mostly in children 1-3 yr of age, results from a deficiency of dietary protein and is usually associated with an infection (3). However in India, Gopalan did not find any difference in diets of children developing marasmus or kwashiorkor (4). In response to infection, amino acids are used for the production of acute phase reactants at the expense of visceral protein synthesis. There is a decrease in blood albumin level, which is partly responsible for development of oedema (5). Beta-lipoprotein is not produced in adequate amounts, resulting in impaired transport of fat from the liver, accumulation of fat and an enlarged fatty liver (6). There is no population-based data on prevalence of oedematous malnutrition. This is due to the fact that large-scale health and nutrition surveys do not make any attempts to detect oedema. Case fatality, however, is very high among children hospitalised with oedematous malnutrition. These observations indicate the need for better information on the global, regional and national prevalence of kwashiorkor and other forms of oedematous malnutrition (7). Mechanism of oedema Oedema is facilitated by two biological processes (8); filtration is the movement of fluid out of the capillary and, reabsorption is the movement of fluid back into the distal end of the capillary and small venules. When capillary fluid filtration exceeds reabsorption, fluid accumulates within the interstitium over time if it were not for the lymphatic system that removes excess fluid from the interstitium and returns it back to the intravascular compartment. Circumstances, however, can arise where net capillary filtration exceeds the capacity of the lymphatics to carry away the fluid (i.e., net filtration > lymph flow). When this occurs, the interstitium will swell with fluid and become oedematous. Decreased plasma oncotic pressure, as occurs in hypoproteinaemia during malnutrition, precipitates oedema (8). How does oedema occur in kwashiorkor? The genesis of oedema of kwashiorkor is multifactorial, with electrolyte disturbance--potassium deficiency and sodium retention playing an important role (9). Nevertheless, the classical theory postulates that an inadequate intake of protein leads to a low plasma albumin concentration which in turn causes oedema (10). Association of protein for genesis of oedema was grounded further by indirect evidences gathered through some of the work of Gopalan and fellow Indian scientists, who found that diets based on protein were associated with satisfactory clinical and biochemical cure of kwashiorkor (11,12). However, this classical hypothesis has been challenged. Golden et al (13) in a study examined the association between plasma albumin and nutritional oedema by observing the changes in albumin during loss of oedema in patients on a restricted diet. Since there was no difference in the concentration of plasma albumin before and after loss of oedema, the association is not causal. In another study, Golden (14) demonstrated that loss of oedema from oedematous malnourished children was strongly associated with dietary energy intake but not with intake of protein. Gopalan et al (4), in a prospective study followed a group of Indian children on poor diet. Some children developed kwashiorkor and some marasmus, but there was no quantitative and qualitative difference between their diets. It was concluded that the difference lay in host's response and that, kwashiorkor represented the theory of dysadaptation, i.e., adaptation failure, and good adaptation resulting in marasmus. Anti-diuretic factor in the urine of children with nutritional oedema: Nutritional oedema is associated with an increased secretion of an anti-diuretic substance (probably anti-diuretic hormone) which prevents the normal excretory response to water administration. Gopalan and Venkatachalam (15) in a study furnished indirect proof of the effect of posture on the urinary response to water load in normal subjects and in cases of nutritional oedema. The normal subjects were found to excrete over 100 per cent of ingested water within 4 h of ingestion in the recumbent posture, while in the erect posture they excreted only 80 per cent. In case of nutritional oedema, the urinary excretion was found to be much lower than in the normal subjects in both recumbent and erect postures. The effect of dietary protein deficiency on the hepatic inactivation of ADH in rats has also been investigated. It was found that the rats maintained on low-protein, low-calorie diets showed a delayed and incomplete response to a water load, and that the livers of these animals showed a reduced capacity for inactivating ADH (Gopalan & Srikantia, unpublished). Role of ferritin and aldosterone: Srikantia observed presence of ferritin in children with kwashiorkor (16). With a view to reveal the precise role of ferritin in the pathogenesis of nutritional oedema, Gopalan and Srikantia (17) investigated the sequence of changes occurring in induced protein and calorie under-nutrition with focus on oedema formation in monkeys. On the basis of the findings, they suggested that calorie-protein undernutrition leads to structural and functional changes in the liver, further leading to defective inactivation of ADH. Active ferritin is released from damaged liver leading to increased secretion of ADH. The net result is water retention. Among other factors, aldosterone, the salt retaining hormone, which is known for influencing water metabolism by altering renal tubular reabsorption of sodium, is also known to be inactivated by the liver. Altered aldosterone metabolism has been reported in diseases of the liver. Associated hyperaldosteronism could account for the sodium retention18. In oedematous children aldosterone secretion becomes higher during loss of oedema (19). Oedema of kwashiorkor--environmental and metabolic factors: Environment, particularly diet, certainly has an important role in the pathogenesis of kwashiorkor; the condition is not seen in children with an adequate nutritional intake. Intrinsic characteristics of the host may also be required for the development of kwashiorkor. It is possible that variant isozymes or variations in concentration of enzymes in the metabolic pathways lead to the development of kwashiorkor in children with poor diets. Differences in the pattern of amino acid concentrations between children with kwashiorkor and marasmus have been used in favour of this assumption (20). The serum amino-acidogram may show distinct differences in cases of marasmus and kwashiorkor. Very high levels of glutamate with low or undetectable levels of alanine are the hallmark of kwashiorkor (21). One possible explanation for this can be the low level of transaminases in kwashiorkor. Low transaminase levels in the liver biopsy specimens in case of kwashiorkor have been reported earlier (22). It has also been shown that they remain low even during recovery. It is possible that this deficiency is present right from birth and is genetically transmitted and is made clinically overt when the child is exposed to stress of dietary inadequacy and may be responsible for development of kwashiorkor. Those children who have normal transaminase function develop marasmus under the same dietary insult. In addition to dietary and nutritional investigations, genetic techniques including genome-wide association to delineate host factors may prove useful in unscrambling the enigma of kwashiorkor. Evidence for free radicals/anti-oxidants Golden and Ramdath (23) proposed that kwashiorkor results from an imbalance between the production of free radicals and their safe disposal. This theory is supported by the observations in other studies where blood concentrations of vitamin E derivatives, glutathione, and red cell antioxidant enzymes are lower in children with kwashiorkor than in marasmic children (24-26). The study of Sive et al (27) shows that, 'free' circulating iron may contribute to oedema in kwashiorkor. Srikantia (17), using a bioassay, had reported that children with kwashiorkor had high levels of circulating ferritin, which was further confirmed by a Jamaican study when immunoassays became available (28). The study of Okunade et al (29) shows that the extent of lipid peroxidation in the erythrocytes of kwashiorkor subjects was three times that found in erythrocytes of normal subjects. This finding was supported by another study which also demonstrated excessive lipid peroxidation in kwashiorkor (30). In a clinical trial, the administration of N-acetylcysteine, a glutathione precursor, resulted in more rapid resolution of oedema in kwashiorkor (31). These associations between oxidative stress and kwashiorkor indicate that antioxidant depletion may cause kwashiorkor which can therefore be prevented with antioxidant supplementation. Challenge to the oxidative stress theory? The study by Ciliberto et al (32) examined the impact of an antioxidant cocktail containing riboflavin, vitamin E, selenium, and N-acetyl cysteine in a dose three times of required daily intakes, as a possible preventive treatment for kwashiorkor in children in a highly endemic area of Malawi but failed to find any protective effect. Although the result may be a deterrent to the antioxidant hypothesis, it would be premature to discard the theory altogether. The specific antioxidants used in the Ciliberto study are known to have a high relative antioxidant capacity, but the amounts taken by the children may have been insufficient to overcome high oxidative stress and prevent kwashiorkor. Since neither antioxidant capacity nor oxidative stress was measured, the adequacy of the antioxidant mix or the dose can be questioned. Moreover, the study did not assess the children's HIV status, which may have contributed to or affected their responses to oxidative stress (33). Thus more than a century has elapsed but the theories on pathogenesis of kwashiorkor oedema continue to unfold. The age old classical theory of dietary protein inadequacy now continues to be challenged. The theory of dysadaptation explains a different perspective related to differential host response leading to different outcomes (kwashiorkor or marasmus) under nutritional stress, and underpins a wider perspective of metabolic and enzymatic variances leading to oedema formation. Hormonal factors (ADH) also demonstrate a plausible explanation of the pathology. Evidence for free radicals / anti-oxidants, which essentially propose an imbalance between free radicals and their disposal, is increasingly becoming strong. Evidence of oxidative changes in the cell membranes of the oedematous kwashiorkor subjects i.e., lipid peroxidation has been established by some studies. Indirect evidences of anti-oxidant therapy improving oedema further consolidate the free radical/anti-oxidant theory; yet this theory is not without question- the enigma of kwashiorkor oedema continues! Received April 16, 2009 (1.) Gopalan C, Ramalingaswami V. Kwashiorkor in India. Indian J Med Res 1955; 43 : 751-73. (2.) Williams CD. Kwashiorkor: a nutritional disease of children associated with a maize diet. Lancet 1935; 2 : 1151-2. (3.) Suskind RM, Murthy KK, Suskind D. The malnourished child: an overview. In: Suskind RM, Suskind LL, editors. The malnourished child. New York: Vevey/Raven Press; 1990. (4.) Gopalan C. Kwashiorkor and marasmus: evolution and distinguishing features. In: McCance RA, Widdowson EM, editors. Calorie deficiencies and protein deficiencies. Boston: Little, Brown; 1968. p. 49-58. (5.) Waterlow JC. Causes of oedema and its relation to kwashiorkor. In: Waterlow JC, editor. Protein-energy malnutrition. London: Edward Arnold; 1992. (6.) Truswell AS Hansen JDL. Fatty liver in protein-calorie malnutrition. South Afr Med J 1969; 43 : 280-3. (7.) Bhutta ZA, Black RE, Cousens S, Ahmed T. Kwashiorkor and severe acute malnutrition in childhood--Authors' reply. Lancet 2008; 371 : 1749. (8.) Klabunde RE. Tissue oedema and general principles of transcapillary fluid exchange, cardiovascular physiology concepts. Available at: www.cvphysiology.com/microcircula tionM010.htm. (9.) Alleyne GAO. The effect of severe protein calorie malnutrition on the renal function of Jamaican children. Paediatrics 1967; 39 : 400-12. (10.) Waterlow JC. Fatty liver disease in infants in the British West Indies. Medical Research Council Special Report Series No. 263. London: Medical Research Council; 1948. (11.) Gopalan C, Srikantia SG. Clinical trials with vegetable protein foods in kwashiorkor. Indian J Med Res 1960; 48 : 637-44. (12.) Gopalan C, Venkatachalam PS, Srikantia SG, Mehta G. Treatment of nutritional oedema syndrome (kwashiorkor) with vegetable protein diets. Am J Clin Nut 1962; 11 : 12733. (13.) Golden MH, Golden BE, Jackson AA. Albumin and nutritional oedema. Lancet 1980; i : 114-6. (14.) Golden MHN. Protein deficiency, energy deficiency and the oedema of malnutrition. Lancet 1982; i : 1261-5. (15.) Gopalan C, Venkatachalam PS. The pathogenesis of nutritional oedema. Indian J Med Sci 1952; 6 : 713. (16.) Srikantia SG. Ferritin in nutritional oedema. Lancet 1958; i : 667-8. (17.) Srikantia SG, Gopalan C. Role of ferritin in nutritional oedema. JApplPhysiol 1959; 14 : 829-33. (18.) Migeon CJ, Beitins IZ, Kowarski A, Graham CG. Plasma aldosterone concentration and aldosterone secretion rate in Peruvian infants with marasmus and kwashiorkor. In: Gardner LI, Amacher P, editors. Endocrine aspects of malnutrition. Santa Yenz: KrocFoundation; 1973. p. 399-424. (19.) Lurie AO, Jackson WPU. Aldosteronuria and the oedema of kwashiorkor. Am J Clin Nutr 1962; 11 : 115-26. (20.) Phadke MA, Khedkar VA, Pashankar D, Kate SL, Mokashi GD, Gambhir PS, et al. Serum amino acids and genesis of protein energy malnutrition. Indian Pediatr 1995; 32 : 301-6. (21.) Lunn PG, Whitehead RG, Hay RW, Baker BA. Aminoacids in protein energy malnutrition. Br J Nutr 1973; 29 : 399-401. (22.) Mclean EM. Hepatic failure in malnutrition. Lancet 1962; 2 : 1292-4. (23.) Golden MHN, Ramdath D. Free radicals in the pathogenesis of kwashiorkor. Proc Nutr Soc 1987; 46 : 53-68. (24.) Jackson AA. Blood glutathione in severe malnutrition in childhood. TransR Soc TropMedHyg 1986; 80 : 911-3. (25.) Sive AA, Subotzky EF, Malan H, Dempster WS, De v, Heese H. Red blood cell antioxidant enzyme concentrations in kwashiorkor and marasmus. Ann Trop Paediatr 1993; 13 : 33-8. (26.) Becker K, Botticher D, Leichsenring M. Antioxidant vitamins in malnourished Nigerian children. Int J Vitam Nutr Res 1994; 64 : 306-10. (27.) Sive AA, Dempster WS, Malan H, Rosseau S, Hesse HD. Plasma free iron: a possible cause of oedema in kwashiorkor. Arch Dis Child 1997; 76 : 54-6. (28.) Ramdadi DD, Golden MH. Non-haematological aspects of iron nutrition. Nutr Res Rev 1989; 2 : 29-49. (29.) Okunade WG, Olorunsogo OO. Effect of reactive oxygen species on the erythrocyte calcium-pump function in proteinenergy malnutrition. Pediatrics 1995; 95 : 874. (30.) Lenhartz H, Ndasi R, Anninos A, Botticher D, Mayatepek E, Tetanye E, et al. The clinical manifestation of the kwashiorkor syndrome is related to increased lipid peroxidation. J Pediatr 1998; 132 : 879-81. (31.) Badaloo A, Reid M, Forrester T, Heird WC, Jahoor F. Cysteine supplementation improves the erythrocyte glutathione synthesis rate in children with severe oedematous malnutrition. Am J Clin Nutr 2002; 76 : 646-52. (32.) Ciliberto H, Ciliberto M, Briend A, Ashorn P, Bier D, Manary M. Antioxidant supplementation for the prevention of kwashiorkor in Malawian children: randomised, double blind, placebo controlled trial. BMJ 2005; 330 : 1109-11. (33.) Fuchs GG. Antioxidants for children with Kwashiorkor. BMJ 2005; 330 : 1095-6. Reprint requests: Dr Tahmeed Ahmed, Head, Nutrition Programme, International Centre for Diarrhoeal Disease Research, Bangladesh (ICDDR, B), GPO Box 128, Dhaka 1000, Bangladesh e-mail: firstname.lastname@example.org Tahmeed Ahmed, Sabuktagin Rahman & Alejandro Cravioto International Centre for Diarrhoeal Disease Research, Bangladesh, ICDDR, B, Dhaka, Bangladesh |Gale Copyright:||Copyright 2009 Gale, Cengage Learning. All rights reserved.|

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The reverse shoulder replacement is a shoulder implant that has been used successfully for over ten years in Europe. It was approved by the FDA for use in the United States in 2004. It specifically designed for use in shoulders that have a deficient rotator cuff and severe arthritis. In addition, it can be used in the setting of complex fractures and failure of previous shoulder replacements in which the rotator cuff has become deficient deficient. The normal shoulder is a ball and socket joint (Figure 1). The ball is called the humeral head and the socket is called the glenoid. The rotator cuff is a series of four muscles that hold the shoulder in the socket and help the shoulder move. When torn, the rotator cuff is usually repaired surgically. In some cases, surgical repair of the rotator cuff is not possible. Over the course of many years, the shoulder can develop a unique type of arthritis due to massive rotator cuff tearing. This end stage of a massively torn, irreparable rotator cuff tear is called cuff tear arthropathy of the shoulder, a difficult to treat combination of arthritis and a massive rotator cuff tear. A normal shoulder has cartilage on the ball and socket to enable smooth gliding motion (Figure 2). In the arthritic shoulder the normal cartilage is worn away instead of cartilage gliding smoothly on cartilage, bone rubs roughly against bone, creating pain and inflammation. On x-ray, the joint space narrows and osteophytes (bone spurs) form (Figure 3). When the rotator cuff is intact, a conventional shoulder replacement replaces the ball and socket joint with metal and plastic, eliminating pain and restoring range of motion (Figure 4). Figure 4. These three x-rays represent a conventional shoulder replacement that is used when the rotator cuff is intact. Conventional shoulder replacement uses a press fit humeral stem and a cemented three pegged polyethylene glenoid component to resurface the shoulder joint and eliminate pain. When an irreparable rotator cuff tear of large size goes untreated for many years, a condition called cuff tear arthropathy gradually develops. The humeral head loses its containment within the rotator cuff and begins to articulate with the acromion. On x-ray, this manifests as not only arthritis between the ball and socket joint (Figure 5). Cartilage wear ensues. In the most severe cases, the patient has intractable pain and is unable to raise the arm. Conventional shoulder replacement with a hemiarthroplasty (half of a shoulder replacement) is unpredictable for pain relief and gain of function. The reverse prosthesis was designed to improve upon the results of conventional shoulder replacement in the setting of a deficient rotator cuff. Figure 5. The Hamada classification of rotator cuff tear arthropathy shows progressive stages of arthritis of both glenohumeral and acromiohumeral spaces. The reverse shoulder replacement (Figure 6) changes the orientation of the shoulder so that the normal socket (glenoid) is replaced with a metal ball, and the normal ball (humeral head) is replaced with a humeral stem with a socket. The humeral socket then rests under the glenoid ball. The mechanics of the shoulder are changed in such a way that the deltoid muscle now has tension, restoring the patient's ability to raise the arm and improving the pain from arthritis. Figure 6. A reverse shoulder replacement consists of a humeral stem with a concave socket attached that articulates with a hemispherical glenoid componenent (glenosphere) in a semiconstrained fashion. This metal on plastic articulation improves pain and range of motion by changing the anatomy of the shoulder to restore deltoid tension. Figure 5A: A typical patient with rotator cuff tear arthropathy has a high riding humeral head with arthritis between glenoid and humerus as well as arthritis between acromion and humerus. Figure 5B: After reverse total shoulder replacement, the acromiohumeral interval and deltoid tension have been restored. Figure 5C+D: Preoperative x-rays of severe rotator cuff tear arthropathy Figure 5E: After treatment with reverse total shoulder replacement Some shoulder fractures are complex and involve the part of the bone where the rotator cuff tendons insert. The goal of the shoulder surgeon in the setting of shoulder fracture surgery is to enable the fracture to heal with a functioning rotator cuff. Displaced shoulder fractures in this setting are usually treated with either a plate and screws or a hemiarthroplasty (shoulder replacement of the humerus alone). When these fractures fail to heal or when the rotator cuff fails to heal to the prosthesis, pain and inability to lift the arm ensues. The reverse prosthesis is a salvage operation for the painful, failed shoulder fracture. Lastly, previous shoulder replacements can become rotator cuff deficient over time and can also be salvaged with a reverse prosthesis. In the setting of previous fracture surgery and/or a previous prosthesis, the complication rate is much higher than in cuff tear arthopathy alone. Figure 6 shows conversion of a failed, dislocated hemiarthroplasty using a reverse total shoulder replacement. Figure 6A+B: Preoperative x-rays of a failed hemiarthroplasty dislocated superiorly. This painful shoulder was treated with a reverse total shoulder replacement (6C). The complication rate for the reverse prosthesis is about 10% in primary surgery (no previous surgery). The complication rate is 30-40% when revising previous surgery in the aforementioned salvage setting. For this reason, the problem being treated with a reverse prosthesis must be significant enough to warrant the high surgical risk. (e.g. daily, debilitating pain and inability to lift the arm). Complications include: The reverse shoulder replacement is for severe pain and inability to lift the arm that affects daily life. Prior to undergoing a reverse replacement, you should have tried physical therapy, injections, medications, activity modification and watchful waiting, all without improvement. Risks are higher for this joint replacement than for conventional joint replacements, but the results can be excellent in the properly selected patient with a debilitating shoulder condition.

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Faculty Peer Reviewed Lung cancer is the most common cause of cancer deaths globally and responsible for an estimated 221,120 new cases and 156,940 deaths in 2011 in the United States. Presently, the United States Preventive Services Task Force, the National Cancer Institute (NCI), the American College of Chest Physicians, and most other evidence-based organizations do not recommend screening for lung cancer with chest x-ray or low-dose helical computed tomography (CT) due to inadequate evidence to support mortality reduction. This recommendation, however, may soon change. LOW-DOSE CT SCREENING REDUCES MORTALITY In October 2010, the NCI announced that the National Lung Screening Trial (NLST) was concluded early because the study showed that low-dose CT screening, when compared with screening by chest radiography, resulted in a 20.0% relative reduction in lung cancer-related mortality and an all-cause mortality reduction of 6.7%. The number needed to screen with low-dose CT to prevent one lung cancer death was 320. This report, published in the August 4th, 2011 issue of the New England Journal of Medicine, is the first randomized controlled trial of lung cancer screening to show a significant mortality benefit. The trial enrolled 53,454 high-risk current and former smokers aged 55 to 74 years who had a history of at least 30 pack-years. Former smokers (52% of the total) had to have quit only recently–within the last 15 years. They underwent three annual screenings with CT or chest X-ray and then were followed for an additional 3.5 years. Suspicious screening results were three-fold higher in the low-dose CT group compared to radiography across all three screening rounds (24.2% vs 6.9%). More than 90% of the positive screening tests in the first round of screening led to follow-up, mainly consisting of further imaging, with invasive procedures rarely performed. More cancers were diagnosed after the screening period in the chest radiography group compared to those screened by low-dose CT, suggesting that radiography missed more cancers during the screening period. Furthermore, cancers detected in the low-dose CT arm were more likely to be early-stage compared to those discovered after chest radiography. NLST STUDY LIMITATIONS Lung cancer-specific deaths were 247 and 309 per 100,000 person-years in the low-dose CT and chest radiography groups, respectively, and this was statistically significant (P=0.004). The internal validity of the study is firm, based on similar baseline characteristics and rates of follow-up between the two study groups.[4-6] Whether these results can be applied to the general population, however, is uncertain. Trial participants were, on average, younger urban dwellers with a higher level of education than a random sample of smokers 55 to 74 years old [4-5], which might have increased adherence in the study. Furthermore, radiologists interpreting the screening images had additional training in reading low-dose CT scans and presumably greater experience due to high workload. One major barrier to implementation of any screening program is its cost. Eventual analysis of the results from the NLST will definitively answer this question; however, a recent Australian study can provide us some with some provisional guidance. Manser and colleagues examined the cost effectiveness of CT screening in a baseline cohort of high-risk male current smokers aged 60 and 64 with an assumed annual incidence of lung cancer of 552 per 100,000 and determined that the incremental cost-effectiveness ratio was $105,090 per quality-adjusted life year (QALY) saved. This is less than the generally accepted upper limit of $113,000 per QALY in the United States, but far above the $50,000 per QALY threshold that many authors of cost-effectiveness are advocating. The NLST study population had an approximate annual incidence of lung cancer of 608.5 per 100,000, which is similar to the incidence rate in the Australian analysis. Though this extrapolation is purely speculative, it suggests that if the upper limit of $113,000 per QALY were the cut-off, low-dose CT screening in the United States may be cost-effective. IMPORTANCE OF IDENTIFYING HIGH-RISK PATIENTS A second important issue to address is the identification of patients most likely to benefit from CT screening. In the Australian study, for the patient risk group with an annual incidence of lung cancer of 283 per 100,000 it costs $278,219 per QALY saved.. The national incidence in the US in 2006 was 63.1 per 100,000 person-years. To screen the average person in the US general population would be an astronomical expenditure of resources (greater than $1 million per QALY saved), dramatically increase the false-positive rates from screening, and promote unnecessary exposure to carcinogenic radiation. Accordingly, only high-risk patients (eg, advanced age, positive family history, and heavy smoking history) should be considered for this screening modality. ADDITIONAL BARRIERS AND ISSUES The United Kingdom Lung Screening Trial investigators listed other issues that will need to be addressed prior to implementation of a screening program: 1. Synchronization of CT technique and scan interpretations 2. Value of the diagnostic work-up techniques for positive screening findings and establishing standards for follow-up 3. Optimal surgical management of detected nodules in patients 4. Optimal screening interval for both screen-negative and screen-positive patients 5. Continued study and collaboration by academic organizations, federal institutions and policymakers. CONCLUSIONS ON HOW TO COUNSEL PATIENTS With all this in mind, how are we to counsel patients interested in lung cancer screening? First, only high-risk patients for lung cancer should be considered for low-dose CT screening. Even in the high-risk NLST cohort, positive images were false roughly 95% of the time in both study arms. In patients at lower risk, these false-positive rates will undoubtedly be much higher. Second, patients should be informed about the potential harms from detection of benign abnormalities requiring follow-up and potential invasive interrogation, which can result in adverse outcomes. Finally, even with the exciting revelation of mortality reduction by a lung cancer screening modality, smoking cessation will remain one of the most important interventions in reducing mortality from lung cancer. Benjamin Lok is a 4th year medical student at NYU School of Medicine Peer reviewed by Craig Tenner, MD, Medicine, NYU Langone Medical Center Image courtesy of Wikimedia Commons 1. Parkin DM, Bray F, Ferlay J, Pisani P. Global cancer statistics, 2002. CA Cancer J Clin. 2005;55(2):74-108. 2. American Cancer Society. Cancer facts and figures 2011. http://www.cancer.org/Research/CancerFactsFigures/CancerFactsFigures/cancer-facts-figures-2011. Accessed July 7, 2011. 3. National Cancer Institute: PDQ® Lung Cancer Screening. 2011; http://cancer.gov/cancertopics/pdq/screening/lung/HealthProfessional. Accessed July 21, 2011. 4. National Lung Screening Trial Research Team. Reduced lung-cancer mortality with low-dose computed tomographic screening. N Engl J Med. 2011;365(5):395-409. 5. National Lung Screening Trial Research Team. Baseline characteristics of participants in the randomized national lung screening trial. J Natl Cancer Inst. 2010;102(23):1771-1779. 6. Sox HC. Better evidence about screening for lung cancer. N Engl J Med. 2011;365(5):455-457. 7. Manser R, Dalton A, Carter R, Byrnes G, Elwood M, Campbell DA. Cost-effectiveness analysis of screening for lung cancer with low dose spiral CT (computed tomography) in the Australian setting. Lung Cancer. May 2005;48(2):171-185. 8. Weinstein MC. How much are Americans willing to pay for a quality-adjusted life year? Med Care. 2008;46(4):343-345. 9. American Lung Association. State of lung disease in diverse communities, 2010. http://www.lungusa.org/assets/documents/publications/lung-disease-data/solddc_2010.pdf. Accessed July 28, 2011. 10. Field JK, Baldwin D, Brain K, et al. CT screening for lung cancer in the UK: position statement by UKLS investigators following the NLST report. Thorax. 2011;66(8):736-737.

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- All > Medicine Information and Evidence for Policy > Medicines Policy - All > Medicine Information and Evidence for Policy > World’s Medicines Situation Report (2011; 176 pages) Noncommunicable diseases (NCDs) are the leading global causes of death, causing more deaths than all others causes combined, and they strike hardest at the world’s low- and middle-income populations. These diseases have reached epidemic proportions, yet they could be significantly reduced, with millions of lives saved and untold suffering avoided, through reduction of their risk factors, early detection and timely treatments. The Global status report on noncommunicable diseases is the first worldwide report on the state of NCDs and ways to map the epidemic, reduce its major risk factors and strengthen health care for people who already suffer from NCDs. This report was prepared by the WHO Secretariat under Objective 6 of the 2008–2013 Action Plan for the Global Strategy for the Prevention and Control of NCDs. It focuses on the current global status of NCDs and will be followed by another report to assess progress in 2013. One of the main objectives of this report is to provide a baseline for countries on the current status of NCDs and their risk factors, as well as the current state of progress countries are making to address these diseases in terms of policies and plans, infrastructure, surveillance and population-wide and individual interventions. It also disseminates a shared vision and road map for NCD prevention and control. Target audiences include policy-makers, health officials, nongovernmental organizations, academia, relevant non-health sectors, development agencies and civil society...Of the 57 million global deaths in 2008, 36 million, or 63%, were due to NCDs, principally cardiovascular diseases, diabetes, cancers and chronic respiratory diseases. As the impacts of NCDs increases, and as populations age, annual NCD deaths are projected to continue to rise worldwide, and the greatest increase is expected to be seen in low- and middle-income regions. While popular belief presumes that NCDs afflict mostly high-income populations, the evidence tells a very different story. Nearly 80% of NCD deaths occur in low-and middle-income countries and are the most frequent causes of death in most countries, except in Africa. Even in African nations, NCDs are rising rapidly and are projected to almost equal communicable, maternal, perinatal, and nutritional diseases as the most common causes of death by 2020. Mortality and morbidity data reveal the growing and disproportionate impact of the epidemic in lower resource settings. Over 80% of cardiovascular and diabetes deaths, and almost 90% of deaths from chronic obstructive pulmonary disease, occur in low- and middle-income countries. More than two thirds of all cancer deaths occur in low- and middle-income countries. NCDs also kill at a younger age in low- and middle-income countries, where 29% of NCD deaths occur among people under the age of 60, compared to 13% in high-income countries. The estimated percentage increase in cancer incidence by 2030, compared with 2008, will be greater in low- (82%) and lower-middle-income countries (70%) compared with the upper-middle- (58%) and high-income countries (40%)...

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Magnetic Resonance Imaging (MRI) Magnetic resonance imaging (MRI) is a superior technique that uses radio waves and a strong magnetic field to provide remarkably clear pictures. As such, it offers an alternative to patients who react to radiopaque intravenous dye. Because of its ability to show soft tissues in exquisite detail, this technology can detect disease and detail blood vessels or other structures. In the kidney system, for example, an MRI can distinguish a hollow cyst from a solid mass, producing excellent three-dimensional images of any tumor's shape. In particular, its super sensitivity can help urologists identify and measure the spread of kidney cancer into the renal vein and inferior vena cava, the large vessel that returns blood to the heart. But while useful in evaluating kidney transplant donors, MRI has limited applicability for the urinary tract since the non-specificity of its signals makes it ineffective in detecting calcifications and bladder abnormalities. MRI is unique among imaging methods because, unlike radiographs (X-rays,), CT scan and even radioisotope studies, it does not use ionizing radiation. Instead, MRI uses a strong magnet, radio waves and computers to create detailed images of the body. More specifically, lying inside a massive hollow magnet, a patient is exposed to short bursts of powerful non-ionizing radio wave energy, directed at protons, the nuclei of hydrogen or water atoms, in the body. Radio signals generated by first "exciting" and then "relaxing" those protons, are computer-processed to form digital images, reflecting different types of tissue. Typical MRI examinations consist of multiple imaging sequences, each lasting from two to 15 minutes. While these techniques continue to evolve, the beauty of current MRI is that it can be tailored for any clinical question. This test is performed in a hospital radiology department or in a health care provider's office by a technician under the supervision of a physician. No patient preparation is necessary prior to this test. The patient will be asked to lie on a narrow table, which slides into a large tunnel-like tube within the scanner. The patient's head will be placed in a padded plastic cradle or on a pillow and the table will then slide into the scanner. The patient will be instructed to breathe quietly and normally but to refrain from any movement, coughing or wiggling. The technician will be able to communicate with the patient during this test through the use of an intercom. While the scanner is taking images, the patient will hear rapidly repeating, loud thumping noises coming from the walls of the scanner, so earplugs are usually provided to the patient to reduce the noise. The entire test usually takes between 30 and 60 minutes to complete. Following the test, the patient may resume their normal daily activities. For generally healthy individuals, MRI poses no risk. But patients with pacemakers, aneurysm clips, ear implants and metallic pieces in vital body locations cannot be imaged safely. Reviewed January 2011 You are leaving UrologyHealth.org. The Urology Care Foundation has no control over the content of this site. Click OK to proceed.

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Scientists at NIAID's Rocky Mountain Laboratories (RML) are examining how abnormal prion protein molecules cause transmissible spongiform encephalopathy (TSE) diseases. RML has had an active TSE research program since the 1960s. RML is one of the world's premiere laboratories for studying TSE diseases. Scientists there co-discovered and were among the first to clone the prion protein gene. NIAID scientists also discovered that abnormal prion protein can convert normal prion protein to the abnormal form. This may account for the disease process in the brain. RML scientists have published findings from significant TSE studies. One study showed that when prion protein was modified to remove a membrane "anchor" in laboratory animals, scrapie infection caused formation of abnormal prion protein, but remarkably, did not result in disease. Researchers believe that without the membrane anchor, the abnormal prion protein is unable to damage the brain cells. These results suggest that drugs aimed at blocking interactions between normal and abnormal prion protein might be able to halt the progress of disease. In these same mice where the membrane anchor was removed, scrapie infection led to an accumulation of abnormal prion protein in heart tissue resulting in heart stiffness and malfunction. This research indicates that cardiac infection may be a new and previously overlooked feature of TSE diseases. In another study, RML scientists used a new methodology to determine the size of the smallest infectious prions. These results demonstrate that the minimal size of the infectious material is equivalent to 5 to 10 prion protein molecules. It is possible, though not yet proven, that these smallest fractions are more infectious than the larger aggregates. At Colorado State University in Fort Collins, NIAID has established an emerging diseases research center focused on studying chronic wasting disease (CWD). This center is investigating the mechanics of CWD infection in deer and elk. Such studies underlie the search for improved diagnostics and therapies. The researchers also will seek to better understand the entire spectrum of disease transmission and under what circumstances CWD might "jump" to other species. One study concluded that infectious prions are present in skeletal muscles of CWD-infected deer, demonstrating that humans eating or handling meat from CWD-infected deer are at risk for prion exposure. Though there is no causal proof that CWD is capable of spreading to humans, researchers suggest that people use caution when handling infectious material or consuming any part of the animal that may be infected. More recently, the research group at Colorado State University has reported that infectious prions capable of transmitting CWD are found in the saliva and blood of affected deer. This helps to explain the ease of transmission of CWD among deer and suggests caution concerning contact with body fluids of infected animals. back to top Last Updated March 04, 2009

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Wild poliovirus in Côte d'Ivoire 21 April 2011 - Côte d'Ivoire is experiencing an outbreak of wild poliovirus type 3 (WPV3) with three new cases reported with onset of paralysis on 27 January, 24 February and 27 February this year. Genetic sequencing of the isolated viruses show that they are linked to WPV3 last detected in mid-2008 in northern Nigeria. They are the first WPV3 recorded in Côte d'Ivoire since 2000. In 2008-2009, Côte d'Ivoire was affected by a wild poliovirus type 1 (WPV1) outbreak affecting west Africa (and which was recently stopped). There is currently a high risk of further spread of WPV3 - both within and from - Côte d'Ivoire. It is the first time since 2000 that WPV3 has been recorded in this part of west Africa (WPV3 transmission has been limited to northern Nigeria and parts of Niger, and since 2008 also in parts of Mali and one case in Benin). The outbreak response may be constrained by the current security situation in Côte d'Ivoire. Due to the persistence of subnational surveillance gaps in Côte d'Ivoire and other areas of west Africa, undetected further circulation cannot be ruled out at this time. Detection of these WPV3 cases underscores the risk suboptimal surveillance poses to the global polio eradication effort. Globally, WPV3 transmission is at its lowest level in history, with only nine cases reported worldwide in 2011 - efforts to rapidly interrupt all remaining chains of WPV3 transmission is a key priority for the global polio eradication effort. The overriding priority is to urgently stop the WPV3 outbreak, while maintaining high population immunity across west Africa to WPV1. Two rounds of coordinated, multi-country supplementary immunization activities (SIAs) with bivalent oral polio vaccine (bOPV) and trivalent oral polio vaccine (tOPV) across west Africa have been/are being implemented on 25 March 2011, and again on 29 April 2011, in 15 countries across west Africa (except Côte d'Ivoire, see next paragraph). A further outbreak response is currently planned in six countries, over and beyond these two multi-country SIAs. Such a further response could see planned SIAs scheduled for the fourth quarter to be brought forward to earlier in the year. In Côte d'Ivoire, the end-March SIA did not take place due to the current security and political situation. A response round is proposed in the affected province using bOPV in late April 2011, to be followed by two National Immunization Days (NIDs), as soon as the situation permits. Planning is underway to ensure capacity (ie technical, vaccine, operational) is in place for this emergency response. Coordination with other United Nations (UN) organizations and non-governmental organizations (NGOs) operating in Côte d'Ivoire is ongoing, to ensure that OPV is added to any planned immunization activity, in particular for displaced populations. Ongoing transmission will be monitored, and mop-ups implemented as epidemiology dictates. An investigation is ongoing to more clearly identify surveillance gaps in the region, including among mobile, migrant and underserved populations. Measures will be implemented to strengthen sub-national surveillance, to ensure that all groups and areas, particularly high-risk populations, are covered by high-quality surveillance. As per recommendations outlined in WHO's International travel and health, travellers to and from Côte d'Ivoire, and other polio-affected countries of west Africa, should be fully protected by vaccination. Travellers who have in the past received three or more doses of OPV should be offered another dose of polio vaccine before departure. Any unimmunized individuals intending to travel to should have a complete course of vaccination. Travellers from Côte d'Ivoire, and other polio-affected countries of west Africa, should have a full course of vaccination against polio before departure, with a minimum one dose of OPV before departure.

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Tubulin (tubul- + -in) is one of several members of a small family of globular proteins. The tubulin superfamily includes five distinct families, the alpha-, beta-, gamma-, delta-, and epsilon-tubulins and a sixth family (zeta-tubulin) which is present only in kinetoplastid protozoa. The most common members of the tubulin family are α-tubulin and β-tubulin, the proteins that make up microtubules. Each has a molecular weight of approximately 55,000 Daltons. Microtubules are assembled from dimers of α- and β-tubulin. These subunits are slightly acidic with an isoelectric point between 5.2 and 5.8. To form microtubules, the dimers of α- and β-tubulin bind to GTP and assemble onto the (+) ends of microtubules while in the GTP-bound state. The β-tubulin subunit is exposed on the plus end of the microtubule while the α-tubulin subunit is exposed on the minus end. After the dimer is incorporated into the microtubule, the molecule of GTP bound to the β-tubulin subunit eventually hydrolyzes into GDP through inter-dimer contacts along the microtubule protofilament. Whether the β-tubulin member of the tubulin dimer is bound to GTP or GDP influences the stability of the dimer in the microtubule. Dimers bound to GTP tend to assemble into microtubules, while dimers bound to GDP tend to fall apart; thus, this GTP cycle is essential for the dynamic instability of the microtubule. Human α-tubulin subtypes include: Class III β-tubulin is a microtubule element expressed exclusively in neurons, and is a popular identifier specific for neurons in nervous tissue. It binds colchicine much more slowly than other isotypes of β-tubulin. β1-tubulin, sometimes called class VI β-tubulin, is the most divergent at the amino acid sequence level. It is expressed exclusively in megakaryocytes and platelets in humans and appears to play an important role in the formation of platelets. Human β-tubulins subtypes include: γ-Tubulin, another member of the tubulin family, is important in the nucleation and polar orientation of microtubules. It is found primarily in centrosomes and spindle pole bodies, since these are the areas of most abundant microtubule nucleation. In these organelles, several γ-tubulin and other protein molecules are found in complexes known as γ-tubulin ring complexes (γ-TuRCs), which chemically mimic the (+) end of a microtubule and thus allow microtubules to bind. γ-tubulin also has been isolated as a dimer and as a part of a γ-tubulin small complex (γTuSC), intermediate in size between the dimer and the γTuRC. γ-tubulin is the best understood mechanism of microtubule nucleation, but certain studies have indicated that certain cells may be able to adapt to its absence, as indicated by mutation and RNAi studies that have inhibited its correct expression. Human γ-tubulin subtypes include: Members of the γ-tubulin ring complex: δ And ε tubulin Delta (δ) and epsilon (ε) tubulin have been found to localize at centrioles and may play a role in forming the mitotic spindle during mitosis, though neither is as well-studied as the α- and β- forms. Human δ- and ε-tubulin subtypes include: Tubulins are targets for anticancer drugs like Taxol, Tesetaxel and the "Vinca alkaloid" drugs such as vinblastine and vincristine. The anti-gout agent colchicine binds to tubulin and inhibits microtubule formation, arresting neutrophil motility and decreasing inflammation. The anti-fungal drug Griseofulvin targets microtubule formation and has applications in cancer treatment. Tubulin/FtsZ family, GTPase domain kif1a head-microtubule complex structure in atp-form In molecular biology, Tubulin/FtsZ family, GTPase domain is an evolutionary conserved protein domain. This GTPase protein domain is found in all tubulin chains, as well as the bacterial FtsZ family of proteins. These proteins are involved in polymer formation. Tubulin is the major component of microtubules, while FtsZ is the polymer-forming protein of bacterial cell division that forms part of a ring in the middle of the dividing cell that is required for constriction of the cell membrane and cell envelope to yield two daughter cells. FtsZ can polymerise into tubes, sheets, and rings in vitro, and is ubiquitous in bacteria and archaea. - NCBI CCD cd2186 - Williams RC Jr, Shah C, Sackett D (November 1999). "Separation of tubulin isoforms by isoelectric focusing in immobilized pH gradient gels". Anal Biochem 275 (2): 265–7. doi:10.1006/abio.1999.4326. PMID 10552916. - Nogales E, Downing KH, Amos LA, Löwe J (June 1998). "Tubulin and FtsZ form a distinct family of GTPases". Nat Struct Biol 5 (6): 451–8. doi:10.1038/nsb0698-451. PMID 9628483. - Heald R, Nogales E (January 2002). "Microtubule dynamics". J Cell Sci 115 (Pt 1): 3–4. PMID 11801717. - Howard J, Hyman AA (April 2003). "Dynamics and mechanics of the microtubule plus end". Nature 422 (6933): 753–8. doi:10.1038/nature01600. PMID 12700769. - Zhou J, Giannakakou P (January 2005). "Targeting Microtubules for Cancer Chemotherapy". Current Medicinal Chemistry - Anti-Cancer Agents 5 (1): 65–71. doi:10.2174/1568011053352569. PMID 15720262. - Luduena RF (May 1993). "Are tubulin isotypes functionally significant". Molecular Biology of the Cell 4 (5): 445–457. doi:10.1091/mbc.4.5.445. PMID 8334301. - Lecine P et al. (August 2000). "Hematopoietic-specific beta 1 tubulin participates in a pathway of platelet biogenesis dependent on the transcription factor NF-E2". Blood 96 (4): 1366–1373. PMID 10942379. - McNally FJ, Vale RD (November 1993). "Identification of katanin, an ATPase that severs and disassembles stable microtubules". Cell 75 (3): 419–29. doi:10.1016/0092-8674(93)90377-3. PMID 8221885. - Nogales E, Wolf SG, Downing KH (January 1998). "Structure of the alpha beta tubulin dimer by electron crystallography". Nature 391 (6663): 199–203. doi:10.1038/34465. PMID 9428769. - Löwe J, Amos LA (January 1998). "Crystal structure of the bacterial cell-division protein FtsZ". Nature 391 (6663): 203–6. doi:10.1038/34472. PMID 9428770. - Tubulin at the US National Library of Medicine Medical Subject Headings (MeSH) - EC 22.214.171.124 - protocol for purification of tubulin from bovine brain

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drugs all have a widespread effect in the brain that can be summed up as decreased neural activity. The behavioral effects are very similar to the effects of alcohol. At low doses these drugs might be prescribed for daytime use to reduce anxiety (as a sedative). At higher doses many of these same drugs are prescribed as sleeping pills (hypnotics). This grouip of prescription drugs is often referred to as sedative-hypnotics, part of a larger group of substances considered to be CNS depressants. * the most widely used depressant is alcohol * the most widely used prescribed types of sedative-hypnotics fall into the chemical grouping called the benzodiapezines, which in the past 30 years have replaced the barbiturates. have a longer history than barbiturates but are less frequently used today The names of barbiturates always end with the letters "al" grouped on the basis of the duration of their activity: short-acting, intermediate-acting, or long-acting (refer to Table 8.1 on page 167 of your textbook). In general, the drugs that are the most lipid-soluble are the ones that have both the shortest time of onset (i.e., they are absorbed and enter the brain rapidly) and the shortest duration of action (i.e., they leave the brain quickly and tend to be more rapidly metabolized). Sedatives are usually low dose of a long-acting barbiturate (like phenobarbital); and sleeping pills are usually of higher dose of a short-acting drug (such as amobarbital and physical dependence, and fatal overdose are possible drawbacks to barbiturates. one of the classes of drugs that stimulate the activity of microsomal enzymes of the liver. Some of the tolerance that develops is the result of an INCREASED rate of deactivation caused by this stimulation. They depress respiration and, in large doses or in combination with alcohol, can completely stop Mechanism of Action: GABA (gamma amino butyric acid) receptor complex, which includes a barbiturate binding site and a benzodiazepine receptor. When these chemicals bind to their receptor respective receptor site, they enhance the normally inhibitory effects of of GABA on its receptors. Because of concerns of addiction liability and the danger of overdose, new sedative or hypnotic agents were accepted and utilized. released in 1955, was the first modern antianxiety agent, was a revolutionary replaced meprobamate and were considered a safer substitute than barbiturates. Chlordiazepoxide (Librium) and Diazapam (Valium). In looking at the differences between barbiturates and so-called safer drugs (like benzodiazapines), we have learned that it is the dose and the time course of individual drugs that make the difference. A drug that has a rapid onset of action will be more likely to produce psychological dependence than a slow-acting drug. Physical dependence occurs when the drug leaves the system more rapidly than the body can adapt. - one way to reduce the severity of withdrawal symptoms is to reduce the dose of a drug slowly over time. Drugs with a shorter duration of action leave the system quickly and are much more likely to produce withdrawal symptoms than longer-acting drugs. There might be a greater difference among the bartiturates and among the benzodiazepines than there are between the two classes. a benzodiazepine sold as a hypnotic in many countries but NOT the U.S. appeared in the late 1950ís and early 1960ís and was incorrectly viewed as safe, nonbarbiturate sleeping pill. Methaqqualone causes the same kind of motor incoordination as alcohol and the barbiturates. USES FOR SEDATIVE-HYPNOTIC not curing neurotic behavior, is the one primary purpose of these drugs. Most psychiatrists refer to the benzodiazepines as antiantiety agents (anxiolytics). For a typical general practitioner, about half of the patients have NO treatable physical ailment. Because of the possibility of tolerance, dependency, rebound insomnia, and hangover effects, the use of hypnotic drugs has decreased - they are usually taken for only a few nights at a time. benzodiazepines are often used for the control of epileptic seizures OF SEDATIVE-HYPNOTIC DRUGS are more likely to lead to dependency than benzodiazepines are can occur with any of the sedative-hypnotic drugs Withdrawal can be These drugs impair judgement and coordination by barbiturates has been reported (especially when used with alcohol) is affected (respiration is depressed), sometimes to the point of respiratory Abuse usually occurs by an older person using these drugs for a long time for sedation or sleeping; or by a young person using these drugs to get high (using sleeping pills from home, etc.) to these fumes makes users intoxicated, often slurring their speech and causing them to have trouble walking Because so many different sovents are involved, it is impossible to characterize the potential harm produced by abuse, except to say that several solvents have been linked to kidney damage, brain damage and peripheral nerve damage and many produce irritation to the respiratory tract and result in severe headaches. However, several users of various inhalants have suffocated as a result of this e.g., nitrous oxide, chloroform, ether, etc. isoamyl nitrite, butyl nitrite, etc. e.g., petroleum distillates, acetone, toluene, etc. nitrous oxide, butane, propane, etc. Use of inhalants

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oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets. Hypoparathyroidism is characterised by hypocalcaemia, hyperphosphataemia and low or inappropriately normal levels of parathyroid hormone (PTH). Pseudohypoparathyroidism is characterised by similar findings but PTH is elevated due to PTH resistance. PTH is a key calcium-regulating hormone essential for calcium homeostasis, vitamin D-dependent calcium absorption, renal calcium reabsorption and renal phosphate clearance. PTH is secreted by the four parathyroid glands, located in the neck behind the thyroid gland. It regulates serum calcium and phosphorus levels and also plays a part in bone metabolism. Low levels of PTH cause serum calcium levels to fall and serum phosphate levels to rise. Calcium and phosphate homeostasis - Maintenance of normal serum calcium levels involves the regulation of the flux of calcium between the intestinal tract, kidneys and bone. - Calcium itself, PTH and 1,25-dihydroxyvitamin D3 all play a role in calcium regulation. - 1,25-dihydroxyvitamin D3 facilitates intestinal calcium absorption, whilst both 1,25-dihydroxyvitamin D3 and PTH stimulate calcium release from bone. - PTH also stimulates the conversion of 25-hydroxyvitamin D3 to 1,25-dihydroxyvitamin D3 enabling distal renal tubular calcium reabsorption. - High concentrations of serum calcium inhibit PTH secretion while low concentrations stimulate it. - Phosphate reabsorption from the kidney is reduced by PTH. Thus if PTH levels are low, serum phosphate will rise (more will be reabsorbed). - This is a rare disorder. - Found equally in males and females. - Age of onset depends on the aetiology. Hypoparathyroidism may be transient, congenital/genetically inherited or acquired. The most common cause of hypoparathyroidism is iatrogenic following anterior neck surgery. Transient hypoparathyroidism in the neonatal period Healthy term neonates undergo a reduction in serum calcium levels by 24-48 hours of age. Some neonates, especially high-risk (eg, infants of mothers with diabetes, preterm infants and infants with perinatal asphyxia), may develop hypocalcaemia. Early-onset hypocalcaemia presents within 72 hours and requires treatment with calcium supplementation for at least 72 hours. Late-onset hypocalcaemia usually presents after seven days and requires longer-term therapy. - Prematurity at birth: very low birth weight infants may not have a normal PTH surge postnatally, thus resulting in hypocalcaemia. - Infants of mothers with diabetes: hypomagnesaemia due to maternal magnesuria impairs PTH release and action. - Delay in PTH surge postnatally: this can occur in otherwise healthy neonates. - Maternal hyperparathyroidism: this results in hypercalcaemia which can cause prolonged PTH suppression in the neonate. Congenital or genetically inherited hypoparathyroidism - Defects in parathyroid gland development: - DiGeorge's syndrome: there is abnormal development of the parathyroid glands from the third and fourth pharyngeal pouches. The thymus gland, aortic arch and parts of the lips and ears also develop from these pouches.There is hypoparathyroidism, T-cell immune deficiency, abnormal facies such as cleft palate, and cardiac anomalies. - Defects in the PTH gene. - Defects in the calcium-sensing receptor gene: - Presents as hypocalcaemia, inappropriately normal levels of PTH and raised phosphate levels. - This is not true hypoparathyroidism but its presentation mimics it. - Can present from birth to adulthood. - Defects in PTH action (pseudohypoparathyroidism): this occurs when the somatic features of pseudohypoparathyroidism are present in patients with normal serum calcium and phosphate levels. PTH is either normal or raised. The patient may fluctuate between hypocalcaemia and normocalcaemia and may develop cataracts: - A rare inherited disorder where there is failure of target cells to respond to PTH, ie there is PTH resistance. - PTH levels are not low but are appropriate for the degree of hypocalcaemia. - There is an association with: - Somatic anomalies. - Short stature. - Round face. - Short neck. - Shortening of the metacarpals and metatarsals. - Diabetes mellitus. - Gonadal dysgenesis. - As part of an autoimmune process: - Autoimmune polyglandular syndrome type 1 (APS-1): autosomal recessive inheritance. Features include hypoparathyroidism, adrenal insufficiency, chronic mucocutaneous candidiasis. Also known as autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED). Presents in childhood. - Autoimmune polyglandular syndrome type 2 (APS-2): features include adrenal insufficiency, insulin-dependent diabetes mellitus and thyroid disease. Presents in adulthood. Autosomal dominant inheritance. - Isolated hypoparathyroidism with a possible autoimmune cause can also be inherited. - Genetic syndromes, including: - Hypoparathyroidism, deafness and renal (HDR) dysplasia syndrome. - Hypoparathyroidism, retardation and dysmorphism (HRD) syndrome. - Neck surgery (thyroid, parathyroid, laryngeal or oesophageal surgery) is the most common cause and includes: - Accidental damage to, or accidental removal of, the parathyroid glands. Most likely during thyroid surgery. May be transient or permanent. Surgeon-dependent. - Removal of parathyroid glands because of potential malignancy. - After surgery for hyperparathyroidism. Transient hypoparathyroidism may occur whilst the body returns to a normal response to PTH. - Radiation or drugs: - Neck or chest irradiation during radiotherapy treatment. - Radioactive iodine treatment for hyperthyroidism: a rare side-effect. - Chemotherapeutic/cytotoxic agents. - Infiltration of the parathyroid glands: - Destruction of the parathyroid glands due to iron deposition can occur in haemochromatosis or multiple blood transfusions. - Destruction of the parathyroid glands due to copper deposition can occur in Wilson's disease. - Infiltration of the parathyroid glands by malignant metastases. - Magnesium deficiency, which can occur in: - Chronic alcoholism. - Hereditary renal or intestinal hypomagnesaemia. - Magnesium excess - eg, when magnesium is used for the treatment of preterm labour or pre-eclampsia. - Autoimmune process: sporadic forms of APS-1 can occur as described above. - Isolated idiopathic hypoparathyroidism: - PTH deficiency is present but no other associated endocrine or developmental disorders. - Usually sporadic but can be familial. - May possibly be a form of autoimmune hypoparathyroidism. Pseudohypoparathyroidism includes a heterogeneous group of rare metabolic disorders that include characteristic morphological features and end-organ resistance to the action of PTH. Plasma concentrations of PTH are elevated and reflect the failure of target tissues to respond appropriately to the biological actions of PTH. - Muscle pains. - Bone pain: bone turnover is abnormally low and bone mineral density is typically increased. - Abdominal pain. - Paraesthesiae (tingling, vibrating, burning and numbness) of the face, fingers and toes. - Facial twitching. - Carpopedal spasm. - Convulsions (usually grand mal). - Emotional lability, anxiety and depression, confusion. - Memory impairment. - Brittle nails. - Dry hair and skin. - Painful menstruation. Important points to elicit in the history include: - History of previous neck surgery. - Family history of any hypoparathyroid disorders. - Chvostek's sign: detects latent tetany: - Tapping of the fifth facial nerve in front of the ear with the patient's mouth slightly open causes contraction of the facial muscles. - Not specific, as about 25% of the normal population have a positive response. - Trousseau's sign: occlude the arterial circulation of the forearm using a blood pressure cuff inflated to the systolic blood pressure for three minutes. Carpopedal spasm is induced. - Raised intracranial pressure with papilloedema. - Dental abnormalities and enamel dysplasia. - Brittle nails with transverse grooves. - Dry, rough skin. Other symptoms and signs depend on the aetiology: - DiGeorge's syndrome: - Recurrent infections due to T-cell immunodeficiency. - Congenital heart disease and its related symptoms, heart murmur. - Speech delay. - Abnormal facies: cleft palate, micrognathia, ear abnormalities. - Familial autoimmune polyglandular syndrome type I (APS-I): - Chronic mucocutaneous candidiasis. - Adrenal failure. - Dental enamel hypoplasia. - Genetic syndromes: - Sensorineural deafness. - Renal dysplasia. - General learning disability. Hypocalcaemia and hyperphosphataemia can also be caused by: - Magnesium deficiency. - Vitamin D deficiency. - Chronic kidney disease: may develop secondary hyperparathyroidism. - Blood tests (to exclude other causes of hypocalcaemia): - Calcium, phosphate, PTH and alkaline phosphatase: Typical blood test results in hypoparathyroidism: - Low serum calcium. - High serum phosphate. - Low PTH. - Normal alkaline phosphatase. - Low serum calcium. - High or normal PTH. - Serum magnesium: may be low. - U&Es: to exclude chronic kidney disease. - 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3: to exclude vitamin D deficiency as a cause of hypocalcaemia. 25-hydroxyvitamin D3 is normal in hypoparathyroidism and pseudohypoparathyroidism but 1,25-dihydroxyvitamin D3 is low because PTH is not available for its activation - Calcium, phosphate, PTH and alkaline phosphatase: - Additional blood tests: If an autoimmune process is suspected, look for co-inciding thyroid and adrenal insufficiency: - Thyroid-stimulating hormone (TSH), thyroxine and thyroid autoantibodies. - Adrenocorticotrophic hormone (ACTH) and adrenal antibodies. - Urine tests: 24-hour urinary calcium is usually low. - Other possible investigations: - ECG: prolonged QT interval which may progress to ventricular fibrillation or heart block. - Echocardiogram: cardiac abnormalities (in DiGeorge's syndrome). - Renal ultrasound: looking for renal calculi. - Hand radiography: looking for shortened metacarpals. - Brain MRI scan: basal ganglia calcification (sign of a long-standing hypocalcaemic state). - Genetic studies: as appropriate. - If severe hypocalcaemia symptoms are present, such as tetany, urgent IV calcium should be given. - A diet rich in dairy products containing calcium and vitamin D is recommended. Calcium and vitamin D3 - The basis of treatment is with calcium and vitamin D. - The doses are tailored to the individual's needs and regular monitoring is needed. - In some people, once adequate doses of vitamin D are achieved, they can absorb all the calcium that they need through the diet. However, in others, calcium levels remain permanently unstable and maintenance doses of calcium and vitamin D will need to be regularly monitored and adjusted. - Treatment is lifelong. - There is no restriction on activities but patients should wear a bracelet to identify themselves as suffering from hypoparathyroidism. - As yet, PTH is not commercially available to treat hypoparathyroidism. - However, recombinant PTH is used for the treatment of postmenopausal osteoporosis. - PTH replacement improves serum calcium and lowers serum phosphate. It has been shown to lower urinary calcium loss. - Careful monitoring of vitamin D, phosphorous, and calcium is necessary during acute and long-term therapy. Parathyroid autotransplantation and allotransplantation - If a patient has a thyroidectomy, one of the parathyroids can be 'autotransplanted' into either the neck or the forearm to give a continuing supply of PTH. - Allotransplantation of cultivated parathyroid tissue is also a possibility. Potential treatment problems - Pregnancy, diuretics, antacids, anticonvulsants, intercurrent illness, ammonium chloride and acetazolamide may alter the requirements for vitamin D. - Close monitoring of calcium levels is needed. - There has been one case report of hypoparathyroidism refractory to vitamin D therapy, treated with multipulse teriparatide. Mostly due to hypocalcaemia: - Laryngospasm can cause stridor and airway obstruction. - Neuromuscular irritability can lead to muscle cramps, tetany and seizures. - Heart: QT interval changes can cause syncope, arrhythmias and death. - Calcium can be deposited in the kidneys, causing calculi. - Stunted growth, malformed teeth and mental impairment can develop if untreated in childhood. - Over-treatment with vitamin D can cause hypercalcaemia and renal impairment. - The regular monitoring required to ensure appropriate calcium levels means that the prognosis is challenging for many people. This may improve if synthetic PTH becomes widely available. - Regular review and blood monitoring programmes within the GP setting are likely to be beneficial. Close monitoring of patients undergoing thyroid or neck surgery, radiotherapy to the neck or chest and chemotherapy treatment for symptoms and signs of hypocalcaemia. Further reading & references - Al-Azem H, Khan AA; Hypoparathyroidism. Best Pract Res Clin Endocrinol Metab. 2012 Aug;26(4):517-22. doi: 10.1016/j.beem.2012.01.004. Epub 2012 May 31. - Jain A, Agarwal R, Sankar MJ, et al; Hypocalcemia in the newborn. Indian J Pediatr. 2010 Oct;77(10):1123-8. doi: 10.1007/s12098-010-0176-0. Epub 2010 Aug 25. - Betterle C, Garelli S, Presotto F; Diagnosis and classification of autoimmune parathyroid disease. Autoimmun Rev. 2014 Apr-May;13(4-5):417-22. doi: 10.1016/j.autrev.2014.01.044. Epub 2014 Jan 11. - Sciume C, Geraci G, Pisello F, et al; Complications in thyroid surgery: symptomatic post-operative hypoparathyroidism incidence, surgical technique, and treatment. Ann Ital Chir. 2006 Mar-Apr;77(2):115-22. - Osmolski A, Frenkiel Z, Osmolski R; Complications in surgical treatment of thyroid diseases, Otolaryngol Pol. 2006;60(2):165-70. - Understanding the Causes of Hypoparathyroidism; Hypoparathyroidism UK - Levine MA; An update on the clinical and molecular characteristics of pseudohypoparathyroidism. Curr Opin Endocrinol Diabetes Obes. 2012 Dec;19(6):443-51. doi: 10.1097/MED.0b013e32835a255c. - Maeda SS, Fortes EM, Oliveira UM, et al; Hypoparathyroidism and pseudohypoparathyroidism. Arq Bras Endocrinol Metabol. 2006 Aug;50(4):664-73. - Lau K, Willig RP, Hiort O, et al; Linear skin atrophy preceding calcinosis cutis in pseudo-pseudohypoparathyroidism. Clin Exp Dermatol. 2012 Aug;37(6):646-8. doi: 10.1111/j.1365-2230.2011.04292.x. Epub 2012 Feb 2. - De Sanctis V, Soliman A, Fiscina B; Hypoparathyroidism: from diagnosis to treatment. Curr Opin Endocrinol Diabetes Obes. 2012 Dec;19(6):435-42. doi: 10.1097/MED.0b013e3283591502. - Shoback D; Clinical practice. Hypoparathyroidism. N Engl J Med. 2008 Jul 24;359(4):391-403. - Rejnmark L, Sikjaer T, Underbjerg L, et al; PTH replacement therapy of hypoparathyroidism. Osteoporos Int. 2013 May;24(5):1529-36. doi: 10.1007/s00198-012-2230-4. Epub 2012 Nov 27. - Michels TC, Kelly KM; Parathyroid disorders. Am Fam Physician. 2013 Aug 15;88(4):249-57. - Fong J, Khan A; Hypocalcemia: updates in diagnosis and management for primary care. Can Fam Physician. 2012 Feb;58(2):158-62. - Walker Harris V, Jan De Beur S; Postoperative hypoparathyroidism: medical and surgical therapeutic options. Thyroid. 2009 Sep;19(9):967-73. - Cusano NE, Rubin MR, Sliney J Jr, et al; Mini-review: new therapeutic options in hypoparathyroidism. Endocrine. 2012 Jun;41(3):410-4. doi: 10.1007/s12020-012-9618-y. Epub 2012 Feb 7. - British National Formulary - Testini M, Rosato L, Avenia N, et al; The impact of single parathyroid gland autotransplantation during thyroid surgery on postoperative hypoparathyroidism: a multicenter study. Transplant Proc. 2007 Jan-Feb;39(1):225-30. - Nawrot I, Wozniewicz B, Tolloczko T, et al; Allotransplantation of cultured parathyroid progenitor cells without immunosuppression: clinical results. Transplantation. 2007 Mar 27;83(6):734-40. - Puig-Domingo M, Diaz G, Nicolau J, et al; Successful treatment of vitamin D unresponsive hypoparathyroidism with multipulse Eur J Endocrinol. 2008 Nov;159(5):653-7. Epub 2008 Aug 14. Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions. Dr Michelle Wright Dr Colin Tidy Dr John Cox

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Volume 10, Number 8—August 2004 Crimean-Congo Hemorrhagic Fever in Bulgaria We report the epidemiologic characteristics of Crimean-Congo hemorrhagic fever in Bulgaria, as well as the first genetic characterization of the virus strains circulating in the country in 2002–2003 that caused disease in humans. Crimean-Congo hemorrhagic fever virus (CCHFV) (genus Nairovirus, family Bunyaviridae) causes severe disease with a fatality rate as high as 30%. CCHFV is endemic in the Balkan Peninsula; a number of cases occur every year, sometimes in an epidemic form. Cases have been reported in Albania (1), Kosovo (2,3), and Bulgaria (4). Mountains approximately 1,500 m to 2,500 m high separate these countries from Greece, where no case of the disease has yet been identified. However, a CCHFV strain was isolated in Greece from Rhipicephalus bursa ticks, collected in May 1975 from goats of a flock in Vergina village, 80 km west of Thessaloniki (5). Antibodies against the virus were detected in the Greek human population (6). CCHFV is also endemic in Russia and in parts of Asia and Africa. The virus is transmitted to humans by the bite of ixodid ticks (primarily of the Hyalomma genus) or by contact with blood or tissues from infected persons or infected livestock. The risk for spread of the virus from person to person is high, which occasionally results in nosocomial outbreaks. After an incubation period of 3 to 7 days, the patient has sudden onset of fever, chills, myalgia, and headache, which rapidly progress to severe illness; a hemorrhagic state follows with bleeding from the mucous membranes and petechiae, associated with thrombocytopenia and leukopenia (7). CCHFV, like all members of the genus, is a negative-stranded RNA virus with a tripartite genome consisting of a small, medium, and large segment encoding the nucleocapsid protein; the glycoprotein precursor, which results in the two envelope glycoproteins G1 and G2; and the putative RNA-dependent polymerase, respectively (8). We report (for the first time in English) the epidemiologic characteristics of the disease in Bulgaria. We also provide the first genetic characterization of the CCHFV strains circulating in the country from 2002 to 2003 that caused disease in humans. Bulgaria is a country of 8 million inhabitants in the eastern part of the Balkans (Figure 1). CCHF was first recognized in the country in 1952 and became a reportable disease in 1953. In 1968, CCHFV was isolated from blood samples of two patients. Results from serologic investigations showed that approximately 20% of patients living in disease-endemic areas who reported a tick bite had antibodies to CCHFV (4). The seropositivity in animals in the disease-endemic areas can be as high as 50%. Most cases were reported from Plovdiv and Pazardgik (central Bulgaria), Haskovo and Kardgali (southeastern Bulgaria), Shumen (northeastern Bulgaria), and Burgass (eastern Bulgaria) (4). The most prevalent tick in Bulgaria is Ixodes ricinus; however CCHFV strains have been isolated from Hyalomma plumbeum (H. marginatum), Rhipicephalus sanguineus, and Boophilus calcaratus (9). From 1953 to 1974, 1,105 CCHFV cases were reported to the Bulgarian Ministry of Health; the fatality rate was approximately 17%. Of them, 20 cases were nosocomial infections and 52% were fatal. In 1974, an immunization program was introduced for medical workers and military personnel in CCHF-endemic areas. The treatment regimen consisted of mouse brain preparation inactivated by chloroform, heated at 58°C, and adsorbed on Al(OH)3. The first two doses were given at day 0 and day 30; a third dose was given 1 year later, and another dose was given 5 years after that (10). As a result, between 1975 and 1996, the number of reported CCHF cases was reduced to 279, with a fatality rate of 11.4%. No infection was reported from vaccinated military personnel (11). Since 1997, a total of 124 cases occurred in Bulgaria, 27 of them fatal (Table 1). Most patients had been bitten by a tick; however, a few were infected through direct contact with CCHF patients. Only the eastern part of the country has been affected; two main foci exist, one in the southeast and a second one in northeast. The mean age of patients is 52 years (range 11–79 years). Most patients were men (74%), probably because they are more frequently exposed to ticks bites during outdoor activities. The disease occurs mainly from March to July when ticks are more active. The main clinical symptoms are fever, malaise, nausea, epistaxis, petechiae, and bleeding from the gastrointestinal tract; the main laboratory findings are leukopenia, thrombocytopenia, and elevated transaminase levels. To investigate the genetic relationships of the CCHFV strains circulating recently in Bulgaria, RNA was extracted from cell culture supernatant from six virus isolates. The virus had been isolated in a Vero E6 cell line from blood samples taken from CCHF patients who were infected in 2002 and 2003. The epidemiologic characteristics of the patients are shown at Table 2. A reverse-transcriptase–nested polymerase chain reaction (PCR) was applied to amplify a partial fragment of the S RNA genome segment by using two sets of primers, F2-R3 and F3-R2 (12). Purified PCR products were sequenced; the nucleotide sequences were submitted to the GenBank database and assigned the accession numbers AY550253–AY550258. After aligning the obtained Bulgarian CCHFV sequences with respective ones retrieved from GenBank, we constructed a phylogenetic tree with PHYLIP software (13) (Figure 2). All Bulgarian isolates were found to cluster together, with a genetic homology of 98.4% to 100% at the nucleotide level. Identical sequences were obtained from isolates originating from the same region in the same year. The Bulgarian CCHFV strains were found to cluster with other Balkan strains from Kosovo and Albania, with a mean genetic difference of 2% and 1.2%, respectively. All Balkan strains clustered in the same branch with CCHFV strains from European Russia, such as STV/HU29223 strain, isolated in 2000 from human blood in Stavropol (mean genetic difference 2.5%), and ROS/TI28044, isolated in 2000 from Hyalomma marginatum ticks in Rostov (mean genetic difference 3.7%) (14). A “European CCHFV group,” distinct from all others, is evident. An exception to the European group is the Greek strain AP92, isolated from R. bursa ticks (5), which forms an independent clade, which differs from the Bulgarian strains by 24%. This genetic difference is likely attributable to the different species of related ticks or to reassortment. Studies on the Greek strain are still in progress; they will help explain the genetic and pathogenic differences among this strain and respective strains from neighboring countries. Although the genetic divergence among European strains is low, a great divergence is seen among European CCHFV strains and strains from other continents (Asia and Africa). As the number of CCHFV sequences derived from the S genome segment is growing, eight distinct clades can be seen: 1) strain AP92 from Greece; 2) strains from Senegal, Mauritania, and Iran; 3) strains from Senegal, Mauritania, and South Africa; 4) strains from Nigeria and Central African Republic; 5) strain from Uganda; 6) strains from Central Asia and China; 7) strains from Madagascar, Iran, and Pakistan; and 8) European strains (Russia, Albania, Kosovo, and Bulgaria) (Figure 2). In conclusion, this report shows that the CCHV is endemic in Bulgaria and causes severe disease in the whole Balkan Peninsula (except Greece) and that the Bulgarian CCHFV strains are genetically similar to other Balkan virus strains (except AP92). CCHFV evolves relatively slowly, which suggests that the great genetic divergence among the strains is not time-dependent. Whether this divergence is because of the different tick species, the different geographic location, or any other reason, remains to be elucidated. - Papa A, Bino S, Llagami A, Brahimaj B, Papadimitriou E, Pavlidou V, Crimean-Congo hemorrhagic fever in Albania, 2001. Eur J Clin Microbiol Infect Dis. 2002;21:603–6. - Drosten C, Minnak D, Emmerich P, Schmitz H, Reinicke T. Crimean-Congo hemorrhagic fever in Kosovo. J Clin Microbiol. 2002;40:1122–3. - Papa A, Bozovic B, Pavlidou V, Papadimitriou E, Pelemis M, Antoniadis A. Genetic detection and isolation of Crimean-Congo hemorrhagic fever virus, Kosovo, Yugoslavia. Emerg Infect Dis. 2002;8:852–4. - Vasilenko S, Chumakov M, Katzarov G, Mihailov A, Levi V, Kebedgiev G, Investigations on Congo-Crimean hemorrhagic fever in Bulgaria II. Serological examinations of people and animals in endemic and nonendemic for CCHF areas. [Bulgarian]. Epidemiology, Microbiology, and Infectious Diseases. 1971;8:150–6. - Papadopoulos O, Koptopoulos G. Crimean-Congo hemorrhagic fever (CCHF) in Greece: isolation of the virus from Rhipicephalus bursa ticks and a preliminary serological survey. Zentbl Bakteriol Hyg Abt 1. 1980;Suppl 9;189–93. - Antoniadis A, Casals J. Serological evidence of human infection with Congo-Crimean hemorrhagic fever virus in Greece. Am J Trop Med Hyg. 1982;31:1066–7. - Swanepoel R, Shepherd AJ, Leman PA, Shepherd SP, McGillivray GM, Erasmus MJ, Epidemiologic and clinical features of Crimean-Congo hemorrhagic fever in southern Africa. Am J Trop Med Hyg. 1987;36:120–32. - Nichol ST. Bunyaviruses. In: Knipe DM, Howley PM, editors. Fields virology, vol. 2. Philadelphia: Lippincott Williams and Wilkins; 2001. p. 1603–33. - Vasilenko SM, Kirov I, Katzarov G, Investigations on CCHF in Bulgaria. [Bulgarian]. Proceedings of Hyg Epidemiol Inst. 1970;22:153–66. - Todorov S, Kovacheva T, Velcheva D, Katzarov G. Congo-Crimean hemorrhagic fever—prophylaxis and treatment. [Bulgarian]. Contemporary Medicine. 2001;42:54–60. - Kovacheva T, Velcheva D, Katzarov G. Studies on the morbidity of Congo-Crimean hemorrhagic fever before and after specific immunoprophylaxis. [Bulgarian]. Infectology. 1997;34:34–5. - Rodriguez LL, Maupin GO, Ksiazek TG, Rollin PE, Khan AS, Schwarz TF, Molecular investigation of a multisource outbreak of Crimean-Congo hemorrhagic fever in the United Arab Emirates. Am J Trop Med Hyg. 1997;57:512–8. - Felsenstein J. PHYLIP (Phylogeny Inference Package) version 3.5c. Seattle: Department of Genetics, University of Washington; 1993. - Yashina L, Petrova I, Seregin S, Vyshemirskii O, Lvov D, Aristova V, Genetic variability of Crimean-Congo hemorrhagic fever virus in Russia and Central Asia. J Gen Virol. 2003;84:1199–206. Suggested citation for this article: Papa A, Christova I, Papadimitriou E, Antoniadis A. Crimean-Congo hemorrhagic fever in Bulgaria. Emerg Infect Dis [serial on the Internet]. 2004 Aug [date cited]. Available from: http://wwwnc.cdc.gov/eid/article/10/8/04-0162.htm Comments to the Authors West Nile Virus RNA in Tissues from Donor Transmission to Organ

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Pubic lice are small, six-legged creatures that infect the pubic hair area and lay eggs. These lice can also be found in armpit hair and eyebrows. Pediculosis - pubic lice; Lice - pubic; Crabs Causes, incidence, and risk factors Pubic lice are known as Phthirus pubis. Lice infestation is found mostly in teenagers and usually spreads during sexual activity. Sometimes, pubic lice can spread through contact with objects such as toilet seats, sheets, blankets, or bathing suits at a store. However, this type of spreading is rare. Animals cannot spread lice to humans. Other types of lice include: - Body lice (Pediculus humanus corporis) - Head lice (Pediculus humanus capitis) Risk factors include: - Having multiple sexual partners - Having sexual contact with an infected person - Sharing bedding or clothing with an infected person Almost anyone with pubic lice will have itching in the area covered by pubic hair (it often gets worse at night). This itching may start soon after getting infected with lice, or it may not start for up to 2 - 4 weeks after contact. - Skin reaction that is bluish-gray in color - Sores (lesions) in the genital area due to bites and scratching Signs and tests An examination of the outer genital area shows small gray-white oval eggs (nits) attached to the hair shaft. It may also reveal adult lice. The health care provider might also see scratch marks or signs of an infection, such as impetigo. Because pubic lice may cause an eye infection (blepharitis) in young children, their eyelashes should be examined for evidence of lice with a high-powered magnifying glass. Adult lice may be easily identified under the microscope. Their crab-like appearance is the reason that pubic lice are referred to as "the crabs." Teenagers with pubic lice may need to be tested for other sexually transmitted infections (STIs). Pubic lice are best treated with a prescription wash containing permethrin, such as Elimite or Kwell: - Thoroughly work the shampoo into the pubic hair and surrounding area for at least 5 minutes. - Rinse well. - Comb the pubic hair with a fine-toothed comb to remove eggs (nits). Applying vinegar to pubic hair before combing may help loosen nits, but the hair should be dry when applying the shampoo. A single treatment is all that is usually needed. If another treatment is recommended, it should be done 4 days to 1 week later. Over-the-counter medications for the treatment of lice include Rid and Nix. Malathione lotion is another treatment option. While you are treating pubic lice, wash all clothing and linens in hot water. Items that cannot be washed may be sprayed with a medicated spray or sealed (suffocated) in plastic bags and not used for 10 - 14 days. It is important for all intimate contacts to be treated at the same time. People with pubic lice should be evaluated for other sexually-transmitted infections at the time of diagnosis. The proper treatment, including thorough cleaning, should get rid of the lice. The constant scratching and digging can cause the skin to become raw, and secondary infections may develop. Calling your health care provider Call for an appointment with your health care provider if: - You or your sexual partner has symptoms of pubic lice - You try over-the-counter lice treatments and they are not effective - Your symptoms continue after treatment Avoid sexual or intimate contact with infected people. If you are sexually active, use safe sex practices to avoid getting lice. Good personal hygiene is always recommended. If possible, avoid trying on bathing suits while you are shopping. However, if you must try them on, be sure to wear your underwear. This may prevent transmission. Habif TP, ed. Clinical Dermatology. 5th ed. Philadelphia, Pa:Mosby Elsevier;2009: pp 590-594. Diaz JH. Lice (pediculosis). In: Mandell GL, Bennett JE, Dolin R. Mendell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 7th ed. Philadelphia, Pa:Churchill Livingstone Elsevier;2009:chap 293.

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Volume 19, Number 3—March 2013 Armillifer armillatus Pentastomiasis in African Immigrant, Germany To the Editor: Pentastomiasis is a parasitic zoonotic disease with an incremental number of reported human infections caused by larval stages (nymphs) of pentastomes (1–3). The vermiform parasites are in their own phylum and are related to branchiuran crustaceans (2). Most human infections with these parasites are caused by Armillifer armillatus (2), a parasite endemic to western and central Africa. Most cases are reported from the Congo region and Nigeria, and occasionally infections in African immigrants to Europe and North America have been reported (4,5). Imported cases to Germany have not been reported. A. grandis, a related parasite from central Africa, has been rarely found (6), but A. moniliformis, a pentastome species from Asia, has recently reemerged and caused a human infection after ≈40 years in Malaysia (1). Adult Armillifer spp. inhabit the respiratory tract of large snakes (Python spp.). These dioecious parasites produce large amounts of ova that are shed into the environment by snake feces and secretions. When intermediate hosts, such as rodents or other small mammals, ingest ova, larvae hatch, migrate to the viscera, encyst, and molt several times (3). Humans become accidental intermediate hosts after uptake of environmental parasite ova or by consumption of contaminated snake meat. We report an infection with A. armillatus in an African immigrant to Germany that was diagnosed by histopathologic analysis and confirmed by PCR. In 2005, a 23-year-old man from Togo who had immigrated to Germany 3 years earlier showed development of acute myeloid leukemia. He subsequently underwent stem cell transplantation, which was followed by graft versus host disease. The patient died of sudden intracerebral hemorrhage and leukencephalopathy. His medical history also included α-thalassemia and a heterocygotous sickle cell trait, chronic hemolytic anemia, splenomegaly, and cardiomyopathy. He had been treated for schistosomiasis and filariasis. An autopsy specimen showed several living pentastome nymphs of ≈2 cm in size, which were found in the subscapular region of liver parenchyma. A presumptive diagnosis of visceral pentastomiasis caused by A. armillatus nymphs was made in accordance with the origin of the patient and the geographic distribution of the parasite. Microscopic slides from patient specimens were retrieved from an archive and reanalyzed (Figure, Technical Appendix Figure [PDF - 132 KB - 1 page]). A pentastome-specific PCR targeting the 18S rRNA gene (2,7) was conducted after DNA extraction from formalin-fixed tissue on a remaining unstained microscope slide. The resulting 383-bp amplicon was sequenced, and BLAST analysis (www.ncbi.nlm.hih.gov/blast) confirmed 100% identity with A. armillatus (GenBank accession no. HM756289.1) and 99% homology with A. agkistrodontis (FJ607339.1) and A. moniliformis (HM048870.1). Visceral pentastomiasis in humans is often asymptomatic and an incidental finding during surgery (1,3) or autopsy (8,9). In a large autopsy series from Malaysia, a pentastomiasis prevalence of 45.5% was found in adult Aborigines (8). In Nigeria, a rate of 33% was seen during autopsies of patients who had died of malignancies (9). However, a few severe and even lethal cases have been described for heavy A. armillatus and A. grandis infections in persons from Africa (4,6). Diagnosis is achieved by gross pathologic and histopathologic analyses. Nymphs are found in the serosa around the liver and spleen, in liver parenchyma, mesenterium, intestine wall, and abdominal lymph nodes. The lungs or pleura are occasionally infected (3). Radiographic analysis may show typical C-shaped chest or abdominal calcifications (10). Species identification is performed by counting annulations (A. armillatus 18–22, A. grandis >25) and measuring the size of larval parasites (3). Recently, PCR has been used for diagnosis in veterinary infections (2,7). For the patient in our study, molecular analysis identified human pentastomiasis by using a formalin-fixed microscope slide that had been stored for 7 years. A difference of 2 nt each was seen when the amplified nucleotide sequence was compared with database sequences of A. agkistrodontis and A. moniliformis. However, there is no database entry in GenBank for A. grandis, the geographically closest Armillifer species. Serologic assays have been developed for identification of A. armillatus (2), but no serum was available for retrospective analysis. In special settings, such as tropical snake farming and pet keeping, pentastomiasis may be a public health concern (2). However, most infections have been linked to consumption of undercooked snake meat or other snake products (1). Most immigrants who were given a diagnosis of visceral pentastomiasis were from Nigeria or the Congo region, and diagnoses were made after death. Molecular analysis is particularly valuable when only autoptic paraffin-embedded patient material is available. For industrialized countries, where experience in morphologic identification of unusual parasite species is limited, molecular analysis is a valuable diagnostic tool. Our case-patient constitutes a record of imported Armillifer species pentastomiasis to Germany. Because of increasing international migration, more cases of pentastomiasis are likely to be seen. - Latif B, Omar E, Heo CC, Othman N, Tappe D. Human pentastomiasis caused by Armillifer moniliformis in Malaysian Borneo. Am J Trop Med Hyg. 2011;85:878–81. - Tappe D, Meyer M, Oesterlein A, Jaye A, Frosch M, Schoen C, Transmission of Armillifer armillatus ova at snake farm, The Gambia, West Africa. Emerg Infect Dis. 2011;17:251–4. - Tappe D, Büttner DW. Diagnosis of human visceral pentastomiasis. PLoS Negl Trop Dis. 2009;3:e320. - Lavarde V, Fornes P. Lethal infection due to Armillifer armillatus (Porocephalida): a snake-related parasitic disease. Clin Infect Dis. 1999;29:1346–7. - Guardia SN, Sepp H, Scholten T, Morava-Protzner I. Pentastomiasis in Canada. Arch Pathol Lab Med. 1991;115:515–7. - Cagnard V, Nicolas-Randegger J, Dago Akribi A, Rain B, Nozais JP, Essoh Nomel P, Generalized and lethal pentastomiasis due to Armillifer grandis (Hett, 1915) [in French]. Bull Soc Pathol Exot. 1979;72:345–52. - Brookins MD, Wellehan JF, Roberts JF, Allison K, Curran SS, Childress AL, Massive visceral pentastomiasis caused by Porocephalus crotali in a dog. Vet Pathol. 2009;46:460–3. - Prathap K, Lau KS, Bolton JM. Pentastomiasis: a common finding at autopsy among Malaysian aborigines. Am J Trop Med Hyg. 1969;18:20–7 . - Smith JA, Oladiran B, Lagundoye SB. Pentastomiasis and malignancy. Ann Trop Med Parasitol. 1975;69:503–12. - Tiendrebeogo H, Levy D, Schmidt D. Human pentastomiasis in Abidjan. A report on 29 cases [in French]. Rev Fr Mal Respir. 1982;10:351–8 . Suggested citation for this article: Tappe D, Haeupler A, Schäfer H, Racz P, Cramer JP, Poppert S. Armillifer armillatus pentastomiasis in African immigrant, Germany [letter]. Emerg Infect Dis [Internet]. 2103 Mar [date cited]. http://dx.doi.org/10.3201/eid1903.121508 - Page created: January 31, 2013 - Page last updated: January 31, 2013 - Page last reviewed: January 31, 2013 - Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Office of the Director (OD)

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Dr. Uma Pradhan* Department of Pediatrics.* | Childhood Glaucoma is a very specialized and challenging subject. It requires accurate knowledge, lot of experience and skill to examine, diagnose and to treat a case of Childhood Glaucoma. It should be a joint endeavor of an ophthalmologist and pediatrician, since pediatrician can be of immense help in diagnosing the associated systemic disorder as well as in management. The objective of management of childhood glaucoma should be to normalize and control intraocular pressure permanently there by preventing loss of visual acuity, and to preserve visual field and ocular integrity and to stimulate the development of stereoscopic vision. Childhood Glaucoma can be broadly divided into two categories: |Salient Features of Childhood Glaucoma| - It is uncommon an average ophthalmologist is likely to see one case per five years - Early suspicion and diagnosis is important - Examination needs patience and skill - Impact on visual development can be extreme - Early effective therapy significantly improves visual future |Epidemiology of Congenital Glaucoma| |By definition if the onset is before the age of 3 years, it is called as congenital glaucoma. It is usually diagnosed by 6-12 months. The incidence is 1 in 30,000 births. It is an autosomal recessive disease with two linkages at chromosomes 2p and 1p. Gene on 2p is CYPIBI. 65% of all cases are male with 70% bilaterality. In primary childhood glaucoma, developmental anomalies like Iridodysgenesis, Familial Iris Hypoplasia, Aniridia, Anomalous iris vessels, Microcornea, Microspherophakia are present. Glaucoma associated with other congenital anomalies are present. - Sturge-Weber Syndrome - Glaucoma is present when upper lid is involved - Vascular tissue in ciliary body causes hyper secretion of aqueous and abnormal vessels in angle causes obstruction to aqueous flow - Marfans syndrome and Homocystinuria Ocular complications like pupil block due to dislocated lens cause glaucoma - Lowe's Syndrome - Glaucoma is caused by defective development of angle. Diagnosis is complicated by Microphathalmos and corneal haze. - Chromosomal defects - Broad thumb syndrome - Goldenhars sequence with associated Juvenile Glaucoma - Turner's syndrome - Rieger's syndrome |Secondary Glaucoma in Infants| - Persistent hyperplastic primary vitreous in which shallow AC, swollen lens with hemorrhage in AC is seen - Retinopathy of prematurity - Rubeosis (abnormal vessels) of angle causes glaucoma 1.Retinoblastoma-forward shift,inflammation and tumour cells in angle. |Photophobia, epiphora and blepharospasm is a classical triad which leads to the suspicion of congenital glaucoma. Enlargement of the eyeball along with clouding and enlargement of the cornea resembles an ox eye, hence called Buphthalmos, Inability to see could be other presenting symptom. Epiphora due to congenital dacryostenosis which is very common at this age should be differentiated. In congenital dacryostenosis, there is fullness of lachrymal sac, chronic purulent discharge and absence of photophobia. Baby constantly keeps it's eyes closed or when exposed to sunlight. To avoid pain and photophobia children bury their head in the pillow.| |Sequelae of raised Intraocular Pressure (IOP)| |Elevated IOP causes enlargement of the eyeball and stretching of tissues. Overall stretch causes progressive myopia. Sclerocorneal stretch causes big cornea with diameter more than 12 mm. Rupture of Descemet's membrane leading to stromal edema, Habb's striae, erosion, ulceration and permanent scarring can occur. Zonular stretch causes subluxation of lens.| |Examination includes external exam, corneal assessment, refraction, tonometry, slit lamp exam, gonioscopy, funduscopy, fundus photography and ultrasound biometry. Visual filed recording in children is not reliable, non reproducible due to short attention span and poor fixation. Ultrasound biometry is done to measure axial length which is 17.5 to 20 mm at birth and reaches to 22 mm by the age of 1 year. Corneal opacification and edema in children due to glaucoma needs to be differentiated from other conditions like sclerocornea, dermoid, corneal dystrophy, inflammations, trauma, anterior chamber cleavage syndrome, trisomy, mucopolysaccharidosis etc. |Intraocular Pressure Measurement| - Accurate IOP measurement is important but difficult and tricky in pediatric situation. - Indentation tonometry with schiotz tonometer is not ideal and is influenced by scleral rigidity and corneal curvature. - Handheld applanation tonometry is ideal in awake and co-operative child. - When IOP is to be measured under general anesthesia, we have to remember that, IOP should be recorded as soon as the child is quiet i.e., under light anesthesia. General anesthesia decreases IOP to variable amount where as ketamine increases IOP slightly. Double check with two instruments is advisable Halothane rapidly decreases IOP. Normal IOP in newborn under Halothane anesthesia is 9-10 mm Hg, 21 mm Hg remains useful upper limit. Gonioscopy with Koeppe 14-16 mm lens and Barken light or hand held microscope can be done to diagnose anomalies of angle of anterior Chamber. Funduscopy is important to determine optic disc cupping which occurs rapidly in childhood glaucoma. Disc in newborn is pink with small cup and C : D ratio is 0.3. Cup is often round, steep and enlarged in glaucoma. Drawings and photographs are useful for serial documentation. Differential diagnosis of glaucomatous cupping in children is congenital pit, coloboma oblique entry, tilting of disc, familial enlarged cup, physiological large cup. |Medical line of treatment has limited place and poor response. Lack of compliance and side effects are added difficulties. Medications are used briefly in pre-operative period for clearing the cornea and improving visualization during the surgery. Beta blockers such as timolol 0.25% or Betaxolol 0.25% may be administered every 12 hours. Prostaglandin analogues like Latanoprost or topical CAI like dorzolamide can be used 12 hourly. Brimonidine should be avoided as it may cause bradycardia, hypotension, apneic in infants. It is out of scope of this article to discuss surgical procedures in detail. Goniotomy, Trabeculotomy, combined Trabeculotomy with Trabeculectomy are the procedures which are preferred Visco-canalostomy or Visco-trabeculotomy are newer procedures. Follow up evaluation and longterm follow up and management is of crucial importance. |How to Cite URL :| |Pradhan U D.. Available From : http://www.pediatriconcall.com/fordoctor/ Conference_abstracts/report.aspx?reportid=173|

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In Depth: Gallbladder and Hepatic Portal System The gallbladder is a small, sac-like muscle that stores bile from the liver. It is located behind the liver. The liver produces bile continuously, but the body only needs it a few times a day. The excess sits in the hepatic and cystic ducts, which are connected to the gallbladder. When signaled, the gallbladder contracts and squeezes bile through the cystic duct and into the common bile duct. The most common ailment that affects the gallbladder is the formation gallstones, or cholelithiasis. These stones are often made up of substances found in bile, namely cholesterol. They can become lodged in the bile ducts and can cause extreme pain. The Hepatic Portal System The hepatic portal system is a series of veins that carry blood from the capillaries of the stomach, intestine, spleen, and pancreas to capillaries in the liver. It is part of the body’s filtration system. Its main function is to deliver de-oxygenated blood to the liver to be detoxified further before it returns to the heart. The hepatic portal system consists of: - Hepatic portal vein: This is the main vein connected to the liver. It forms at the connection of the inferior and superior mesenteric veins. - Inferior mesenteric vein: This vein takes blood from the colon and rectum and connects with the portal vein. - Superior mesenteric vein: This drains blood from the small intestine and connects with the hepatic portal vein. - Gastrosplenic vein: This tributary is formed by the union of the splenic vein from the spleen and the gastric vein from the stomach. It joins with the mesenteric vein inside the pancreas. The hepatic portal system is designed to rid the body of toxins, and it cannot detect those that are designed to help it. Some drugs must be taken under the tongue, through the skin, or via suppository to avoid entering the hepatic portal system and being prematurely metabolized in the liver before reaching general circulation.