query: an example of a type iii hypersensitivity is

pos: Type III hypersensitivity antibody aggregation, tissues that are associated with blood filtration at considerable osmotic and hydrostatic gradient (e.g. sites of urinary and synovial fluid formation, kidney glomeruli and joint tissues respectively) bear the brunt of the damage. Hence, vasculitis, glomerulonephritis and arthritis are commonly associated conditions as a result of type III hypersensitivity responses. As observed under methods of histopathology, acute necrotizing vasculitis within the affected tissues is observed concomitant to neutrophilic infiltration, along with notable eosinophilic deposition (fibrinoid necrosis). Often, immunofluorescence microscopy can be used to visualize the immune complexes. Skin response to a hypersensitivity of this type is referred to

pos: Immune complex Immune complexes may themselves cause illness when they are deposited in organs, for example, in certain forms of vasculitis. This is the third form of hypersensitivity in the Gell-Coombs classification, called type III hypersensitivity. Such hypersensitivity progressing to disease states produces the immune complex diseases. Immune complex deposition is a prominent feature of several autoimmune diseases, including systemic lupus erythematosus, cryoglobulinemia, rheumatoid arthritis, scleroderma and Sjögren's syndrome. Immune complex An immune complex, sometimes called an antigen-antibody complex, is a molecule formed from the integral binding of an antibody to a soluble antigen. The bound antigen and antibody act as a

pos: Arthus reaction fibrinoid necrosis with ischemia-aggravating thrombosis in the tissue vessel walls. The end result is a localized area of redness and induration that typically lasts a day or so. Arthus reactions have been infrequently reported after vaccinations containing diphtheria and tetanus toxoid. The CDC's description: Arthus reactions (type III hypersensitivity reactions) are rarely reported after vaccination and can occur after tetanus toxoid–containing or diphtheria toxoid–containing vaccines. An Arthus reaction is a local vasculitis associated with deposition of immune complexes and activation of complement. Immune complexes form in the setting of high local concentration of vaccine antigens and high circulating antibody concentration.

pos: Drug eruption Some of the most severe and life-threatening examples of drug eruptions are erythema multiforme, Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), hypersensitivity vasculitis, drug induced hypersensitivity syndrome (DIHS), erythroderma and acute generalized exanthematous pustulosis (AGEP). These severe cutaneous drug eruptions are categorized as hypersensitivity reactions and are immune-mediated. There are four types of hypersensitivity reactions and many drugs can induce one or more hypersensitivity reactions. The most common type of eruption is a morbilliform (resembling measles) or erythematous rash (approximately 90% of cases). Less commonly, the appearance may also be urticarial, papulosquamous, pustular, purpuric, bullous (with blisters) or lichenoid. Angioedema

pos: Arthus reaction the in situ formation of antigen/antibody complexes after the intradermal injection of an antigen. If the animal/patient was previously sensitized (has circulating antibody), an Arthus reaction occurs. Typical of most mechanisms of the type III hypersensitivity, Arthus manifests as local vasculitis due to deposition of IgG-based immune complexes in dermal blood vessels. Activation of complement primarily results in cleavage of soluble complement proteins forming C5a and C3a, which activate recruitment of PMNs and local mast cell degranulation (requiring the binding of the immune complex onto FcγRIII), resulting in an inflammatory response. Further aggregation of immune complex-related processes induce a local

pos: Glomerulonephritis developing shunt nephritis, which frequently produces MGN. Microscopically, MGN is characterized by a thickened glomerular basement membrane without a hyperproliferation of the glomerular cells. Immunofluorescence demonstrates diffuse granular uptake of IgG. The basement membrane may completely surround the granular deposits, forming a "spike and dome" pattern. Tubules also display the symptoms of a typical Type III hypersensitivity reaction, which causes the endothelial cells to proliferate, which can be seen under a light microscope with a PAS stain. Prognosis follows the rule of thirds: one-third remain with MGN indefinitely, one-third remit, and one-third progress to end-stage kidney failure. As the glomerulonephritis

neg: Type III hypersensitivity Type III hypersensitivity Type III hypersensitivity occurs when there is accumulation of immune complexes (antigen-antibody complexes) that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and attraction of leukocytes. Such reactions may progress to immune complex diseases. Type III hypersensitivity occurs when there is an excess of antigen, leading to small immune complexes being formed that fix complement and are not cleared from the circulation. It involves soluble antigens that are not bound to cell surfaces (as opposed to those in type II hypersensitivity). When these antigens bind antibodies, immune complexes of different

neg: Type III hypersensitivity as an Arthus reaction, and is characterized by local erythema and some induration. Platelet aggregation, especially in microvasculature, can cause localized clot formation, leading to blotchy hemorrhages. This typifies the response to injection of foreign antigen sufficient to lead to the condition of serum sickness. Some clinical examples: Other examples are: Type III hypersensitivity Type III hypersensitivity occurs when there is accumulation of immune complexes (antigen-antibody complexes) that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and attraction of leukocytes. Such reactions may progress to immune complex diseases. Type III hypersensitivity occurs when

neg: Type I hypersensitivity the entire body is involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal. Some examples: Type I hypersensitivity Type I hypersensitivity (or immediate hypersensitivity) is an allergic reaction provoked by reexposure to a specific type of antigen referred to as an allergen. Type I is not to be confused with type II, type III, or type IV hypersensitivities, nor is it to be confused with Type I Diabetes or Type I of any other disease or reaction. Exposure may be by ingestion, inhalation, injection, or direct contact. In type 1 hypersensitivity, B-cells are

neg: Type I hypersensitivity Type I hypersensitivity Type I hypersensitivity (or immediate hypersensitivity) is an allergic reaction provoked by reexposure to a specific type of antigen referred to as an allergen. Type I is not to be confused with type II, type III, or type IV hypersensitivities, nor is it to be confused with Type I Diabetes or Type I of any other disease or reaction. Exposure may be by ingestion, inhalation, injection, or direct contact. In type 1 hypersensitivity, B-cells are stimulated (by CD4+TH2 cells) to produce IgE antibodies specific to an antigen. The difference between a normal infectious immune response and a

neg: Hypersensitivity pneumonitis present within or outside granulomas. In addition, many patients have hypoxemia at rest, and all patients desaturate with exercise. Hypersensitivity pneumonitis involves inhalation of an antigen. This leads to an exaggerated immune response (hypersensitivity). Type III hypersensitivity and type IV hypersensitivity can both occur depending on the cause. The diagnosis is based upon a history of symptoms after exposure to the allergen and clinical tests. A physician may take blood tests, seeking signs of inflammation, a chest X-ray and lung function tests. The sufferer shows a restrictive loss of lung function. Precipitating IgG antibodies against fungal or avian antigens can

neg: Type II hypersensitivity Type II hypersensitivity In type II hypersensitivity (also tissue-specific, or cytotoxic hypersensitivity) the antibodies produced by the immune response bind to antigens on the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self" antigen, innately part of the patient's cells) or extrinsic (adsorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen. An example of type II hypersensitivity

neg: Arthus reaction Arthus reactions are characterized by severe pain, swelling, induration, edema, hemorrhage, and occasionally by necrosis. These symptoms and signs usually occur 4–12 hours after vaccination. ACIP has recommended that persons who experienced an Arthus reaction after a dose of tetanus toxoid–containing vaccine should not receive Td more frequently than every 10 years, even for tetanus prophylaxis as part of wound management. Arthus reaction In immunology, the Arthus reaction () is a type of local type III hypersensitivity reaction. Type III hypersensitivity reactions are immune complex-mediated, and involve the deposition of antigen/antibody complexes mainly in the vascular walls, serosa (pleura, pericardium,

neg: Severe cutaneous adverse reactions benign morbilliform rash hypersensitivity drug reactions such as MPR. However, they also include more serious reactions: a) pseudo-allergic reactions in which a drug directly stimulates mast cells, basophils, and/or eosinophils to release pro-allergic mediators (e.g. histamine); b) Type I, Type II, and Type III hypersensitivity reactions of the adaptive immune system mediated by IgE, IgG, and/or IgM antibodies; and c) SCARs and MPR which are Type IV hypersensitivity reactions of the innate immune system initiated by lymphocytes of the T cell type and mediated by various types of leukocytes and cytokines. Type IV hypersensitivity reactions are off-target drug reactions, i.e.

neg: Type II hypersensitivity cells. Type II hypersensitivity In type II hypersensitivity (also tissue-specific, or cytotoxic hypersensitivity) the antibodies produced by the immune response bind to antigens on the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self" antigen, innately part of the patient's cells) or extrinsic (adsorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen. An example of type II

neg: Immune system and IgM antibodies. Immune complexes (aggregations of antigens, complement proteins, and IgG and IgM antibodies) deposited in various tissues trigger Type III hypersensitivity reactions. Type IV hypersensitivity (also known as cell-mediated or "delayed type hypersensitivity") usually takes between two and three days to develop. Type IV reactions are involved in many autoimmune and infectious diseases, but may also involve "contact dermatitis" (poison ivy). These reactions are mediated by T cells, monocytes, and macrophages. Inflammation is one of the first responses of the immune system to infection, but it can appear without known cause. Inflammation is produced by eicosanoids and cytokines,

neg: Arthus reaction Arthus reaction In immunology, the Arthus reaction () is a type of local type III hypersensitivity reaction. Type III hypersensitivity reactions are immune complex-mediated, and involve the deposition of antigen/antibody complexes mainly in the vascular walls, serosa (pleura, pericardium, synovium), and glomeruli. This reaction is usually encountered in experimental settings following the injection of antigens. The Arthus reaction was discovered by Nicolas Maurice Arthus in 1903. Arthus repeatedly injected horse serum subcutaneously into rabbits. After four injections, he found that there was edema and that the serum was absorbed slowly. Further injections eventually led to gangrene. The Arthus reaction involves

neg: Serum sickness an alternate antitoxin if it's appropriate or continue with prophylactic measures. Serum sickness Serum sickness in humans is a reaction to proteins in antiserum derived from a non-human animal source, occurring 5–10 days after exposure. It is a type of hypersensitivity, specifically immune complex hypersensitivity (type III). The term serum sickness–like reaction (SSLR) is occasionally used to refer to similar illnesses that arise from the introduction of certain non-protein substances, such as penicillin. It was first characterized by Clemens von Pirquet and Béla Schick in 1906. When an antiserum is given, the human immune system can mistake the proteins present

neg: Type II hypersensitivity autoimmune hemolytic anemia and acetylcholine receptors in myasthenia gravis. Another example of type II hypersensitivity reaction is Goodpasture's syndrome where the basement membrane (containing collagen type IV) in the lung and kidney is attacked by one's own antibodies. Another form of type II hypersensitivity results from misdirected antibody-dependent cell-mediated cytotoxicity (ADCC). Here, native cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by natural killer cells (NK) and macrophages (recognised via IgG bound (via the Fc region) to the effector cell surface receptor, CD16 (FcγRIII)), which in turn kill these tagged

neg: Penicillin neurotoxicity, urticaria, and superinfection (including candidiasis). Infrequent adverse effects (0.1–1% of people) include fever, vomiting, erythema, dermatitis, angioedema, seizures (especially in people with epilepsy), and pseudomembranous colitis. Penicillin can also induce serum sickness or a serum sickness-like reaction in some individuals. Serum sickness is a type III hypersensitivity reaction that occurs one to three weeks after exposure to drugs including penicillin. It is not a true drug allergy, because allergies are type I hypersensitivity reactions, but repeated exposure to the offending agent can result in an anaphylactic reaction. Anaphylaxis will occur in approximately 0.01% of patients. Pain and inflammation at

neg: Inflammation because urethral microbial invasion is the most common cause of urethritis. It is useful to differentiate inflammation and infection as there are many pathological situations where inflammation is not driven by microbial invasion – for example, atherosclerosis, type III hypersensitivity, trauma, and ischemia. There are also pathological situations where microbial invasion does not result in classic inflammatory response—for example, parasitosis, eosinophilia. Acute inflammation is a short-term process, usually appearing within a few minutes or hours and begins to cease upon the removal of the injurious stimulus. It involves a coordinated and systemic mobilization response locally of various immune, endocrine and

neg: Serum sickness Serum sickness Serum sickness in humans is a reaction to proteins in antiserum derived from a non-human animal source, occurring 5–10 days after exposure. It is a type of hypersensitivity, specifically immune complex hypersensitivity (type III). The term serum sickness–like reaction (SSLR) is occasionally used to refer to similar illnesses that arise from the introduction of certain non-protein substances, such as penicillin. It was first characterized by Clemens von Pirquet and Béla Schick in 1906. When an antiserum is given, the human immune system can mistake the proteins present for harmful antigens. The body produces antibodies, which combine with these

neg: Hapten groups present, one of the two main strategies could be employed: Hapten inhibition or "semi-hapten" is the inhibition of a type III hypersensitivity response. In inhibition, free hapten molecules bind with antibodies toward that molecule without causing the immune response, leaving fewer antibodies left to bind to the immunogenic hapten-protein adduct. An example of a "hapten inhibitor" is dextran 1, which is a small fraction (1 kilodalton) of the entire dextran complex, which is enough to bind anti-dextran antibodies, but insufficient to result in the formation of immune complexes and resultant immune responses. Hapten Haptens are minute molecules that elicit

neg: Immune system that damages the body's own tissues. They are divided into four classes (Type I – IV) based on the mechanisms involved and the time course of the hypersensitive reaction. Type I hypersensitivity is an immediate or anaphylactic reaction, often associated with allergy. Symptoms can range from mild discomfort to death. Type I hypersensitivity is mediated by IgE, which triggers degranulation of mast cells and basophils when cross-linked by antigen. Type II hypersensitivity occurs when antibodies bind to antigens on the patient's own cells, marking them for destruction. This is also called antibody-dependent (or cytotoxic) hypersensitivity, and is mediated by IgG

neg: Rheumatoid arthritis can be seen as a form of Type III hypersensitivity. As of 1999, if TNF release is stimulated by T cell products such as interleukin-17 it might be closer to type IV hypersensitivity although this terminology may be getting somewhat dated and unhelpful. Although TNF appears to be the dominant chemical mediator other cytokines are involved in inflammation in RA, because blocking TNF does not benefit all persons and all tissues, particularly lung disease and nodules may get worse. Blocking IL-1, IL-15 and IL-6 have beneficial effects and IL-17 may be important. X-rays of the hands and feet are generally

neg: Hypersensitivity Hypersensitivity Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity. They are usually referred to as an over-reaction of the immune system and these reactions may be damaging, uncomfortable, or occasionally fatal. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. They are classified in four groups after the proposal of P. G. H. Gell and Robin Coombs in 1963. This is an additional type that is sometimes (especially in the UK) used as a distinction from Type 2. Instead of binding to cell surfaces, the antibodies

neg: Allergic bronchopulmonary aspergillosis E, or IgE) and a type III hypersensitivity response (with formation of immunoglobulin G, or IgG). The reaction of IgE with "Aspergillus" antigens results in mast cell degranulation with bronchoconstriction and increased capillary permeability. Immune complexes (a type III reaction) and inflammatory cells are deposited within the mucous membranes of the airways, leading to necrosis (tissue death) and eosinophilic infiltration. Type 2 T helper cells appear to play an important role in ABPA due to an increased sensitivity to interleukin (IL) 4 and IL-5. These cytokines up-regulate mast cell degranulation, exacerbating respiratory decline. "Aspergillus" also utilises a number of factors

neg: MELISA metal sensitivity in metal-sensitive patients. A MELISA test measures a so-called type-IV delayed hypersensitivity reaction. In contrast to a type-I allergy, which is mediated by IgE antibodies and is often tested using an ELISA test, a type-IV hypersensitivity reaction is mediated by T-lymphocytes (or memory lymphocytes) that have had prior contact with a given allergen. In genetically predisposed individuals, an ongoing everyday exposure to allergens can induce the type-IV hypersensitivity with a resulting allergic reaction. The test procedure is a cell culture and requires live memory lymphocytes. Lymphocytes are isolated and cultured in an incubator for five days. A portion

neg: Rabeprazole meaningful. Rabeprazole is contraindicated in the following populations and situations: An allergy to a PPI like rabeprazole may take the form of type I hypersensitivity or delayed hypersensitivity reactions. A selective (pattern C—see below for a discussion of cross-reactivity patterns) type I hypersensitivity reaction to rabeprazole resulting in anaphylaxis has been reported, as well as several whole group hypersentivities. Hypersensitivity to PPIs can take the form of whole group hypersensitivity, pattern A, B, or C. Whole group hypersentivity occurs when a person is cross-reactive to all PPIs; that is, all PPIs will induce the allergy. In pattern A, a person

neg: Farmer's lung have set in. This disease is most prevalent in damp climates. Farmer's lung Farmer's lung (not to be confused with silo-filler's disease) is a hypersensitivity pneumonitis induced by the inhalation of biologic dusts coming from hay dust or mold spores or any other agricultural products. It results in a type III hypersensitivity inflammatory response and can progress to become a chronic condition which is considered potentially dangerous. These symptoms develop between four and eight hours after exposure to the antigens. In acute attacks, the symptoms mimic pneumonia or flu. In chronic attacks, there is a possibility of the victim going

neg: Farmer's lung Farmer's lung Farmer's lung (not to be confused with silo-filler's disease) is a hypersensitivity pneumonitis induced by the inhalation of biologic dusts coming from hay dust or mold spores or any other agricultural products. It results in a type III hypersensitivity inflammatory response and can progress to become a chronic condition which is considered potentially dangerous. These symptoms develop between four and eight hours after exposure to the antigens. In acute attacks, the symptoms mimic pneumonia or flu. In chronic attacks, there is a possibility of the victim going into shock and dying from the attack. Permanent lung damage can

neg: Hypersensitivity recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling. Some clinical examples: <br> The use of Type 5 is rare. These conditions are more frequently classified as Type 2, though sometimes they are specifically segregated into their own subcategory of Type 2. Hypersensitivity Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity. They are usually referred to as an over-reaction of the immune system and these reactions may

neg: Type IV hypersensitivity Type IV hypersensitivity Type 4 hypersensitivity is often called delayed type hypersensitivity as the reaction takes several days to develop. Unlike the other types, it is not antibody-mediated but rather is a type of cell-mediated response. CD4+ T1 helper T cells recognize foreign antigen in a complex with the MHC class II major histocompatibility complex on the surface of antigen-presenting cells. These can be macrophages that secrete IL-12, which stimulates the proliferation of further CD4+ T1 cells. CD4+ T cells secrete IL-2 and interferon gamma, inducing the further release of other T1 cytokines, thus mediating the immune response. Activated CD8+

neg: Type IV hypersensitivity with IFN-gamma, the macrophages become capable of killing "M. tuberculosis" by forming phagolysosomes and nitric oxide radicals. The hyper-activated macrophages secrete TNF-α which recruits multiple monocytes to the site of infection. These cells differentiate into epithelioid cells which wall off the infected cells, but results in significant inflammation and local damage. Some other clinical examples: Type IV hypersensitivity Type 4 hypersensitivity is often called delayed type hypersensitivity as the reaction takes several days to develop. Unlike the other types, it is not antibody-mediated but rather is a type of cell-mediated response. CD4+ T1 helper T cells recognize foreign antigen in

neg: Mosquito common to all mosquito species, whereas others are specific to certain species. There are both immediate hypersensitivity reactions (types I and III) and delayed hypersensitivity reactions (type IV) to mosquito bites. Both reactions result in itching, redness and swelling. Immediate reactions develop within a few minutes of the bite and last for a few hours. Delayed reactions take around a day to develop, and last for up to a week. Several anti-itch medications are commercially available, including those taken orally, such as diphenhydramine, or topically applied antihistamines and, for more severe cases, corticosteroids, such as hydrocortisone and triamcinolone. A common

neg: Solar urticaria can range from 320–400 nm. The wavelength range of type III and IV spans from 400 to 500 nm, while type V can be caused by UVB radiation to visible light (280–600 nm). Type VI has only been known to occur at 400 nm. Another classification distinguishes two types. The first is a hypersensitivity caused by a reaction to photoallergens located only in people with SU; while the second is caused by photoallergens that can be found in both people with SU and people without it. A subgroup of solar urticaria, fixed solar urticaria, has also been identified. It is

neg: Drug eruption human adult is exposed to a large number of drugs over longer treatment periods throughout a lifetime. This unprecedented rise in pharmaceutical use has led to an increasing number of observed adverse drug reactions. There are two broad categories of adverse drug reactions. Type A reactions are known side effects of a drug that are largely predictable and are called, pharmatoxicologic. Whereas Type B or hypersensitivity reactions, are often immune-mediated and reproducible with repeated exposure to normal dosages of a given drug. Unlike type A reactions, the mechanism of type B or hypersensitivity drug reactions is not fully elucidated. However,

neg: Subacute bacterial endocarditis Brooklyn Jewish Hospital was the first to successfully treat subacute bacterial endocarditis with penicillin. Loewe reported at the time seven cases of subacute bacterial endocarditis in 1944. Subacute bacterial endocarditis Subacute bacterial endocarditis (also called endocarditis lenta) is a type of endocarditis (more specifically, infective endocarditis). Subacute bacterial endocarditis can be considered a form of type III hypersensitivity. Among the signs of subacute bacterial endocarditis are: It is usually caused by a form of streptococci viridans bacteria that normally live in the mouth ("Streptococcus mutans, mitis, sanguis "or "milleri"). Other strains of streptococci can also cause subacute endocarditis, streptococcus intermedius:

neg: Subacute bacterial endocarditis Subacute bacterial endocarditis Subacute bacterial endocarditis (also called endocarditis lenta) is a type of endocarditis (more specifically, infective endocarditis). Subacute bacterial endocarditis can be considered a form of type III hypersensitivity. Among the signs of subacute bacterial endocarditis are: It is usually caused by a form of streptococci viridans bacteria that normally live in the mouth ("Streptococcus mutans, mitis, sanguis "or "milleri"). Other strains of streptococci can also cause subacute endocarditis, streptococcus intermedius: acute and subacute infection (causes about 15% of cases pertaining to infective endocarditis). Additional enterococci (urinary tract infections) and coagulase negative staphylococci can also be causative agents.

neg: Type I hypersensitivity type 1 hypersensitivity response is that in type 1 hypersensitivity, the antibody is IgE instead of IgA, IgG, or IgM. During sensitization, the IgE antibodies bind to FcεRI receptors on the surface of tissue mast cells and blood basophils. Mast cells and basophils coated by IgE antibodies are "sensitized". Later exposure to the same allergen cross-links the bound IgE on sensitized cells, resulting in anaphylactic degranulation, which is the immediate and explosive release of pharmacologically active pre-formed mediators from storage granules and concurrent synthesis of inflammatory lipid mediators from arachidonic acid; some of these mediators include histamine, leukotriene (LTC4 and

neg: Booster dose or determine the prevalence of the disease in vaccinated populations. If a patient receives a booster dose but already has a high level of antibody, then a reaction called an Arthus reaction could develop, a localized form of Type III hypersensitivity induced by high levels of IgG antibodies causing inflammation. The inflammation is often self-resolved over the course of a few days, but could be avoided altogether by increasing the length of time between the primary vaccine and the booster dose. It is not yet fully clear why some vaccines such as hepatitis A and B are effective for life,

neg: Allergy second injections. Pirquet called this phenomenon "allergy" from the Ancient Greek words ἄλλος "allos" meaning "other" and ἔργον "ergon" meaning "work". All forms of hypersensitivity used to be classified as allergies, and all were thought to be caused by an improper activation of the immune system. Later, it became clear that several different disease mechanisms were implicated, with the common link to a disordered activation of the immune system. In 1963, a new classification scheme was designed by Philip Gell and Robin Coombs that described four types of hypersensitivity reactions, known as Type I to Type IV hypersensitivity. With this

neg: Cochliobolus lunatus that the underlying disease is controlled, and immune modulators such as granulocyte-macrophage colony-stimulating factor and gamma interferon can be indicated when surgery or antifungals are not feasible alternatives. Allergic fungal manifestations include asthma, rhinitis, sinusitis and bronchopulmonary mycoses caused by a variety of etiological fungal agents including "C. lunatus". These agents provoke humoral immune responses, characterized by type I (immediate) and type III (immune complex mediated) hypersensitivity reactions. Prevalence of these diseases among the atopic population is 20-30 % and 6% in the general population. Allergic rhinitis, more commonly known as hay fever, is less frequently encountered in clinic compared

neg: Systemic lupus erythematosus will now produce antibodies against these nuclear-related proteins. These antibodies clump into antibody-protein complexes which stick to surfaces and damage blood vessels in critical areas of the body, such as the glomeruli of the kidney; these antibody attacks are the cause of SLE. Researchers are now identifying the individual genes, the proteins they produce, and their role in the immune system. Each protein is a link on the autoimmune chain, and researchers are trying to find drugs to break each of those links. SLE is a chronic inflammatory disease believed to be a type III hypersensitivity response with potential type

neg: Experimental autoimmune encephalomyelitis onset. Since the discovery of the four lucchinetti patterns, new EAE models have been published, specifically mimicking the patterns I and II. DTH-EAE for pattern I (T cell and macrophage-mediated delayed-type hypersensitivity) and fMOG-EAE for pattern II (antibody-mediated focal myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalitis) Also a model for pattern III lesions has been developed in which mitochondrial metabolism is impaired, resulting in a tissue energy deficiency, a mechanism later termed “virtual hypoxia”. The demyelination, characterized by loss of myelin-associated glycoprotein, has been described as “hypoxia-like”. Thanks to these pattern III models some specific experimental treatments have appeared The model

neg: Allergic contact dermatitis primes and sensitizes the immune system for an allergic response, and an "elicitation phase", in which this response is triggered. As it involves a cell-mediated allergic response, ACD is termed a Type IV delayed hypersensitivity reaction, making it an exception in the usage of the designation "allergic," which otherwise usually refers to type I hypersensitivity reactions. Contact allergens are essentially soluble haptens (low in molecular weight) and, as such, have the physico-chemical properties that allow them to cross the stratum corneum of the skin. They can only cause their response as part of a complete antigen, involving their association with

neg: Gemtuzumab ozogamicin of stem cells. Common side effects of administration included shivering, fever, nausea and vomiting. Serious side effects included severe myelosuppression (suppressed activity of bone marrow, which is involved in formation of various blood cells [found in 98% of patients]), disorder of the respiratory system, tumor lysis syndrome, Type III hypersensitivity, venous occlusion, and death. Gemtuzumab ozogamicin was created in a collaboration between Celltech and Wyeth that began in 1991. The same collaboration later produced inotuzumab ozogamicin. Celltech was acquired by UCB in 2004 and Wyeth was acquired by Pfizer in 2009. In the United States, it was approved under an

neg: Type III hypersensitivity the action of cleaved complement anaphylotoxins C3a and C5a, which, respectively, mediate the induction of granule release from mast cells (from which histamine can cause urticaria), and recruitment of inflammatory cells into the tissue (mainly those with lysosomal action, leading to tissue damage through frustrated phagocytosis by PMNs and macrophages). The reaction can take hours, days, or even weeks to develop, depending on whether or not there is immunological memory of the precipitating antigen. Typically, clinical features emerge a week following initial antigen challenge, when the deposited immune complexes can precipitate an inflammatory response. Because of the nature of the

neg: Stevens–Johnson syndrome IV, subtype IVc, delayed hypersensitivity reaction dependent in part on the tissue-injuring actions of natural killer cells. This contrasts with the other types of SCARs disorders, i.e. The DRESS syndrome which is a Type IV, Subtype IVb, hypersensitivity drug reaction dependent in part on the tissue-injuring actions of eosinophils and acute generalized exanthematous pustulosis which is a Type IV, subtype IVd, hypersensitivity reaction dependent in part on the tissue-injuring actions of neutrophils. Like other SCARs-inducing drugs, SJS-inducing drugs or their metabolites stimulate CD8 T cells or CD4 T cells to initiate autoimmune responses. Studies indicate that the mechanism by which

neg: Serum sickness–like reaction subsides. Serum sickness–like reaction is named for its clinical similarity to serum sickness, in which immune complexes are deposited in the skin, joints, and other organs. True serum sickness, a type III hypersensitivity reaction, results in fever, lymphadenopathy, arthralgias, cutaneous eruptions, gastrointestinal disturbances, proteinuria, and significant decreases in serum complement levels; it was originally described after patients were infused with equine immunoglobulins. In contrast, serum sickness–like reactions are specific drug reactions that are not associated with circulating immune complexes. Although the exact pathogenesis is poorly understood, serum sickness–like reactions are thought to originate from an abnormal inflammatory reaction that occurs

neg: Group A streptococcal infection throat or a streptococcal skin infection. It is classified as a type III hypersensitivity reaction. Symptoms of PSGN develop within 10 days following a strep throat or 3 weeks following a GAS skin infection. PSGN involves inflammation of the kidney. Symptoms include pale skin, lethargy, loss of appetite, headache, and dull back pain. Clinical findings may include dark-colored urine, swelling of different parts of the body (edema), and high blood pressure. Treatment of PSGN consists of supportive care. A subset of children with acute, rapid-onset of tic disorders and obsessive compulsive disorder (OCD) are hypothesized to be due to an

neg: Type III hypersensitivity sizes form. Large complexes can be cleared by macrophages but macrophages have difficulty in the disposal of small immune complexes. These immune complexes insert themselves into small blood vessels, joints, and glomeruli, causing symptoms. Unlike the free variant, a small immune complex bound to sites of deposition (like blood vessel walls) are far more capable of interacting with complement; these medium-sized complexes, formed in the slight excess of antigen, are viewed as being highly pathogenic. Such depositions in tissues often induce an inflammatory response, and can cause damage wherever they precipitate. The cause of damage is as a result of

neg: Dogger Bank itch live in colonies. "A. diaphanum" is a gelatinous, smooth, sponge-like colony up to long, growing on rocks and shells from lower shore down to approximately ; superficially, they resemble seaweed. The distribution of this animal is from the North Sea to the Mediterranean. The disease is especially prevalent among trawlermen working in the Dogger Bank, an important fishing bank in the North Sea. It has also been reported from the Baie de la Seine in France. The rash is caused by a type of cell-mediated hypersensitivity reaction; this type of hypersensitivity normally occurs in people who become sensitized to volatile

neg: Serum sickness–like reaction clearly defined in the literature, discontinuation of the suspected agent combined with use of antihistamines and corticosteroids for symptom control is an appropriate therapeutic route. Case reports have shown that treatment with prednisone, 60 mg daily, and high doses of H1 and H2 antihistamines help resolve the arthralgias and myalgias within 24 hours and the remaining symptoms within 48–72 hours Serum sickness–like reaction Serum sickness–like reactions (SSLRs) refer to adverse reactions that have symptoms similar to those of serum sickness (type III immune complex hypersensitivity) but in which immune complexes are not found. Agents that have been implicated in serum

neg: Hypersensitivity pneumonitis be detected in the laboratory using the traditional Ouchterlony immunodiffusion method wherein 'precipitin' lines form on agar plate. The ImmunoCAP technology has replaced this time consuming, labor-intensive method with their automated CAP assays and FEIA (Fluorescence enzyme immunoassay) that can detect IgG antibodies against Aspergillus fumigatus (Farmer's lung or for ABPA) or avian antigens (Bird Fancier's Lung). Although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it is not restricted to only occupational exposure, and that asthma generally is classified as a type I hypersensitivity. Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than

neg: Allergy that more correctly corresponds to a type IV hypersensitivity reaction. In type IV hypersensitivity, there is activation of certain types of T cells (CD8+) that destroy target cells on contact, as well as activated macrophages that produce hydrolytic enzymes. Effective management of allergic diseases relies on the ability to make an accurate diagnosis. Allergy testing can help confirm or rule out allergies. Correct diagnosis, counseling, and avoidance advice based on valid allergy test results reduces the incidence of symptoms and need for medications, and improves quality of life. To assess the presence of allergen-specific IgE antibodies, two different methods can

neg: Dermatitis return. The type of dermatitis is generally determined by the person's history and the location of the rash. For example, irritant dermatitis often occurs on the hands of people who frequently get them wet. Allergic contact dermatitis occurs upon exposure to an allergen, causing a hypersensitivity reaction in the skin. Treatment of atopic dermatitis is typically with moisturizers and steroid creams. The steroid creams should generally be of mid- to high strength and used for less than two weeks at a time as side effects can occur. Antibiotics may be required if there are signs of skin infection. Contact dermatitis

neg: Anti-neutrophil cytoplasmic antibody in autoimmune diseases – the classical example in post group A streptococcal rheumatic heart disease, where there is similarity between M proteins of "Streptococcus pyogenes" to cardiac myosin and laminin. It has also been shown that up to 70% of patients with granulomatosis with polyangiitis (previously known as Wegener's granulomatosis) are chronic nasal carriers of "Staphylococcus aureus", with carriers having an eight times increased risk of relapse. This would therefore be considered a type II hypersensitivity reaction. Neutrophil apoptosis, or programmed cell death, is vital in controlling the duration of the early inflammatory response, thus restricting damage to tissues by

neg: Bisulfite common additives to the drug epinephrine in order to prevent its oxidation to adrenochrome and resulting inactivation. Bisulfites can sometimes cause an allergic reaction. This is different from the common sulfa drugs allergy. The quantity of bisulfite in medical pain blockers that initiates Type 1 hypersensitivity has been determined by Fraser and Huang. Bisulfite Bisulfite ion (IUPAC-recommended nomenclature: hydrogen sulfite) is the ion HSO. Salts containing the HSO ion are termed bisulfites also known as sulfite lyes. For example, sodium bisulfite is NaHSO. Some evidence may suggest that the proton in bisulfite ion is located on sulfur, giving rise to

neg: Acute generalized exanthematous pustulosis drug-induced SCARs disorders, AGEP is a type IV hypersensitivity reaction in which a drug or its metabolite stimulates cytotoxic T cells (i.e. CD8 T cells) or T helper cells (i.e. CD4 T cells) to initiate autoimmune reactions that attack self tissues. SCARs are type IV, subtype IVb (DRESS syndrome), type IV, subtype IVc (SJS, SJS/TEN, TEN), or type IV, subtype IVd (AGEP) hypersensitivity reactions. AGEP therefore differs from the other SCARs disorders in that it involves the tissue-injuring action of inappropriately activated neutrophils and the excessive production of cytokines which stimulate production of, recruit to tissues, and/or activation of neutrophils

neg: Atopy allergies. Atopy may appear associated with an undiagnosed non-celiac gluten sensitivity. Atopic syndrome can be fatal for those who experience serious allergic reactions, such as anaphylaxis, brought on by reactions to food or environment. The individual components of atopy are all caused at least in part by allergy (type I hypersensitivity reactions). Therefore, atopic responses appear after the body is exposed to various allergens, for example pollen, dander, dust mites, certain foods, or chemical/physical irritants. Although atopy has various definitions, in general, it is defined by the presence of elevated levels of total and allergen-specific IgE in the serum, leading

neg: Serum sickness–like reaction Serum sickness–like reaction Serum sickness–like reactions (SSLRs) refer to adverse reactions that have symptoms similar to those of serum sickness (type III immune complex hypersensitivity) but in which immune complexes are not found. Agents that have been implicated in serum sickness–like reactions include cefaclor, amoxicillin, sulfonamides, tetracyclines, ciprofloxacin, nonsteroidal anti-inflammatory drugs, barbiturates, carbamazepine, propranolol, thiouracil, and allopurinol. Metabolites of these drugs might bind with tissue proteins inappropriately, eliciting an acute inflammatory response that typically develops 7–14 days after initiation of the offending agent. Acute hepatitis B will sometimes be complicated with this syndrome, often resolving as soon as the jaundice

neg: Type I hypersensitivity LTD4 and LTB4), and prostaglandin, which act on proteins (e.g., G-protein coupled receptors) located on surrounding tissues. The principal effects of these products are vasodilation and smooth-muscle contraction. Type 1 hypersensitivity can be further classified into immediate and late-phase reactions. The immediate hypersensitivity reaction occurs minutes after exposure and includes release of vasoactive amines and lipid mediators, whereas the late-phase reaction occurs 2–4 hours after exposure and includes the release of cytokines. The reaction may be either local or systemic. Symptoms vary from mild irritation to sudden death from anaphylactic shock. Treatment usually involves adrenaline (epinephrine), antihistamines, and corticosteroids. If

neg: Fibrinoid necrosis necrosis is a special form of necrosis usually seen in immune reactions involving blood vessels, known as Type III hypersensitivity reactions. This pattern of necrosis typically occurs when complexes of antigens and antibodies are deposited in the walls of arteries. Deposits of these immune complexes, together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologists. Ultimately, in the living patient most necrotic cells and their contents disappear by phagocytosis of the debris and enzymatic digestion by leukocytes. If necrotic cells and cellular debris are not

neg: Glybuzole used to treat diabetes type 1, because they are ineffective if insulin production is inhibited, in such cases as diabetes type 1 and post-pancreatectomy. The main side effects of glybuzole and other sulphonylureas are induction of hypoglycaemia, weight gain, abdominal upset, headache, and hypersensitivity reactions. Hypoglycaemia is mainly caused by excesses in insulin production due to doses that are too high, or due to the eating habits of the patient. It should not be taken if the patient has a hypersensitivity for sulphonylureas. There are some drugs that prolong the effects of drugs such as glybuzole and thereby increase the

neg: Urushiol-induced contact dermatitis "Ginkgo biloba." As is the case with all contact dermatitis, urushiol-induced rashes are a Type IV hypersensitivity reaction, also known as delayed-type hypersensitivity. Symptoms include itching, inflammation, oozing, and, in severe cases, a burning sensation. The American Academy of Dermatology estimates that there are up to 50 million cases of urushiol-induced dermatitis annually in the United States alone, accounting for 10% of all lost-time injuries in the United States Forest Service. Poison oak is a significant problem in the rural Western and Southern United States, while poison ivy is most rampant in the Eastern United States. Dermatitis from poison sumac

neg: Type IV hypersensitivity T cells destroy target cells on contact, whereas activated macrophages produce hydrolytic enzymes and, on presentation with certain intracellular pathogens, transform into multinucleated giant cells. An example of a tuberculosis (TB) infection that comes under control: "M. tuberculosis" cells are engulfed by macrophages after being identified as foreign, but due to an immuno-escape mechanism peculiar to mycobacteria, TB bacteria are able to block the fusion of their enclosing phagosome with lysosomes which would destroy the bacteria. Thereby TB can continue to replicate within macrophages. After several weeks, the immune system somehow [mechanism as yet unexplained] ramps up and, on stimulation

neg: Stichodactyla toxin considered to be models of atopic dermatitis. ShK, ShK-170, ShK-186, ShK-192 and ShK-IgG-Fc were all effective in the ovalbumin-induced delayed type hypersensitivity model, while a topical formulation of ShK-198 was effective in treating oxazolone-induced dermatitis. Even where compensation by K3.1 channels was reported to over-ride K1.3 block, ShK administered alone suppressed delayed type hypersensitivity significantly in 2 of 3 studies, albeit modestly. Psoriasis is a severe autoimmune disease of the skin that afflicts many people worldwide. Despite the success of recent biologics in ameliorating disease, there is still a search for safe and effective drugs for psoriasis. K1.3 inhibitors (ShK,

neg: Food allergy harmful proteins are those that do not break down due to the strong bonds of the protein. IgE antibodies bind to a receptor on the surface of the protein, creating a tag, just as a virus or parasite becomes tagged. Why some proteins do not denature and subsequently trigger allergic reactions and hypersensitivity while others do is not entirely clear. Hypersensitivities are categorized according to the parts of the immune system that are attacked and the amount of time it takes for the response to occur. The four types of hypersensitivity reaction are: type 1, immediate IgE-mediated; type 2, cytotoxic;

neg: Casoni test hydatid disease affecting the liver, but positive in less than 50% of patients with hydatid disease elsewhere in the body; false positive results are also common. Precaution – Being a type I hypersensitivity reaction, anaphylactic reaction tray must be kept ready before carrying out the test.Consequently, serological tests are now generally used. The test was described in 1912 by Tomaso Casoni. Casoni test The Casoni test is an immediate hypersensitivity skin test used in the diagnosis of hydatid disease introduced by casoni. The test involves the intradermal injection of 0.25 ml of sterilised fluid from hydatid cysts/human cyst and sterilised

neg: Drug reaction with eosinophilia and systemic symptoms to 1996, there were numerous reports on individuals presenting with a medication-induced disorder now recognized as the DRESS syndrome. For example, anticonvulsants in the 1930s, dilantin in 1950, and other medications in the ensuing years were reported to do so. The reports often named the disorder based on the drug evoking it, e.g. the anticonvulsant hypersensitivity syndrome, dilantin hypersensitivity syndrome, allopurinol hypersensitivity syndrome, dapsone syndrome, and dapsone hypersensitivity syndrome. In 1996, however, the term DRESS syndrome was coined in a report attempting to simplify the terminology and consolidate these various clearly related syndromes into a single underlying disorder. The symptoms

neg: Dental emergency inform the orthodontist as soon as possible so that appropriate actions are taken to address the de-bonded brackets immediately. The most common allergy in orthodontics is to nickel. Nickel is found in multiple orthodontic components, such as nickel-titanium (NiTi) archwires and stainless steel brackets. If patients are previously exposed to nickel, for example with nickel-containing jewellery, the re-exposure with orthodontic components are more likely to lead to a Type IV delayed hypersensitivity immune response. This response is usually delayed for a few days or weeks. In this case, the orthodontist must be informed immediately to make arrangements for patient to

neg: Alkene reactive oxygen species generated by the photosensitiser, such as hydroxyl radicals, singlet oxygen or superoxide ion. These reactive photochemical intermediates are generated in what are known as Type I, Type II, and Type III processes, respectively. These various alternative processes and reactions can be controlled by choice of specific reaction conditions, leading to a wide range of different products. A common example is the [4+2]-cycloaddition of singlet oxygen with a diene such as cyclopentadiene to yield an endoperoxide: Another example is the Schenck ene reaction, in which singlet oxygen reacts with an allylic structure to give a transposed allyl peroxide:

neg: Dental anesthesia medical history. Genuine allergy to LA will manifest either as Type 1 or Type 4 hypersensitivity. Signs and symptoms will vary depending on the type of allergy. Type 1 reactions have a rapid onset of symptoms which include swelling, redness, rashes, itchiness, chest tightness, breathing problems. A Type 4 reaction has a delayed onset of symptoms and is usually localized to the site of injection. If a genuine allergic reaction to LA should occur, the patient should be treated as an emergency for anaphylaxis, according to the guidelines in the respective areas. For the UK, the section on medical emergencies

neg: Organoiron chemistry and studies have exploited the chiral derivatives CpFe(PPh)(CO)acyl. The simple peralkyl and peraryl complexes of iron are less numerous than are the Cp and CO derivatives. One example is tetramesityldiiron. Compounds of the type [(η-allyl)Fe(CO)X are allyl cation synthons in allylic substitution. Complexes of the type Fe(SR)(CO) and Fe(PR)(CO) form, usually by the reaction of thiols and secondary phosphines with iron carbonyls. The thiolates can also be obtained from the tetrahedrane FeS(CO). Some organoiron(III) compounds are prepared by oxidation of organoiron(II) compounds. A long-known example being ferrocenium [(CH)Fe]. Organoiron(III) porphyrin complexes are numerous. In Fe(norbornyl), Fe(IV) is stabilized by an

neg: Taspoglutide serious hypersensitivity reactions and gastrointestinal side effects. Taspoglutide is the peptide with the sequence HN-His-2-methyl-Ala-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Val-Ser-Ser-Tyr-Leu-Glu-Gly-Gln-Ala-Ala-Lys-Glu-Phe-Ile-Ala-Trp-Leu-Val-Lys-2-methyl-Ala-Arg-CONH. In other words, it is the 8-(2-methylalanine)-35-(2-methylalanine)-36--argininamide derivative of the amino acid sequence 7–36 of human glucagon-like peptide I. Taspoglutide Taspoglutide is a pharmaceutical drug, a glucagon-like peptide-1 agonist (GLP-1 agonist), under investigation for treatment of type 2 diabetes being codeveloped by Ipsen and Roche. Two phase II trials reported it was effective and well tolerated. Of the eight planned phase III clinical trials of weekly taspoglutide (four against exenatide, sitagliptin, insulin glargine, and pioglitazone), at least five were active in 2009. Preliminary results in

neg: Anticonvulsant hypersensitivity syndrome Anticonvulsant hypersensitivity syndrome Anticonvulsant/sulfonamide hypersensitivity syndrome is a potentially serious hypersensitivity reaction that can be seen with drugs with an aromatic amine chemical structure, such as aromatic anticonvulsants (e.g. diphenylhydantoin, phenobarbital, phenytoin, carbamazepine, lamotrigine), sulfonamides, or other drugs with an aromatic amine (procainamide). Cross-reactivity should not occur between drugs with an aromatic amine and drugs without an aromatic amine (e.g., sulfonylureas, thiazide diuretics, furosemide, and acetazolamide); therefore, these drugs can be safely used in the future. The hypersensitivity syndrome is characterized by a skin eruption that is initially morbilliform. The rash may also be a one of the potentially lethal

neg: Allergen Allergen An allergen is a type of antigen that produces an abnormally vigorous immune response in which the immune system fights off a perceived threat that would otherwise be harmless to the body. Such reactions are called allergies. In technical terms, an allergen is an antigen that is capable of stimulating a type-I hypersensitivity reaction in atopic individuals through Immunoglobulin E (IgE) responses. Most humans mount significant Immunoglobulin E responses only as a defense against parasitic infections. However, some individuals may respond to many common environmental antigens. This hereditary predisposition is called atopy. In atopic individuals, non-parasitic antigens stimulate inappropriate

neg: Type punning verify portability expectations, helps to keep the code maintainable. For a practical example popularized by Quake III, see fast inverse square root. In addition to the assumption about bit-representation of floating-point numbers, the previous floating-point type-punning example also violates the C language's constraints on how objects are accessed:<ref name="ISOs6.5/7">ISO/IEC 9899:1999 s6.5/7</ref> the declared type of codice_13 is codice_12 but it is read through an expression of type codice_18. On many common platforms, this use of pointer punning can create problems if different pointers are aligned in machine-specific ways. Furthermore, pointers of different sizes can alias accesses to the same memory,

neg: Allergy a type I hypersensitivity reaction against an allergen encountered for the first time and presented by a professional antigen-presenting cell causes a response in a type of immune cell called a T2 lymphocyte; a subset of T cells that produce a cytokine called interleukin-4 (IL-4). These T2 cells interact with other lymphocytes called B cells, whose role is production of antibodies. Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific

neg: Latex allergy trigger a reaction. People with latex allergies may also have or develop allergic reactions to some fruits, such as bananas. Natural rubber latex is known to cause allergic reactions of Type I (e.g. anaphylaxis) and Type IV (e.g. allergic contact dermatitis) as well as non-allergic irritant contact dermatitis. The most serious and rare form of latex allergy, Type I hypersensitivity can cause an immediate and potentially life-threatening reaction, not unlike the severe reaction some people have to bee stings. Such reactions account for a significant proportion of perioperative anaphylactic reaction, especially in children with myelomeningocele. Type I natural rubber latex

neg: Anticonvulsant hypersensitivity syndrome anticonvulsants, the general term "anticonvulsant hypersensitivity syndrome" (AHS) is favored over the original descriptive term "dilantin hypersensitivity syndrome." As of 2015, two cases of AHS have been reported that manifested during long-term treatment with multiple anti-seizure medications. Death due to multiple organ failure can occur; symptoms also mimic lymphoma, AHS has been called "pseudolymphoma" as a result. Changing the medications involved to those in a different class can avoid further problems. Anticonvulsant hypersensitivity syndrome Anticonvulsant/sulfonamide hypersensitivity syndrome is a potentially serious hypersensitivity reaction that can be seen with drugs with an aromatic amine chemical structure, such as aromatic anticonvulsants (e.g.

neg: Major royal jelly protein fungi, and viruses. They also show an ability to lower blood pressure, fats in the blood (hypercholesterolemia), stop tumour growth "in vitro", and anti-inflammation. Royal jelly has been associated with allergic reactions such as contact dermatitis, acute asthma, and anaphylaxis, which can lead to death. In a clinical diagnosis, MRJP1 and MRJP2 are found to be the main allergens. They induce IgE-mediated hypersensitivity reactions thereby causing type 1 hypersensitivity. Major royal jelly protein Major royal jelly proteins (MRJPs) are a family of proteins secreted by honey bee. The family consists of nine proteins, of which MRJP1 (also called royalactin), MRJP2,

neg: Breguet Type IV arrangement and in the engine fitted. Although Breguet's earlier aircraft were referred to using a type number, the aircraft produced after the Type III were generally referred to using an airframe number and a letter/number combination denoting the type of engine fitted. An example, an R.U.1, is on display at the Musée des Arts et Métiers in Paris. Breguet Type IV The Breguet Type IV was an aircraft built by Breguet Aviation. It was first flown in 1911, and was the first Breguet aircraft to be produced in quantity. It was used by the French Army and the R.F.C.. It

neg: Immune tolerance same mechanisms of peripheral tolerance that limit inflammation to bacterial antigens in the microbiome, since both involve the gut-associated lymphoid tissue. It may also have evolved to prevent hypersensitivity reactions to food proteins. It is of immense immunological importance, since it is a continuous natural immunologic event driven by exogenous antigen. Allergy and hypersensitivity reactions in general are traditionally thought of as misguided or excessive reactions by the immune system, possibly due to broken or underdeveloped mechanisms of peripheral tolerance. Usually, Treg cells, TR1, and Th3 cells at mucosal surfaces suppress type 2 CD4 helper cells, mast cells, and eosinophils,

neg: Glimepiride Glimepiride Glimepiride (original trade name Amaryl) is an orally available medium-to-long-acting sulfonylurea antidiabetic drug. It is sometimes classified as either the first third-generation sulfonylurea, or as second-generation. Glimepiride is indicated to treat type 2 diabetes mellitus; its mode of action is to increase insulin secretion by the pancreas. However it requires adequate insulin synthesis as prerequisite to treat appropriately. It is not used for type 1 diabetes because in type 1 diabetes the pancreas is not able to produce insulin. Its use is contraindicated in patients with hypersensitivity to glimepiride or other sulfonylureas. Side effects from taking glimepiride include gastrointestinal

neg: Chromium(III) chloride solutions of [CrCl(HO)] are accelerated by chromium(II) catalysts. With molten alkali metal chlorides such as potassium chloride, CrCl gives salts of the type MCrCl and KCrCl, which is also octahedral but where the two chromiums are linked via three chloride bridges. CrCl is a Lewis acid, classified as "hard" according to the Hard-Soft Acid-Base theory. It forms a variety of adducts of the type [CrClL], where L is a Lewis base. For example, it reacts with pyridine () to form an adduct: Treatment with trimethylsilylchloride in THF gives the anhydrous THF complex: Chromium(III) chloride is used as the precursor to

neg: Tetrazepam marketing authorisations of tetrazepam-containing medicines across the European Union (EU) in April 2013. The European Commission has confirmed the suspension of the marketing authorisations for Tetrazepam in Europe because of cutaneous toxicity, effective from the 1 August 2013. Delayed type 4 allergic hypersensitivity reactions including maculopapular exanthema, erythematous rash, urticarial eruption, erythema multiforme, photodermatitis, eczema and Stevens–Johnson syndrome can occasionally occur as a result of tetrazepam exposure. These hypersensitivity reactions to tetrazepam share no cross-reactivity with other benzodiazepines. Tetrazepam is used therapeutically as a muscle relaxant. The indicated adult dose for muscle spasm is 25 mg to 150 mg per

neg: Aspirin exacerbated respiratory disease Aspirin exacerbated respiratory disease Aspirin exacerbated respiratory disease (AERD), also termed aspirin-induced asthma, is a medical condition initially defined as consisting of three key features: asthma, respiratory symptoms exacerbated by aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and nasal polyps. The symptoms of respiratory reactions in this syndrome are hypersensitivity reactions to NSAIDs rather than the typically described true allergic reactions that trigger other common allergen-induced asthma, rhinitis, or hives. The NSAID-induced reactions do not appear to involve the common mediators of true allergic reactions, immunoglobulin E or T cells. Rather, AERD is a type of NSAID-induced hypersensitivity syndrome. EAACI/WHO

neg: Tenascin C An example of this interaction is the adhesion of SW80 carcinoma cells to the third FN-III repeat of TN-C via the αβ integrin receptor leads to cell spreading, phosphorylation of focal adhesion kinase, paxillin and ERK2 MAPK, and proliferation. In contrast, when these same cells use either αβ or αβ integrins to adhere to the same third FN type III repeat, cell spreading is attenuated and activation of these signaling mediators and cell growth is suppressed or fails to occur. Tenascin C is a very diverse protein that can produce different functions within the same cell type. This myriad of

neg: Sulfamethoxazole immunoglobulin E (IgE)-mediated reactions such as urticaria, angioedema, and anaphylaxis. In contrast, non-type 1 hypersensitivities are believed to be caused by metabolites of sulfonamides. Therefore, the liver and kidney are the determining factors of these other hypersensitivity reactions; alterations in kidney or liver functions may increase or decrease the frequencies of these reactions. One study has shown the allergic reaction rate to be about 3.0% over 359 courses of therapy. Of the allergic reactions, skin rashes, eosinophilia and drug fever were the most common, while serious reactions were less common. Sulfamethoxazole is contraindicated in people with a known hypersensitivity to

neg: Localizer type directional aid as an offset localizer. If the offset angle is greater than thirty degrees, the facility is classified as a localizer-type directional aid (LDA). As a "directional aid," and only a Category I (CAT I) approach, rather than a full-fledged instrument landing system (ILS), the LDA is more commonly used to help the pilot safely reach a point near the runway environs, where he or she hopefully can see the runway, at which point he or she will proceed and land visually, as opposed to (for example) full Category III (CAT III) ILS systems that allow a pilot to fly, without

neg: Copper protein 1 water or substrate molecule in this type-II blue copper protein. Examples for Type-II bluer copper protein are galactose oxidase, amine oxidase and doparmine monooxidase. The figure 3 is showing the structure of Type-III blue copper protein. In this structure oxygen bridged dimer with a Cu-Cu distance of ca 360 PM. Example for type-III blue copper protein are haemocyanin and tyrosinase . Electronic Structure of D(CuCl) The Jahn –Teller (JT) distortion basically happens in copper ion compounds is at tetragonal elongation. The figure A explains geometric structure that the bigger JT effect bring it to square planar D(CuCl) structure. Based

neg: T helper cell cells, IgG B cells, and IL-10 CD4 T cells. The key THαβ transcription factors are STAT1 and STAT3 as well as IRFs. IL-10 from CD4 T cells activate NK cells' ADCC to apoptose virus-infected cells and to induce host as well as viral DNA fragmentation. IFN alpha/beta can suppress transcription to avoid virus replication and transmission. Overactivation of THαβ against autoantigen will cause type 2 antibody-dependent cytotoxic hypersensitivity. Myasthenia gravis or Graves' disease belong to this category. The interactions between cytokines from the T1/T2 model can be more complicated in some animals. For example, the T2 cytokine IL-10 inhibits cytokine

neg: Idiosyncrasy They considered each disease as a unique condition, related to each patient. This understanding began to change in the 1870s, when discoveries made by researchers in Europe permitted the advent of a "scientific medicine", a precursor to the evidence-based medicine that is the standard of practice today. The term idiosyncratic drug reaction denotes an aberrant or bizarre reaction or hypersensitivity to a substance, without connection to the pharmacology of the drug. It is what is known as a Type B reaction. Type B reactions have the following characteristics: They are usually unpredictable, might not be picked up by toxicological screening,

neg: CCL18 CCL18 seems to play a part in both activation of the immune system and the induction of tolerance and homeostasis at steady-state conditions. The production of CCL18 is induced by T-helper 2 type cytokines, namely IL-4 and IL-13. Coupled with the fact that CCL18 is highly expressed in patients with allergic asthma and other hypersensitivity diseases, CCL18 seems to play an important role for generating and maintaining a T-helper 2 (Th2) type response. Furthermore, the addition of CCL18 as an adjuvant for a malaria vaccine have shown efficacy, perhaps by recruiting immune cells to the site of vaccination. Finally, CCL18

neg: Poppy seed floral arrangements, but is sold illegally from some meat markets. White poppy seeds called khashkhash (خشخاش) are essential for a type of cookies called Kulcha (کولچہ). Kulcha can be salty (namkeen) or sweet (Qandi). Both kinds are covered on top with a layer of white poppy seeds. Eating large quantities of poppy seeds can cause a phytobezoar which can block the bowels. But, if the seeds are consumed in moderation as an ingredient in cooked or baked foods, phytobezoar formation is very unlikely. Allergy (type 1 hypersensitivity) to poppy seeds is rare, but has been reported and can cause anaphylaxis.

neg: Hypersensitivity pneumonitis Hypersensitivity pneumonitis Hypersensitivity pneumonitis (HP; also called allergic alveolitis, bagpipe lung, or extrinsic allergic alveolitis, EAA) is an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled organic dusts. Sufferers are commonly exposed to the dust by their occupation or hobbies. Hypersensitivity pneumonitis (HP) is categorized as acute, subacute, and chronic based on the duration of the illness. In the acute form of HP, symptoms may develop 4–6 hours following heavy exposure to the provoking antigen. Symptoms include fever, chills, malaise, cough, chest tightness, dyspnea, rash, swelling and headache. Symptoms resolve within 12 hours to several days

neg: Incident Command System generator or a truck. The "type" of resource describes a performance capability for a kind of resource for instance, In both type and kind, the objective must be included in the resource request. This is done to widen the potential resource response. As an example, a resource request for a "small aircraft for aerial reconnaissance of a search and rescue scene" may be satisfied by a [[National Guard of the United States|National Guard]] [[OH-58 Kiowa]] helicopter (Type & Kind: Rotary-wing aircraft, Type II/III) or by a [[Civil Air Patrol]] [[Cessna 182]] (Type & Kind: Fixed-wing aircraft, Type I). In this

neg: Usher syndrome function of these genes is still poorly understood. Usher syndrome is a variable condition; the degree of severity is not tightly linked to whether it is Usher I, II or III. For example, someone with type III may be unaffected in childhood but go on to develop a profound hearing loss and a very significant loss of sight by early-to-mid adulthood. Similarly, someone with type I, who is therefore profoundly deaf from birth, may keep good central vision until the sixth decade of life or even beyond. People with type II, who have useful hearing with a hearing aid, can