Reaction, allergic complexation

Attempts continue to predict metal sensitivity in the individual patient so that the choice of material can be made accordingly. In vitro tests for metal allergies have been developed on the basis of lymphokine (MIF) release from sensitized T lymphocytes exposed to metal-protein complexes (11). About 6% of patients without a previous metal implant had positive reactions to nickel, chromium, or cobalt. However, it is still not clear whether such a positive reaction is a reliable predictor of clinical problems. In practice few patients have either local or systemic reactions when symptoms occur and other causes are ruled out, the implant should be removed. Some workers recommend removal of an implant whenever there is both a positive MIF test and a positive skin test, even in the current absence of a serious reaction. Allergic dermatitis will clear up as soon as the metal has begun to be cleared from the tissue. The type of metal and the amount released into the tissue will affect the time taken for the disappearance of toxic dermatological phenomena. 

A Type III allergic reaction occurs when antibodies of the immunoglobulin G class (IgG) form immune complexes which are slowly eliminated and thus may elicit an inflammatory reaction by binding to the Fey receptors of leukocytes resulting in their activation. 

Development of models to assess chemical-induced allergic or autoimmune reactions is difficult in that both types of reactions are subject to complex processes, and are idiosyncratic in nature. Factors that must be considered include a large number of genetic as well as phenotypic, neuroendocrine, or environmental factors that are only in part related to the immune system. 

MSG (monosodium- glutamate) flavour enhancer for foods may cause allergic reaction known as MSG symptom complex, with symptoms such as nausea and headache may worsen already severe asthma... 

The interaction of a chemical (hapten) with epidermal proteins (carrier) can result in a hapten-carrier complex capable of activating skin-associated lymphoid tissue (sensitisation) and dissemination of antigen-specific T l)unphocytes (induction). Subsequent encoimter with the same or cross-reactive chemicals can result in the elicitation of a characteristic inflammatory skin reaction. The clinical condition is referred to as allergic contact dermatitis and is characterised by erythema, oedema, vesiculation and pruritus. Allergic contact sensitisation is, therefore, classed as a cell-mediated immunological response to chemicals that contact and penetrate the skin. 

Antibodies Formation of antihirudin antibodies was observed in approximately 40% of HIT patients treated with lepirudin. This may increase the anticoagulant effect of lepirudin possibly because of delayed renal elimination of active lepirudin-antihirudin complexes. Therefore, strict monitoring of aPTT is necessary also during prolonged therapy. No evidence of neutralization of lepirudin or of allergic reactions associated with positive antibody test results was found. 

Honey bees Complex proteins Swelling, allergic reaction... 

Most anaphylactoid reactions are due to a direct or chemical release of histamine, and other mediators, from mast cells and basophils. Immune-mediated hypersensitivity reactions have been classified as types I-IV. Type I, involving IgE or IgG antibodies, is the main mechanism involved in most anaphylactic or immediate hypersensitivity reactions to anaesthetic drugs. Type II, also known as antibody-dependent hypersensitivity or cytotoxic reactions are, for example, responsible for ABO-incompatible blood transfusion reactions. Type III, immune complex reactions, include classic serum sickness. Type IV, cellular responses mediated by sensitised lymphocytes, may account for as much as 80% of allergic reactions to local anaesthetic. 

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