Immune complex reactions

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. 

Adverse Effects. Enfuvirtide must be administered by subcutaneous injection, and local pain and irritation occurs at the injection site in most patients. Other common side effects include peripheral neuropathy and immune complex reactions that can lead to serious problems including respiratory distress syndrome, kidney dysfunction, and possibly Guillain-Barre syndrome. 

Higashi GI, Farid Z. Oxamniquine fever—drug-induced or immune-complex reaction BMJ 1979 2(6194) 830. 

Immune Complex Reaction This is referred to as serum sickness and results in angioedema, arthralgia (sore joints), fever, swollen lymph nodes, and splenomegaly (large spleen). The Immune complex reaction can appear up to 3 weeks after the drug is administered. 

Type 3 immune complex reaction Other drugs can form immune complexes with antibodies, IgG or IgM, which circulate in the blood and can be deposited in particular areas of the body, for example in the joints, skin or kidneys. See Figure 3.3c. Here the immune complexes can cause a local inflammation by activation of the complement system. 

The exact mechanism of metal fume fever (a syndrome consisting of a leukocytosis with chills, fever, cough, myalgias, headache, weakness, and dyspnea) is unknown (Ellenhorn and Barceloux 1988), but respiratory tract inflammation and the development of an immune complex reaction have been proposed (McCord 1960). Treatment is supportive (e.g., bed rest, analgesics, and antipyretics) (Mueller and Seger 1985). 

The pathophysiology of immune complex reactions occurs in several stages formation of immune complexes in antigen excess, deposition of complexes in tissue, activation of complement followed by attraction at the site of plynuclear neutrophils, and liberation in tissue of proteolytic lysosomal enzymes and inflammatory cationic proteins. The importance of concomitant increase in vascular permeability for the deposition of immune complexes has been shown in vivo by the preventive effect of antihistaminic and antiserotonin drugs on the development of serum sickness to horse antidiphteric serum (Kniker et al. 1971). 

The patho-mechanism of these papular and urticarial eruptions is unknown. An immune complex reaction may be the basis of the clinical manifestation here. Goh postulated that the allergen is absorbed percutaneously and evoked an allergic contact dermatitis at the primary site, while concurrently forming immune complexes with a circulating antibody (Goh 1989). The immune complexes were probably deposited in the microvasculature and triggered by an inflammatory process that led to the UPPE. Occupational allergens reported to cause UPPE include woods and/or plants, and chemicals. 

Despite their anti-inflammatory and immunosuppressive properties, CSs can provoke both immunological and inflammatory responses, occasionally inducing immediate type 1 and delayed type IV allergic reactions. Type 11 cytotoxic and type III immune complex reactions do not appear to have been reported. 

Chloroalkylamine leukemia alkylating agents immune hemolytic anemia bms Tc immune complex reactions Diagnosis"... 

Type III reactions (immune-complex reactions) In type III reactions, formation of an immune complex and its deposition on tissue surface serve as primary initiators. Occasionally, immune complexes bind to endothelial cells and lead to immune-complex deposition with subsequent complement activation in the linings of blood vessels. Circumstances that govern immune formation or immune-complex disease remain unclear to date, and it usually occurs without symptoms. The clinical symptoms of a type III reaction include serum sickness (e.g. 3-lactams), drug-induced lupus erythematosus (e.g. quinidine) and vasculitis (e.g. minocycline). Type III reactions can result in acute interstitial nephritis or serum sickness (fever, arthritis, enlarged lymph nodes, urticaria and maculopapular rashes) [1-3]. 

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