Type III Allergic Reaction

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. 

Hachimi-Idrissi S, de Schepper J, de Waele M, Dab I, Otten J. Type III allergic reaction after infusion of immunoglobulins. Lancet 1990 336(8706) 55. 

Sulphonamides are usually the cause of type III or type IV allergic reactions, such as serum-sickness syndrome, or probably, the majority of maculopapular rashes. 

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. 

Currently allergic reactions are classified into four types on the basis of different reaction patterns. Whereas types I—III are dependent on antibodies, the type IV reaction is mediated by cellular immune reactions. 

Type II, III, and IV allergic reactions are variants of physiologic defense mechanisms only relevant in special situations, which follow a common pathologic pattern. In general, treatment of these forms require antiinflammatory ( inflammation) or immunosuppressive strategies ( immunosuppression). Therefore, only therapy of Type I reactions will be described here. 

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. 

GAGs are classified into several major types based on the nature of the repeating disaccharide unit heparan sulfate, chondroitin sulfate, dermatan sulfate, keratan sulfate, and hyaluronan. A hypersulfated form of heparan sulfate called heparin, produced mostly by mast cells, plays a key role In allergic reactions. It is also used medically as an anticlotting drug because of its ability to activate a natural clotting inhibitor called antlthrombln III. 

In some of these, for example, in allergic bronchopulmonary aspergillosis there is evidence to support a type III reaction (Pepys 1977 b). No skin reactions were elicited in either of the two subjects with other oxidizing agents such as potassium permanganate, potassium chlorate, sodium perchlorate, and potassium sulphate. Ammonium persulphate has also been reported to cause urticaria and dermatitis, giving both immediate and non-immediate skin test reactions (Calnan and Shuster 1963). 

Penicillins and cephalosporins are prototypes for allergic reactions of type I by the classification of Coombs and Gell (1963), based on the pathogenetic mechanisms. They are mostly IgE mediated. But type III and type IV reactions also occur. 

Coombs and Gell (1963) have classified all immunologic (allergic) reactions into four types (I to IV). The classification of Types I to III depends on whether antigen or antibody is cell-fixed or in solution. Type IV is cell-mediated and is typified in the skin by responses such as the tuberculin reaction which develops macroscopically over 36-48 hr and lasts for 72-96 hours. This is the classical delayed hypersensitivity reaction. 

In the Gell and Coombs classification of allergic reactions, four types of hypersensitivities designated types I, n. III, and IV are distinguished. 

The answer is 3 [Chapter 8 III A 21. Type II (idiosyncratic, unpredictable, drug-related) hepatotoxicosis is probably caused by irxlivkl-ual differences in the ability to metabolize atx) detoxify xenobiotics. These diflierences may be hereditary arxl are txrt detected by routine experimoilal toxicity testing. Thus, excessive suscepfibilHy tttay occur at very low dosages arx] a dose-response relationship is rxrt demonstrable. Prior sensitization (e.g., by an allergic-type reaction) may also be a factor. 

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