Hypersensitivity type III

Pain at the injection site is one of the most commonly reported adverse effects of vaccination. The reaction is usually mild with complaints of pain and tenderness at the injection site that may or may not be accompanied by erythema. Local reactions tend to be more frequent with repeated doses or booster doses of vaccine. The frequency and degree of the reactions appear to be related to the amount of preformed antibodies and rapid immunologic responses reflective of priming from previous doses. More serious Arthus reactions are infrequently reported. Arthus reactions are classified as type III hypersensitivity reactions, and are characterized by a massive local response involving the entire thigh or deltoid. Arthus reactions are also related to preformed antibody complexes that induce an inflammatory lesion.14... 

Type III hypersensitivity is due to the presence of elevated levels of antigen-antibody complexes that deposit on basement membranes in tissues and vessels. Immune complex deposition activates complement to produce components with anaphylatoxic and chemotactic activities (C5a, C3a, C4a) that increase vascular permeability and recruit neutrophils to the site of complex deposition. Complex deposition and the action of lytic enzymes released by neutrophils can cause skin rashes, glomerulonephritis, and arthritis in these individuals. If patients have type III hypersensitivity against a particular antigen, clinical symptoms usually occur 3-4 days after exposure to the antigen. 

The adverse effects of ALG are mostly those associated with injection of a foreign protein. Local pain and erythema often occur at the injection site (type III hypersensitivity). Since the humoral antibody mechanism remains active, skin-reactive and precipitating antibodies may be formed against the foreign IgG. Similar reactions occur with monoclonal antibodies of murine origin, and reactions thought to be caused by the release of cytokines by T cells and monocytes have also been described. 

Immunologic reactions to drugs resulting in serum sickness are more common than immediate anaphylactic responses, but type II and type III hypersensitivities often overlap. The clinical features of serum sickness include urticarial and erythematous skin eruptions, arthralgia or arthritis, lymphadenopathy, glomerulonephritis, peripheral edema, and fever. The reactions generally last... 

Figure 6.33 The basis of type III hypersensitivity reactions. These are mediated by immune complexes formed between antigen and IgG antibodies, which accumulate in capillaries and in tissues.

Trimellitic anhydride, used in chemical synthesis. Type II hypersensitivity manifested by adverse effects on blood, including hemolytic anemia and bone marrow depression, may be caused by exposure to trimellitic anhydride. This agent may also cause type III hypersensitivity, resulting from deposition of antigen-antibody complexes in tissue and causing symptoms such as rheumatoid disease or pneumonitis. 

A case of urticarial vasculitis, a type III hypersensitivity reaction, has been reported after cocaine use (222). 

Cytolytic (type II) hypersensitivity Arthus-immune complex (type III) hypersensitivity Cell-mediated (type IV) hypersensitivity Immunosuppression... 

P-ARK An enzyme that phosphoylates the occupied form of a G-protein coupled receptor, e.g. the 6-adrenoceptor, leading to uncoupling of that receptor and desensitization. ARMI age-related memory impairment, arrhythmia (dysrhythmia) An abnormality of heart rhythm or rate of heartbeat, usually caused by disturbance of the electrical impulses and their conduction within the heart. They include ectopic beats (isolated irregular beats), tachycardias (too fast a heartbeat), bradycardias (too slow a heartbeat) and atrial flutter and ventricular fibrillation. Arthus reaction A severe local inflammatory response, a skin reaction characterized by erythema, oedema, necrosis, local haemorrhage. A type III hypersensitivity reaction. Arunlakshana and Schild plot See Schild plot, ascites fluid The fluid that accumulates in the peritoneal cavity during certain pathological conditions, aspiration The withdrawal of fluid or tissue from the body by suction. 

C. Type III Drug Allergy Type III hypersensitivity is a complex type of drug allergy reaction that involves complement-fixing IgM or IgG antib ies and—possibly—IgE antibodies. Drug-induced serum sickness and vasculitis are examples of type III reactions Stevens-Johnson syndrome (associated with sulfonamide therapy) may also result from type III mechanisms. 

B cells Form plasma cells that secrete immunoglobulins (IgG, IgA, and IgE) Participate in antigen-antibody complex-mediated tissue damage (type III hypersensitivity)... 

Arthus reaction A local reaction seen in the skin after subcutaneous or intradermal injection of an antigenic substance, immune complex (Type-III) hypersensitivity. 

Known also as immune complex (Type-III) hypersensitivity. 

Presentation of current knowledge of the mechanisms underlying the various systemic and cutaneous drug reactions including mechanisms of immediate, late, and delayed reactions, type II and type III hypersensitivities, and some important drug-induced sensitivities lacking an immune basis. 

Type in hypersensitivity is mediated by soluble immune complexes mostly involving IgG antibodies. Drug-induced serum sickness-like reaction is the prototype example of type III drug hypersensitivity. Hypersensitivity vascu-Ms is another example of a type III hypersensitivity response induced by drugs. 

Reactions to the platinum drags are mainly type I or type IV hypersensitivity responses with a few cases of type II and type III hypersensitivities. 

HP is an airway-centered ILD that may be acute or chronic. Acute HP is a type III hypersensitivity reaction, and chronic HP is a type IV hypersensitivity reaction. In both cases, the antigen is introduced to the lung through the airways and results in airway inflammation of some degree (23). Bronchioles may show features of constrictive bronchiolitis with subepithelial granulation tissue and fibrosis however, complete luminal obliteration is not seen. As the disease progresses, peribronchiolar metaplasia develops via the canals of Lambert, also called Lambertosis (24). 

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