Excerpt from Serum Sickness

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Background

Serum sickness is a type III hypersensitivity reaction that results from the injection of heterologous or foreign protein or serum. Reactions secondary to the administration of nonprotein drugs are clinically similar to serum sickness reactions.

Pathophysiology

Not all substances that are recognized as foreign by the immune system elicit an immune response. The antigen must be of characteristic size or have specific antigenic determinants and physiological properties to be an effective stimulator of the immune system. After an appropriate antigen is introduced, an individual's immune system responds by synthesizing antibodies after 4-10 days. The antibody reacts with the antigen, forming soluble circulating immune complexes that may diffuse into the vascular walls, where they may initiate fixation and activation of complement. Complement-containing immune complexes generate an influx of polymorphonuclear leukocytes into the vessel wall, where proteolytic enzymes that can mediate tissue damage are released. Immune complex deposition and the subsequent inflammatory response are responsible for the widespread vasculitic lesions seen in serum sickness.

Frequency

United States

The incidence of serum sickness is decreasing as a result of public health vaccination programs that have decreased the need for specific antitoxins. Also, many horse serum antitoxins have been refined of the antigenic components that cause serum sickness. Products derived from human serum have replaced the most frequently used antitoxins, which are rabies and tetanus horse serum antitoxins. When these were used, the incidences of serum sickness were 2-5% in patients receiving tetanus antitoxin and 16% in patients receiving rabies antitoxin. The frequency and severity of reactions were directly related to the amount and type of antiserum administered.

Currently, nonprotein drugs are the most common causes of serum sickness–like reactions. The incidence of serum sickness–like reactions caused by nonprotein drugs is difficult to determine. From 1972-1985, the adverse drug reactions reported to the US Food and Drug Administration (FDA) included 10 cases of serum sickness related to amoxicillin (Amoxil, Polymox), 638 cases related to cefaclor (Ceclor), 28 cases related to cephalexin (Keflex), and 51 cases related to trimethoprim-sulfamethoxazole (Bactrim, Cotrim, Septra, Sulfatrim).

Mortality/Morbidity

Symptoms usually last 1-2 weeks before spontaneously subsiding. Long-lasting sequelae generally do not occur. Fatalities are rare and usually are due to continued administration of the antigen.

Age

Individuals older than 15 years may experience more frequent and more severe disease because they receive larger volumes of antitoxin.

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