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Serum sickness - Overview

Definition of Serum sickness:

Serum sickness is a reaction similar to an allergy. Specifically, it is an immune system reaction to certain medications, injected proteins used to treat immune conditions, or antiserum, the liquid part of blood that contains antibodies that help protect against infectious or poisonous substances.

See also: Immune response

Causes, incidence, and risk factors:

Serum is the clear fluid portion of blood. It does not contain blood cells, but it does contain many proteins, including antibodies, which are formed as part of the immune response to protect against infection.

Antiserum is taken from a person or animal with immunity against a particular infection or poisonous substance. Antiserum may be used to protect a person who has been exposed to a potentially dangerous microorganism against which the person has not been immunized. For example, you may receive a certain type of antiserum injection if you have been exposed to tetanus or rabies. This is called passive immunization. It gives you immediate, but temporary, protection while your body develops a personal immune response against the toxin or microorganism.

During serum sickness, the immune system misidentifies a protein in antiserum as a potentially harmful substance (antigen). The result is a faulty immune system response that attacks the antiserum, causing inflammation and other symptoms.

Certain medications (such as penicillin, cefaclor, and sulfa) can cause a similar reaction. Unlike other drug allergies, which occur very soon after receiving the medication for the second (or subsequent) time, serum sickness develops 7 - 21 days after the first exposure to a medication.

Injected proteins such as antithymocyte globulin (used to treat transplant rejection) and rituximab (used to treat immune disorders and cancers) cause serum sickness reactions.

Blood products may also cause serum sickness.

  • Reviewed last on: 5/1/2008
  • Stuart I. Henochowicz, MD, FACP, Associate Clinical Professor of Medicine, Division of Allergy, Immunology, and Rheumatology, Georgetown University Medical School; and David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.
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