Pediatric emergency medicine trisk 1681 1681
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Background
Serum sickness, an immune complex–mediated disease, was first described in
1905 among patients receiving heterologous antisera to treat various infectious
diseases. Although use of these therapies has declined, they are still found in
antithymocyte globulins used to prevent organ transplant rejection, antitoxins
(clostridia, diphtheria, tetanus), and antivenoms (arachnid, snake, scorpion).
Serum sickness-like reactions, now more common than classic serum sickness,
are caused by different mechanisms and may be triggered by infections, or
administration of medications or vaccines. Frequently implicated medications
include penicillins, sulfonamides, cephalosporins, streptomycin, hydantoins,
griseofulvin, bupropion, fluoxetine, and thiouracil. Serum sickness may also be
induced by monoclonal antibodies including infliximab (used to treat psoriasis
and inflammatory bowel disease) and rituximab (used to treat autoimmune
disorders and lymphomas), and the humanized anti-IgE antibody omalizumab
(used to treat allergic disorders and asthma).
Pathophysiology
In classical serum sickness, characteristic symptoms develop 7 to 14 days after
exposure to foreign serum protein. After initial protein exposure there is a period
of antigen excess followed by an antibody response leading to the formation of
antibody–antigen complexes. Immune complexes deposit in tissues causing local
inflammation and complement activation, including anaphylactic toxins C3a and
C5a which promote vascular permeability, histamine release, and bronchospasm.
Immune complex clearance is dependent on complex size and effectiveness of the
reticuloendothelial system. The organs most vulnerable to injury include the
kidneys and vascular system.
Although the pathogenesis of serum sickness–like reactions is not well
understood, reactions are not dependent on high levels of antibody or circulating
immune complexes. Medication (e.g., cefaclor) metabolites may cause direct
toxic effects or bind with serum proteins (e.g., albumin) with resultant antibody
response.
Goals of Treatment
The mainstay of serum sickness management includes removing the offending
antigen (if known), treating arthralgias/arthritis and pruritis with nonsteroidal
anti-inflammatory drugs and antihistamines, and evaluating whether there is
organ dysfunction (particularly renal involvement).
Clinical Considerations
