Serum Sickness

Descriptive text is not available for this imageBASICS

DESCRIPTION

  • Classic serum sickness
    • Type III hypersensitivity reaction that occurs 7 to 21 days after administration of foreign protein or serum (e.g., biologic drug or streptokinase)
    • Clinical syndrome consists of skin rash, itching, fever, malaise, proteinuria, edema, joint pain lymphadenopathy, and vasculitis.
  • Serum sickness–like reactions
    • Similar reaction to classic serum sickness, most commonly associated with medications
    • Etiology is not well understood.
    • Immune complexes, vasculitis, and hypocomplementemia are absent.
    • Characterized by fever, rash, lymphadenopathy, and arthralgia
    • Occur 1 to 3 weeks after drug exposure, can be sooner if previously sensitized to the drug
    • Significantly more common than classic serum sickness
  • Clinically, these entities present and are treated in a similar manner.

EPIDEMIOLOGY

  • Limited information is available regarding the incidence of adverse drug reactions in children; generally believed to occur less frequently in children than in adults
  • >90% of serum sickness cases are drug-induced.
  • <5% of serum sickness cases are fatal.

ETIOLOGY

  • Common causative agents for classic serum sickness:
    • Horse or rabbit antithymocyte globulins (ATGs)
    • Biologics (especially infliximab and rituximab)
    • Human diploid-cell rabies vaccine
    • Streptokinase
    • Insect stings (Hymenoptera venom)
    • Antivenom (snake, spider)
    • Antitoxins (diphtheria, rabies, botulinum)
  • Common causative agents for serum sickness–like reactions
    • Penicillins
    • Cephalosporins (especially cefaclor)
    • Sulfonamides
    • Nonsteroidal anti-inflammatory drugs (NSAIDs)
    • Carbamazepine
    • Bupropion
    • Minocycline
    • Metronidazole
    • Fluoxetine

GENERAL PREVENTION

  • No known way to prevent first occurrence
  • Obtain careful history of previous allergic reactions.

PATHOPHYSIOLOGY

  • Serum sickness—type III immune complex, antigen–antibody complement reaction
    • Antibodies form 6 to 10 days after the introduction of foreign material.
    • Antibodies interact with antigens, forming immune complexes that deposit in the skin, joints, kidneys, and other organs.
    • They become fixated in tissue and activate the complement cascade.
    • C3a and C5a are produced, resulting in increased vascular permeability and activated inflammatory cells.
    • Polymorphonuclear cells and monocytes cause diffuse vasculitis.
  • Serum sickness–like reaction
    • Abnormal inflammatory reaction in response to defective metabolism of drug by-products
    • Drugs and/or their metabolites may act as haptens to bind plasma proteins and may elicit an abnormal immune response.

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