Serum Sickness
Basics
Description
- Serum sickness
- Type III hypersensitivity reaction that occurs 7 to 21 days after injection of foreign protein or serum (e.g., biologics or streptokinase)
- Immune complexes deposit in the skin, joints, kidneys, and other organs
- Clinical syndrome consists of skin rash, itching, fever, malaise, proteinuria, edema, joint pain, lymphadenopathy, and vasculitis.
- Serum sickness–like reactions
- Characterized by fever, rash, lymphadenopathy, and arthralgia
- Occur 1 to 3 weeks after drug exposure, can be sooner if previously sensitized to the drug
- Immune complexes, vasculitis, and hypocomplementemia are absent.
- This type of reaction, most commonly associated with medications, is commonly referred to as serum sickness as well.
- More common than true serum sickness because equine serum antitoxins have been replaced with human antitoxin sera
- Clinically, these entities present and are treated in the same 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.
Risk Factors
Genetics
People with a genetic predisposition to produce IgE are more susceptible.
General Prevention
- No known way to prevent first occurrence
- Obtain careful history of previous allergic reactions.
- Skin testing prior to antiserum administration will prevent anaphylaxis but not serum sickness.
- When the need for antiserum arises, consider prophylactic antihistamines.
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 diffuse across the vascular walls.
- 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
Etiology
- Common causative agents:
- Horse antithymocyte globulins
- Biologics (especially infliximab and rituximab)
- Human diploid-cell rabies vaccine
- Streptokinase
- Insect stings (Hymenoptera venom)
- Antivenom
- Penicillins
- Cephalosporins (especially cefaclor)
- Sulfonamides
- Hydralazine
- Thiouracils
- Metronidazole
- Naproxen
- Dextrans
- Case-reported agents:
- Minocycline
- Carbamazepine
- IVIG
- Bupropion
- H1N1 vaccination
There's more to see -- the rest of this topic is available only to subscribers.
Citation
Cabana, Michael D., editor. "Serum Sickness." 5-Minute Pediatric Consult, 8th ed., Wolters Kluwer, 2019. Pediatrics Central, peds.unboundmedicine.com/pedscentral/view/5-Minute-Pediatric-Consult/617395/all/Serum_Sickness.
Serum Sickness. In: Cabana MDM, ed. 5-Minute Pediatric Consult. Wolters Kluwer; 2019. https://peds.unboundmedicine.com/pedscentral/view/5-Minute-Pediatric-Consult/617395/all/Serum_Sickness. Accessed October 13, 2024.
Serum Sickness. (2019). In Cabana, M. D. (Ed.), 5-Minute Pediatric Consult (8th ed.). Wolters Kluwer. https://peds.unboundmedicine.com/pedscentral/view/5-Minute-Pediatric-Consult/617395/all/Serum_Sickness
Serum Sickness [Internet]. In: Cabana MDM, editors. 5-Minute Pediatric Consult. Wolters Kluwer; 2019. [cited 2024 October 13]. Available from: https://peds.unboundmedicine.com/pedscentral/view/5-Minute-Pediatric-Consult/617395/all/Serum_Sickness.
* Article titles in AMA citation format should be in sentence-case
TY - ELEC
T1 - Serum Sickness
ID - 617395
ED - Cabana,Michael D,
BT - 5-Minute Pediatric Consult
UR - https://peds.unboundmedicine.com/pedscentral/view/5-Minute-Pediatric-Consult/617395/all/Serum_Sickness
PB - Wolters Kluwer
ET - 8
DB - Pediatrics Central
DP - Unbound Medicine
ER -