Pediatric Serum Sickness Workup

Updated: Sep 29, 2023
  • Author: Tova Ronis, MD; Chief Editor: Harumi Jyonouchi, MD  more...
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Laboratory Studies

The following studies are indicated in patients with serum sickness:

  • CBC with differential - Leukocytosis or leukopenia, eosinophilia, or mild thrombocytopenia

  • Erythrocyte sedimentation rate and C-reactive protein levels - Usually slightly elevated

  • Urinalysis - Proteinuria, hematuria, active sediment

  • Blood urea nitrogen (BUN) and creatinine levels - May be transiently elevated

  • C3, C4, CH50 - Depressed complement levels due to complement consumption

  • Quantitative immunoglobulins - Hypergammaglobulinemia that results from prolonged course of antithymocyte globulin (ATG)

  • Immune complexes - C1q binding or Raji cell assays for elevated levels of immune complexes (These test can be confirmatory but are not essential for diagnosis.)



Skin biopsy is usually not indicated for serum sickness but may be considered to further evaluate for vasculitis if the etiology is unclear.


Histologic Findings

Biopsy of serum sickness skin lesions reveals a perivascular lymphohistiocytic infiltrate and may show edema of perivascular stroma. [14] Immune deposits (IgM, IgE, C3, and IgA) are found in superficial small blood vessels and renal glomeruli with direct immunofluorescence (DIF).

Results from biopsy of skin lesions in serum sickness–like reactions have noted interstitial inflammatory infiltrate with neutrophils and eosinophils, perivascular lymphocytic, eosinophilic, histiocytic, or neutrophilic infiltrate, typically consistent with urticaria without evidence of vasculitis. [49]

Because of the high rate of blood flow and the filtration effect at the renal glomeruli, the immune complexes with serum sickness are deposited at the glomerular basement membrane. These deposits can be visualized with electron microscopy in the subendothelial and mesangial areas. These deposits lead to the activation of the complement system and the recruitment of neutrophils. Inflammatory mediators are released, resulting in a histologic picture of glomerulonephritis. [50]