Serum Sickness

Content of This Page

1- Definition and Classification

2-Pathophysiology

3-Triggers and Causes

4- Clinical Features and Timeline

5– Serum Sickness–Like Reactions (SSLR)

6- Schistosomiasis and ‘Serum Sickness’

7- Laboratory Findings

8- Laboratory Findings

9- Differential Diagnosis

10- Treatment and Prognosis

11- Prevention Strategies

Definition and Classification

Serum sickness is a type III hypersensitivity reaction caused by immune complexes formed after exposure to foreign proteins.
It is a systemic immune reaction, distinct from immediate allergic (type I) reactions.

Pathophysiology

  • Antigen–antibody complexes form in circulation.

  • These complexes deposit in blood vessels, joints, kidneys.

  • Complement activation → vasculitis, inflammation, and tissue damage.

Triggers and Causes

Common causes include:

  • Heterologous antiserum (e.g. equine anti-venom, anti-diphtheria)

  • Monoclonal antibodies (e.g. rituximab, infliximab)

  • Penicillin (rare but classic)

  • Infections (e.g. schistosomiasis, particularly in acute stages)

Clinical Features and Timeline

Typical onset: 7–12 days after antigen exposure.

Symptoms:

  • Fever

  • Urticarial or morbilliform rash

  • Arthralgia and arthritis

  • Lymphadenopathy

  • Myalgia, malaise

  • Occasionally: nephritis, neurological symptoms

Serum Sickness–Like Reactions (SSLR)

  • Similar symptoms but not true type III hypersensitivity.

  • Often seen in children after antibiotics (e.g. cefaclor).

  • Less complement consumption, no circulating immune complexes.

Schistosomiasis and 'Serum Sickness'

Acute phase (Katayama fever) of S. mansoni / japonicum can mimic serum sickness:

  • Fever, rash, myalgia, eosinophilia.

  • Due to immune complex formation and systemic inflammation

Laboratory Findings

  • ↑ ESR and CRP

  • ↓ Complement levels (C3, C4)

  • Mild proteinuria or haematuria (if renal involvement)

  • Circulating immune complexes (if tested)

Diagnosis

  • History of exposure to foreign protein or biologic agent

  • Onset of typical symptoms in 1–2 weeks

  • Supportive labs (↑ inflammatory markers, ↓ complement)

Differential Diagnosis

  • Anaphylaxis (immediate, type I, IgE-mediated)

  • Drug rash (exanthema)

  • Viral exanthems

  • Systemic autoimmune diseases (e.g. SLE)

Treatment and Prognosis

  • Withdraw the offending agent

  • Supportive care:

    • Antihistamines for rash

    • NSAIDs or corticosteroids for severe symptoms

  • Usually self-limiting (resolves in 1–2 weeks)

  • Monitor renal function if glomerulonephritis suspected

Prevention Strategies

  • Avoid re-exposure to known triggers

  • Caution with repeat use of non-human antiserum

  • Screen for hypersensitivity before administering biologic drugs

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