What laboratory abnormalities are associated with Kawasaki disease?

Laboratory Abnormalities in Kawasaki Disease

Kawasaki disease presents with characteristic laboratory abnormalities that, while nonspecific, strongly support the diagnosis when combined with clinical features—most notably marked elevations in inflammatory markers (ESR often >40 mm/hr and CRP ≥3 mg/dL), leukocytosis with left shift, and thrombocytosis in the second week of illness. 1, 2

Acute Phase Reactants (Most Diagnostically Useful)

Erythrocyte Sedimentation Rate (ESR):

• Elevated in nearly all cases, typically >40 mm/hr 1
• Commonly reaches ≥100 mm/hr in many patients 1
• Critical caveat: IVIG therapy artificially elevates ESR, making it unreliable for monitoring treatment response 1, 2
• ESR remains elevated longer than CRP during disease resolution 2

C-Reactive Protein (CRP):

• Nearly universally elevated, typically ≥3 mg/dL (30 mg/L) 1
• More accurate than ESR after IVIG therapy for monitoring treatment response 1, 2
• Normalizes more quickly than ESR during resolution 2
• Important discrepancy: 44% of patients may show discordance between ESR and CRP elevations (high ESR with low CRP or vice versa), so both tests should be obtained 3

Hematologic Abnormalities

White Blood Cell Count:

• Leukocytosis is typical during acute stage with predominance of immature and mature granulocytes 1, 2
• Approximately 50% of patients have WBC >15,000/mm³ 1, 2
• Pitfall: Leukopenia is rare and should prompt consideration of alternative diagnoses 1, 2

Platelet Count:

• Timing is critical: Thrombocytosis typically does not occur until the second week of illness 2
• Peaks in the third week with mean counts around 700,000/mm³ 2
• Normalizes by 4-6 weeks 2
• Thrombocytopenia in the first 1-2 weeks is rare but concerning—may indicate disseminated intravascular coagulation and is a risk factor for coronary artery abnormalities 2

Anemia:

• Common, typically normochromic and normocytic 1, 2
• Develops particularly with prolonged duration of active inflammation 1
• Resolves with resolution of inflammation 2

Hepatic and Protein Abnormalities

Transaminases:

• Mild to moderate elevations in AST, ALT, or gamma-glutamyl transpeptidase occur in 40-60% of patients 2

Albumin:

• Hypoalbuminemia is common and becomes quite pronounced with more severe and prolonged illness 1, 2
• Albumin <3.0 g/dL is a supplemental laboratory criterion supporting diagnosis 2
• Associated with more severe acute disease 2

Bilirubin:

• Mild hyperbilirubinemia occurs in approximately 10% of patients 2

Urinalysis

Sterile Pyuria:

• Present in up to 80% of children, though lacks specificity for KD 2
• ≥10 WBC/hpf is a supplemental laboratory criterion 2
• Common pitfall: May be mistaken for partially treated urinary tract infection with sterile cultures 1, 2

Cerebrospinal Fluid (if obtained)

• Approximately 30% demonstrate pleocytosis with mononuclear cell predominance 2
• Normal glucose and generally normal protein levels 2
• Diagnostic pitfall: May lead to misdiagnosis as viral meningitis 2

Diagnostic Algorithm for Laboratory Testing

For patients with fever ≥5 days and 2-3 principal clinical features: 1

1. First-line tests: Measure CRP and ESR 1
2. If inflammatory markers are elevated: Obtain complete blood count, serum albumin, serum transaminases, and urinalysis 1, 2
3. Supplemental laboratory criteria supporting diagnosis (≥3 of the following): 2
   • Anemia for age
   • Platelet count ≥450,000/mm³ after day 7 of fever
   • Albumin <3.0 g/dL
   • Elevated ALT
   • WBC ≥15,000/mm³
   • Urine ≥10 WBC/hpf

Critical timing consideration: KD is unlikely if ESR, CRP, and platelet count are all normal after day 7 of illness 2

Key Clinical Caveats

• No single diagnostic test exists for KD—diagnosis remains clinical with laboratory support 2, 4
• A minimally elevated ESR in the setting of severe clinical disease should prompt investigation for disseminated intravascular coagulation 2
• Both ESR and CRP should be obtained given the high rate of discordance between these markers 3
• Laboratory abnormalities become more pronounced with more severe and prolonged illness 1