A neonate treated with chloramphenicol develops vomiting, hypothermia, ash-gray skin color, abdominal distension and cardiovascular collapse within days of starting high-dose therapy. The pathogenesis of this syndrome is best explained by:
- A Immature hepatic glucuronyl transferase leading to drug accumulation ✓
- B Idiosyncratic immune-mediated marrow aplasia
- C Hemolysis due to glutathione deficiency
- D Displacement of bilirubin causing kernicterus
Explanation
Gray baby syndrome results from inadequate hepatic glucuronidation of chloramphenicol in neonates combined with reduced glomerular filtration, causing toxic accumulation that impairs myocardial function. This is a dose-related toxicity, distinct from the rare idiosyncratic aplastic anemia seen weeks after exposure in older patients. Kernicterus is associated with sulfonamide displacement, not chloramphenicol.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
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Written and medically reviewed by the StethoPrep medical team.