A 3-day-old full-term neonate receiving chloramphenicol for suspected meningitis becomes lethargic, refuses feeds, turns ashen grey, and develops hypotension and abdominal distension. The underlying cause of this presentation is:
- A Deficiency of glucose-6-phosphate dehydrogenase causing hemolysis
- B Immature hepatic glucuronidation leading to drug accumulation ✓
- C Displacement of bilirubin from albumin causing kernicterus
- D Inhibition of mitochondrial protein synthesis in the bone marrow
Explanation
The gray baby syndrome results from deficient hepatic UDP-glucuronosyltransferase activity in neonates, so chloramphenicol is not conjugated and accumulates. It also causes direct cellular toxicity. The classic picture is vomiting, ashen gray color, hypotension, and cardiovascular collapse within days of starting therapy. Option D describes dose-related marrow suppression seen later in therapy, and option C is the mechanism by which sulfonamides cause kernicterus.
Reference: Katzung Basic and Clinical Pharmacology, 16th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.