A 38-year-old woman with chronic cholestatic liver disease presents with progressive proprioceptive loss, peripheral neuropathy, and retinitis pigmentosa. Serum studies show very low levels of a specific fat-soluble vitamin. Biochemically, this vitamin acts as a chain-breaking antioxidant protecting cellular membranes. Which mechanism best explains the neurological damage in this deficiency?
- A Impaired gamma-carboxylation of clotting factors
- B Accumulation of lipid peroxides due to failure of free radical scavenging ✓
- C Failure of 25-hydroxylation in the liver
- D Impaired conversion of procollagen to collagen
Correct answer: B. Accumulation of lipid peroxides due to failure of free radical scavenging
Explanation
The patient has vitamin E deficiency. Vitamin E (alpha-tocopherol) is the principal chain-breaking antioxidant in cell membranes. It scavenges free radicals and prevents peroxidation of polyunsaturated fatty acids in neuronal and erythrocyte membranes. In deficiency, lipid peroxides accumulate, causing spinocerebellar ataxia, neuropathy, and retinopathy. Option A describes vitamin K function and is the most tempting distractor for a fat-soluble vitamin question.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.