A patient on long-term isoniazid therapy develops peripheral neuropathy. The BIOCHEMICAL basis of pyridoxine (B6) deficiency in this context is:
- A Isoniazid forms a hydrazone complex with pyridoxal phosphate (PLP), inactivating it and increasing urinary excretion of the complex ✓
- B Isoniazid directly destroys pyridoxal phosphate in peripheral neurons
- C Isoniazid inhibits pyridoxal kinase, preventing conversion of B6 to its active form
- D Isoniazid causes malabsorption of B6 from the GI tract
Explanation
Isoniazid (isonicotinic acid hydrazide) contains a hydrazide group that condenses with the aldehyde group of pyridoxal phosphate (PLP), forming an isonicotinoyl-PLP hydrazone. This complex is biologically inactive and is excreted in urine, depleting cellular PLP. PLP is the coenzyme for >100 reactions including aminotransferases, decarboxylases (DOPA decarboxylase, GAD for GABA synthesis), and cystathionine beta-synthase. Depletion causes peripheral neuropathy (reduced GABA, abnormal amino acid metabolism), sideroblastic anemia (blocked ALA synthase — first enzyme in heme synthesis). Pyridoxine 25–50 mg/day is co-prescribed to prevent this.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.