A 50-year-old man started on carbamazepine for trigeminal neuralgia returns after 4 weeks with fatigue, nausea, and confusion. Serum sodium is 122 mEq/L, urine osmolality is high, and urine sodium is elevated. Thyroid and adrenal function are normal. What is the most likely explanation?
- A Carbamazepine-induced pseudohypoaldosteronism with renal salt wasting
- B Carbamazepine potentiation of ADH action causing syndrome of inappropriate antidiuresis ✓
- C Carbamazepine-induced central diabetes insipidus with secondary water intoxication
- D Autoimmune adrenalitis triggered by carbamazepine
Correct answer: B. Carbamazepine potentiation of ADH action causing syndrome of inappropriate antidiuresis
Explanation
Carbamazepine enhances the effect of vasopressin on renal collecting ducts, producing dilutional hyponatraemia indistinguishable from SIADH, typically within the first weeks of therapy. The euvolaemic pattern with concentrated urine fits this. Diabetes insipidus causes dilute urine and hypernatraemia, the opposite picture. Pseudohypoaldosteronism is associated with drugs like lithium in some reports but not carbamazepine, and adrenalitis is not a recognised carbamazepine toxicity.
Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.
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