A 45-year-old woman on carbamazepine for trigeminal neuralgia presents with fatigue and mild confusion. Serum sodium is 122 mEq/L, urine osmolality is elevated, and euvolemia is present. The mechanism of this adverse effect is:
- A Direct nephrogenic diabetes insipidus from collecting duct injury
- B Stimulation of ADH release and potentiation of its renal action, producing a state like SIADH ✓
- C Inhibition of renal carbonic anhydrase causing sodium wasting
- D Osmotic diuresis from the inactive metabolite carbamazepine epoxide
Correct answer: B. Stimulation of ADH release and potentiation of its renal action, producing a state like SIADH
Explanation
Carbamazepine is the antiepileptic most associated with hyponatremia. It enhances ADH secretion from the posterior pituitary and sensitizes the renal tubules to ADH, producing a syndrome indistinguishable from SIADH with euvolemic hypo-osmolar hyponatremia and concentrated urine. Oxcarbazepine carries an even higher risk. Carbonic anhydrase inhibition is a property of topiramate and acetazolamide, and nephrogenic diabetes insipidus would cause dilute urine with hypernatremia, the opposite picture.
Reference: Katzung Basic and Clinical Pharmacology, 15th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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