TITLE:
Carbamazepine-Induced SIADH: A Case Report
AUTHORS:
Imran Sheriff, Madeeha Sheriff, Zarah Shabir, Ilana Stukal, Aayan Sheriff
KEYWORDS:
Carbamazepine, SIADH, Hyponatremia, Antiepileptic Drugs, Drug-Induced Endocrine Disorder
JOURNAL NAME:
Open Journal of Clinical Diagnostics,
Vol.16 No.1,
March
17,
2026
ABSTRACT: Introduction: Carbamazepine is an anticonvulsant widely used for epilepsy, trigeminal neuralgia, and bipolar disorder. While effective, it has been implicated in the development of the syndrome of inappropriate antidiuretic hormone secretion (SIADH), leading to hyponatremia. Case Presentation: We report the case of a 66-year-old man with a history of hypertension, hyperlipidemia, schizophrenia, and epilepsy who presented with confusion, blurry vision, and bilateral hand paresthesia. Laboratory evaluation revealed hyponatremia (serum sodium 118 mEq/L), low serum osmolality, elevated urine osmolality, and elevated urine sodium, consistent with SIADH. Despite the therapeutic range of carbamazepine, symptoms persisted for several years due to delayed recognition of the drug-induced etiology. Gradual tapering and eventual discontinuation of carbamazepine resulted in normalization of serum sodium. Discussion: Carbamazepine-induced SIADH is a well-documented but often underrecognized complication of antiepileptic therapy. The mechanism involves direct stimulation of vasopressin V2 receptors, resulting in increased aquaporin-2 expression and water reabsorption. Conclusion: This case highlights the importance of recognizing medication-induced SIADH as a potential cause of refractory hyponatremia. Early identification and discontinuation of the offending agent are crucial to prevent morbidity and ensure optimal outcomes.