Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is one of the most common causes of hyponatremia. The usual causes are malignancies, central nervous system, pulmonary disorders, and drugs. Amiodarone is a broad spectrum antiarrhythmic agent widely used in the management of arrhythmias. The different side effects include thyroid dysfunction, visual disturbances, pulmonary infiltrates, ataxia, cardiac conduction abnormalities, drug interactions, corneal microdeposits, skin rashes, and gastrointestinal disturbances. SIADH is a rare but lethal side effect of amiodarone. We describe a 62-year-old male who was suffering from advanced prostatic malignancy, taking amiodarone for underlying heart disease. He developed SIADH which was initially thought to be paraneoplastic in etiology, but later histopathology refuted that. This case emphasizes the importance of detailed drug history and the role of immunohistochemistry in establishing the diagnosis and management of hyponatremia due to SIADH. 1. Introduction Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is one of the most common causes of hyponatremia. This syndrome is caused by various malignancies, lung diseases, central nervous system disorders, and drugs. The commonest malignancy associated with SIADH is small cell carcinoma of the lung [1]. There are a few case reports of SIADH in patients with small cell and anaplastic carcinoma of prostate [2]. Amongst various drugs selective serotonin reuptake inhibitors, carbamazepine, thiazide diuretics, chlorpropamide, and alkylating agents are commonly associated with SIADH [3–6]. Amiodarone is extensively used in clinical practice for a wide variety of arrhythmias. The adverse effect profile is very broad; however, there are very few cases of hyponatremia due to SIADH reported with this drug [7–16]. We describe one such case in an elderly male which was initially thought to be due to ectopic secretion of vasopressin by an anaplastic carcinoma of prostate but later refuted by immunohistochemistry of the tumor and normalization of serum sodium level following omission of amiodarone. 2. Case Report A 63-year-old male, known to be hypothyroid for the past three years, on treatment with 100？μg of L-thyroxine presented to his primary care physician with history of 3 episodes of syncopal attacks 8 months back. He was a smoker with history suggestive of chronic bronchitis. He was also hypertensive for the last 4 years. His blood pressure was stable on 100？mg of losartan per day. Electrocardiogram and 24-hour holter revealed runs of ill
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