PROLONGED TACHYCARDIA, HYPOKALEMIA, AND HYPOPHOSPHATEMIA AFTER CLENBUTEROL INGESTION: CONFIRMATION BY QUANTITATIVE CLENBUTEROL LEVELS

Objective: Clenbuterol is a long acting [beta.sub.2] adrenoreceptor agonist used clinically in the treatment of pulmonary disorders. Due to its unique ability to shunt metabolic energy from lipid production to protein and muscle production, clenbuterol is used illicitly as an anabolic agent in livestock and human bodybuilders. We report a case of clenbuterol toxicity confirmed and correlated with qualitative and quantitative serum clenbuterol assays. Case Report: A 28-year-old healthy female tasted a small amount of clenbuterol powder that belonged to a friend. Two to three hours later she presented to the ED with tremor, palpitations, and vomiting. Vital signs included: pulse 140/min and BP 120/80 mm Hg. A fine hand tremor was noted. An ECG revealed sinus tachycardia, and serum chemistries were remarkable only for hypokalemia (2.4 mmol/L), and hypophosphatemia (0.9 mg/dL). Metoprolol (50 mg PO) was given, and her pulse slowed to 115/min, but returned to 130/min within 30 minutes. Twice subsequently, metoprolol (5mg IV) was administered, with only a transient response each time. Hypokalemia was supplemented with KCl (40 mEq PO and 10 mEq IV). After 10 hours of persistent tremor and tachycardia, she refused further treatment and left against medical advice. She returned seven hours later, still symptomatic. Her pulse was 123/min and a fine hand tremor was again noted. The ECG was unchanged, and hypokalemia (3.3 mmol/L) and hypophosphatemia (2.0 mg/dL) persisted. Metoprolol (50 mg PO) was given, and again she refused further treatment. Qualitative and quantitative serum clenbuterol assays were performed on blood samples taken at each presentation, 3 hours and 20 hours after the clenbuterol ingestion, respectively. The qualitative technique, ELISA, was positive for the first and indeterminate for the second serum sample. Liquid chromatography/mass spectrometry (LC/MS) quantitation revealed a serum clenbuterol concentration of 2.93 mcg/L in the first sample and was undetectable ([is less than] 1 mcg/L) in the second sample. Conclusion: Clenbuterol toxicity resembles other [beta.sub.2] adrenoreceptor agonist toxicities. Most reported cases describe patients who ate livestock illicitly treated with clenbuterol. In this case, the clenbuterol belonged to a bodybuilder who used clenbuterol for the purpose of increasing muscle mass and decreasing body fat. Although acute clenbuterol toxicity has been rarely reported following illicit use in humans, this is the first such case to provide confirmatory toxicological analysis. This patient developed sustained tachycardia, hypokalemia and hypophosphatemia after ingesting an apparently small quantity of clenbuterol. It is noteworthy that even at a serum concentration below the limit of detection by LC/MS, the patient remained symptomatic for several hours. Hoffman RJ, Hoffman RS, Freyberg C, Poppinga R, Nelson L. New York City Poison Control Center, New York City, New York, USA