Clinical implications of appetite suppressants

Abstract

A 41-YEAR-OLD woman with a past medical history significant for asthma, tubal ligation, and mild systemic hypertension presented with the chief complaint of severe exertional dyspnea. She was essentially well until 6 weeks before presentation when she began to experience exertional dyspnea that progressed rapidly over the next few weeks. Her systemic hypertension had been wellcontrolled by lisinopril 10 mg/d and she was using inhaled bronchodilators and occasional steroid therapy to treat her asthma. Approximately 7 months before presentation, the patient, who was a long-time smoker (10 pack-year), had asked her primary care physician to prescribe an appetite suppressant. Although not markedly overweight, she intended to quit smoking and was concerned about possible weight gain following smoking cessation. Fen-phen (fenfluramine with phentermine) was prescribed, which the patient took daily for approximately 4 months. The drug was discontinued by the patient when she began experiencing nausea and vomiting, which she associated with drug intake. There was no history of illicit drug use, human immunodeficiency virus risk factors, connective tissue disease, or liver disease. Physical examination revealed a moderately overweight woman (92 kg and 163 cm), but was otherwise normal. A chest x-ray film revealed clear lungs and a significantly enlarged cardiac silhouette compared with a normal examination obtained 1.5 years previously. An echocardiogram revealed a markedly dilated right atrium and ventricle, septal paradoxical motion, 3+ tricuspid regurgitation, and an estimated pulmonary systolic pressure greater than 80 mm Hg. The left ventricular function was normal. The diagnosis of pulmonary hypertension was confirmed by right heart catheterization. Mean pulmonary arterial pressure was 50 mm Hg and pulmonary vascular resistance index 824 dynes, s/cmS/m 2. A ventilation-perfusion scan and Doppler studies of the lower extremities were normal. Acute drug testing with oral calcium channel blocker, performed under hemodynamic monitoring, resulted in a 30% reduction in mean pulmonary artery pressure and pulmonary vascular resistance index. The patient was given 120 mg of diltiazem slow release twice a day, which significantly improved her tolerance to exercise as assessed by a 6-minute walk test. She was also given warfarin daily. She remains stable on therapy 10 months after diagnosis, although a repeat echocardiogram has revealed no change in estimated pulmonary artery pressure.