Introduction. Sibutramine is an amphetamine-like drug used for its weight reducing effect. Sibutramine-induced acute coronary syndrome has rarely been reported. We report a case of myocardial infarction associated with the use of sibutramine. Case Report. A 37-year-old woman presented to an Emergency Department (ED) with intermittent retrosternal chest pain, nausea, and sweating for 3 days. She reported taking one sibutramine tablet each day for 3 days. Blood pressure was 128/89 mm Hg and pulse 66 beats/min. An electrocardiogram revealed ST elevation over the inferior leads and ST depression over leads AVR and V1, the other leads were normal. Serum troponin T was 0.65 μg/L, and sibutramine was identified in her urine. Echocardiography revealed mild hypokinesia over the inferior wall without evidence of acute aortic dissection. The ST segment changes resolved spontaneously within 24 h of cardiac care unit (CCU) admission, a coronary angiogram performed 1 week later was unremarkable, and echocardiography performed 4 weeks after the event showed normal resting regional wall motion. Discussion. Seventeen medications containing sibutramine as an active ingredient were registered in Hong Kong in 2007. Sibutramine was introduced in the United States in 1997 and in Australia, United Kingdom, and Italy in 2001. Hypertension, tachycardia, dry mouth, and headache are the most commonly reported adverse reactions. Cardiovascular toxicities include tachycardia, palpitation, hypertension, and tachyarrhythmia. Conclusions. We postulate that the myocardial infarction was the result of coronary vasospasm associated with the therapeutic use of sibutramine-containing slimming pills.

Letters to the editor 913Due to deterioration in the condition of the patient and progressing neurological symptoms the patient was transferred to the Department of Nephrology, Transplantology, and Internal Medicine at Pomeranian Medical University in Szczecin, with the initial diagnosis of thallium intoxication. On admission to our department, the patient complained of pain in his legs that interfered with normal walking. He reported nausea, dysgeusia, and severe epigastric pain. Oliguria was noted and the patient experienced growing weakness, insomnia, nocturnal anxiety, and audiovisual hallucinations. Physical examination done on the third day after ingestion revealed general paleness, psoriatic lesions on the left calf and head, elevated temperature, and sweating. There were no abnormalities in the subcutaneous tissues. Lymph nodes were not enlarged, sense organs were normal, and the respiratory system was normal. His heart rate was 50 beats/minute and his blood pressure was 200/100 mmHg. The examination of the abdomen was normal. There were limitations in active and passive mobility of the ankles, as well as superficial and deep paresthesias of the feet and calves.Laboratory tests revealed a white blood cell count of 10.4 × 10 9 /L with normal erythrocyte and platelet values. Urine pH and specific gravity were 5.5 and 1.015, respectively. Urinalysis showed glucose, protein, and erythrocytes. A 24-hour urine collection had a volume of 3100 mL and protein of 1.12 g. Capillary blood gases analysis disclosed pH 7.456, pCO 2 33.6 mmHg, pO 2 88.0 mmHg, HCO 3 at 23.1 mmol/L, and Base Excess 0.0 mmol/L. Serum electrolytes were normal, creatinine was 1.57 mg/dL, and urea was 35 mg/dL. Other laboratory results were aspartate aminotranferase 51 U/L (reference 0 to 35 U/L), alanine aminotransferase 40 U/L (reference 0 to 35 U/L), creatine kinase 526 U/L (reference 0 to 130 U/L), lactate dehydrogenase 616 U/L (reference 50 to 150 U/L); serum and urine amylase, γ-glutamyl transferase, and alkaline phosphatase were normal. No abnormalities in abdominal ultrasound and chest radiograph were noted. An electrocardiogram (ECG) revealed a normal sinus rhythm and a rate of 54 beats/minute. No ophthalmologic abnormalities were disclosed. Electromyography (EMG) disclosed distal axonal-demyelinization polyneuropathy with loss of innervation of foot muscles, absence of response to stimulation of peroneal nerves, and significant neurographic abnormalities of tibial nerves.Gastroduodenoscopy revealed acute gastritis and mucosal biopsy provided evidence for Helicobacter pylori infection. The patient was given one dose of carbamazepine (200 mg). Diuresis was stimulated, and Vitamin B complex and atropine were administered. At this point, the thallium concentration in the urine sample collected at the county hospital was reported to be 11,600 μg/L (reference blood and urine value ≤1μg/L or 5 nmol/L), measured using flame atomic absorption spectrometry. The diagnosis of thallium intoxication was made, the patient was given Prussian blue 4 ...