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Presents letters to the editor on medical topics as of July 3, 2002. Raloxifene and risk of cardiovascular events; Diagnosis and treatment of cutaneous anthrax; Camphor intoxication after cao gio (coin rubbing).

Abstract Introduction Chronic hypokalemia is the main finding in patients with Gitelman's syndrome. Exogenous factors can trigger deterioration of the patient's condition and provoke clinical symptoms. We discuss the pathophysiology of and therapy for Gitelman's syndrome, with a focus on dietary factors which may aggravate the disease. Case presentation We describe the case of a 31-year-old, previously apparently healthy Caucasian Swiss man who presented to our hospital with gait disturbance of subacute onset and a potassium level of 1.5 mmol/L. A detailed medical history revealed that he had been consuming large amounts of licorice (in the form of Fisherman's Friend menthol eucalyptus lozenges). Despite discontinuing the intake of glycyrrhizinic acid, his potassium level remained low. Biochemical investigations showed refractory hypokalemia and secondary hyperaldosteronism, suggestive of Gitelman's syndrome. Despite treatment with supplementation of potassium and magnesium in combination with an aldosterone antagonist, further clinically symptomatic episodes occurred. Triggers could be identified only by repeated detailed history taking. In response to the patient's dietary excesses (ingestion of relevant amounts of alcohol, lemon juice and iced tea), his hypokalemia was aggravated and provoked clinical symptoms. Finally, vomiting and failure to replace salt led to volume depletion and hypokalemic crisis, with a plasma potassium level of 1.0 mmol/L and paralysis with respiratory failure necessitating not only infusion of saline and potassium but also temporary mechanical ventilation. Conclusion Dietary preferences may have a much larger impact than any drug treatment on the symptoms of this chronic syndrome. Individual (mainly dietary) preferences must be monitored closely, and patients should be given dietary advice to avoid recurrent aggravation of hypokalemia with muscular weakness.

Abstract This case report describes for the first time acute coronary syndrome in a 67-year old patient after oral intake of naratriptan for migraine. So far in the literature, only sumatriptan, zolmitriptan and frovatriptan have been described to cause acute coronary syndromes. A 67-year old Swiss woman with thoracic pain after intake of 2.5 mg naratriptan presented with T-wave inversions in the ECG and a positive troponin-T at our hospital. Coronary angiography showed normal coronary arteries. Naratriptan-induced coronary vasospasms were thought to have caused the acute coronary syndrome. Triptans should not be prescribed in patients with pre-existing coronary heart disease. However, triptans can also cause acute coronary syndromes in patients without coronary heart disease – as described in our case report. Severe or persistent thoracic pain after intake of triptans should therefore be investigated accordingly.