A clinical trial to evaluate the efficiency of oral zinc sulphate in the treatment of cutaneous leishmaniasis was conducted. One-hundred and four patients with parasitologically proven cutaneous leishmaniasis were included in the trial. Patients were assigned randomly to receive 2.5, 5 or 10 mg/kg of zinc sulphate orally, and a control group of patients did not receive any treatment. All patients were followed up for 45 days. At the end of the follow-up period, lesions were assessed and parasitological proof of cure or otherwise was sought. Results showed that the cure rate for the 2.5 mg/kg group was 83.9%, for the 5 mg/kg treatment group it was 93.1% and for the 10 mg/kg treatment group it was 96.9%. No lesions in the control group showed any sign of healing during the follow-up period. Therefore, oral zinc sulphate can be recommended as a very safe therapy for cutaneous leishmaniasis.

A comparative clinical trial between two newly introduced intralesional treatments for acute leishmaniasis and the established treatment of intralesionally-administered pentavalent antimony compounds was performed. Treatments were allocated randomly to a total of 63 patients who received 2% zinc sulphate, 7% sodium chloride solutions or sodium stibogluconate intralesionally. A number of patients were left without treatment as controls. Patients were followed-up for 45 days, the results showing that the three treatments gave comparable cure rates by the end of the follow-up period. However, zinc sulphate gave a high cure rate (94.8%) usually with a single injection.

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The protective effects of drugs acting at the benzodiazepine receptors against ethanol-induced gastric damage were investigated using a newly developed in vitro model of the ethanol-induced gastric damage. The rat stomachs were isolated from the whole animal and kept in Kreb's solution at 37 degrees C. Gastric damage was induced by administration of 1 mL of 50% V/V ethanol into the isolated rat stomach. Administration of the benzodiazepine agonist, clonazepam (25, 50, 100 microg), or the partial benzodiazepine inverse agonist Ro15-4513 (50 or 100 microg), significantly protected against ethanol-induced gastric damage when these agents were administered 15 min before ethanol. The protective effects of these drugs were blocked by the benzodiazepine receptor antagonist flumazenil (200-400 microg). Flumazenil alone was found to aggravate ethanol-induced gastric damage (200-400 microg). The results of this study give evidence for the involvement of central-type benzodiazepine receptors located in the stomach in the protective action of benzodiazepines against ethanol-induced gastric damage.