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Retrieved 30 September Archived from the original on 13 May Archived from the original on 23 October Archived from the original on 7 September Encyclopedic reference of parasitology. World Health Organization model list of essential medicines: 21st list Geneva: World Health Organization. Tarascon pocket pharmacopoeia 13 ed. McGraw-Hill, New York. Archived from the original on 22 February Harrison's Principles of Internal Medicine, 18th ed.

 

Annals of Internal Medicine. Archived from the original on 6 February If acute overdosage of mebendazole occurs, vomiting and purging should be induced. Activated charcoal may be administered. Mebendazole does not inhibit glucose uptake in mammals. Mebendazole appears to cause degenerative changes in the intestine of nematodes and in the absorptive cells of cestodes. Microtubular deterioration results in inhibition of organelle movement and interferes with the absorptive and secretory function.

 

As a result of excessive accumulation of intracellular transport secretory granules, hydrolytic and proteolytic enzymes are released and cause cellular autolysis. The presence of food in the digestive tract of the definitive host does not affect the action of the drug during treatment of intestinal helminthic infections. Peak plasma concentrations of mebendazole occur approximately 0. Mebendazole is highly bound to plasma proteins. It is not known if mebendazole is distributed into milk.

 

Although the exact metabolic fate of mebendazole has not been fully determined, the drug is metabolized via decarboxylation to 2-amino-5 6 -benzimidazolyl phenylketone; this metabolite does not have anthelmintic activity. The metabolic fate and rate of excretion of unabsorbed mebendazole have not been determined. Mebendazole is a synthetic, benzimidazole-derivative anthelmintic agent. All benzimidazoles can cause mild and reversible rises in transaminases, but even in high doses withdrawal is justified in only a few patients.

 

A year-old man with ascariasis took two 3-day cycles of mebendazole mg bd with a 2-week interval. Ten days later he had tender hepatomegaly. The serum alkaline phosphatase and bilirubin were normal and the gamma-glutamyl transferase mildly raised. The white blood cell count was Antimitochondrial antibodies were negative but anti-nuclear antibodies and antibodies against smooth muscle were positive.

 

Extensive tests to exclude other causes of granulomatous hepatitis were all negative. There was slight fibrosis around the granulomata. There was no evidence of cholestasis. No helminthic ova were found.

 

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