Hepatotoxicity of sodium stibogluconate therapy for American cutaneous leishmaniasis

Abstract

Sodium stibogluconate is the mainstay of treatment for all forms of leishmaniasis. Therapy is associated with an increase in serum aminotransferases. In this study liver damage was assessed during treatment of American cutaneous leishmaniasis with sodium stibogluconate and also in a control group given aminosidine. In addition to standard liver function tests, acute hepatocellular damage was assessed by measuring plasma glutathione S-transferase B1 (GST), and hepatic metabolic capacity was assessed by a caffeine clearance (CCL) test, before, during and after treatment. Thirteen patients were treated; 5 received sodium stibogluconate, 6 received aminosidine and a further 2 patients received aminosidine followed by sodium stibogluconate. Treatment with sodium stibogluconate was associated with an increase in both alanine aminotransferase (ALT) and GST and a fall in the CCL, indicating both hepatocellular damage and functional impairment. Six weeks after treatment had stopped ALT and GST had returned to pre-treatment levels and the CCL remained depressed in only one patient. Patients given aminosidine did not show any evidence of liver damage. Sodium stibogluconate is associated with significant hepatocellular damage and hepatic functional impairment. However, this is rapidly reversible on drug withdrawal. We suggest that liver function is monitored throughout treatment and that patients with pre-existing liver disease receive alternative treatment.