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Hepatotoxicity of sodium stibogluconate therapy for American cutaneous leishmaniasis
N C Hepburn1, I Siddique, A F Howie
1Departments of Dermatology, Royal Infirmary, Edinburgh.
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.
Insights
Sodium stibogluconate, a key leishmaniasis treatment, can cause liver damage and functional impairment. This effect is reversible upon drug cessation, suggesting careful liver function monitoring during therapy.
Area of Science:
- Hepatology
- Pharmacology
- Infectious Diseases
Background:
- Sodium stibogluconate is a primary treatment for leishmaniasis.
- Aminotransferase elevation is a known side effect of sodium stibogluconate therapy.
Purpose of the Study:
- To assess liver damage during American cutaneous leishmaniasis treatment with sodium stibogluconate.
- To evaluate hepatic functional impairment and hepatocellular damage using specific biomarkers.
Main Methods:
- Liver function tests, plasma glutathione S-transferase B1 (GST), and caffeine clearance (CCL) were measured before, during, and after treatment.
- Patients received either sodium stibogluconate or aminosidine.
Main Results:
- Sodium stibogluconate treatment increased alanine aminotransferase (ALT) and GST, and decreased CCL, indicating hepatocellular damage and functional impairment.
- Aminosidine treatment did not result in liver damage.
- Liver function markers returned to baseline six weeks after sodium stibogluconate withdrawal, with minimal residual CCL depression.
Conclusions:
- Sodium stibogluconate causes significant, but rapidly reversible, hepatocellular damage and hepatic functional impairment.
- Liver function should be monitored during treatment.
- Alternative treatments are recommended for patients with pre-existing liver disease.