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Open Access Research article

Pharmacokinetic and metabolic effects of American ginseng (Panax quinquefolius) in healthy volunteers receiving the HIV protease inhibitor indinavir

Adriana SA Andrade1*, Craig Hendrix2, Teresa L Parsons2, Benjamin Caballero3, Chun-Su Yuan4, Charles W Flexner2, Adrian S Dobs5 and Todd T Brown5

Author Affiliations

1 Division of Infectious Diseases, The Johns Hopkins University, Baltimore, MD 21287, USA

2 Division of Clinical Pharmacology, The Johns Hopkins University, Baltimore, MD 21287, USA

3 Department of Human Nutrition, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA

4 Tang Center for Herbal Medicine Research, Department of Anesthesia and Critical Care, Pritzker School of Medicine, University of Chicago, Chicago, IL 60637, USA

5 Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University, Baltimore, MD 21287, USA

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BMC Complementary and Alternative Medicine 2008, 8:50  doi:10.1186/1472-6882-8-50

Published: 19 August 2008

Abstract

Background

Complementary and alternative medicine (CAM) use is prevalent among HIV-infected patients to reduce the toxicity of antiretroviral therapy. Ginseng has been used for treatment of hyperglycemia and insulin resistance, a common side effect of some HIV-1 protease inhibitors (PI). However, it is unknown whether American ginseng (AG) can reverse insulin resistance induced by the PI indinavir (IDV), and whether these two agents interact pharmacologically. We evaluated potential pharmacokinetic interactions between IDV and AG, and assessed whether AG improves IDV-induced insulin resistance.

Methods

After baseline assessment of insulin sensitivity using the insulin clamp technique, healthy volunteers received IDV 800 mg q8 h for 3 days and then IDV and AG 1g q8h for 14 days. IDV pharmacokinetics and insulin sensitivity were assessed before and after AG co-administration.

Results

There was no difference in the area-under the plasma-concentration-time curve after the co-administration of AG, compared to IDV alone (n = 13). Although insulin-stimulated glucose disposal per unit of insulin (M/I) decreased by an average of 14.8 ± 5.9% after 3 days of IDV (from 0.113 ± 0.012 to 0.096 ± 0.014 mg/kgFFM/min per μU/ml of insulin, p = 0.03, n = 11), M/I remained unchanged after co-administration of IDV and AG.

Conclusion

IDV decreases insulin sensitivity, which is unaltered by AG co-administration. AG does not significantly affect IDV pharmacokinetics.