Hyperlipidemia associated with protease inhibitor therapy

OBJECTIVE: To report a case of extreme hyperlipidemia associated with protease inhibitor-based antiretroviral therapy and review the relevant literature concerning lipid abnormalities with HIV infection and antiretroviral therapy. CASE SUMMARY: A 35-year-old HIV-infected man developed a serum cholesterol of 1472 mg/dL and fasting serum triglycerides of 8660 mg/dL after initiation of antiretroviral therapy consisting of ritonavir, saquinavir, nevirapine, and didanosine. All other medications had been stable during this time period and the abnormality resolved after discontinuation of antiretroviral therapy and initiation of lipid-lowering therapy. The elevated cholesterol and triglyceride concentrations did not recur when therapy was reinstituted with nelfinavir, saquinavir, nevirapine, and didanosine. The hyperlipidemia then was attributed to ritonavir. DISCUSSION: Lipid abnormalities are common in patients with HIV infection and usually consist of hypocholesterolemia and moderate hypertriglyceridemia. Hypercholesterolemia and hypertriglyceridemia have been reported with ritonavir and, less commonly, with other currently available protease inhibitors. Some cases of ritonavir-associated hyperlipidemia have been extreme. Although an association between hyperlipidemia and clinical consequences such as pancreatitis and atherosclerotic disease has not been well described with protease inhibitor therapy, pancreatitis is common in HIV-infected patients. It is possible that in some cases, protease inhibitor-induced hypertriglyceridemia may contribute to the development of pancreatitis. CONCLUSIONS: Optimal management of lipid abnormalities in HIV-infected patients is controversial. The potential benefit of reducing the incidence of pancreatitis and atherosclerotic events must be weighed against the risk of intolerance, toxicity, and drug interactions.

This article has been cited by other articles:

				J. Fuller A 39-Year-Old Man With HIV-Associated Lipodystrophy JAMA, September 3, 2008; 300(9): 1056 - 1066. [Abstract] [Full Text] [PDF]

				M. E Temple, K. I Koranyi, and M. C Nahata Lipodystrophy in HIV-Infected Pediatric Patients Receiving Protease Inhibitors Ann. Pharmacother., September 1, 2003; 37(9): 1214 - 1218. [Abstract] [Full Text] [PDF]

				M. K. S. Leow, C. L. Addy, and C. S. Mantzoros Human Immunodeficiency Virus/Highly Active Antiretroviral Therapy-Associated Metabolic Syndrome: Clinical Presentation, Pathophysiology, and Therapeutic Strategies J. Clin. Endocrinol. Metab., May 1, 2003; 88(5): 1961 - 1976. [Full Text] [PDF]

				L. G. DePAOLA Managing the care of patients infected with bloodborne diseases J Am Dent Assoc, March 1, 2003; 134(3): 350 - 358. [Abstract] [Full Text] [PDF]

				P. G. Yeni, S. M. Hammer, C. C. J. Carpenter, D. A. Cooper, M. A. Fischl, J. M. Gatell, B. G. Gazzard, M. S. Hirsch, D. M. Jacobsen, D. A. Katzenstein, et al. Antiretroviral Treatment for Adult HIV Infection in 2002: Updated Recommendations of the International AIDS Society-USA Panel JAMA, July 10, 2002; 288(2): 222 - 235. [Abstract] [Full Text] [PDF]

				T. M. Riddle, D. G. Kuhel, L. A. Woollett, C. J. Fichtenbaum, and D. Y. Hui HIV Protease Inhibitor Induces Fatty Acid and Sterol Biosynthesis in Liver and Adipose Tissues Due to the Accumulation of Activated Sterol Regulatory Element-binding Proteins in the Nucleus J. Biol. Chem., September 28, 2001; 276(40): 37514 - 37519. [Abstract] [Full Text] [PDF]