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Are HIV positive patients resistant to statin therapy?
Lipids Health Dis. 2007 Oct 24; 6:27.LH

Abstract

BACKGROUND

Patients with HIV are subject to development of HIV metabolic syndrome characterized by dyslipidemia, lipodystrophy and insulin resistance secondary to highly active antiretroviral therapy (HAART). Rosuvastatin is a highly potent HMG-CoA reductase inhibitor. Rosuvastatin is effective at lowering LDL and poses a low risk for drug-drug interaction as it does not share the same metabolic pathway as HAART drugs. This study sought to determine the efficacy of rosuvastatin on lipid parameters in HIV positive patients with HIV metabolic syndrome.

RESULTS

Mean TC decreased from 6.54 to 4.89 mmol/L (25.0% reduction, p < 0.001). Mean LDL-C decreased from 3.39 to 2.24 mmol/L (30.8% reduction, p < 0.001). Mean HDL rose from 1.04 to 1.06 mmol/L (2.0% increase, p = ns). Mean triglycerides decreased from 5.26 to 3.68 mmol/L (30.1% reduction, p < 0.001). Secondary analysis examining the effectiveness of rosuvastatin monotherapy (n = 70) vs. rosuvastatin plus fenofibrate (n = 43) showed an improvement of 21.3% in TG and a decrease of 4.1% in HDL-C in the monotherapy group. The rosuvastatin plus fenofibrate showed a greater drop in triglycerides (45.3%, p < 0.001) and an increase in HDL of 7.6% (p = 0.08).

CONCLUSION

This study found that rosuvastatin is effective at improving potentially atherogenic lipid parameters in HIV-positive patients. The lipid changes we observed were of a smaller magnitude compared to non-HIV subjects. Our results are further supported by a small, pilot trial examining rosuvastatin effectiveness in HIV who reported similar median changes from baseline of -21.7% (TC), -22.4% (LDL-C), -30.1% (TG) with the exception of a 28.5% median increase in HDL. In light of the results revealed by this pilot study, clinicians may want to consider a possible resistance to statin therapy when treating patients with HIV metabolic syndrome.

Authors+Show Affiliations

Department of Medicine, University of British Columbia, Vancouver, Canada. kevinwjohns@gmail.comNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17958912

Citation

Johns, Kevin W., et al. "Are HIV Positive Patients Resistant to Statin Therapy?" Lipids in Health and Disease, vol. 6, 2007, p. 27.
Johns KW, Bennett MT, Bondy GP. Are HIV positive patients resistant to statin therapy? Lipids Health Dis. 2007;6:27.
Johns, K. W., Bennett, M. T., & Bondy, G. P. (2007). Are HIV positive patients resistant to statin therapy? Lipids in Health and Disease, 6, 27.
Johns KW, Bennett MT, Bondy GP. Are HIV Positive Patients Resistant to Statin Therapy. Lipids Health Dis. 2007 Oct 24;6:27. PubMed PMID: 17958912.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Are HIV positive patients resistant to statin therapy? AU - Johns,Kevin W, AU - Bennett,Matthew T, AU - Bondy,Gregory P, Y1 - 2007/10/24/ PY - 2007/08/13/received PY - 2007/10/24/accepted PY - 2007/10/26/pubmed PY - 2008/3/4/medline PY - 2007/10/26/entrez SP - 27 EP - 27 JF - Lipids in health and disease JO - Lipids Health Dis VL - 6 N2 - BACKGROUND: Patients with HIV are subject to development of HIV metabolic syndrome characterized by dyslipidemia, lipodystrophy and insulin resistance secondary to highly active antiretroviral therapy (HAART). Rosuvastatin is a highly potent HMG-CoA reductase inhibitor. Rosuvastatin is effective at lowering LDL and poses a low risk for drug-drug interaction as it does not share the same metabolic pathway as HAART drugs. This study sought to determine the efficacy of rosuvastatin on lipid parameters in HIV positive patients with HIV metabolic syndrome. RESULTS: Mean TC decreased from 6.54 to 4.89 mmol/L (25.0% reduction, p < 0.001). Mean LDL-C decreased from 3.39 to 2.24 mmol/L (30.8% reduction, p < 0.001). Mean HDL rose from 1.04 to 1.06 mmol/L (2.0% increase, p = ns). Mean triglycerides decreased from 5.26 to 3.68 mmol/L (30.1% reduction, p < 0.001). Secondary analysis examining the effectiveness of rosuvastatin monotherapy (n = 70) vs. rosuvastatin plus fenofibrate (n = 43) showed an improvement of 21.3% in TG and a decrease of 4.1% in HDL-C in the monotherapy group. The rosuvastatin plus fenofibrate showed a greater drop in triglycerides (45.3%, p < 0.001) and an increase in HDL of 7.6% (p = 0.08). CONCLUSION: This study found that rosuvastatin is effective at improving potentially atherogenic lipid parameters in HIV-positive patients. The lipid changes we observed were of a smaller magnitude compared to non-HIV subjects. Our results are further supported by a small, pilot trial examining rosuvastatin effectiveness in HIV who reported similar median changes from baseline of -21.7% (TC), -22.4% (LDL-C), -30.1% (TG) with the exception of a 28.5% median increase in HDL. In light of the results revealed by this pilot study, clinicians may want to consider a possible resistance to statin therapy when treating patients with HIV metabolic syndrome. SN - 1476-511X UR - https://www.unboundmedicine.com/medline/citation/17958912/Are_HIV_positive_patients_resistant_to_statin_therapy L2 - https://lipidworld.biomedcentral.com/articles/10.1186/1476-511X-6-27 DB - PRIME DP - Unbound Medicine ER -