Abstract
IntroductionHIV infection is a disease associated with chronic inflammation and immune activation. Antiretroviral therapy reduces inflammation, but not to levels in comparable HIV-negative individuals. The HMG-coenzyme A reductase inhibitors (statins) inhibit several pro-inflammatory processes and suppress immune activation, and are a logical therapy to assess for a possible salutary effect on HIV disease progression and outcomes.MethodsEligible patients were patients enrolled in the Johns Hopkins HIV Clinical Cohort who achieved virologic suppression within 180 days of starting a new highly active antiretroviral therapy (HAART) regimen after January 1, 1998. Assessment was continued until death in patients who maintained a virologic suppression, with right-censoring of their follow-up time if they had an HIV RNA > 500 copies/ml. Cox proportional hazards regression was used to assess statin use as a time-varying covariate, as well as other demographic and clinical factors.ResultsA total of 1538 HIV-infected patients fulfilled eligibility criteria, of whom 238 (15.5%) received a statin while taking HAART. There were 85 deaths (7 in statin users, 78 in non-users). By multivariate Cox regression, statin use was associated with a relative hazard of 0.33 (95% CI: 0.14, 0.76; P = 0.009) after adjusting for CD4, HIV-1 RNA, hemoglobin and cholesterol levels at the start of HAART, age, race, HIV risk group, prior use of ART, year of HAART start, NNRTI vs. PI-based ART, prior AIDS-defining illness, and viral hepatitis coinfection. Malignancy, non-AIDS-defining infection and liver failure were particularly prominent causes of death.DiscussionStatin use was associated with significantly lower hazard of dying in these HIV-infected patients who were being effectively treated with HAART as determined by virologic suppression. Our results suggest the need for confirmation in other observational cohorts, and if confirmed, the need for a clinical trial of statin use in HIV infection.
Highlights
HIV infection is a disease associated with chronic inflammation and immune activation
By multivariate Cox regression, statin use was associated with a relative hazard (RH) of 0.33, adjusting for CD4, HIV-1 RNA, hemoglobin and cholesterol levels at the start of highly active antiretroviral therapy (HAART), age, race, HIV risk group, prior use of antiretroviral therapy (ART), year of HAART start, nucleoside reverse transcriptase inhibitor (NNRTI) vs. protease inhibitor (PI)-based ART, prior AIDS-defining illness, and viral hepatitis coinfection (Table 2)
We found that statin use was associated with a significantly decreased hazard of dying
Summary
HIV infection is a disease associated with chronic inflammation and immune activation. The HMG-coenzyme A reductase inhibitors (statins) inhibit several pro-inflammatory processes and suppress immune activation, and are a logical therapy to assess for a possible salutary effect on HIV disease progression and outcomes. It is well-recognized that HIV infection causes chronic inflammation and immune activation. Untreated HIV infection is associated with persistently high levels of pro-inflammatory cytokines such as IL-1, IL-6, and TNF-alpha, coagulation biomarkers and acute phase proteins such as fibrinogen, Ddimer and high-sensitivity C-reactive protein [1,2] These markers of inflammation decline with the use of effective antiretroviral therapy (ART), suggesting that active HIV replication is responsible for this inflammatory response. Cardiovascular disease, malignancy, chronic kidney and liver disease all appear to be occurring earlier and more frequently in HIVinfected individuals, and have each been associated with this process [10,11,12,13]
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