Statin Therapy Does Not Reduce Liver Fat Scores in Patients Receiving Antiretroviral Therapy for HIV Infection

Kamari, Vanessa El; Hileman, Corrilynn Olesky; Gholam, Pierre M.; Kulkarni, Milind V.; Funderburg, Nicholas T.; McComsey, Grace A.

doi:10.1016/j.cgh.2018.05.058

Cited by 9 publications

(10 citation statements)

References 30 publications

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“…Despite effective viral suppression with ART, gut damage is not reversed 3,4 . Much of the current research effort is looking at therapeutic strategies to restore gut structural integrity, in the hope of reducing non-AIDS related comorbidities 1,5 . The underlying mechanisms of gut structural damage are not completely understood.…”

Section: Introductionmentioning

confidence: 99%

Brief Report: Gut Structural Damage: an Ongoing Process in Chronically Untreated HIV Infection

Kamari

Sattar

McComsey

2019

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Objective: To investigate the longitudinal changes of gut structural damage in chronically untreated HIV infection. Design: This is a 96-week prospective, single site, cohort study of antiretroviral therapy (ART)naïve HIV-infected participants. Methods: Intestinal fatty acid-binding proteins (I-FABP) was used as a surrogate marker of gut structural damage. We assessed changes in I-FABP over 96 weeks and examined the associations between I-FABP, HIV variables, and inflammation. Spearman's correlations and linear mixed effect models were used to study relationships among variables. Results: A total of 63 HIV-infected, ART-naïve patients were included in this analysis. At baseline, 76% were male; 62% were African American, with median age and BMI of 40 years and 27kg/m 2. Median HIV-RNA and CD4+ T cell counts were 5520 copies/mL and 588 cells/mm 3. I-FABP significantly increased from baseline to week 96 (mean change +333.9 pg/mL; p=0.03), and this increase was associated with viral replication (rho=+0.4; p=0.03). I-FABP levels were found to be associated with markers of inflammation: sTNFR-II (rho=0.4, p=0.02) and sVCAM-1 (rho=0.04; p<0.01) at all study time points. Lower baseline CD4+ T cells counts was found to be independently associated with I-FABP progression after adjusting for baseline characteristics variables (p=0.02). Conclusion: Gut structural damage is an ongoing process in the chronic phase of untreated HIV infection, and is largely dependent on viral replication. I-FABP was found to be associated with worse immune function, increase inflammation, and viremia in chronically untreated HIV infection, supporting its role as a biomarker of intestinal barrier dysfunction.

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Section: Introductionmentioning

confidence: 99%

Brief Report: Gut Structural Damage: an Ongoing Process in Chronically Untreated HIV Infection

Kamari

Sattar

McComsey

2019

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…Another trial showed that 24 weeks of vitamin E treatment decreased ALT and the degree of hepatic steatosis in HIV mono‐infected patients with non‐alcoholic steatohepatitis and showed no change in triglycerides, total cholesterol, HDL cholesterol, and HOMA‐IR 20 . Nevertheless, a randomized controlled trial of statin versus placebo, 147 HIV‐infected individuals with 96‐week follow‐up had hepatic steatosis increased over time, regardless of statin treatment 21 . Future clinical trials would take into consideration disease heterogeneity and target patients with specific characteristics, such as sex, hormonal status, genetic predisposition, metabolic and microbiota signatures, and the presence or absence of comorbid conditions 2 .…”

Section: Discussionmentioning

confidence: 99%

Prevalence and risk factors of metabolic associated fatty liver disease among people living with HIV in China

Liu

Shen

Zhang

et al. 2021

J of Gastro and Hepatol

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Background and Aim The new definition for metabolic associated fatty liver disease (MAFLD), formerly named non‐alcoholic fatty liver disease (NAFLD), would undoubtedly have significant influence on diagnosis, epidemiology, and new drug research. We investigated the prevalence and risk factors of MAFLD among people living with HIV (PLWH). Methods In this cross‐sectional study, transient elastography was performed in PLWH without significant alcohol intake and hepatitis B virus and hepatitis C virus infection. NAFLD was diagnosed as controlled attenuation parameter (CAP) ≥ 248 dB/m by transient elastography, and MAFLD was defined according to the 2020 international consensus. Advanced fibrosis was defined as liver stiffness measurement (LSM) ≥ 10 kPa. Results Among the 361 PLWH enrolled, the prevalence of NAFLD and MAFLD were 37.67% and 34.90%, respectively. Compared with the non‐MAFLD group, the prevalence of elevated alanine aminotransferase (ALT) level (44.44% vs 16.17%, P < 0.001) and advanced fibrosis (19.05% vs 2.55%, P < 0.001) were significantly higher in the MAFLD group. A positive correlation between LSM and CAP values was found in the MAFLD group (rs = 0.350, P < 0.001) but not in the non‐MAFLD group. In multivariate analysis, independent risk predictors for MAFLD were higher ALT level (odds ratio [OR] 1.015, 95% confidence interval [CI] 1.003–1.028, P = 0.018), higher uric acid (OR 1.005, 95% CI 1.002–1.009, P = 0.003), higher total cholesterol (OR 1.406, 95% CI 1.029–1.921, P = 0.032), and greater waist–height ratio (OR 1.291, 95% CI 1.196–1.393, P < 0.001). Conclusions A third of PLWH had MAFLD, which was highly accordant with the prevalence of NAFLD. Routine screening for MAFLD is necessary in PLWH.

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“…The comprehensive search for the literature from these databases yielded 795 records that were screened and evaluated at the title, abstract and keywords level (Figure 1). Finally, 20 studies [12][13][14]16,[19][20][21][22][23][41][42][43][44][45][46][47][48][49][50][51][52] were included, of which 12 trials used rosuvastatin of either 10, 20 or 80 mg, four used atorvastatin of 10, 30 and 40 mg, four used pravastatin at 40 mg and one used pitavastatin of 2 mg. These studies were published in peer-reviewed journals between 2004 and 2021, thus tracing old and advanced evidence on statins in PLHIV taking ART.…”

Section: Search General Characteristics and Quality Of Included Trialsmentioning

confidence: 99%

“…This problem has prompted other researchers to conduct clinical trials investigating this paradigm. Surprisingly, researchers have reported contradicting findings, with some showing consistently improved HIV surrogate markers [11][12][13][14][15][16][17][18] and others showing negative findings [19][20][21][22][23]. HIV as a chronic infection is closely associated with inflammation due to the continuously rising viral load [24,25].…”

Section: Introductionmentioning

confidence: 99%

A Systematic Review and Meta-Analysis on the Impact of Statin Treatment in HIV Patients on Antiretroviral Therapy

Mokgalaboni

Phoswa

Yates

et al. 2023

IJERPH

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The rate of new human immunodeficiency virus (HIV) infections globally is alarming. Although antiretroviral therapy (ART) improves the quality of life among this group of patients, ARTs are associated with risk of cardiovascular diseases (CVD). Moreover, virally suppressed patients still experience immune activation associated with HIV migration from reservoir sites. Statins are widely recommended as therapeutic agents to control ART-related CVD; however, their impacts on the cluster of differentiation (CD)4 count and viral load are inconsistent. To assess the effect of statins on markers of HIV infections, immune activation and cholesterol, we thoroughly reviewed evidence from randomised controlled trials. We found 20 relevant trials from three databases with 1802 people living with HIV (PLHIV) on statin–placebo treatment. Our evidence showed no significant effect on CD4 T-cell count standardised mean difference (SMD): (−0.59, 95% confidence intervals (CI): (−1.38, 0.19), p = 0.14) following statin intervention in PLHIV on ART. We also found no significant difference in baseline CD4 T-cell count (SD: (−0.01, 95%CI: (−0.25, 0.23), p = 0.95). Our findings revealed no significant association between statins and risk of viral rebound in PLHIV with undetectable viral load risk ratio (RR): (1.01, 95% CI: (0.98, 1.04), p = 0.65). Additionally, we found a significant increase in CD8+CD38+HLA-DR+ T-cells (SMD (1.10, 95% CI: (0.93, 1.28), p < 0.00001) and CD4+CD38+HLA-DR+ T-cells (SMD (0.92, 95% CI: (0.32, 1.52), p = 0.003). Finally, compared to placebo, statins significantly reduced total cholesterol (SMD: (−2.87, 95% CI: (−4.08, −1.65), p < 0.0001)). Our results suggest that the statin lipid-lowering effect in PLHIV on ART may elevate immune activation without influencing the viral load and CD4 count. However, due to the limited evidence synthesised in this meta-analysis, we recommend that future powered trials with sufficient sample sizes evaluate statins’ effect on CD4 count and viral load, especially in virally suppressed patients.

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Statin Therapy Does Not Reduce Liver Fat Scores in Patients Receiving Antiretroviral Therapy for HIV Infection

Cited by 9 publications

References 30 publications

Brief Report: Gut Structural Damage: an Ongoing Process in Chronically Untreated HIV Infection

Brief Report: Gut Structural Damage: an Ongoing Process in Chronically Untreated HIV Infection

Prevalence and risk factors of metabolic associated fatty liver disease among people living with HIV in China

A Systematic Review and Meta-Analysis on the Impact of Statin Treatment in HIV Patients on Antiretroviral Therapy

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