2139. Long-term LDL-cholesterol trajectories in virologically suppressed HIV patients: effect of liver fibrosis and statin use.
Session: Poster Abstract Session: HIV Cardiovascular Disease, Lipids, and Diabetes
Saturday, October 29, 2016
Room: Poster Hall
Posters
  • ID Week 2016 - Final.pdf (449.9 kB)
  • Background: HIV infection and initiation of highly active antiretroviral therapy (HAART) alter low-density lipoprotein- cholesterol (LDL-c). HIV infection is also associated with increased incidence and progression of liver fibrosis even in the absence of hepatitis C (HCV) co-infection. However, it is unclear whether liver fibrosis modifies LDL-c serum levels over time and whether the anti-inflammatory effect of statins protects against fibrosis progression.

    Methods: We used the US VA HIV Clinical Case Registry to generate a medication exposure model for HAART and statins. We identified all HCV-negative patients who initiated HAART after 1/1/2003, and had at least three LDL-c and liver fibrosis index-4 (FIB-4) measurements over time. We selected LDL-c and FIB-4 values recorded during periods of viral suppression (HIV-1 RNA<500 copies/mL) and HAART use ratio >80% (days on HAART/days since HAART initiation). We fit fractional polynomials curves stratified by FIB-4 category and current statin use at the time of LDL-c measurement. We used multilevel linear regression to assess the effect of FIB-4 on LDL-c changes over time adjusting for age, time since HAART initiation, initial LDL-c level, sex, race, statin prescription and CD4 count. We used the same methods to assess the effect statin use ratio quartiles and LDL-c on FIB-4 score changes.

    Results: The analysis included 2551 individuals with an average of 8 LDL-c and 5 FIB-4 measurements per person. Overall, LDL-c decreased by 0.7 (0.6, 1.1) mg/dl with each additional year on HAART. Higher FIB-4 (indicating greater likelihood of liver fibrosis) was associated with lower LDL-c over time regardless of statin use (see Figures 1 and 2).  Compared to those with FIB-4<1.45, average LDL-c was 7.9 (5.5-10.4) mg/dL lower in patients with FIB-4>3.25 (advanced fibrosis), and 2.3 (1.4-3.3) mg/dL lower in those with FIB-4 between 1.45-3.25. Statin use ratio was not significantly associated with FIB-4 changes over time regardless of initial LDL-c.

    Conclusion: Among HIV-infected patients with suppressed viremia on stable HAART, LDL-c declined over time regardless of statin use and the decline was greater in those with higher liver fibrosis score. FIB-4 score changes did not differ by statin use categories.

     

     

     

     

     

    Macintosh HD:private:var:folders:5k:wgk9xhqn14bd3jzxcvrg6wlh0000gn:T:TemporaryItems:LDL by time since HAART initiation (no statin) 10 yrs .pdfMacintosh HD:private:var:folders:5k:wgk9xhqn14bd3jzxcvrg6wlh0000gn:T:TemporaryItems:LDL by time since HAART initiation (on statin) 10yrs [1].pdf

    Roger Bedimo, MD, Medicine, VA N Texas Health Care Systems, University of Texas, Dallas, TX, Henning Drechsler, MD, Infectious Diseases, University of Texas Southwestern Medical School, Dallas, TX and Kaku So-Armah, PhD, School of Public Health, Boston University, Boston, MA

    Disclosures:

    R. Bedimo, Merck & Co.: Scientific Advisor , Research grant
    Theratechnologies: Scientific Advisor , Research grant
    Bristol Myers Squibb: Scientific Advisor , Research grant
    Gilead: Scientific Advisor , Consulting fee

    H. Drechsler, None

    K. So-Armah, None

    Findings in the abstracts are embargoed until 12:01 a.m. CDT, Wednesday Oct. 26th with the exception of research findings presented at the IDWeek press conferences.