Showing posts with label Liver Fibrosis. Show all posts
Showing posts with label Liver Fibrosis. Show all posts

Wednesday, March 23, 2016

Poorly Controlled HIV Infection: An Independent Risk Factor for Liver Fibrosis

BACKGROUND:
Liver disease is a major cause of mortality among HIV-infected persons. There is limited information about the extent to which HIV disease severity impacts liver disease progression.

METHODS:
We determined the incidence and predictors of advanced hepatic fibrosis measured by the FIB-4 index (≥3.25) in a large diverse population of HIV-infected patients without significant liver disease at baseline (FIB-4<1.45) in care between January 2000 and March 2014. We used Cox proportional hazards analysis to examine factors associated with progression to FIB-4 ≥3.25.

RESULTS:
Among 14,198 HIV-infected patients, HCV coinfection (adjusted hazard ratio [aHR] 1.9, 95% CI 1.6-2.1), HBV coinfection (aHR 1.5, 95% CI 1.2-1.8), alcohol use disorder (aHR 1.4, 95% CI 1.2-1.6) and diabetes (aHR 1.9, 95% CI 1.6-2.3) were associated with progression to advanced fibrosis in multivariable analysis. In addition, patients at each lower level of time-varying CD4 count had a significantly greater risk of progression, with a nearly 7-fold higher risk in those with CD4 <100 cells/mm (aHR 6.9, 95% CI 5.8-8.3) compared with CD4 ≥500 cells/mm. An increasing gradient of risk was also observed among patients with higher time-varying HIV viral load (VL), with the greatest risk noted with VL ≥100,000 copies/ml (aHR 2.6, 95% CI 2.2-3.1) compared with VL <500 copies/ml.

CONCLUSION:
Lower CD4 count and higher HIV VL were significantly associated with progression to advanced hepatic fibrosis in a dose-dependent manner, independent of the risk associated with traditional factors: HCV or HBV coinfection, alcohol, and diabetes. Our findings suggest that early treatment of HIV infection could mitigate liver disease.

Purchase full article at:   http://goo.gl/HVfMN5

  • 1Department of Medicine, University of Washington 
  • 2 Department of Epidemiology, University of Washington 
  • 3 Department of Medicine, University of California San Diego 
  • 4 Department of Medicine, University of California San Francisco 
  • 5 Fenway Health, Boston MA 
  • 6 Department of Medicine, Case Western University 
  • 7 Department of Medicine, University of North Carolina Chapel Hill 
  • 8 Department of Medicine, University of Alabama, Birmingham 
  • 9 Department of Medicine, Johns Hopkins University.
  •  2016 Mar 16. 



Friday, December 25, 2015

Liver Fibrosis in HIV Patients Receiving a Modern cART: Which Factors Play a Role?

Liver-related death in human immunodeficiency virus (HIV)-infected individuals is about 10 times higher compared with the general population, and the prevalence of significant liver fibrosis in those with HIV approaches 15%. 

The present study aimed to assess risk factors for development of hepatic fibrosis in HIV patients receiving a modern combination anti-retroviral therapy (cART).This cross-sectional prospective study included 432 HIV patients, of which 68 (16%) patients were anti-hepatitis C virus (HCV) positive and 23 (5%) were HBsAg positive.Health trajectory including clinical characteristics and liver fibrosis stage assessed by transient elastography were collected at inclusion. Liver stiffness values >7.1 kPa were considered as significant fibrosis, while values >12.5 kPa were defined as severe fibrosis. Logistic regression and Cox regression uni- and multivariate analyses were performed to identify independent factors associated with liver fibrosis.

Significant liver fibrosis was detected in 10% of HIV mono-infected, in 37% of HCV co-infected patients, and in 18% of hepatitis B virus co-infected patients. The presence of diabetes mellitus (odds ratio [OR] = 4.6) and FIB4 score (OR = 2.4) were independently associated with presence of significant fibrosis in the whole cohort. Similarly, diabetes mellitus (OR = 5.4), adiposity (OR = 4.6), and the FIB4 score (OR = 3.3) were independently associated with significant fibrosis in HIV mono-infected patients. Importantly, cumulative cART duration protected, whereas persistent HIV viral replication promoted the development of significant liver fibrosis along the duration of HIV infection.

Our findings strongly indicate that besides known risk factors like metabolic disorders, HIV may also have a direct effect on fibrogenesis. Successful cART leading to complete suppression of HIV replication might protect from development of liver fibrosis.

Below:  FIGURE 1. (A) Distribution of fibrosis among subgroups. (B–D) Association between LS and HIV duration, time naive, and DM. (E–H) Association between LS and BMI, DM, HIV duration, and time naive in HIV mono-infected patients compared with coinfected patients. Data are presented as mean ± SEM. BMI = body mass index, DM = diabetes mellitus, HIV = human immunodeficiency virus, LS = liver stiffness, SEM = standard error of the mean.



Full article at:   http://goo.gl/1el3nx

  • 1From the Department of Medicine I, University Hospital Bonn, Bonn, Germany (RM, RS, CS-Z, CB, J-CW, JT, JKR); German Centre for Infection Research (DZIF), Partner Site Bonn-Cologne, Bonn, Germany (RM, CS-Z, CB, J-CW, JKR); and Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark (JT).