title: Outcomes in HIV/HBV-Coinfected Patients in the Tenofovir Era Are Greatly Affected by Immune Suppression.
abstract: OBJECTIVE
  HIV-infected patients have higher mortality when coinfected with hepatitis B virus (HBV). With potent highly active antiretroviral therapy (HAART) and the use of tenofovir (TDF), outcomes may improve. Our objective was to determine the clinical and virological outcomes of a HIV/HBV-Coinfected cohort at our center since TDF became available.
  
  
  METHODS
  We retrospectively studied all HIV/HBV-Coinfected adults followed between 2002 and 2012 for ≥3 months. Outcome measurements included HBV DNA suppression, HBV e-antigen (HBeAg) and HBV surface antigen (HBsAg) clearance, cirrhosis diagnosis, development of liver complications, and overall and liver-related mortality. Predicting factors were assessed with log-rank test and logistic regression.
  
  
  RESULTS
  Median time to follow-up of the 99 patients included was 5 years. Undetectable HBV DNA and HBsAg loss were achieved by 65% and 18%, respectively. Overall and liver-related mortality rates were 4.58 and 0.91 per 100 person-years, respectively. Most patients died of causes unrelated to the liver. Four patients died from hepatocellular carcinoma (HCC) and one, hepatitis C virus (HCV) coinfected, from liver failure. Higher CD4 counts at last follow-up were associated with HBV suppression (odds ratio [OR] 1.004, 95% confidence interval [CI] 1.001-1.006, P=.007), HBeAg loss (OR 1.003, 95% CI 1-1.005, P=.02), HBsAg loss (CD4 count>700 cells/mm3, OR 3.80, 95% CI 1.06-13.58, P=.04), and survival (OR .994, 95% CI 0.990-0.997, P<.0001). HCV coinfection was associated with higher overall mortality (OR 7.74, 95% CI 1.47-40.81, P=.02).
  
  
  CONCLUSIONS
  Mortality was high and most often unrelated to liver disease in this HIV/HBV-Coinfected cohort treated predominantly with TDF-containing HAART. Optimal CD4 counts predicted survival and the achievement of HBV virological end points. Tenofovir prevented liver decompensation but not HCC, which was the predominant cause of liver death.
authors.affiliation: Wake Forest University School of Medicine, Winston-Salem, NC, USA.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Huang
authors.affiliation: Division of Infectious Disease, Department of Internal Medicine, Wake Forest University Health Sciences, Winston-Salem, NC, USA mnunez@wakehealth.edu.
authors.forename: Marina
authors.initials: M
authors.lastname: Núñez
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D060085:Coinfection / Q000188:drug therapy / Q000821:virology*; D004279:DNA, Viral / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy* / Q000276:immunology / Q000821:virology*; D019694:Hepatitis B, Chronic / Q000097:blood / Q000188:drug therapy* / Q000276:immunology / Q000821:virology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D063065:Organophosphonates / Q000627:therapeutic use*; D012189:Retrospective Studies; D000068698:Tenofovir
chemical_list: D019380:Anti-HIV Agents; D004279:DNA, Viral; D063065:Organophosphonates; D000068698:Tenofovir; D000225:Adenine
keywords: HIV infection; chronic hepatitis B; outcomes