- Category: Acute Hepatitis C
- Published on Wednesday, 28 May 2014 00:00
- Written by Liz Highleyman
Liver disease was found to progress slowly in studies of both HIV negative people with newly acquired hepatitis C virus (HCV) and HIV/HCV coinfected people with acute HCV, according to a pair of studies presented at the recent Conference on Retroviruses and Opportunistic Infections.
Over years or decades, chronic hepatitis C virus infection can lead to serious liver disease including cirrhosis and liver cancer. People with HIV -- especially those with advanced immune suppression -- tend to experience more rapid disease progression.
Some researchers have found that people who are already HIV positive when they become infected with HCV may experience very fast liver fibrosis progression over a short term, even during acute or early infection. Others, however, have not seen this effect.
Adeel Butt from the University of Pittsburgh and colleagues described fibrosis progression among HIV negative people with recently acquired HCV infection.
The researchers analyzed data from the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES) database. The analysis included more than 4000 U.S. veterans who initially tested HCV antibody negative followed by a subsequent positive test, allowing an estimate of when infection occurred (the mid-point between the negative and positive tests).
Almost all included patients were men, about 60% were white, about one-quarter were black, and the mean age was approximately 54 years. People who were previously treated for hepatitis C, HIV/HCV coinfected people, and patients with less than 2 years of follow-up were excluded. Liver fibrosis was estimated using the APRI biomarker index prior to and annually after the presumed HCV seroconversion date; a score >1.5 indicates significant fibrosis.
The mean APRI score was 0.40 at baseline, rising to 0.60 after 10 years of follow-up. The average increase was 0.023 units per year, indicating slow progression. After 10 years, 7% of participants had APRI scores indicating significant fibrosis. Patient age, sex, race, body mass index, and HCV genotype were not associated with higher likelihood of APRI >1.5.
"Fibrosis progression in persons with recently acquired HCV infection is slow, particularly in the first 5 years," the researchers summarized. "Over 10 years only 6.5% developed significant fibrosis. These data can help in deciding whether to defer treatment while awaiting more potent and more tolerable newer regimens to treat HCV infection."
Turning to coinfected people, Christoph Boesecke and Jürgen Rockstroh from the University of Bonn and fellow investigators with the NEAT study group looked at liver disease progression among HIV positive gay and bisexual men with presumed sexually transmitted HCV infection.
The NEAT team evaluated the evolution of liver fibrosis among 41 HIV positive patients in Germany, Austria, and France who had persistent HCV viremia after acute infection -- that is, a chronic course of infection (27%) or unsuccessful early hepatitis C treatment (73%). Participants were diagnosed with hepatitis C after 2003 and followed for at least 1 year (median 179 weeks). Liver fibrosis was estimated over time using FibroScan transient elastometry, which measures liver stiffness using ultrasound.
Almost all participants were men who have sex with men (MSM) and the mean age was 43 years; only 2% reported injection drug use. 78% had HCV genotype 1 and 22% had genotype 4. Most participants (80%) did not have a record of clinical symptoms of acute HCV infection. Most were on antiretroviral therapy (ART) with undetectable HIV viral load, and the median CD4 T-cell count was approximately 500 cells/mm3.
Overall, there was no significant change in median liver stiffness over a maximum follow-up period of 8 years. No significant correlations were observed between liver stiffness and factors including body mass index, alcohol or drug use, diabetes or lipodystrophy, ART duration or use of "d-drugs" (e.g., ddI [didanosine or Videx] or d4T [stavudine or Zerit], which can cause liver toxicity), or reason for HCV persistence (chronic course or unsuccessful treatment).
"An episode of acute hepatitis C in HIV positive MSM does not appear to lead towards early advanced liver fibrosis," the investigators concluded. "This finding is particularly reassuring for clinicians and patients in whom HCV persists due to a chronic course or unsuccessful early treatment."
C Boesecke, P Ingiliz, M Mandorfer, JK Rockstroh, et al (NEAT Study Group). Is There Long-Term Evidence of Advanced Liver Fibrosis After Acute Hepatitis C in HIV Coinfection? 21st Conference on Retroviruses and Opportunistic Infections (CROI 2014). Boston, March 3-6, 2014. Abstract 644.
AA Butt, P Yan, V Lo Re, et al. Liver Fibrosis Progression Among Persons With Recently Acquired HCV Infection. 21st Conference on Retroviruses and Opportunistic Infections (CROI 2014). Boston, March 3-6, 2014. Abstract 649.