Liver fibrosis progression in hepatitis C virus infection after seroconversion.

IMPORTANCE Knowing the rate of liver fibrosis progression in hepatitis C virus (HCV)-infected persons can help inform patients and providers (clinicians, medical institutions or organizations, and third-party payers) in making treatment decisions. OBJECTIVE To determine the rate and factors associated with liver fibrosis progression and hepatic decompensation in persons after acquiring HCV infection. DESIGN, SETTING, AND PARTICIPANTS Secondary data analysis of persons in the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES), a national Veterans Affairs (VA) database, between 2002 and 2012. Among 610 514 persons in ERCHIVES (half were HCV positive), we identified those with an initial negative and subsequent positive test result for HCV antibody and positive HCV RNA test result (HCV+). Controls had 2 negative HCV antibody test results (HCV-) in a comparable time frame and were matched 1:1 on age (in 5-year blocks), race, and sex. We excluded persons with human immunodeficiency virus, hepatitis B, less than 24 months of follow-up, hepatocellular carcinoma, and cirrhosis at baseline. MAIN OUTCOMES AND MEASURES Progression of liver fibrosis as estimated by the Fibrosis-4 (FIB-4) index; development of cirrhosis, defined by a FIB-4 score greater than 3.5; and development of hepatic decompensation. RESULTS The evaluable data set consisted of 1840 persons who were HCV+ and 1840 HCV- controls. The HCV+ persons were younger and had a lower mean (SD) body mass index (27.39 [5.51] vs 29.49 [6.16]; P < .001), a higher prevalence of alcohol and drug abuse and dependence diagnoses, and higher serum aminotransferase levels, but had a lower prevalence of diabetes and hypertension. Fibrosis progression started early after infection among HCV+ persons and tapered off after 5 years. A total of 452 cirrhosis and 85 hepatic decompensation events were recorded. After 10 years of follow-up, HCV+ persons were more likely to have a diagnosis of cirrhosis compared with HCV- controls (18.4% vs 6.1%). Nine years after diagnosis of cirrhosis, hepatic decompensation events were uncommon but had a higher rate in the HCV+ group (1.79% vs 0.33%). CONCLUSIONS AND RELEVANCE Persons who seroconverted for HCV have a more rapid progression of liver fibrosis and accelerated time to development of cirrhosis after seroconversion compared with HCV- controls. Fibrosis progression occurs early after infection; however, hepatic decompensation is uncommon after diagnosis of cirrhosis.

[1]  G. Dusheiko,et al.  Natural history of hepatitis C. , 2014, Journal of hepatology.

[2]  S. Wild,et al.  Development of new fatty liver, or resolution of existing fatty liver, over five years of follow-up, and risk of incident hypertension. , 2014, Journal of hepatology.

[3]  M. Vinciguerra,et al.  Sympathetic Nervous System Catecholamines and Neuropeptide Y Neurotransmitters Are Upregulated in Human NAFLD and Modulate the Fibrogenic Function of Hepatic Stellate Cells , 2013, PloS one.

[4]  A. Moorman,et al.  Noninvasive serum fibrosis markers for screening and staging chronic hepatitis C virus patients in a large US cohort. , 2013, Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.

[5]  M. Freiberg,et al.  Hepatitis C virus treatment and survival in patients with hepatitis C and human immunodeficiency virus co‐infection and baseline anaemia , 2013, Journal of viral hepatitis.

[6]  M. Freiberg,et al.  Therapy for hepatitis C virus infection increases survival of patients with pretreatment anemia. , 2013, Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association.

[7]  Farah Kidwai,et al.  Validity of diagnostic codes and liver‐related laboratory abnormalities to identify hepatic decompensation events in the Veterans Aging Cohort Study , 2011, Pharmacoepidemiology and drug safety.

[8]  L. Fried,et al.  HCV infection and the incidence of CKD. , 2011, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[9]  E. Ridruejo Hepatitis C treatment completion rates in routine clinical care , 2010, Liver international : official journal of the International Association for the Study of the Liver.

[10]  A. Butt,et al.  Effect of hepatitis C virus and its treatment on survival , 2009, Hepatology.

[11]  J. Tsevat,et al.  Rates of HCV Treatment Eligibility Among HCV-Monoinfected and HCV/HIV-Coinfected Patients in Tertiary Care Referral Centers , 2009 .

[12]  M. Budoff,et al.  Hepatitis C virus infection and the risk of coronary disease. , 2008, Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.

[13]  C. Chang,et al.  Impact of hepatitis C virus infection and other comorbidities on survival in patients on dialysis , 2007, Journal of viral hepatitis.

[14]  A. Butt,et al.  Co-morbid medical and psychiatric illness and substance abuse in HCV-infected and uninfected veterans. , 2007, Journal of viral hepatitis.

[15]  Melissa Skanderson,et al.  Development and Verification of a “Virtual” Cohort Using the National VA Health Information System , 2006, Medical care.

[16]  J. Montaner,et al.  Development of a simple noninvasive index to predict significant fibrosis in patients with HIV/HCV coinfection , 2006, Hepatology.

[17]  A. Justice,et al.  Relative prevalence of comorbidities and treatment contraindications in HIV-mono-infected and HIV/HCV-co-infected veterans , 2005, AIDS.

[18]  H. El‐Serag,et al.  Hepatitis C coinfection increases the risk of fulminant hepatic failure in patients with HIV in the HAART era. , 2005, Journal of hepatology.

[19]  C. Kwoh,et al.  Risk of diabetes in HIV infected veterans pre‐ and post‐HAART and the role of HCV coinfection , 2004, Hepatology.

[20]  J. Crowe,et al.  The natural course of hepatitis C virus infection after 22 years in a unique homogenous cohort: spontaneous viral clearance and chronic HCV infection , 2001, Gut.

[21]  L. Seeff,et al.  Natural history of hepatitis C , 1997, Hepatology.

[22]  M. Leal,et al.  Human immunodeficiency virus infection modifies the natural history of chronic parenterally-acquired hepatitis C with an unusually rapid progression to cirrhosis. , 1997, Journal of hepatology.

[23]  M. Tong,et al.  Clinical outcomes after transfusion-associated hepatitis C. , 1995, The New England journal of medicine.

[24]  O. Weiland,et al.  Outcome of acute symptomatic non-A, non-B hepatitis: a 13-year follow-up study of hepatitis C virus markers. , 2008, Liver.

[25]  Richard E. Sampliner,et al.  The Natural History of Community-Acquired Hepatitis C in the United States , 1993 .

[26]  R. Koretz,et al.  Non-A, Non-B Post-Transfusion Hepatitis: Looking Back in the Second Decade , 1993, Annals of Internal Medicine.

[27]  A. Alberti,et al.  Long-term follow-up of non-A, non-B (type C) post-transfusion hepatitis. , 1993, Journal of hepatology.

[28]  K. Ishak,et al.  Long‐term clinical and histopathological follow‐up of chronic posttransfusion hepatitis , 1991, Hepatology.

[29]  R. Purcell,et al.  Interrelationship of blood transfusion, non‐A, non‐B hepatitis and hepatocellular carcinoma: Analysis by detection of antibody to hepatitis C virus , 1990, Hepatology.

[30]  H. Blum,et al.  Long-term follow-up of posttransfusion and sporadic chronic hepatitis non-A, non-B and frequency of circulating antibodies to hepatitis C virus (HCV). , 1990, Journal of hepatology.

[31]  R. W. Mccollum The natural history of hepatitis. , 1969, Bulletin of the New York Academy of Medicine.