Gregory D. Kirk, MD, MPH, PhD; Shruti H. Mehta, PhD, MPH; Jacquie Astemborski, MS; Noya Galai, PhD; Jonathan Washington, BA; Yvonne Higgins, PA; Ashwin Balagopal, MD; David L. Thomas, MD, MPH
This article was published at www.annals.org on 26 February 2013.
Acknowledgment: All persons who have contributed substantially to this work have been recognized.
Grant Support: By United States Public Health Service, National Institute of Drug Abuse (R01-DA-016078, R01-DA-04334, and R01-DA-12568). Dr. Kirk was supported by the American Cancer Society (MRSG-07-284-01-CCE). Support of reagents for HCV RNA testing was generously provided by Abbott Molecular.
Potential Conflicts of Interest: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M12-1085.
Reproducible Research Statement: Study protocol and data set: Not available. Statistical code: Available from Dr. Kirk (address below).
Requests for Single Reprints: David L. Thomas, MD, Stanhope Bayne Jones Professor of Medicine, Chief, Division of Infectious Diseases, Johns Hopkins School of Medicine, Room 437, 1830 Monument Street, Baltimore, MD 21205.
Current Author Addresses: Dr. Kirk: 615 North Wolfe Street, E-6533, Baltimore, MD 21205.
Dr. Mehta: 615 North Wolfe Street, E-6535, Baltimore, MD 21205.
Ms. Astemborski: 2213 McElderry Street, 1st Floor, Baltimore, MD 21205.
Dr. Galai: 615 North Wolfe Street, E-6529, Baltimore, MD 21205, and University of Haifa, Department of Statistics, Haifa, Israel.
Mr. Washington, Ms. Higgins, and Drs. Balagopal and Thomas: Division of Infectious Diseases, Johns Hopkins School of Medicine, Room 437, 1830 Monument Street, Baltimore, MD 21205.
Author Contributions: Conception and design: G.D. Kirk, S.H. Mehta, D.L. Thomas.
Analysis and interpretation of data: G.D. Kirk, S.H. Mehta, J. Astemborski, N. Galai, D.L. Thomas.
Drafting of the article: G.D. Kirk, J. Astemborski, D.L. Thomas.
Critical revision of the article for important intellectual content: G.D. Kirk, S.H. Mehta, N. Galai, A. Balagopal, D.L. Thomas.
Final approval of the article: G.D. Kirk, S.H. Mehta, J. Astemborski, D.L. Thomas.
Provision of study materials or patients: G.D. Kirk, S.H. Mehta, D.L. Thomas.
Statistical expertise: G.D. Kirk, S.H. Mehta.
Obtaining of funding: G.D. Kirk, S.H. Mehta, D.L. Thomas.
Administrative, technical, or logistic support: G.D. Kirk, Y. Higgins, D.L. Thomas.
Collection and assembly of data: G.D. Kirk, S.H. Mehta, J. Astemborski, Y. Higgins, J. Washington, D.L. Thomas.
Kirk GD, Mehta SH, Astemborski J, Galai N, Washington J, Higgins Y, et al. HIV, Age, and the Severity of Hepatitis C Virus–Related Liver Disease: A Cohort Study. Ann Intern Med. 2013;158:658-666. doi: 10.7326/0003-4819-158-9-201305070-00604
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Published: Ann Intern Med. 2013;158(9):658-666.
Persons with HIV infection have been reported to develop age-related diseases at younger ages than those without HIV. Whether this finding is related to HIV infection or failure to control for other risk factors is unknown.
To investigate whether persons with HIV infection develop hepatitis C virus (HCV)–related liver disease at younger ages than similar persons without HIV.
Comparison of the severity of liver fibrosis by age among persons who have HCV with and without HIV followed concurrently in the same protocol.
Observational cohort from Baltimore, Maryland, participating in the ALIVE (AIDS Linked to the IntraVenous Experience) study.
1176 current and former injection drug users with antibodies to HCV.
Liver fibrosis assessed semiannually from 2006 to 2011 by elastography (FibroScan, Echosens, Paris, France) and using previously validated thresholds for clinically significant fibrosis and cirrhosis; concurrent assessment of medical history, alcohol and illicit drug use, HCV RNA levels, hepatitis B virus surface antigen level, body mass index, and (for those with HIV) CD4+ lymphocyte count and HIV RNA levels.
Among 1176 participants with antibodies to HCV, the median age was 49 years and 34% were coinfected with HIV and HCV. Participants contributed 5634 valid liver fibrosis measurements. The prevalence of clinically significant fibrosis without cirrhosis (12.9% vs. 9.5%) and of cirrhosis (19.5% vs. 11.0%) was greater in persons coinfected with HIV and HCV than in those with only HCV (P < 0.001). Increasing age and HIV infection were independently associated with liver fibrosis, as were daily alcohol use, chronic hepatitis B virus infection, body mass index greater than 25 kg/m2, and greater plasma HCV RNA levels. When these factors were kept constant, persons with HIV had liver fibrosis measurements equal to those of persons without HIV, who were, on average, 9.2 years older.
The process of liver fibrosis began before the study in most persons.
In this cohort, persons who have HCV with HIV have liver fibrosis stages similar to those without HIV who are nearly a decade older.
National Institute on Drug Abuse.
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Gastroenterology/Hepatology, Infectious Disease, HIV, Viral Hepatitis, Liver Disease.
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