scholarly journals Morbidity and Mortality Among Community-Based People Who Inject Drugs With a High Hepatitis C and Human Immunodeficiency Virus Burden in Chennai, India

2016 ◽  
Vol 3 (3) ◽  
Author(s):  
Shruti H. Mehta ◽  
Allison M. McFall ◽  
Aylur K. Srikrishnan ◽  
M. Suresh Kumar ◽  
Paneerselvam Nandagopal ◽  
...  

Abstract Background.  There are limited data on clinical outcomes of hepatitis C virus (HCV) infection from low- and middle-income countries. We characterize mortality and liver disease progression in a cohort of people who inject drugs (PWID) with high HCV burden. Methods.  In a cohort of PWID in Chennai, India, 851 persons were observed semiannually. Information on death was obtained through verbal autopsy and liver disease progression, which was defined as an incident liver stiffness measurement of ≥12.3 kPa if it was <12.3 at baseline. Poisson and Cox regression were used to identify factors associated with mortality and disease progression, respectively. Results.  At baseline, 36.9% of cases were infected with HCV, 16.7% were infected with human immunodeficiency virus (HIV), 71.6% had no or mild stiffness, 14.9% had moderate stiffness, and 13.5% had severe stiffness or cirrhosis. Mortality was significantly higher among those with moderate (mortality rate ratio [MRR] = 2.31) and severe stiffness (MRR = 4.86) at baseline, those with ongoing substance use, those who were HIV monoinfected and not on antiretroviral therapy (ART) (MRR = 6.59), and those who were HIV/HCV coinfected regardless of ART status (MRR for no ART = 5.34; MRR for ART = 4.51). Of those with no or mild stiffness, 25.9% and 6.4% had evidence of progression to moderate and severe stiffness or cirrhosis, respectively; 38.3% of those with moderate stiffness had evidence of progression to severe stiffness or cirrhosis. Factors associated with progression included age, alcohol use, body mass index, and chronic HCV infection. Conclusions.  We observed significant morbidity and mortality primarily driven by untreated HIV, HIV/HCV coinfection, and alcohol use. Even with improved access to HIV treatment, in the absence of HCV treatment, outcomes are unlikely to improve for HIV/HCV-coinfected persons.

2015 ◽  
Vol 2 (1) ◽  
Author(s):  
Jeffrey P. Anderson ◽  
C. Robert Horsburgh ◽  
Paige L. Williams ◽  
Eric J. Tchetgen Tchetgen ◽  
David Nunes ◽  
...  

Abstract Background.  Human immunodeficiency virus (HIV) coinfection accelerates liver disease progression in individuals with chronic hepatitis C. We evaluated the associations of CD4, HIV RNA, and antiretroviral therapy (ART)-induced CD4 recovery with liver diagnoses in a prospective cohort of injecting drug users (IDUs). Methods.  We evaluated 383 coinfected IDUs in the Boston area, prospectively observed for a median of 1.8 years. Liver disease progression included the first occurrence of hepatocellular carcinoma, variceal bleeding, ascites, encephalopathy, or death due to hepatic failure. Multivariable-adjusted extended Cox models were specified to estimate hazard ratios (HRs) for comparisons of CD4, change in CD4 (from nadir), and HIV RNA with respect to liver disease progression events. Results.  Twenty-four persons experienced a liver disease progression event over 1155 person-years (2.1 per 100 person-years), including 20 deaths attributed to end-stage liver disease (1.7 per 100 person-years). CD4 at baseline and over follow-up strongly predicted liver disease progression (baseline CD4 <200 vs ≥200: HR = 5.23, 95% confidence interval [CI], 2.30–11.92; time-updated CD4 <200 vs ≥200: HR = 11.79, 95% CI, 4.47–31.07). Nadir CD4 was also a strong indicator (<100 vs ≥100: HR = 3.52, 95% CI, 1.54–8.06). A lack of CD4 recovery (failure to increase 100 cells over nadir) among ART initiators was associated with increased risk (HR = 7.69; 95% CI, 2.60–22.69). Human immunodeficiency virus RNA was not significantly associated with liver disease progression. Conclusions.  Impaired immune function was highly predictive of liver disease progression in this cohort of IDUs, and a lack of CD4 recovery on ART was associated with increased risk of progression to HCV-associated liver disease.


2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Amy S. Baranoski ◽  
Deborah Cotton ◽  
Timothy Heeren ◽  
David Nunes ◽  
Rachel W. Kubiak ◽  
...  

Abstract Background.  Hepatitis C virus (HCV) infection is a leading cause of liver-related morbidity and mortality in the United States, and injection drug users are at particularly high risk. Methods.  This prospective observational cohort study assessed the rate of, and risk factors for, clinical liver disease progression in a cohort of HCV monoinfected and human immunodeficiency virus (HIV)/HCV coinfected drug users using unadjusted and multivariate Cox proportional hazards regression analyses. Results.  Of 564 subjects including 421 (75%) with HIV/HCV coinfection and 143 with HCV monoinfection, 55 (10%) had clinical liver disease progression during follow-up with a rate of 25.3 events per 1000 person-years. In unadjusted analysis, there was an interaction between sex and HIV status. In sex-stratified multivariate analysis, HIV/HCV-coinfected women with CD4 <200 cells/mm3 had 9.99 times the risk of liver disease progression as HCV-monoinfected women (confidence interval [CI], 1.84–54.31; P = .008), and white women had a trend towards increased risk of liver disease progression compared with non-white women (hazard ratio, 2.84; CI, .93–8.68; P = .07). Human immunodeficiency virus/HCV-coinfected men with CD4 <200 cells/mm3 had 2.86 times the risk of liver disease progression as HCV-monoinfected men (CI, 1.23-6.65; P = .01). Conclusions.  Hepatitis C virus-monoinfected and HIV/HCV-coinfected drug users had high rates of clinical liver disease progression. In those with HIV infection, liver disease progression was associated with advanced immune suppression. This effect was strikingly more pronounced in women than in men.


2017 ◽  
Vol 66 (1) ◽  
pp. S711-S712
Author(s):  
W. Zanjir ◽  
R. Maan ◽  
B. Hansen ◽  
O. Cerocchi ◽  
H. Janssen ◽  
...  

2001 ◽  
Vol 33 (2) ◽  
pp. 240-247 ◽  
Author(s):  
Harpreet K. Monga ◽  
Maria C. Rodriguez‐Barradas ◽  
Katharine Breaux ◽  
Kamran Khattak ◽  
Catherine L. Troisi ◽  
...  

Author(s):  
Boun Kim Tan ◽  
Mathieu Chalouni ◽  
Dominique Salmon Ceron ◽  
Alexandre Cinaud ◽  
Laure Esterle ◽  
...  

Abstract Background An increased risk of cardiovascular disease (CVD) was reported in patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV), without identifying factors associated with atherosclerotic CVD (ASCVD) events. Methods HIV–HCV coinfected patients were enrolled in the ANRS CO13 HEPAVIH nationwide cohort. Primary outcome was total ASCVD events. Secondary outcomes were coronary and/or cerebral ASCVD events, and peripheral artery disease (PAD) ASCVD events. Incidences were estimated using the Aalen-Johansen method. Factors associated with ASCVD were identified using cause-specific Cox proportional hazards models. Results At baseline, median age of the study population (n=1213) was 45.4 (interquartile range [IQR] 42.1−49.0) years and 70.3% were men. After a median follow-up of 5.1 (IQR 3.9−7.0) years, the incidence was 6.98 (95% confidence interval [CI] 5.19−9.38) per 1000 person-years for total ASCVD events, 4.01 (2.78−6.00) for coronary and/or cerebral events, and 3.17 (2.05−4.92) for PAD ASCVD events. Aging (hazard ratio [HR] 1.06, 95% CI 1.01−1.12), prior CVD (HR 8.48, 95% CI 3.14−22.91), high total cholesterol (HR 1.43, 95% CI 1.11−1.83), high-density lipoprotein cholesterol (HR 0.22, 95% CI 0.08−0.63), statin use (HR 3.31, 95% CI 1.31−8.38), and high alcohol intake (HR 3.18, 95% CI 1.35−7.52) were independently associated with total ASCVD events, while undetectable baseline viral load (HR 0.41, 95%CI 0.18−0.96) with coronary and/or cerebral events. Conclusion HIV–HCV coinfected patients experienced a high incidence of ASCVD events. Some traditional cardiovascular risk factors were the main determinants of ASCVD. Controlling cholesterol abnormalities and maintaining undetectable HIV viral load are essential to control cardiovascular risk.


Hepatology ◽  
2009 ◽  
Vol 50 (5) ◽  
pp. 1360-1369 ◽  
Author(s):  
Neal D. Freedman ◽  
James E. Everhart ◽  
Karen L. Lindsay ◽  
Marc G. Ghany ◽  
Teresa M. Curto ◽  
...  

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