October 14, 2016
Crude incidence of hepatocellular carcinoma (HCC) rose 11% yearly from 2001 through 2014 in an analysis of 7,229 HIV/hepatitis C (HCV)-coinfected people in Europe and Canada. Cirrhosis largely explained climbing incidence of HCC. Over the same years, incidence of other liver complications dropped, according to the study.
Although liver-related deaths declined in recent years among people with HIV or HCV, some evidence indicates that HCC incidence rose in some HIV populations. To get a better understanding of HCC incidence in HIV/HCV-coinfected people, collaborators in Europe and Canada conducted this multicohort study.
The analysis involved HCV antibody-positive adults with HIV in four cohorts: EuroSIDA, the Swiss HIV Cohort Study, the Southern Alberta Clinic Cohort and the Canadian Co-infection Cohort over the years 2001-2014. The researchers checked records to identify new diagnoses of HCC and other liver events, defined as liver decompensation or liver-related death. They used Poisson regression analysis to estimate incidence rate ratios (IRR) and Poisson generalized estimating equations to identify predictors of HCC or other liver events.
From 2001 through 2014, the collaborators counted 72 new cases of HCC to yield an incidence of 1.6 per 1000 person-years and 375 new cases of other liver events for an incidence of 8.6 per 1000 person-years. HCC incidence rose 11% yearly (95% confidence interval [CI] 4% to 19%, P = .002) from 0.4 per 1000 in 2001-2002 to 2.3 per 1000 in 2013-2014. Incidence of other liver events dropped 4% yearly (95% CI 2% to 7%, P = .002) from 9.9 per 1000 in 2003-2004 to 5.2 per 1000 in 2013-2014. People with cirrhosis had a higher incidence of HCC (7.9 per 1000, 95% CI 5.9 to 10.5) and a higher incidence of other liver events (35.9 per 1000, 95% CI 31.1 to 41.4). Regardless of cirrhosis status, incidence of HCC or other liver events was lower in people with a current CD4 count above 350 cells/mm3.
Although HCC incidence rose with later calendar year in univariate analysis, that association lost significance in multivariate analysis, a finding indicating that other variables explained rising HCC incidence over time. Further analysis showed that cirrhosis largely explained rising HCC incidence. Three factors independently raised the risk of incident HCC: cirrhosis (IRR 12.92, 95% CI 6.97 to 23.95, P < .01), hepatitis B coinfection (IRR 2.46, 95% CI 1.03 to 5.87, P = .04) and every additional 10 years of age (IRR 2.36, 95% CI 1.89 to 2.94, P < .01). Every 10-fold higher current CD4 count lowered the risk (IRR 0.78, 95% CI 0.65 to 0.95, P = .01).
Older age, lower current CD4 count, cirrhosis, being underweight and ever smoking independently predicted other liver event incidence. Factors that did not contribute to risk of either HCC or other liver events included alcohol abuse, diabetes mellitus and detectable HIV RNA.
Because cirrhosis mostly explained the rising incidence of HCC, the researchers suggest that increasing survival with HIV allows development of HCV-related cirrhosis and subsequent HCC. They propose that falling incidence of other liver events (hepatic decompensation and liver-related death) may be explained by increasing use of antiretroviral therapy and improved HCV therapy, along with falling use of older hepatotoxic antiretrovirals. The seemingly paradoxical coincidence of improving liver-related morbidity but rising HCC incidence, the authors suggest, may mean improved management of cirrhosis and HIV boosts the threshold for liver decompensation in cirrhotics with HIV/HCV and thus increases longevity and allows HCC to develop.
Mark Mascolini writes about HIV infection.
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