HIV appears to promote the progression of liver disease in people co-infected with hepatitis C (HCV), researchers found.
In a prospective observational cohort of people with HCV, those who also had HIV showed liver fibrosis similar to that seen in people who had only HCV — but who are almost a decade older, according to David Thomas, MD, of Johns Hopkins School of Medicine, and colleagues.
The finding is “consistent” with the notion that HIV infection and aging both drive HCV-related liver disease, possibly through common mechanisms, Thomas and colleagues reported online in Annals of Internal Medicine.
In general, the researchers noted, people with HIV have been reported to develop age-related diseases – such as heart disease and some cancers – at a younger-than-expected age.
But it has not been clear whether those observations can be blamed on HIV infection itself or on other, unmeasured risk factors, they added.
To help clarify the issue, they turned to the AIDS Linked to the IntraVenous Experience (ALIVE) cohort of current and former injection drug users in Baltimore.
They compared the severity of liver fibrosis by age (assessed every six months by liver stiffness measurements) among HCV-positive participants with and without HIV, who were followed over time with the same protocol.
The 1,176 participants had a median age of 49 and 34% were co-infected with HIV. Overall, the participants contributed 5,634 valid liver fibrosis measurements – a median of five tests per person over 2.9 years of follow-up.
At the beginning of the study, those with both viruses were significantly more likely (at P<0.001) than mono-infected participants to have cirrhosis (19.5% versus 11.0%) or clinically significant fibrosis without cirrhosis (12.9% versus 9.5%).
Liver fibrosis was independently associated with older age (at P<0.001) and HIV infection (atP=0.005).
In a multivariate model, the researchers calculated the expected liver fibrosis value by age and found that – if age was held constant — it was from 1.17 to 2.02 kilopascals greater in people with HIV than in those without HIV.
Put another way, they found that people with HIV had liver fibrosis measurements equal to those of HIV-negative people, who were, on average, 9.2 years older.
Thomas and colleagues also found that liver fibrosis among people with HIV was associated with lower nadir or current counts of CD4-positive T cells and with higher levels of HIV RNA.
One implication is that effective HIV treatment might reduce the risk of liver disease progression among co-infected people, but the study so far has not found such a link, they reported.
They cautioned that liver stiffness is “only a proxy” for fibrosis.
They also noted that, in most cases, they do not have any data on the duration of HCV infection, although their estimates of duration did not differ by HIV status.
But if HIV-positive drug users tend to get infected with HCV earlier than others, they cautioned, “it may seem that HIV causes liver fibrosis at younger ages.”