Spanish research shows that liver stiffness can predict outcomes in people co-infected with HIV and hepatitis C

Liver stiffness is a strong predictor of hepatic complications and all-cause mortality in people co-infected with HIV and hepatitis C virus (HCV), Spanish investigators report in the online edition of AIDS. Liver stiffness was assessed using an ultrasound-based technique called transient elastometry (FibroScan). This can assess liver stiffness, an accurate proxy for fibrosis without the need for a liver biopsy.

“We found that baseline liver stiffness was the strongest predictor of developing hepatic events and of all-cause mortality and death in HIV/HCV-coinfected patients,” write the investigators. “The strength of our study is the large size of the study population…and the long follow-up.”

The availability of safe and potent antiretroviral therapy means that the prognosis for many people with HIV is now a normal life expectancy. However, people co-infected with HIV and hepatitis C continue to have markedly elevated mortality rates and liver disease is an important cause of death in these patients.

Liver fibrosis is a predictor of the risk of liver disease and death in co-infected people. The standard assessment tool for fibrosis is liver biopsy. However, this is an invasive procedure, has a risk of complications and is unpopular with patients. Therefore, alternative tests have been developed, one of which is FibroScan. This test uses a handheld ultrasound scanning device to measure the stiffness of the liver. A liver scarred by fibrosis is stiffer than a healthy liver.

Investigators at the Hospital Carlos III in Madrid wanted to see if liver stiffness as assessed by FibroScan was a predictor of liver disease and death in their co-infected patients. FibroScan has been in routine use at their centre since 2004.

Their observational, retrospective study involved 545 co-infected patients. Most (71%) were men, their mean age was 41 years, 81% had a history of injecting drug use and 4% were also infected with hepatitis B. All but three of the participants were taking antiretroviral therapy and 88% had an undetectable viral load. The mean duration of follow-up was 71 months.

Liver stiffness below 7.5 kPa was considered to equate to the Metavir F0-F1 stages (no or very mild fibrosis); 7.5-9.4 to Metavir F2 (mild fibrosis); 9.5-12.4 kPa to Metavir 3; and above 14.5 kPa as Metavir F4. Advanced fibrosis was classified Metavir F3-F4.

The investigators explored the relationship between baseline liver stiffness and the incidence of death and liver-related events (defined as ascites – fluid in the abdominal cavity; encephalopathy – damage to the brain; oesophageal varices – enlarged veins in the oesophagus; and hepatocellular carcinoma).

Over a third of participants (34%) had advanced fibrosis at baseline. Almost two-thirds of individuals received hepatitis C therapy during follow-up and 39% achieved a sustained virological response. Twelve participants (2%) died. Four deaths were attributed to liver disease. Liver-related events occurred in 53% participants (10%).

After taking into account potential confounders, the investigators established that baseline liver stiffness was the strongest predictor of liver-complications (OR = 1.12; 95% CI, 1.08-1.16; p < 0.0001). Moreover, liver stiffness was the only factor associated with all-cause mortality (OR = 1.09; 95% CI, 1.01-1.19; p = 0.02).

Other factors associated with liver-related events were male gender (p = 0.01), CD4 cell count (p = 0.02) and glucose levels (p = 0.006).

Hepatitis C therapy that achieved a sustained virological response was protective against liver events (p = 0.01).

“Baseline liver stiffness is the strongest predictor of liver-related complications and of all-cause mortality in HIV/HCV-coinfected patients on antiretroviral therapy,” conclude the authors. “Clearance of HCV with antiviral therapy significantly reduces the risk of developing liver decompensation events in this population.”