In the Journals

Liver stiffness can predict decompensation, mortality in HCV/HIV coinfected patients

Liver stiffness as measured by transient elastography was found to be a predictive factor of hepatic decompensation and liver-related mortality in patients with HCV and HIV coinfection in a recent study.

In the prospective cohort study, researchers evaluated 239 patients with HIV, HCV and recently diagnosed cirrhosis with no previous decompensation, over a median follow-up of 20 months (range 9-34 months). The times for each patient between initial diagnosis to first decompensation and death from liver disease were recorded, and potential predictors for these results were determined. All instances of cirrhosis were diagnosed through transient elastography (TE).

After follow-up, 31 patients had developed decompensation and/or hepatocellular carcinoma (13%; 95% CI, 9%-17%), with a median development time of 19 months (range 3-37) and an incidence rate of 6.7 per 100 person-years (95% CI, 4.7-9.6). Among 181 patients with a baseline liver stiffness (LS) of less than 40 kPa, 14 (8%) developed a decompensation compared with 17 (29%) patients of the 58 with baseline LS of 40 kPa or higher (P=.001).

Patients in Child-Turcotte-Pugh (CTP) class B were at significantly greater risk for decompensation than those in class A (HR=7.7; 95% CI, 3.3-18.5). Other factors independently associated with decompensation included log-plasma HCV RNA load (HR=2.1; 95% CI, 1.2-3.6), coinfection with HBV (HR=10.3; 95% CI, 2.1-50.4) and baseline LS (HR=1.03; 95% CI, 1.01-1.05).

Across the entire cohort, 15 patients (6%; 95% CI, 3.5%-9.9%) died, with 10 deaths attributed to liver disease. Factors independently associated with liver disease-related death included previous HCV therapy (HR=7.4; 95% CI, 1.7-32.4) and CTP class B (HR=16.5; 95% CI, 3.4-68.2), with baseline LS near statistical significance (HR=1.03; 95% CI, 0.98-1.07). Liver transplantation or death because of any cause were associated with HBV coinfection (HR=5.1; 95% CI, 0.9-26.4), previous HCV therapy (HR=5.7; 95% CI, 1.7-19.7) and MELD score of 14 or more (HR=1.3; 95% CI, 1.1-1.5), along with other factors.

Researchers also compared the ability of LS, CTP and MELD to predict decompensation and/or HCC, and found an AUROC of 0.76 for CTP stage (95% CI, range 0.65-0.88) compared with 0.72 for LS (95% CI, 0.62-0.82) and 0.71 for MELD (95% CI, 0.61-0.81) (P>.2 for all comparisons). LS and MELD were found to perform better than CTP after assessment of the average improvement in the predicted probability of decompensation. Net improvement of LS over CTP was 11% (P=.01) and MELD was 9% over CTP (P=.02).

“This observation provides new evidence to consider incorporating sequential measurements of LS by TE to the routine daily clinical care of HIV/HCV coinfected patients,” the researchers concluded. “In fact, the measurement of LS may help us to identify those patients at very high risk of decompensation and death. … future studies should evaluate if LS is also an independent prognostic marker in patients with decompensated cirrhosis and if sequential assessment of LS in patients with cirrhosis results in a mortality benefit.”

Liver stiffness as measured by transient elastography was found to be a predictive factor of hepatic decompensation and liver-related mortality in patients with HCV and HIV coinfection in a recent study.

In the prospective cohort study, researchers evaluated 239 patients with HIV, HCV and recently diagnosed cirrhosis with no previous decompensation, over a median follow-up of 20 months (range 9-34 months). The times for each patient between initial diagnosis to first decompensation and death from liver disease were recorded, and potential predictors for these results were determined. All instances of cirrhosis were diagnosed through transient elastography (TE).

After follow-up, 31 patients had developed decompensation and/or hepatocellular carcinoma (13%; 95% CI, 9%-17%), with a median development time of 19 months (range 3-37) and an incidence rate of 6.7 per 100 person-years (95% CI, 4.7-9.6). Among 181 patients with a baseline liver stiffness (LS) of less than 40 kPa, 14 (8%) developed a decompensation compared with 17 (29%) patients of the 58 with baseline LS of 40 kPa or higher (P=.001).

Patients in Child-Turcotte-Pugh (CTP) class B were at significantly greater risk for decompensation than those in class A (HR=7.7; 95% CI, 3.3-18.5). Other factors independently associated with decompensation included log-plasma HCV RNA load (HR=2.1; 95% CI, 1.2-3.6), coinfection with HBV (HR=10.3; 95% CI, 2.1-50.4) and baseline LS (HR=1.03; 95% CI, 1.01-1.05).

Across the entire cohort, 15 patients (6%; 95% CI, 3.5%-9.9%) died, with 10 deaths attributed to liver disease. Factors independently associated with liver disease-related death included previous HCV therapy (HR=7.4; 95% CI, 1.7-32.4) and CTP class B (HR=16.5; 95% CI, 3.4-68.2), with baseline LS near statistical significance (HR=1.03; 95% CI, 0.98-1.07). Liver transplantation or death because of any cause were associated with HBV coinfection (HR=5.1; 95% CI, 0.9-26.4), previous HCV therapy (HR=5.7; 95% CI, 1.7-19.7) and MELD score of 14 or more (HR=1.3; 95% CI, 1.1-1.5), along with other factors.

Researchers also compared the ability of LS, CTP and MELD to predict decompensation and/or HCC, and found an AUROC of 0.76 for CTP stage (95% CI, range 0.65-0.88) compared with 0.72 for LS (95% CI, 0.62-0.82) and 0.71 for MELD (95% CI, 0.61-0.81) (P>.2 for all comparisons). LS and MELD were found to perform better than CTP after assessment of the average improvement in the predicted probability of decompensation. Net improvement of LS over CTP was 11% (P=.01) and MELD was 9% over CTP (P=.02).

“This observation provides new evidence to consider incorporating sequential measurements of LS by TE to the routine daily clinical care of HIV/HCV coinfected patients,” the researchers concluded. “In fact, the measurement of LS may help us to identify those patients at very high risk of decompensation and death. … future studies should evaluate if LS is also an independent prognostic marker in patients with decompensated cirrhosis and if sequential assessment of LS in patients with cirrhosis results in a mortality benefit.”