HCC incidence nearly 5-times higher among HBV, HDV coinfected patients with cirrhosis
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Key takeaways:
- The cumulative incidence of hepatocellular carcinoma at 1, 3 and 5 years was higher among patients coinfected with HBV and HDV.
- HDV infection was an independent risk factor for HCC occurrence.
Incidence of hepatocellular carcinoma was significantly higher among cirrhotic patients coinfected with hepatitis B and D viruses compared with those with HBV alone, with researchers suggesting HDV “plays a direct role” in HCC occurrence.
“Because HDV infection requires simultaneous HBV infection, and HBV on its own can cause HCC in patients with chronic hepatitis B, the direct impact of HDV coinfection on HCC risk remains debated,” Dominique Roulot, MD, of the department of hepatology and hepatic oncology at Avicenna Hospital in Paris, and colleagues wrote. “Potential biases in the analysis of the HCC-promoting role of HDV in patients with HBV-HDV cirrhosis might arise from the limited number of investigated patients, the absence of histologically proven cirrhosis and the ethnic origin of patients.”
Using data from two French cohorts, Roulot and colleagues compared the incidence of HCC among 142 patients (mean age, 55.1 years; 65.5% men) coinfected with HBV-HDV and 271 patients (mean age, 35.7 years; 83% men) with HBV alone. All patients had histologically proven cirrhosis with no history of decompensation.
According to study results published in Clinical Gastroenterology and Hepatology, 13.4% of patients with HBV-HDV developed HCC after a median follow-up of 54 months, as did 10.7% of those with HBV after a median follow-up of 84 months. After adjusting for age, the researchers reported that the cumulative incidence of HCC among coinfected vs. monoinfected patients was higher at 1 year (5.2% vs. 1.1%), 3 years (11.8% vs. 2.5%) and 5 years (20.2% vs. 4.4%; sub HR = 4.99; 95% CI, 2.36-10.52).
Multivariate analysis also showed that HDV infection was an independent risk factor for HCC (HR = 2.94; 95% CI, 1.19-7.25), as were age (HR = 1.08; 95% CI, 1.05-1.11), overweight (HR = 0.45; 95% CI, 0.22-0.93), smoking (HR = 2.26; 95% CI, 1.23-4.16) elevated gamma-glutamyl transferase (HR = 2.73; 95% CI, 1.24-6), total bilirubin higher than 17 µmol/L (HR = 2.68; 95% CI, 1.33-5.42) and platelet count less than 150,000 per mm3 (HR = 3.11; 95% CI, 1.51-6.41).
Further, although HDV coinfection was associated with occurrence of HCC, it was not linked to decompensation (HR = 2.4; 95% CI, 0.57-10.09) or liver transplant/death (HR = 4.26; 95% CI, 0.6-30.02).
“After adjustment for age, the incidence of HCC at 1 and 5 years was 4.6-times higher in HBV-HDV cirrhosis compared with HBV cirrhosis,” Roulot and colleagues wrote. “HDV infection was an independent risk factor for HCC, suggesting that HDV plays a direct role in HCC independently of HBV infection.”
They continued, “In the clinical practice, ultrasound hepatic surveillance of coinfected patients must be reinforced. Cirrhotic coinfected patients should be treated in priority aiming at the HDV-RNA negativity, the persistence of which increases the risk of HCC.”
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