Interference of hepatitis B virus dual infection in platelet count recovery in chronic hepatitis C patients with curative antiviral therapy.

Abstract

Hepatitis C virus infection is associated with thrombocytopenia. Thrombocytopenia recovers after viral eradication. The current study explored the rate and factors associated with platelet (PLT) recovery, which may represent the degree of liver fibrosis regression. A total of 466 patients who achieved a sustained virological response were enrolled to compare the PLT change after a mean follow-up period of 85.5months (range 12-163months). Platelet counts increased significantly after achieving sustained virological response (from 166±55×103 to 201±61×103 u/L, P<0.001). The median PLT count increment was 5.03×103 u/L per year. Logistic regression analysis revealed that factors associated with slow PLT count recovery were high pretreatment PLT counts (odds ratio [OR]/ 95% confidence intervals [CI]: 0.992/0.989-0.996, P<0.001) and hepatitis B virus (HBV) co-infection (OR/CI: 0.416/0.220-0.785, P=0.007). High PLT counts were the only factor associated with slow PLT recovery in patients with mild liver disease (F0-2) (OR/CI: 0.992/0.987-0.996, P<0.001). On the other hand, HBV co-infection was the only factor associated with slow PLT recovery in patients with advanced fibrosis (OR/CI: 0.207/0.054-0.789, P=0.02). Linear regression analysis of factors correlated to the delta PLT count change per year in patients with F0-2 included pretreatment white blood cell (β: -0.001; CI: -0.002-0.000; P=0.01) and pretreatment PLT counts (β: -0.037; CI: -0.061 to -0.013; P=0.003). HBsAg seropositivity was the only factor correlated to the delta PLT count change per year (β: -10.193; CI: -16.752-3.635; P=0.003) among patients with F3-4. Platelet counts recovered after hepatitis C virus eradication. HBV dual infection disrupted PLT count recovery, especially in CHC patients with advanced liver disease.