Effect of direct‐acting antivirals on platelet‐associated immunoglobulin G and thrombocytopenia in hepatitis C virus‐related chronic liver disease

Abstract

Background & Aims Hepatitis C virus (HCV) infection has been known to cause various extrahepatic autoimmune disorders. The prevalence of platelet‐associated immunoglobulin G (PA‐IgG) has been high in patients with HCV infection. Because thrombocytopenia in HCV‐related liver diseases is a notable problem, we performed prospective study on the effect of direct‐acting antivirals (DAAs) treatment on PA‐IgG and platelet count. Methods A total of 215 patients with HCV‐related liver disease were enrolled in this study. The patients who discontinued DAAs or did not undergo adequate laboratory examinations and who did not achieve sustained virologic response were excluded and finally a total of 187 patients were investigated. Results A total of 171 patients (91.4%) were PA‐IgG positive (>46 ng/107 cells) before starting DAAs (baseline). The PA‐IgG level elevation was significantly correlated with higher liver inflammation and fibrosis markers (P < 0.05) and lower platelet count (P = 0.000019). The platelet count of the patients with low PA‐IgG titer tended to be higher at baseline, end of treatment (EOT), and at 12 and 24 weeks after EOT. The platelet count increased at EOT (P < 0.05) and 24 weeks after EOT (P < 0.01). The PA‐IgG levels were significantly decreased at EOT, 12 and 24 weeks after EOT (P < 0.01). Multiple regression analysis found that only platelet count at baseline was closely associated with negative conversion of PA‐IgG at 24 weeks after EOT (P = 0.004). Conclusions Eradication of HCV by DAAs treatment successfully decreased PA‐IgG level and increased platelet count.

Platelet count increases after viral elimination in chronic HCV, independent of the presence or absence of cirrhosis

“…Furthermore, it has been shown that about two-thirds of patients with HCV cirrhosis and clinically significant portal hypertension prior to antiviral therapy remain with this degree of portal hypertension 6 months after viral elimination 20. In further support of our study and providing an explanation for the results, a recent study by Honma et al performed in mostly non-cirrhotic patients with HCV demonstrated that PLT count increases significantly after viral eradication and that it correlated with a decrease in platelet-associated immunoglobulin G (PA-IgG), thereby implicating an HCVassociated immune mechanism in the genesis of thrombocytopenia 21. Therefore, our observation and that of others indicate that the increase in PLT observed in our study is most likely the effect of viral elimination itself and, importantly, indicates that scoring systems that include PLT count as one of the variables should not be used in the evaluation of the degree of fibrosis (or presence or absence of cirrhosis) in the post-SVR setting.…”

“…In further support of our study and providing an explanation for the results, a recent study by Honma et al performed in mostly non‐cirrhotic patients with HCV demonstrated that PLT count increases significantly after viral eradication and that it correlated with a decrease in platelet‐associated immunoglobulin G (PA‐IgG), thereby implicating an HCV‐associated immune mechanism in the genesis of thrombocytopenia …”

Pathogenesis of Thrombocytopenia in Chronic HCV Infection: A Review

“…Honma et al 19 prospectively studied 187 patients who were treated with direct-acting antivirals. PAIgG levels as well as Plt counts were measured prior to treatment and post-treatment.…”

Successful Treatment with Crushed Sofosbuvir/Velpatasvir of a Patient with Decompensated Cirrhosis C and Thrombocytopenia

“…PA-IgG is frequently elevated in HCV-infected patients due to the presence of various autoantibodies [ 12 , 13 ]. Because ITP may be induced by HCV infection itself [ 14 , 15 , 16 ], HCV eradication with DAA may improve ITP [ 16 ]. The etiology of thrombocytopenia accompanying HCV infection is complex, requiring careful examination in individual patients.…”