All‐oral direct‐acting antiviral therapy in HCV‐advanced liver disease is effective in real‐world practice: observations through HCV‐TARGET database

Abstract

All-oral therapies are effective among patients with advanced liver disease with high levels of success in GT2 and GT1b, and may serve to reduce the severity of liver disease after SVR. Treatment for GT3 patients remains an unmet need. Clinical trial number: NCT01474811.

Rates of sustained virological response 12 weeks after the scheduled end of direct‐acting antiviral (DAA)‐based hepatitis C virus (HCV) therapy from the National German HCV registry: does HIV coinfection impair the response to DAA combination therapy?

“…The authors discuss a higher frequency of liver cirrhosis in the HIV‐coinfected patients as a possible explanation for their findings . Liver cirrhosis has indeed been described as a risk factor for lower response rates in some studies, especially in GT 3 patients . Interestingly, in our study cohort we found that more HCV‐monoinfected patients presented with liver cirrhosis, which might be the reason for these different findings.…”

The management of chronic hepatitis C: 2018 guideline update from the Canadian Association for the Study of the Liver

“…Identifying patients with cirrhosis is particularly important because of their increased risk of hepatic complica tions, lower treatment response and requirement for hepato cellular carcinoma surveillance, even after achievement of sus tained virologic response. 12,47,48 In those without overt evidence of cirrhosis on history or exam (e.g., ascites, encephalopathy) or routine tests (e.g., nodular shrunken liver or splenomegaly on ultrasound), an additional dedicated fibrosis assessment is required. Notably, absence of clinical signs or symptoms and even normal radiological findings do not adequately rule out cirrhosis.…”

Racial Disparity in Gastrointestinal Cancer Risk

“…alpha-1 antitrypsin, Wilson’s, hemachromatosis, glycogen storage diseases, autoimmune chronic active hepatitis, primary biliary cirrhosis) in addition to HBV) can cause HCC [107]. New nucleotide/nucleoside and protease inhibitors that clear HCV viral loads theoretically should reduce HCC over time for those who can obtain the expensive treatment [108,109], but other conditions such as NAFLD will likely become the dominant etiology among populations in the U.S. Rates of NAFLD are highest among Hispanic patients compared to NHWs and Blacks [110,111], and without a clear definitive treatment path for NAFLD to date, a relative increased disparity could develop for HCC in Hispanics in the future. Variants for NAFLD risk exist in single nucleotide polymorphisms in or near PNPLA3 and PPP1R3B genes in Hispanic Americans and PNPLA3 , NCAN , GCKR , and PPP1R3B genes in Blacks [112].…”