Even with HCV cure, surveillance for portal hypertension, HCC ‘should be mandatory’
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Key takeaways:
- Sustained virologic response occurred in 81.8% of patients after the first DAA treatment course.
- Despite this, further decompensation occurred in 19% of patients and 2.9% developed hepatocellular carcinoma.
Despite achieving cure with direct-acting antivirals, patients with chronic hepatitis C virus-related decompensated cirrhosis remain at risk for progression of portal hypertension, further decompensation and hepatocellular carcinoma.
“The introduction of pan-genotypic, highly effective DAAs has transformed the therapeutic paradigm towards HCV elimination,” Madhumita Premkumar, MD, DM, associate professor of hepatology at the Postgraduate Institute of Medical Education and Research in Chandigarh, India, and colleagues wrote in Gastroenterology. “In this study, we assessed the real-world efficacy of a programmatic provision of free-of-charge DAA therapy for management of decompensated chronic HCV-related cirrhosis in a public health care setting in the Punjab state, India.”
From July 2018 to July 2023, Premkumar and colleagues enrolled 1,152 patients (mean age, 53.2 years; 63% men) with chronic HCV and decompensated cirrhosis who completed DAA therapy, with follow-ups every 6 months.
Studied outcomes included rates of recompensation after achieving sustained virologic response, progression of portal hypertension, further decompensation events and development of hepatocellular carcinoma. Mortality and liver transplantation outcomes were also investigated.
At enrollment, 87% of patients had genotype 3 HCV and MELD-Na and Child Pugh Turcotte scores were 16.2 and 12.3, respectively.
After a median follow-up of 48.3 months, the researchers reported that 81.8% of patients achieved SVR 12 weeks after the first DAA treatment regimen, with 90.8% achieving SVR after additional treatment courses. The most common decompensation event was ascites (95.3%), which resolved in 86% of patients, followed by variceal bleeding (24.7%) and hepatic encephalopathy (16.6%).
Nearly a quarter of patients (24.7%) experienced recompensation, with a median time to occurrence of 16.5 months. Based on multivariable analysis, low bilirubin (adjusted HR = 0.6; 95% CI, 0.5-0.8), international normalized ratio (aHR = 0.2; 95% CI, 0.1-0.3), absence of large esophageal varices (aHR = 0.4; 95% CI, 0.2-0.9) and gastric varices (aHR = 0.5; 95% CI, 0.3-0.7) were associated with recompensation.
However, 13.7% of patients exhibited portal hypertension progression, with rebleeding in 4%, linked to previous decompensation with variceal bleeding (aHR= 1.6; 95% CI,1.2-2.8) as well as the presence of large varices (aHR = 2.9; 95% CI,1.3-6.5). The researchers also reported further decompensation in 19% of patients and development of HCC in 2.9%.
Further, 12.5% of patients died and six patients required liver transplantation.
“Decompensated cirrhosis has cure rates exceeding 81% using all-oral DAAs in a genotype-3 enriched population of decompensated cirrhosis, with nearly a fourth meeting criteria for recompensation and more than a third improving to Child A status over an average period of 4 years,” Premkumar and colleagues wrote. “However, they remain at risk of further decompensation or progression of portal hypertension, with 0.72% having annual risk of HCC after cure.”
They continued, “Therefore, surveillance for portal hypertension progression and HCC should be mandatory even after apparent improvement in liver disease severity.”
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