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HCV-Related Liver Transplantation

Since its approval in 2013, DAA therapy has been prioritized in patients with HCV-related cirrhosis in an effort to slow clinical progression and induce regression of hepatic histologic damage.

Perumpail and colleagues[13] analyzed the impact of DAA therapy on new waitlist registrations (NWRs) for liver transplantation in the setting of HCV-related cirrhosis. Using the most up-to-date United Network for Organ Sharing data, they evaluated HCV-specific NWR trends for 15 months prior to and following the US Food and Drug Administration's approval of DAA agents. The proportion of all NWRs for liver transplantation represented by HCV patients declined 23%, and the proportion represented by HCV patients without HCC declined 33%.

SVR Before Liver Transplantation

Martini and colleagues[14] used combined immunogenetic markers to identify HCV liver recipients with lower graft survival. HLA variants and the interleukin 28B (IL28B) gene are known to be associated with recurrence and the progression of HCV in the transplant setting. Therefore, the authors investigated the impact of these immunogenetic factors on graft survival in 1228 adult patients after liver transplantation for HCV-related cirrhosis. Ten-year graft survival was lower in HCV-positive recipients compared with HCV-negative recipients. Among HCV-positive recipients, concurrent absence of HLA DRB1*11 and IL28B C/C determined a significantly worse survival and was evident as early as 1 year after transplantation. In a multivariate Cox analysis among HCV-positive recipients, concomitant absence of both immunogenetic markers ranked third as a risk factor for graft survival, inferior only to a MELD score of greater than or equal to 25 and a donor's age of 70 years or older. In the current era of safe and effective all-oral antiviral agents, peritransplant viral eradication might counteract the negative genetic profile of these patients.

HCV Recurrence After Liver Transplantation

Carrai and colleagues[15] evaluated the virologic and clinical efficacy of the combination of SOF/RBV given for 24 weeks in treating recurrent HCV after liver transplantation. HCV genotype frequencies were: 1a (19%), 1b (58%), 2 (5%), 3 (14%), and 4 (4%). Previous treatments failed in 77% of patients, and 69% had cirrhosis. SVR12 was achieved in 97% of patients. No significant drug interactions and no deaths related to antivirals were reported.

Herve and colleagues[16] found that immunosuppression affects the efficacy of antiviral therapy for de novo or recurrent HCV. In a study of a large cohort of liver transplant patients who were treated with SOF plus daclatasvir with or without RBV for 12 or 24 weeks, nearly 50% of patients who received mycophenolate had a slow virologic response, which may indicate that this subgroup may require longer antiviral treatment.

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