Journal
LIVER TRANSPLANTATION
Volume 11, Issue 10, Pages 1235-1241Publisher
WILEY
DOI: 10.1002/lt.20432
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Funding
- NCRR NIH HHS [RR000046] Funding Source: Medline
- NHLBI NIH HHS [R01 HL 64817-01] Funding Source: Medline
- NIDDK NIH HHS [K24 DK066144-01] Funding Source: Medline
- NIEHS NIH HHS [P30ES10126] Funding Source: Medline
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Recurrent hepatitis C after liver transplantation is a serious problem faced by liver transplant recipients. Activation of hepatic stellate cells is an early step in hepatic fibrogenesis. The aim of this study was to evaluate hepatic stellate cell activation, early after liver transplantation, as a predictor for the subsequent development of advanced fibrosis. Forty-six patients who underwent liver transplantation for hepatitis C and protocol liver biopsies were divided into rapid fibrosers (n = 21), defined as recipients who developed bridging fibrosis or cirrhosis within 2 years of liver transplantation, and slow fibrosers (n = 25). The protocol liver biopsy obtained 4 months after transplantation was stained and quantitated for hepatic stellate cell activation with antibody to alpha smooth muscle actin. Hepatic stellate cell activity was independently associated with rapid fibrosis (odds ratio: 1.6 [95% CI: 1.1,2.2], P = 0.013). The c-statistics for the receiver operating characteristic curve for stellate cell activity and fibrosis were 0.78 and 0.67, respectively, P = 0.36. The receiver operating characteristic curve for a model including stellate cell activity, histology activity index, and alanine aminotransferase. obtained at month 4 had the best c-statistic (0.88). In recipients with stage 0 or I fibrosis on the month 4 liver biopsy who subsequently developed advanced fibrosis, the c-statistic for the receiver operating characteristic curves was significantly better for stellate cell activity than for stage of fibrosis (0.77 and 0.51, respectively; P = 0.004). In conclusion, hepatic stellate cell activation early after liver transplantation complements traditional testing for identifying liver transplant recipients with hepatitis C at greatest risk for developing advanced fibrosis.
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