European journal of gastroenterology & hepatology · 2021
Liver fibrosis regression correlates with downregulation in liver angiogenesis in chronic hepatitis C through viral eradication.
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Chen Sheng-Hung, Huang Chia-Lin, Chiang I-Ping, Chang Tzu-Ching, Wang Hung-Wei, Hsu Wei-Fan, Tsai Tsung-Yu, Peng Cheng-Yuan
Аннотация
OBJECTIVES: The impact of viral eradication on hepatic angiogenesis is unknown. This study aimed to analyze the correlations of liver angiogenesis with liver fibrosis progression or regression in chronic hepatitis C (CHC) after viral eradication.
METHODS: From 2003 to 2020, a cohort of 130 eligible participants underwent paired percutaneous liver biopsies (median = 48 months apart; range = 46-62) at the treatment baseline and after sustained virological response to CHC treatment at the tertiary referral center. The collagen proportionate area (CPA) of liver tissue sections was determined using picrosirius red staining through digital image analysis. CD34 and α-smooth muscle actin (α-SMA) phenotypically quantitated liver angiogenesis and myofibroblasts, respectively, through immunohistochemistry staining, to correlate the total, portal, and extraportal liver angiogenesis with fibrogenesis.
RESULTS: Paired histology manifested significant regressions in fibrosis stages, and necroinflammatory grades (both P < 0.001). The median of changes in CPAs (follow-up minus baseline) was -6.12% (interquartile range = -12.35 to -2.05%). The median of CPA changes per year was -1.38%/year (interquartile range = -2.98 to -0.51%/year). The significance of declines in total CD34 [coefficient (95% confidence interval), 5.577 (3.286-7.868); P < 0.001] outweighed α-SMA declines, when explaining (R2 = 0.522; adjusted R2 = 0.502) the CPA declines through multiple regression analysis adjusting for other histological variables.
CONCLUSION: Through viral eradication in CHC, the downregulated liver angiogenesis significantly explains the CPA regression.
METHODS: From 2003 to 2020, a cohort of 130 eligible participants underwent paired percutaneous liver biopsies (median = 48 months apart; range = 46-62) at the treatment baseline and after sustained virological response to CHC treatment at the tertiary referral center. The collagen proportionate area (CPA) of liver tissue sections was determined using picrosirius red staining through digital image analysis. CD34 and α-smooth muscle actin (α-SMA) phenotypically quantitated liver angiogenesis and myofibroblasts, respectively, through immunohistochemistry staining, to correlate the total, portal, and extraportal liver angiogenesis with fibrogenesis.
RESULTS: Paired histology manifested significant regressions in fibrosis stages, and necroinflammatory grades (both P < 0.001). The median of changes in CPAs (follow-up minus baseline) was -6.12% (interquartile range = -12.35 to -2.05%). The median of CPA changes per year was -1.38%/year (interquartile range = -2.98 to -0.51%/year). The significance of declines in total CD34 [coefficient (95% confidence interval), 5.577 (3.286-7.868); P < 0.001] outweighed α-SMA declines, when explaining (R2 = 0.522; adjusted R2 = 0.502) the CPA declines through multiple regression analysis adjusting for other histological variables.
CONCLUSION: Through viral eradication in CHC, the downregulated liver angiogenesis significantly explains the CPA regression.