Effects of direct-acting antiviral therapy (DAAS) on the ultrasound parameters of portal hypertension

Abstract

Background:Among the endpoints of antiviral therapy with DAAs in HCV related liver cirrhosis (LC-HCV) in addition to the eradication of the virus there are the regression of fibrosis and of portal hypertension. For this reason we evaluated in LC-HCV patients and sustained virological response (SVR) to DAAs therapy the behavior of the AST to Platelet Ratio Index (APRI) (indirect marker of fibrosis) and of two ultrasound (US) signs of portal hypertension: caliber of the portal vein (cPV ) and longitudinal diameter of the spleen (LDS) Methods:132 patients with LC-HCV at baseline (BL), at three months (PostT3) and 12 months (PostT12) after the end of therapy, performed liver function tests and platelet count, US at BL, at PostT3 and at PostT12 and the liver stiffness (LS) measurement with Fibroscan at BL. The diagnosis of LC was histological in 12% of patients, in 88% was done by LS, US and endoscopy. Genotype 1b was present in 79% of the patients. When we performed the statistical analysis, 90 patients included in the study were at PostT12. We used the t-Student test for paired data, the Spearman's rho and the chi-square test when appropriated. Results: cPV at BL was significantly higher than at postT3 (P<0.03) and at postT12 (P<0.0001), no difference was detected between postT3 and postT12. LDS showed a decreasing trend and in particular was significantly higher at PostT12 compared to BL (P <0.04). APRI decreased in BL vs PostT3 and BL vs PostT12 (P <0.001), but not between PostT3 vs PostT12 (P = ns). The correlations between the evaluation times BL, PostT3 and PostT12 (indicated as 0,1,2) and the parameters studied were: APRI = -0.7 (P <0.0001), cPV = -0.18 (P <0.02), LDS = -0.16 (P <0.05). Patients who at BL had LS <20 kPa presented a more frequent reduction in cPV (P <0.05) at PostT3, a difference that disappeared at PostT12 (P = ns). Conclusion. Our data suggest that therapy with DAAs eradicates HCV and leads to an improvement in portal hypertension, evidenced by the reduction of cPV and LDS; the cPV and APRI early reduction, the inverse correlation found for APRI and cPV and LDS in the three evaluation times and finally the higher frequency of cPV reduction at PostT3 in patients with LS <20 kPa leads us to suppose that at the beginning the decrease of necroinflammation is the predominant factor. Later, fibrosis reduction would be predominant as suggested by the absence of difference between patients with LS <20 kPa at T12 and the trend of LDS reduction that could be late as more related to fibrosis.