Impact of SVR to IFN-free DAA regimens on steatosis in HIV/HCV coinfected patients

Background and Aims:

Hepatic steatosis (HS) contributes to liver disease among HIV/hepatitis C (HCV) coinfected patients (HIVHCV). Previous studies suggested a steatogenic effect of HCV. We evaluated the impact of sustained virologic response (SVR) to direct-acting antivirals (DAAs) on HS and dyslipidemia in HIVHCV.

Method:

HIVHCV with paired controlled attenuation parameter (CAP®, FibroScan®, Echosens, France) measurements pre and post SVR to DAA treatment were included. CAP® values were adjusted according to Karlas et al (J Hepatol 2017).

Results:

Patient characteristics: 76% male (82/107), median age at baseline (BL): 49 (IQR 16) years; BMI: 22.9 (IQR 4.86)kg*m^-2; PNPLA3 genotype (GT): C/G 51% (52/101) and G/G 3% (3/101); HCV-GT-1a 55% (59/107), HCV-GT-1b 10% (11/107), HCV-GT2 1% (1/107); HCV-GT-3 20% (21/107) and HCV-GT-4 14% (15/107). Total cholesterol (153 (IQR 154) vs. 174 (IQR 59)IU/mL; p < 0.001) and low density lipoprotein (82.4 (IQR 44.3) vs. 104 (IQR 47.6) IU/mL; p < 0.001) levels increased significantly after SVR, while no changes in triglycerides, high density lipoprotein levels, or CAP were observed. The prevalence of HS (defined by CAp ≥248dB/m) at BL and SVR was 33% (35/107) and 41% (44/107), respectively. Predictive factors for a regression of HS after SVR were high BL CAP values (253 ± 55.6 vs. 209 ± 48.1dB/m; p < 0.001), high age (52.0 (12.8) vs. 45.2 (17.2) years; p = 0.015), as well as HIV protease inhibitor intake (47% (20/43) vs. 19% (12/63); p = 0.002) at BL.

Conclusions:

In HIVHCV, achieving SVR to IFN-free therapies had no significant impact on CAP values and the proportion of HIVHCV affected by HS remained high after SVR. HCV eradication significantly increased cholesterol and low density lipoprotein levels. Further studies investigating metabolic changes and cardiovascular risk in HIVHCV after SVR are warranted.