Hepatitis C virus (HCV) is a common cause of cirrhosis, leading to increased morbidity and mortality. Treatment of the underlying etiology has been shown to improve fibrosis and cirrhosis.Aim
We sought to evaluate the impact of a sustained virologic response on liver chemistries, model for end stage liver disease (MELD) score, Child–Pugh–Turcotte score (CPT), and fibrosis 4 score (FIB4) in patients with liver cirrhosis secondary to HCV with portal hypertension, with or without decompensation.Methods
Patients with HCV seen in our transplant clinic between June 2013 and September 2015 were identified using ICD-9 code 573.3. Charts were reviewed retrospectively.Results
We collected data from 92 patients with a mean pretreatment MELD score of 9.16±2.98. The most common genotype was Ia, n=79 (86%). The mean duration of follow-up was 7.52±2.25 months. Transaminitis improved significantly at follow-up versus pretreatment [mean aspartate transaminase from 81.2±62.9 to 32.4±12.0 (P<0.0001); alanine transaminase 74.7±77.8 to 27.7±19.4 (P<0.0001)]. Albumin, bilirubin, and α-fetoprotein improved significantly. MELD scores improved in patients with pretreatment scores greater than 10 (P<0.0003), but not in patients with pretreatment scores less than 10 (P=0.501). The CPT score decreased from 6.1±0.9 to 5.8±0.9 (P<0.0024). The FIB4 score improved significantly in patients with baseline FIB4 more than 3.24, but not with higher baseline FIB4.Conclusion
Use of direct antivirals in patients with decompensated cirrhosis because of HCV leads to improved MELD, FIB4, and CPT scores.