Published online Jun 16, 2022. doi: 10.12998/wjcc.v10.i17.5566
Peer-review started: August 10, 2021
First decision: November 17, 2021
Revised: December 16, 2021
Accepted: April 21, 2022
Article in press: April 21, 2022
Published online: June 16, 2022
Processing time: 302 Days and 19.3 Hours
Liver fibrosis is a common pathway of liver injury and is a feature of most chronic liver diseases. Fibrosis progression varies markedly in patients with hepatitis C virus (HCV), and the severity of liver fibrosis is associated with the prognosis of liver disease. Liver stiffness has been recommended as a parameter of fibrosis progression/regression in patients with HCV.
To investigate the changes in liver stiffness measured by transient elastography (TE) in a large, racially diverse cohort of U.S. patients with chronic hepatitis C (CHC).
We evaluated the differences in liver stiffness between patients treated with direct-acting antiviral (DAA) therapy and untreated patients. In addition, we performed a longitudinal, retrospective observational study investigating changes in liver stiffness measured by TE in a racially diverse cohort of United States patients with CHC.
We conducted a longitudinal retrospective study of patients with confirmed CHC infection seen at Johns Hopkins Health System (JHHS) and Kaiser Permanente Mid-Atlantic States (KPMAS). Patients had ≥ 2 TE measurements and no prior DAA exposure. We used linear regression to measure the change in liver stiffness between first and last TE in response to treatment, controlling for age, sex, race, diabetes, smoking status, HIV status, baseline ALT, and baseline liver stiffness.
Of 813 patients, 84% were at least 50 years of age, 79% were Black, 79% were current or former smokers, 37% were coinfected with HIV, 3% were coinfected with HBV, 19% had diabetes, and 52% initiated treatment with a DAA. The median time between first and last TE was 11.7 and 12.7 mo among treated and untreated patients, respectively. There was no significant change in liver stiffness observed over time in either the group initiating DAA treatment (0.016 kPa/month; CI: -0.051, 0.084) or in the untreated group (0.001 kPa/month; CI: -0.090, 0.092), controlling for covariates. A higher baseline kPa score was independently associated with decreased liver stiffness.
DAA treatment was not associated with a differential change in liver stiffness over time, as measured by TE, in patients with CHC compared to untreated patients. Our study underscores the imperfect characteristics of any single noninvasive test for assessing liver fibrosis, which continues to be compared to the gold standard of liver biopsy and histopathology, despite the impetus to avoid invasive testing for CHC infection in clinical practice.
Direct-acting antiviral therapy was not associated with a differential change in liver stiffness over time in patients with CHC compared to untreated patients. Further longitudinal prospective studies are needed to evaluate the clinical utility of obtaining TE measurements in patients with CHC who have achieved sustained virologic response and assess liver fibrosis progression in diverse populations.