Mezina Anya, Krishnan Arunkumar, Woreta Tinsay A, Rubenstein Kevin B, Watson Eric, Chen Po-Hung, Rodriguez-Watson Carla
Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD 21287, United States.
Division of Gastroenterology and Hepatology, Johns Hopkins School of Medicine, Baltimore, MD 21231, United States.
World J Clin Cases. 2022 Jun 16;10(17):5566-5576. doi: 10.12998/wjcc.v10.i17.5566.
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). Liver stiffness has been recommended as a parameter of fibrosis progression/regression in patients with HCV.
To investigate changes in liver stiffness measured by transient elastography (TE) in a large, racially diverse cohort of United States 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. 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, human immunodeficiency virus status, baseline alanine aminotransferase, and baseline liver stiffness. Separate regression models analyzed the change in liver stiffness as measured by kPa, stratified by cirrhosis status.
Of 813 patients, 419 (52%) initiated DAA treatment. Baseline liver stiffness was 12 kPa in 127 (16%). 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/mo; 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 in patients with CHC compared to untreated patients.
肝纤维化是肝损伤的常见途径，也是大多数慢性肝病的特征。丙型肝炎病毒（HCV）患者的纤维化进展差异显著。肝脏硬度已被推荐作为HCV患者纤维化进展/消退的参数。
在一个种族多样的美国慢性丙型肝炎（CHC）患者大群体中，研究通过瞬时弹性成像（TE）测量的肝脏硬度变化。
我们评估了接受直接抗病毒药物（DAA）治疗的患者与未治疗患者之间肝脏硬度的差异。患者进行了≥2次TE测量且之前未接触过DAA。我们使用线性回归来测量治疗后首次和末次TE之间肝脏硬度的变化，并控制年龄、性别、种族、糖尿病、吸烟状况、人类免疫缺陷病毒状况、基线丙氨酸转氨酶和基线肝脏硬度。单独的回归模型分析了以kPa为单位测量的肝脏硬度变化，并按肝硬化状态分层。
813例患者中，419例（52%）开始接受DAA治疗。127例（16%）患者的基线肝脏硬度为12 kPa。治疗组和未治疗组首次和末次TE之间的中位时间分别为11.7个月和12.7个月。在控制协变量的情况下，接受DAA治疗的组（0.016 kPa/月；可信区间：-0.051，0.084）或未治疗组（0.001 kPa/月；可信区间：-0.090，0.092）中，均未观察到肝脏硬度随时间有显著变化。较高的基线kPa评分与肝脏硬度降低独立相关。
与未治疗的患者相比，CHC患者接受DAA治疗后，肝脏硬度随时间没有差异变化。
