Usefulness of pemafibrate for non-alcoholic fatty liver disease with hypertriglyceridemia.

Abstract

Aim of the study: Non-alcoholic fatty liver disease (NAFLD) is a pathological condition associated with inflammation owing to fat deposition in the liver. Managing hypertriglyceridemia is essential for patients with NAFLD, including treatment with pemafibrate. However, whether pemafibrate affects fat deposition in the liver and whether hypertriglyceridemia is the primary treatment target remain unclear. Thus, in this single-arm, retrospective study, we explored how pemafibrate treatment affects fat deposition in the liver in patients with NAFLD using FibroScan, the only insurance-covered device in Japan for quantitatively measuring fat in the liver.

Material and methods: Patients with NAFLD and hypertriglyceridemia were administered 0.2 mg/day of pemafibrate for either three (n = 51) or six (n = 42) months. The primary endpoint was the FibroScan (FibroScan 430 Mini, Echosens, France) controlled attenuation parameter (CAP) measurement. The secondary endpoints were liver transaminase levels, the FibroScan-aspartate aminotransferase (FAST) score, the hepatic steatosis index (HSI), the fibrosis-4 (FIB-4) index, the aspartate aminotransferase-to-platelet ratio index (APRI), and the albumin-bilirubin (ALBI) score.

Results: Three months of pemafibrate administration significantly improved the CAP values. The FAST score and HSI also significantly improved after three months, suggesting fatty liver improvements. Furthermore, the alanine aminotransferase and γ-glutamyl transpeptidase levels (indicators of hepatitis) decreased, and fibrosis improved in the liver fibrosis prediction assessments, such as the FIB-4 index, APRI, and ALBI score, after three months of pemafibrate administration. Most of these improvements remained after six months.

Conclusions: Oral pemafibrate treatment improved NAFLD in patients with hypertriglyceridemia, indicating that pemafibrate may be a new treatment option for NAFLD.