The effect of nintedanib on health-related quality of life in Japanese patients with progressive fibrosing interstitial lung diseases: A subset analysis of the INBUILD trial.

Background: In previous Japanese subgroup/subset analyses of the global INBUILD trial, nintedanib reduced the annual rate of forced vital capacity (FVC) decline and the risk of disease progression in patients with progressive fibrosing interstitial lung diseases (PF-ILDs). This exploratory subset analysis assessed the effect of nintedanib on symptoms and impacts of pulmonary fibrosis in Japanese patients with PF-ILDs, including those with usual interstitial pneumonia (UIP)-like fibrotic pattern on high-resolution computed tomography (HRCT).
Methods: This analysis included Japanese patients who received at least one dose of study treatment in the randomized, double-blind, placebo-controlled INBUILD trial. The Living with Pulmonary Fibrosis (L-PF) questionnaire was used to assess pulmonary fibrosis symptoms and impacts (higher scores indicated greater impairment) at baseline and weeks 12-52.
Results: In total, 108 Japanese patients (nintedanib: n = 52; placebo: n = 56) were included; 84 patients had UIP-like fibrotic pattern on HRCT. In the total Japanese subgroup and in those with UIP-like fibrotic pattern, numerically greater increases in L-PF total, symptoms total, symptoms fatigue domain, and impacts scores were observed in the placebo group than in the nintedanib group at all timepoints, starting from week 12. A numerically greater increase in the symptoms dyspnea domain score was observed with placebo versus nintedanib starting from week 36. Throughout the study, the symptoms cough domain score increased in the placebo group but decreased in the nintedanib group.
Conclusions: Our findings demonstrate that nintedanib has the potential to reduce the worsening of symptoms and impacts of pulmonary fibrosis in Japanese patients with PF-ILDs.
Competing Interests: Declaration of competing interest Yoshikazu Inoue received lecture fees from Nippon Boehringer Ingelheim Co. Ltd.; Masaki Okamoto received lecture fees from Nippon Boehringer Ingelheim Co. Ltd. and research funding from Nippon Boehringer Ingelheim Co. Ltd., Japan Respiratory Society Nippon Boehringer-Ingelheim research grant and Grant-in-Aid for Scientific Research (C) (no. 22K08274); Takashi Ogura received honoraria from Nippon Boehringer Ingelheim Co. Ltd.; Yasuhiko Nishioka received lecture fees from Nippon Boehringer Ingelheim Co. Ltd.; Masataka Kuwana received honoraria form Nippon Boehringer Ingelheim Co. Ltd., Asahi Kasei Pharma Co. Ltd., Chugai Pharmaceutical Co., Ltd., Kissei Pharmaceutical Co., Ltd., Mochida Pharmaceutical Co., Ltd., research funding from Nippon Boehringer Ingelheim Co. Ltd. and subsidies or donations from Asahi-Kasei Pharma Co. Ltd. and Nippon Boehringer-Ingelheim Co. Ltd.; Atsushi Taniguchi and Tomohiro Ito are employed by Nippon Boehringer Ingelheim Co. Ltd.; Klaus B. Rohr is employed by Boehringer Ingelheim International GmbH.; Takafumi Suda received honoraria from Nippon Boehringer Ingelheim Co. Ltd.; Hideya Kitamura has no conflict of interest.
(Copyright © 2024 The Author. Published by Elsevier B.V. All rights reserved.)