Hisao Higo1, Nobuaki Miyahara2, Akihiko Taniguchi3, Satoru Senoo4, Junko Itano5, Hiromi Watanabe6, Naohiro Oda7, Hiroe Kayatani8, Hirohisa Ichikawa9, Takuo Shibayama10, Kazuhiro Kajimoto11, Yasushi Tanimoto12, Arihiko Kanehiro13, Yoshinobu Maeda14, Katsuyuki Kiura15. 1. Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. Electronic address: h_hisao_430@yahoo.co.jp. 2. Department of Allergy and Respiratory Medicine, Okayama University Hospital, Okayama, Japan; Department of Medical Technology, Okayama University Graduate School of Health Sciences, Okayama, Japan. Electronic address: miyahara@okayama-u.ac.jp. 3. Department of Allergy and Respiratory Medicine, Okayama University Hospital, Okayama, Japan. Electronic address: atgcuacg@gmail.com. 4. Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. Electronic address: shuttle1126@gmail.com. 5. Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. Electronic address: crisis042725@yahoo.co.jp. 6. Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. Electronic address: hwatanabe9724@yahoo.co.jp. 7. Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. Electronic address: dancingqueen121212@gmail.com. 8. Department of Respiratory Medicine, National Hospital Organization Okayama Medical Center, Okayama, Japan. Electronic address: hk85hk64@yahoo.co.jp. 9. Department of Respiratory Medicine, KKR Takamatsu Hospital, Takamatsu, Japan. Electronic address: ichikawa@kkr-ta-hp.gr.jp. 10. Department of Respiratory Medicine, National Hospital Organization Okayama Medical Center, Okayama, Japan. Electronic address: shibayamat@okayamamc.jp. 11. Department of Respiratory Medicine, Kobe Red Cross Hospital, Kobe, Japan. Electronic address: k-kajimoto@kobe.jrc.or.jp. 12. Department of Respiratory Medicine, National Hospital Organization Minami-Okayama Medical Center, Okayama, Japan. Electronic address: tanimoto.yasushi@momc.jp. 13. Department of Allergy and Respiratory Medicine, Okayama Rosai Hospital, Okayama, Japan. Electronic address: akanehir@okayama-u.ac.jp. 14. Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. Electronic address: yosmaeda@md.okayama-u.ac.jp. 15. Department of Allergy and Respiratory Medicine, Okayama University Hospital, Okayama, Japan. Electronic address: kkiura@md.okayama-u.ac.jp.
Abstract
BACKGROUND: Pirfenidone suppresses the decline of forced vital capacity (FVC) in patients with idiopathic pulmonary fibrosis (IPF). However, IPF progresses in some patients despite treatment. We analyzed patients with meaningful FVC declines during pirfenidone treatment and explored the factors predictive of disease progression after FVC decline. METHODS: This study was a retrospective, multicenter, observational study conducted by the Okayama Respiratory Disease Study Group. We defined initial decline in %FVC as 5% or greater per 6-month period during pirfenidone treatment. IPF patients who were treated with pirfenidone and experienced an initial decline from December 2008 to September 2017 were enrolled. RESULTS: We analyzed 21 patients with IPF. After the initial decline, 4 (19.0%) patients showed improvement in disease, 11 (52.4%) showed stable disease, and 6 (28.6%) showed progressive disease. There was no significant correlation between %FVC reduction on initial decline and subsequent %FVC change (p = 0.475). Deterioration of high-resolution computed tomography (HRCT) findings on initial decline was observed significantly more often in the progressive versus improved/stable disease groups (100% vs 20.0%, p = 0.009). CONCLUSIONS: We revealed that deterioration of HRCT findings may predict disease progression after the initial decline in %FVC in IPF patients treated with pirfenidone.
BACKGROUND:Pirfenidone suppresses the decline of forced vital capacity (FVC) in patients with idiopathic pulmonary fibrosis (IPF). However, IPF progresses in some patients despite treatment. We analyzed patients with meaningful FVC declines during pirfenidone treatment and explored the factors predictive of disease progression after FVC decline. METHODS: This study was a retrospective, multicenter, observational study conducted by the Okayama Respiratory Disease Study Group. We defined initial decline in %FVC as 5% or greater per 6-month period during pirfenidone treatment. IPFpatients who were treated with pirfenidone and experienced an initial decline from December 2008 to September 2017 were enrolled. RESULTS: We analyzed 21 patients with IPF. After the initial decline, 4 (19.0%) patients showed improvement in disease, 11 (52.4%) showed stable disease, and 6 (28.6%) showed progressive disease. There was no significant correlation between %FVC reduction on initial decline and subsequent %FVC change (p = 0.475). Deterioration of high-resolution computed tomography (HRCT) findings on initial decline was observed significantly more often in the progressive versus improved/stable disease groups (100% vs 20.0%, p = 0.009). CONCLUSIONS: We revealed that deterioration of HRCT findings may predict disease progression after the initial decline in %FVC in IPFpatients treated with pirfenidone.
Authors: Minna Mononen; Eeva Saari; Hannele Hasala; Hannu-Pekka Kettunen; Sanna Suoranta; Hanna Nurmi; Miia Kärkkäinen; Tuomas Selander; Jukka Randell; Jari Laurikka; Toomas Uibu; Heikki Koskela; Riitta Kaarteenaho; Minna Purokivi Journal: BMC Pulm Med Date: 2022-08-14 Impact factor: 3.320