Yukiko Miura1, Takefumi Saito2, Toru Tanaka3, Hiroyuki Takoi4, Yohei Yatagai5, Minoru Inomata6, Takahito Nei7, Yoshinobu Saito8, Akihiko Gemma9, Arata Azuma10. 1. Department of Respiratory medicine, National Hospital Organization Ibarakihigashi Hospital, 825, Terunuma, Tokai-mura, Naka-gun, Ibaraki 3191113, Japan; Department of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo 1138603, Japan. Electronic address: s7081@nms.ac.jp. 2. Department of Respiratory medicine, National Hospital Organization Ibarakihigashi Hospital, 825, Terunuma, Tokai-mura, Naka-gun, Ibaraki 3191113, Japan. Electronic address: takefumisaito@yahoo.co.jp. 3. Department of Respiratory medicine, National Hospital Organization Ibarakihigashi Hospital, 825, Terunuma, Tokai-mura, Naka-gun, Ibaraki 3191113, Japan. Electronic address: toru10302000@nms.ac.jp. 4. Department of Respiratory medicine, National Hospital Organization Ibarakihigashi Hospital, 825, Terunuma, Tokai-mura, Naka-gun, Ibaraki 3191113, Japan. Electronic address: taco155485@hotmail.com. 5. Department of Respiratory medicine, National Hospital Organization Ibarakihigashi Hospital, 825, Terunuma, Tokai-mura, Naka-gun, Ibaraki 3191113, Japan. Electronic address: yohei820yatagai@yahoo.co.jp. 6. Department of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo 1138603, Japan. Electronic address: inomataminoru@nms.ac.jp. 7. Department of Infection Control and Prevention, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo 1138603, Japan. Electronic address: takahitonei@gmail.com. 8. Department of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo 1138603, Japan. Electronic address: yo-saito@nms.ac.jp. 9. Department of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo 1138603, Japan. Electronic address: agemma@nms.ac.jp. 10. Department of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo 1138603, Japan. Electronic address: azuma_arata@yahoo.co.jp.
Abstract
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a disease with a worse prognosis than some types of cancer. In patients with IPF, lung cancer is critical because of the associated high mortality rate from its progression and fatal complications from anticancer treatments. Therefore, preventing lung cancer in patients with IPF is primordial. Pirfenidone is an anti-fibrotic agent that reduces the decline in forced vital capacity. This study aimed to assess the effect of pirfenidone in the development of lung cancer in patients with IPF. METHODS: Data from 261 patients with IPF with and without pirfenidone were retrospectively reviewed, and the incidence of lung cancer was analyzed. RESULTS: In the pirfenidone group, the incidence of lung cancer was significantly lower than in the non-pirfenidone group (2.4% vs. 22.0%, P < 0.0001). Multivariate Cox proportional hazards regression analysis demonstrated that pirfenidone decreased the risk of lung cancer (hazard ratio, 0.11; 95% confidence interval, 0.03 to 0.46; P = 0.003), whereas coexisting emphysema increased the incidence of lung cancer (hazard ratio, 3.22; 95% confidence interval, 1.35 to 7.70; P = 0.009). CONCLUSIONS: Pirfenidone might correlate with a decreased risk of lung cancer in patients with IPF. However, no definite conclusion can be drawn from this retrospective study, and a multicenter, prospective cohort study is still warranted to confirm the effect of pirfenidone on lung cancer in patients with IPF.
BACKGROUND:Idiopathic pulmonary fibrosis (IPF) is a disease with a worse prognosis than some types of cancer. In patients with IPF, lung cancer is critical because of the associated high mortality rate from its progression and fatal complications from anticancer treatments. Therefore, preventing lung cancer in patients with IPF is primordial. Pirfenidone is an anti-fibrotic agent that reduces the decline in forced vital capacity. This study aimed to assess the effect of pirfenidone in the development of lung cancer in patients with IPF. METHODS: Data from 261 patients with IPF with and without pirfenidone were retrospectively reviewed, and the incidence of lung cancer was analyzed. RESULTS: In the pirfenidone group, the incidence of lung cancer was significantly lower than in the non-pirfenidone group (2.4% vs. 22.0%, P < 0.0001). Multivariate Cox proportional hazards regression analysis demonstrated that pirfenidone decreased the risk of lung cancer (hazard ratio, 0.11; 95% confidence interval, 0.03 to 0.46; P = 0.003), whereas coexisting emphysema increased the incidence of lung cancer (hazard ratio, 3.22; 95% confidence interval, 1.35 to 7.70; P = 0.009). CONCLUSIONS:Pirfenidone might correlate with a decreased risk of lung cancer in patients with IPF. However, no definite conclusion can be drawn from this retrospective study, and a multicenter, prospective cohort study is still warranted to confirm the effect of pirfenidone on lung cancer in patients with IPF.
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Authors: Myung Jin Song; Dae Jun Kim; Hyo Chae Paik; Sukki Cho; Kwhanmien Kim; Sanghoon Jheon; Sang Hoon Lee; Jong Sun Park Journal: PLoS One Date: 2020-06-29 Impact factor: 3.240
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