The Role of Hypertension and Renin-angiotensin-aldosterone System Inhibitors in Bleomycin-induced Lung Injury.


Journal

Clinical lymphoma, myeloma & leukemia
ISSN: 2152-2669
Titre abrégé: Clin Lymphoma Myeloma Leuk
Pays: United States
ID NLM: 101525386

Informations de publication

Date de publication:
04 2021
Historique:
received: 26 06 2020
revised: 03 10 2020
accepted: 04 10 2020
pubmed: 1 11 2020
medline: 11 1 2022
entrez: 31 10 2020
Statut: ppublish

Résumé

The risk factors for bleomycin-induced lung injury (BLI), a fatal complication of cancer chemotherapy, are not well-established. The renin-angiotensin-aldosterone system (RAAS) has recently been suggested to play a role in the development of lung injury. This study clarified the impact of hypertension (HTN) and the administration of RAAS inhibitors on BLI occurrence in patients treated with bleomycin-containing regimens. We retrospectively analyzed the data of 190 patients treated with a bleomycin-containing regimen for Hodgkin lymphoma or germ cell tumors at our institutions from 2004 to 2018. Overall, 190 patients received bleomycin, and symptomatic BLI occurred in 21 (11.1%) cases. In the multivariate analysis, age ≥ 65 years (odd ratio, 10.90; 95% confidence interval, 3.72-32.20; P < .001) and history of HTN (odds ratio, 3.32; 95% confidence interval, 1.07-10.30; P = .04) were found to be significant risk factors for BLI onset. BLI occurred in 3.6% (n = 5) of patients with no risk, 11.8% (n = 2) of those whose only risk factor was HTN, 31.6% (n = 6) of those whose only risk factor was age ≥ 65 years, and 57.1% (n = 8) of those with both risk factors (P < .001). BLI-induced mortality rates in each group were 0.0% (n = 0), 5.9% (n = 1), 10.5% (n = 2), and 42.9% (n = 6) (P < .001), respectively. Among 31 patients with HTN, BLI incidence was 12.5% in patients who were administered RAAS inhibitors and 53.3% in those who were not (P = .02). Older age and history of HTN were independent risk factors for the development of BLI, and the administration of RAAS inhibitors might reduce the onset of BLI.

Identifiants

pubmed: 33127326
pii: S2152-2650(20)30556-5
doi: 10.1016/j.clml.2020.10.004
pii:
doi:

Substances chimiques

Angiotensin II Type 2 Receptor Blockers 0
Angiotensin-Converting Enzyme Inhibitors 0
Bleomycin 11056-06-7

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e321-e327

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Ryujiro Hara (R)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan. Electronic address: ryujirohara@tokai-u.jp.

Makoto Onizuka (M)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Sawako Shiraiwa (S)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Kaito Harada (K)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Yasuyuki Aoyama (Y)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Daisuke Ogiya (D)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Masako Toyosaki (M)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Rikio Suzuki (R)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Sinichiro Machida (S)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Ken Ohmachi (K)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Yoshiaki Ogawa (Y)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Hiroshi Kawada (H)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Shigeki Watanabe (S)

Department of Hematology, Ebina General Hospital, Ebina, Kanagawa, Japan.

Akira Miyajima (A)

Department of Urology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Ryota Masuda (R)

Department of General Thoracic Surgery, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Masayuki Iwazaki (M)

Department of General Thoracic Surgery, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Mikio Mikami (M)

Department of Obstetrics and Gynecology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Takashi Koike (T)

Department of Pediatrics, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Hiroyuki Mochizuki (H)

Department of Pediatrics, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Kiyoshi Ando (K)

Division of Hematology/Oncology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

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