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Peer-reviewedCC BYCureus

Risk Factors and Pathophysiological Mechanisms in Drug-Induced Interstitial Lung Disease Associated With Novel Anticancer Agents: A Scoping Review (2016-2026)

  1. 1Department of Pharmacy, The Institute of Medical Science, The University of Tokyo (IMSUT) Hospital, Tokyo, JPN

Abstract

Drug-induced interstitial lung disease (DI-ILD) associated with novel anticancer agents, such as immune checkpoint inhibitors (ICIs), tyrosine kinase inhibitors (TKIs), and antibody-drug conjugates (ADCs), is a severe adverse event that can lead to fatal outcomes. Effective clinical management requires integrating host-specific risk factors with drug-specific biological mechanisms. This scoping review, conducted following the PRISMA Extension for Scoping Reviews (PRISMA-ScR) guidelines, systematically searched PubMed and Ichushi-Web databases for peer-reviewed articles published between January 2016 and April 2026. Data from 65 included articles were synthesized into a conceptual framework. Pre-existing ILD or subclinical interstitial lung abnormalities (ILA) emerged as highly prevalent and potent class-transcending risk factors, particularly across novel anticancer drug classes. Distinct temporal patterns of injury were identified: TKIs typically induced DI-ILD within the first one to two months via diffuse alveolar damage (DAD) resulting from epithelial repair blockade, whereas ICI-induced pneumonitis peaked between two and four months due to a breakdown of self-tolerance. To transition from reactive drug interruption to a proactive "Precision Clinical Safety" strategy, we propose a risk-adaptive monitoring protocol centered on mandatory pre-treatment screening with thin-section high-resolution computed tomography (HRCT) to detect subclinical ILA. While low-to-intermediate-risk patients follow standard protocols, high-risk patients require enhanced surveillance, including clinical consultations every two weeks during the initial treatment phase.

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BibTeX
@article{kuroda2026risk,
  title = {{Risk Factors and Pathophysiological Mechanisms in Drug-Induced Interstitial Lung Disease Associated With Novel Anticancer Agents: A Scoping Review (2016-2026)}},
  author = {Seiichiro Kuroda and Hidetoshi Ishii and Masaaki Ishibashi and Yohei Iimura},
  journal = {Cureus},
  year = {2026},
  month = oct,
  doi = {10.7759/cureus.117422},
  url = {https://europepmc.org/article/PMC/PMC13730288},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Risk Factors and Pathophysiological Mechanisms in Drug-Induced Interstitial Lung Disease Associated With Novel Anticancer Agents: A Scoping Review (2016-2026)
AU  - Seiichiro Kuroda
AU  - Hidetoshi Ishii
AU  - Masaaki Ishibashi
AU  - Yohei Iimura
PY  - 2026
DA  - 2026/10/04
JO  - Cureus
DO  - 10.7759/cureus.117422
UR  - https://europepmc.org/article/PMC/PMC13730288
AB  - Drug-induced interstitial lung disease (DI-ILD) associated with novel anticancer agents, such as immune checkpoint inhibitors (ICIs), tyrosine kinase inhibitors (TKIs), and antibody-drug conjugates (ADCs), is a severe adverse event that can lead to fatal outcomes. Effective clinical management requires integrating host-specific risk factors with drug-specific biological mechanisms. This scoping review, conducted following the PRISMA Extension for Scoping Reviews (PRISMA-ScR) guidelines, systematically searched PubMed and Ichushi-Web databases for peer-reviewed articles published between January 2016 and April 2026. Data from 65 included articles were synthesized into a conceptual framework. Pre-existing ILD or subclinical interstitial lung abnormalities (ILA) emerged as highly prevalent and potent class-transcending risk factors, particularly across novel anticancer drug classes. Distinct temporal patterns of injury were identified: TKIs typically induced DI-ILD within the first one to two months via diffuse alveolar damage (DAD) resulting from epithelial repair blockade, whereas ICI-induced pneumonitis peaked between two and four months due to a breakdown of self-tolerance. To transition from reactive drug interruption to a proactive "Precision Clinical Safety" strategy, we propose a risk-adaptive monitoring protocol centered on mandatory pre-treatment screening with thin-section high-resolution computed tomography (HRCT) to detect subclinical ILA. While low-to-intermediate-risk patients follow standard protocols, high-risk patients require enhanced surveillance, including clinical consultations every two weeks during the initial treatment phase.
SN  - 2168-8184
ER  -