Pathological Roles of Pulmonary Cells in Acute Lung Injury: Lessons from Clinical Practice

Enomoto, Noriyuki

doi:10.3390/ijms232315027

Cited by 6 publications

(2 citation statements)

References 179 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Research has shown that heat shock protein-70 (HSP-70) exerts a protective effect against pulmonary fibrosis. However, EGFR-TKIs have been found to suppress HSP-70 expression in the lungs, which may potentially promote pulmonary fibrosis ( Enomoto, 2022 ). Furthermore, the efficacy of EGFR-TKI-induced glucocorticoid treatment in ILD implies a possible link to immune mediation ( Kodama et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Case report: EGFR-TKI rechallenge after osimertinib-induced interstitial lung disease: a case report and literature review

Gu,

Zhong,

Huang

2024

Front. Pharmacol.

View full text Add to dashboard Cite

BackgroundOsimertinib, a third-generation tyrosine kinase inhibitor (TKI), has demonstrated significant efficacy in treating non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations. However, EGFR-TKI-induced interstitial lung disease (ILD), a well-known adverse effect, can seriously affect the treatment outcome. There is currently no international consensus on the efficacy and safety of re-administration of EGFR-TKI after EGFR-TKI-induced ILD.Case summaryWe report a case of a 62-year-old male with stage IV lung adenocarcinoma and EGFR L858R mutation who was treated with osimertinib at a dose of 80 mg/day as first-line therapy. On the sixth day of treatment, the patient developed grade 4 ILD, chest tightness, shortness of breath, and paroxysmal dry cough. Arterial blood gas analysis indicated the presence of type I respiratory failure, while the chest CT scan revealed newly developed ground-glass opacities in both lungs and a considerable amount of pleural effusion on the left side. Subsequently, the patient was administered methylprednisolone for anti-inflammatory therapy, in conjunction with oxygen therapy, anti-infection treatment, and closed thoracic drainage, which resulted in a favourable recovery and discharge after 18 days. During this period, the patient adhered to third-generation EGFR-TKI oral targeted therapy. Nevertheless, within a week of discharge, the patient was readmitted due to the recurrence of chest tightness and shortness of breath. A chest CT scan indicated a recurrent ILD. Despite the administration of high-dose methylprednisolone for 9 days, the patient’s condition continued to deteriorate, ultimately resulting in death.ConclusionIt is of the utmost importance to conduct a meticulous evaluation of the severity of osimertinib-induced ILD in order to ascertain the potential risks and benefits of EGFR-TKI rechallenge. Particularly, for patients with grade 4 ILD, firm drug discontinuation should be considered.

show abstract

Section: Discussionmentioning

confidence: 99%

Case report: EGFR-TKI rechallenge after osimertinib-induced interstitial lung disease: a case report and literature review

Gu,

Zhong,

Huang

2024

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…Another example is DM-ILD. Previous studies reported that ferritin was produced by macrophages [26] and correlated with lung function parameters and survival [27]. IL-18 was also secreted by macrophages [28], elevated in DM-ILD compared with DM without ILD [29], and correlated with the severity of pulmonary disease [30].…”

Section: Introductionmentioning

confidence: 93%

The Role of Macrophages in Connective Tissue Disease-Associated Interstitial Lung Disease: Focusing on Molecular Mechanisms and Potential Treatment Strategies

Tseng

Sung

Chen

et al. 2023

IJMS

View full text Add to dashboard Cite

Connective tissue disease-associated interstitial lung disease (CTD-ILD) is a severe manifestation of CTD that leads to significant morbidity and mortality. Clinically, ILD can occur in diverse CTDs. Pathologically, CTD-ILD is characterized by various histologic patterns, such as nonspecific interstitial pneumonia, organizing pneumonia, and usual interstitial pneumonia. Abnormal immune system responses have traditionally been instrumental in its pathophysiology, and various changes in immune cells have been described, especially in macrophages. This article first briefly overviews the epidemiology, clinical characteristics, impacts, and histopathologic changes associated with CTD-ILD. Next, it summarizes the roles of various signaling pathways in macrophages or products of macrophages in ILD, helped by insights gained from animal models. In the following sections, this review returns to studies of macrophages in CTD-ILD in humans for an overall picture of the current understanding. Finally, we direct attention to potential therapies targeting macrophages in CTD-ILD in investigation or in clinical trials, as well as the future directions regarding macrophages in the context of CTD-ILD. Although the field of macrophages in CTD-ILD is still in its infancy, several lines of evidence suggest the potential of this area.

show abstract

Relationship between idiopathic interstitial pneumonias (IIPs) and connective tissue disease-related interstitial lung disease (CTD-ILD): A narrative review

Enomoto

2024

Respiratory Investigation

View full text Add to dashboard Cite

Pathological Roles of Pulmonary Cells in Acute Lung Injury: Lessons from Clinical Practice

Cited by 6 publications

References 179 publications

Case report: EGFR-TKI rechallenge after osimertinib-induced interstitial lung disease: a case report and literature review

Case report: EGFR-TKI rechallenge after osimertinib-induced interstitial lung disease: a case report and literature review

The Role of Macrophages in Connective Tissue Disease-Associated Interstitial Lung Disease: Focusing on Molecular Mechanisms and Potential Treatment Strategies

Relationship between idiopathic interstitial pneumonias (IIPs) and connective tissue disease-related interstitial lung disease (CTD-ILD): A narrative review

Contact Info

Product

Resources

About