Endocrine Abstracts

Rationale/Objective: Diabetes Mellitus (DM) and Interstitial lung Disease (ILD) share common pathogenetic pathways involving inflammatory cells and in particular monocytes and macrophages. Diabetic patients are at higher risk of developing pulmonary fibrosis, whereas DM is a major comorbidity in ILD patients. In our study, we analyzed retrospectively patients with ILD and aimed to examine differential characteristics between patients with and without DM, including disease parameters and alveolar macrophage evaluation.

Material and methods: 256 patients with Pulmonary Fibrosis (Idiopathic or not) seen in the Department of Respiratory Medicine and in Endocrinology and Diabetes Clinic the University Hospital of Heraklion from January 2014 to July 2022, were enrolled; 76 with DM and 180 without DM. Clinical characteristics of all patients including age, smoking habits, BMI, pulmonary function at baseline and disease progression up to 2 years follow-up, were collected. In all of the included patients, bronchoscopy was performed and bronchoalveolar lavage (BAL) was obtained. The levels of mtROS were measured in fresh BAL alveolar macrophages by flow cytometry using MitoSOXRed (Invitrogen) superoxide indicator.

Results: Our results showed that ILD patients with DM had a statistically increased smoking history, and a tendency to rapid disease progression, although not significant. In accordance with previous reports, we did not find any other significant difference between disease baseline characteristics or disease progression and mortality between ILD patients with or without DM. Interestingly, we observed a significantly increased macrophage population in BAL of patients with DM. In the subgroup analysis of IPF patients, there was a trend of increased percentage of alveolar macrophages in BAL of patients with DM, while there were decreased levels of oxidized mitochondria in macrophages of these patients.

Conclusions: Our preliminary results showed increased macrophage population in BAL of ILD patients with DM, while there were reduced levels of oxidized mitochondria in the alveolar macrophages of IPF patients with DM. It is unknown if targeted anti-diabetic treatment results in these observations, and further studies are required to assess whether antidiabetic medications could decrease mitochondrial ROS in alveolar macrophages of ILD patients.

Keywords: Pulmonary fibrosis, interstitial lung disease, alveolar macrophages, diabetes mellitus