PF, Other Respiratory Disorders May Be Linked to Type 2 Diabetes, Study Reports
Pulmonary fibrosis (PF) and other lung diseases may be late complications in patients with Type 2 diabetes, according to a German study.
The study, “Breathlessness and Restrictive Lung Disease: An Important Diabetes-Related Feature in Patients with Type 2 Diabetes,” was published in the journal Respiration.
Breathlessness is reported by 1 in 4 patients in outpatient treatment settings. Acute and chronic lung diseases are usually the main causes of breathlessness. In particular, pulmonary disorders such as chronic obstructive pulmonary disease (COPD) and restrictive lung diseases, which includes PF, may be relevant contributors to shortness of breath.
Since both PF and diabetes patients exhibit epithelial damage with inflammation leading to fibrosis, or scarring, researchers have been discussing whether PF may be a diabetes-related complication. This correlation is supported by the observation that a significant portion of patients with interstitial lung disease also have Type 2 diabetes, and the fact that patients with both idiopathic PF and diabetes have a worse prognosis than patients without this condition.
However, no study so far had explored if breathlessness may result from pulmonary dysfunction in patients with diabetes, and its potential association with diabetic complications.
A research team from the German Centre for Diabetes Research and the German Centre for Lung Research at Heidelberg University Hospital hypothesized that patients with Type 2 diabetes and late diabetic complications may be at a greater risk of restrictive lung diseases and PF.
The study involved 29 patients with newly diagnosed Type 2 diabetes, 110 with long-term Type 2 diabetes, 68 with prediabetes, and 48 non-diabetic individuals used as controls. Participants were assessed for breathlessness, lung function, metabolic control, and diabetes-related complications.
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Results revealed that patients with Type 2 diabetes and those with prediabetes were more likely to experience breathlessness and restrictive lung disease than controls.
Restrictive lung disease was observed in 27% of patients with long-term Type 2 diabetes, in 20% of those with newly diagnosed diabetes, and in 9% with prediabetes. Patients with pronounced Type 2 diabetes symptoms and restrictive lung disease showed evidence of PF on radiological and histological analyses.
Data also showed that having diabetes was associated with changes in the lung’s tissue structure.
“Increased breathlessness, RLD [restrictive lung disease], and interstitial lung anomalies can be associated with type 2 diabetes,” Stefan Kopf, MD, the study’s first author, of the Department of Endocrinology, Diabetology and Clinical Chemistry at Heidelberg University Hospital, said in a press release.
“We therefore suspect that lung disease is a late consequence of type 2 diabetes,” added Peter P. Nawroth, MD, the study’s senior author and medical director of the Department of Endocrinology, Diabetology and Clinical Chemistry at Heidelberg University Hospital.
Findings also revealed that restrictive lung disease was associated with albuminuria, which refers to the presence of a protein called albumin in urine and is a typical sign of kidney disease. This suggests that lung and kidney disease may be linked with diabetic kidney disease, or nephropathy.
Overall, “the current study as well as findings from animal experiments show a significant connection between restrictive lung diseases and diabetes mellitus,” said Michael Kreuter, MD, the study’s co-author, of the Thorax Clinic at Heidelberg University Hospital.
According to the team, patients with Type 2 diabetes nephropathy, and breathlessness should be screened frequently for lung diseases.
This research is part of an ongoing clinical trial (NCT03022721) on diabetes-related complications being conducted in Germany.
The association between diabetes and PF has been the subject of increasing studies. Scientists recently reported that metformin, a common oral medication for Type 2 diabetes, reversed PF in a mouse model and reduced fibrosis in the lung tissue of PF patients.