Abstract

At present, the important role of comorbid diseases, including diabetes
mellitus, in the course of COPD has been determined. Concomitant diabetes
mellitus accelerates the progression of ventilation disorders and worsens the
prognosis, increasing the risk of mortality from COPD. Diabetes mellitus is
associated with COPD from 2 to 16%. Potential mechanisms underlying the
high incidence of the combined course of COPD and type 2 diabetes mellitus
include: chronic systemic inflammation, oxidative stress, and chronic
hyperglycemia.
Purpose. determination of clinical, functional and radiological features
of COPD in diabetes mellitus.
Materials and methods. We examined 75 patients and studied the
features of the course of COPD in combination with diabetes mellitus in
comparison with the results of examining patients with COPD and patients
with diabetes mellitus by X-ray and MSCT.
Results. Patients with COPD in combination with diabetes mellitus are
characterized by more pronounced respiratory failure and chronic cor
pulmonale, frequent exacerbations and more pronounced hypoxemia in
comparison with patients with COPD. Standard radiography did not reveal
pronounced differences between the examined groups of patients with COPD.
COPD is formed as a result of damage to the small bronchi, which determines
the characteristic clinical and radiological symptom complex. In the structure
of COPD, there is a pulmonary component and systemic manifestations that
aggravate the disease. The manifestations of diabetes mellitus are based on
micro- and macroangiopathies that affect pulmonary microcirculation.
Conclusions. Diagnostically significant for COPD during MSCT is a
symptom of expiratory "air trap", combined with expansion and deformation of
the bronchi, up to bronchioectasis. At MSCT in patients with COPD and
diabetes mellitus, pathognomic changes characterizing microangiopathy:
dilated parenchymal vessels, focal-like shadows of vascular origin with a
diameter of 2-5 mm, a clear-cut shape of the vessels, which are considered as a
consequence of specific microangiopathy and fibrotic changes in COPD.