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.