Pulmonary function and circulating adhesion molecules in patients with diabetes mellitus

Abstract

Background: Lung function in diabetes has been reported in several studies with contradictory results. Diabetes mellitus increases expression of adhesion molecules through hyperglycemia. These molecules play an important role in the pathophysiological dysfunction of the vasculature.

Objective: To explore the possible relationship between lung function and circulating levels of adhesion molecules in diabetes.

Methods: Sixteen type 1 diabetic patients, 33 type 2 diabetic patients and 22 healthy subjects matched for age and sex were studied. Spirometry measurements were performed and pulmonary diffusion capacity for carbon monoxide (DLco) was measured in sitting and supine positions by the single-breath method corrected by alveolar volume (VA). Glycosylated hemoglobin, retinopathy and nephropathy were included as parameters of metabolic control and diabetic complications. Circulating levels of soluble E-selectin and vascular cell adhesion molecule-1 (VCAM-1) were determined in all subjects.

Results: Diabetic subjects showed lower variation in DLco and DLco/VA by changing posture from sitting to supine position (P=0.043 and P<0.001, respectively), and showed reduced total lung capacity (P<0.001) and forced expiratory volume in 1 s/forced vital capacity (P=0.009) compared with healthy control subjects. Serum concentrations of E-selectin were elevated in diabetic patients (P<0.001). There was no difference in serum VCAM-1 concentrations between diabetic and control subjects. On stepwise regression analysis, E-selectin concentrations were the most important contributing factor to the variation in DLco/VA.

Conclusions: Diabetic patients show lower pulmonary volumes and variation in DLco by changing posture from sitting to supine position, and they also show increased levels of E-selectin. A possible explanation is impaired pulmonary microvasculature, because adhesion molecules seem to be sensitive markers of endothelial activation and damage seen in diabetes.