Postural variation of pulmonary diffusing capacity as a marker of lung microangiopathy in Indian patients with type 2 diabetes mellitus

Abstract

Introduction:Diabetes mellitus (DM) is characterized by the presence of chronic hyperglycemia and formation of advanced glycation end products (AGEs). Interaction between AGE and its receptor leads to endothelial damage and microangiopathy. This study was undertaken to investigate the possibility of using a postural variation of diffusing capacity as an early marker of lung microangiopathy and its correlation with the level of adhesion molecules, HbA1c, duration of diabetes, and insulin resistance in type 2 DM (T2DM) patients with and without microangiopathy.Materials and Methods:Forty patients having T2DM without any microangiopathy (n = 20) as well as with microangiopathy (n = 20), and 22 age and sex matched healthy controls were enrolled in this cross-sectional study. Measurement of lung volumes and capacities were done. DLco was measured in sitting and supine position. Levels of vascular cell adhesion molecule-1 (VCAM-1), E-selectin, fasting glucose, and insulin were estimated in plasma of the patients and compared with controls.Results:Restrictive type of ventilatory change was observed in DM patients. Diffusing capacity (% predicted) in the supine position (P < 0.0001), postural change in DLco (P < 0.0001), and coefficient of diffusion were significantly less in DM patients as compared to controls. Plasma levels of VCAM-1 were significantly higher in DM patients without microangiopathy and negatively correlated (r = −0.4054, P = 0.0094) with Δ DLco in all diabetic subjects. All patients had significantly higher insulin resistance.Conclusion:Lack of postural increase in diffusing capacity in type 2 diabetic patients along with increased VCAM-1 levels could reflect the presence of an early microangiopathy of the small pulmonary vessels.

Twenty-Four week Taichi training improves pulmonary diffusion capacity and glycemic control in patients with Type 2 diabetes mellitus

“…Diffusion capacity of the lungs for carbon monoxide is a sensitive measure of pulmonary diffusion capacity and commonly applied to assess the function of the transfer of gas across the respiratory membrane between the alveoli and capillaries of the lungs [ 35 , 36 ]. It is reported that DLCO in patient with T2DM is significantly impaired, which is likely associated with the thickening of the gas exchange membrane of the lungs [ 6 ], resulting from chronic hyperglycemia [ 37 , 38 ], dyslipidemia and insulin resistance [ 39 ]. Possible pathological processes associated with impaired pulmonary function in T2DM may include non-enzymatic glycosylation of lung elastin structures, which could stiff the lung [ 40 ] and cause a restrictive impact on ventilation; and diabetes-induced microvascular complications, which could impair the diffusion [ 37 , 41 ] and diminish gas exchange.…”

“…It is reported that DLCO in patient with T2DM is significantly impaired, which is likely associated with the thickening of the gas exchange membrane of the lungs [6], resulting from chronic hyperglycemia [37,38], dyslipidemia and insulin resistance [39]. Possible pathological processes associated with impaired pulmonary function in T2DM may include non-enzymatic glycosylation of lung elastin structures, which could stiff the lung [40] and cause a restrictive impact on ventilation; and diabetes-induced microvascular complications, which could impair the diffusion [37,41] and diminish gas exchange. It is reported that lung function assessed by forced vital capacity and forced expiratory volume in 1 sec (FEV-1) are inversely correlated with HbA1c [42][43][44] and DLCO is significantly impaired in patients with T2DM [44].…”

Development and validation of a risk nomogram model for predicting pulmonary hypertension in patients with stage 3–5 chronic kidney disease

“…These patients were at high risk for the relatively rapid deterioration of kidney function [ 27 ]. DM can cause damage to the pulmonary vascular endothelium and decrease the release of vasodilators, thus aggravating the degree of atherosclerosis, further increasing blood pressure, and eventually leading to high pressure load in the right ventricle and increased pulmonary vascular resistance, resulting in PAH [ 28 , 29 ]. Agarwal R et al found that ambulatory systolic blood pressure (BP) was strongly associated with the progression of chronic kidney disease (CKD) and was an independent predictor of ESRD [ 30 ].…”

Tuberculosis-diabetes co-morbidity is characterized by heightened systemic levels of circulating angiogenic factors

“…Moreover, in DM, there are two tissue specific paradoxical events in the vasculature with excessive formation of premature blood vessels afflicting the retina, while deficiency of small blood vessels in the skin, contributes to impaired wound healing [6]. Hence, the use of angiogenic inhibitors is a common treatment modality for diabetic retinopathy [27, 28]. Similarly, abnormal angiogenesis and vascular dysfunction are also prominent features of active TB and utilization of host-directed therapies aimed at inhibition of these pathways has been proposed as an adjunct measure for TB treatment [16, 17].…”