Journal
RESPIRATION
Volume 68, Issue 3, Pages 268-272Publisher
KARGER
DOI: 10.1159/000050509
Keywords
microangiopathy, diabetic renal; non-insulin-dependent diabetes mellitus pulmonary function; pulmonary diffusion capacity
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Background: In type I diabetes mellitus, lung function has been investigated in several clinical studies, but there are few data concerning pulmonary function abnormalities in patients with non-insulin-dependent diabetes mellitus (NIDDM). Objectives: The aim of this study was to assess the presence of pulmonary function abnormalities in patients with NIDDM and to verify the possible associations between diabetic renal microangiopathy, retinopathy and diabetes control. Method and Patients: Thirty patients with NIDDM were collected and divided into two similar groups: subjects with retinopathy and/or diabetic glomerulopathy (group 1, n = 15) and patients without any complications (group 2, n = 15). 17 were males and 13 females, aged from 45 to 81 years. They had had diabetes for 3-23 years and were studied at the Division of Internal Medicine, with an outpatient service for diabetic patients. All patients were non-smokers. The presence of diabetic glomerulopathy was determined by measuring the 24-hour protein excretion rate using the nephelometric method. The presence of retinopathy was determined by using ophthalmoscopy. Glycosylated hemoglobin was measured as an indicator of glycemic control. We performed a global spirometry and measured pulmonary diffusion capacity by the single-breath method corrected by alveolar volume. Results: We found a significant reduction in lung diffusion capacity for carbon monoxide (DLCO) in the group of patients with other signs of diabetic microangiopathy (p < 0.005) and a significative correlation between DLCO and the grade of albumin uria (r = -0.83, p < 0.001). Conclusions: Pulmonary function abnormalities, in particular a reduction in diffusion capacity, are common in patients with NIDDM and signs of diabetic microangiopathy. A possible explanation is related to an impaired pulmonary microvasculature and alveolar epithelial basal lamina. Copyright (C) 2001 S. Karger AG, Basel.
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