Lung Involvement in Diabetes

Abstract

Dyspnea upon exertion in a diabetic patient readily arouses suspicion of cardiovascular disease and/or physical deconditioning. As reviewed in our previous publications (1), a solid body of literature in the 1980s and 1990s established the occurrence of ventilatory restriction in type 1 diabetes; however, diabetic lung involvement did not gain wide recognition among internists until two recent developments helped change that perception. The first development is the cumulative data that demonstrate a pattern of modest lung restriction in type 2 diabetes qualitatively similar to that in type 1 diabetes, with proportional decreases in forced vital capacity (FVC) and forced expiratory flow in 1 s (FEV1) that are directly related to glycemia (2–5) and a corresponding reduction in lung diffusing capacity (DLCO) (6,7), the primary noninvasive measure of alveolar gas exchange capacity. As the prevalence of type 2 diabetes approaches epidemic proportions and pulmonary function emerges as an independent predictor of incident diabetes (8), pathophysiology of lung involvement also assumes greater relevance. The second development was the finding that chronic use of inhaled insulin could potentially trigger or exacerbate pulmonary dysfunction. Though shown to be efficacious and well tolerated, inhaled insulin has also been reported to cause a small early drop in spirometry and DLCO at rest that did not progress during 2 years of follow-up (9). Its effects over longer duration of use and in the presence of primary lung disease, inflammation, or tobacco exposure are not clear. As inhaled insulin products continue to be developed, the spectacular collapse of Exubera notwithstanding, the issue of …