Nodular fibrosis of the lung in diabetes mellitus

Abstract

The target organs in diabetes mellitus include the kidneys, the eyes and the small vessels. In these organs some specific histopathological changes have been described but there are few reports of histopathoogical changes in the lung in diabetic patients. Several reports describe abnormal pulmonary function in diabetic patients and consider these abnormalities to be due to histopahtological changes found in the pulmonary vessels. We have studied the histopathological changes in the diabetic lung comparing the findings in the autopsies of 61 diabetic and 50 non-diabetic patients. Statistically significant differences in the incidence of chronic obstructive lung disease and pulmonary haemorrhage exist. There are no differences in the incidence of fibrosis of the alveolar walls or intimal and medial thickening of small vessels, changes associated with diabetes according to the literature. We have found a specific type of nodular fibrosis not previously reported which we believe to be typical of diabetes.

The Diabetic Lung - A New Target Organ?

“…The degree of thickening did not correlate significantly with patient age or with duration of diabetes, but correlated significantly with the thickness of basal laminas in renal tubules and muscle capillaries [21,22]. These microvascular abnormalities are frequently associated with histological changes in the lung parenchyma, such as nodular fibrosis [23], and with increased extracellular matrix and connective tissue synthesis in the lung parenchyma of animals [24]. Experimental data obtained in rats with streptozotocin-induced diabetes have shown that hyperglycemia increased the content of collagen and elastin in the lung [24].…”

“…Data on anatomic lung abnormalities reported in patients with diabetes can, at least in part, explain the pulmonary functional deficit. In addition to the alterations in the pulmonary vascular system and the alveolarcapillary membrane, parenchymal damages to lungs of diabetes patients has also been reported [8,[23][24][25]. Farina et al demonstrated the presence of areas of lung fibrosis with specific nodular fibrosis pattern [23].…”

“…In addition to the alterations in the pulmonary vascular system and the alveolarcapillary membrane, parenchymal damages to lungs of diabetes patients has also been reported [8,[23][24][25]. Farina et al demonstrated the presence of areas of lung fibrosis with specific nodular fibrosis pattern [23]. To support the hypothesis of a link between diabetes and lung fibrosis, a casecontrol study, estimating the odds ratio of diabetes as a risk factor for idiopathic fibrosis, found a correlation between these two diseases [70].…”

Glycemic Exposure Is Associated With Reduced Pulmonary Function in Type 2 Diabetes

“…Reduced spirometric measurements do not identify a specific underlying pathology, but there have been preliminary reports of histopathologic changes in the lungs of diabetic patients, including basal lamina thickening (25) and fibrosis (26). Other possible contributory factors include glycation of chest wall/bronchial tree proteins (27,28), autonomic and/or phrenic neuropathy causing alterations in bronchial reactivity and respiratory muscle function (29), and an increased propensity to, and severity of, respiratory infections (30,31).…”

The clinical effectiveness and cost-effectiveness of inhaled insulin in diabetes mellitus: a systematic review and economic evaluation

“…128 Hence, in patients with diabetes there is definite histopathological evidence of thickened alveolar epithelial and pulmonary capillary basal laminae, vascular hyalinosis, granulomas, intraseptal nodular fibrosis and emphysema-like septal obliteration. [129][130][131][132] Experimental data in mice and hamsters, rendered diabetic by streptozotocin, have shown that hyperglycaemia induces basal laminar thickening, focal nodule formation, and capillary narrowing in both the lung and the glomerulus. 133,134 Animal studies have also suggested possible mechanisms for these changes, such as increased synthesis and degradation of collagen and elastin, altered type 2 pneumocyte morphology, enhanced pulmonary endothelial permeability and structural endothelial changes.…”