Pulmonary function changes in diabetic lung

Diabetes mellitus is a chronic and debilitating disease. Its complications give rise to micro and macrovascular diseases which affect eyes, kidneys, heart, blood vessels, nerves and also lungs. There may be a relationship between diabetes and reduced lung function, so this study was designed to evaluate the impairment of lung function on spirometry among diabetic patients. To study the effect of diabetes mellitus on the evolution of respiratory function parameters. Hundred subjects were enrolled in the study, 30 patients with type I, another 30 patients with type II and 40 subjects were controls. Mean age was 42.78 +/- 3.14 years, 45 were males and 55 were females. Mean HbAlC was 8.9 +/- 1.1%. 22 patients with diabetes duration from 5 to 10 years, 38 patients with a duration of more than 10 years. Spirometric tests were done for all groups by computerized Spirometry with six parameters Forced vital capacity [FVC], Forced expiratory volume in first second [FEV1], Peak expiratory flow rate [PEFR], Forced expiratory volume in first second to forced vital capacity [FEV1/FVC], Peak expiratory flow rate [FEFR 25-75] and Diffusing capacity for carbon monoxide [DLCO]. There was a predominant reduction in all the Spirometric parameters of diabetic patients toward the restrictive pattern as there was significant deterioration in DLCO in comparison with healthy controls. FVC [p < 0.01], and FEV1/FVC% [p < 0.001] were significantly lower in typel diabetic patients in comparison to those of type II. Impairment of lung functions was obvious with a longer duration of diabetes. Conclusion: Diabetes is associated with a significant impaired pulmonary function in a restrictive pattern as compared to non diabetics. The pulmonary function impairment was found to be more marked with diabetic duration especially after 10 years. Subjects with type I diabetes had lower FVC and FEV1/FVC% than predicted; it could be related to poor glycemic control

effect of chronic intermittent hypoxia in the evolution of NASH

Obstructive sleep apnea [OSA] causes chronic intermittent hypoxia [CIH] during sleep. OSA is associated with nonalcoholic steatohepatitis [NASH] in obese individuals and may contribute to progression of nonalcoholic fatty liver disease [NAFLD] from steatosis to steatohepatitis. To assess the potential role of hypoxia in the development of NASH in obstructive sleep apnea patients. Nocturnal polysomnography was performed in 60 consecutive patients for clinical suspicion of OSA. We investigated fasting blood glucose, serum insulin, TNF-alpha, ABG and liver enzymes for 30 patients with nocturnal polysomnographic recording of OSA and for 15 patients without recording OSA used as controls. Liver biopsy was offered to 15 of 30 patients with elevated liver enzymes. Patients with OSA had significantly higher levels of insulin and were more insulin-resistant according to HOMA-IR than in controls. We found that the parameters which significantly correlated with AHI were elevated liver enzyme, BMI, ultrasound grading, TNF-alpha and HOMA-IR in patients group but did not find a similar correlation in controls. Liver biopsy showed steatosis with lobular necrosis or hepatocyte ballooning in the 15 patients, associated with fibrosis in 5 patients. Hypoxic stress of obstructive sleep apnea may be implicated in the evolution of insulin resistance and steatohepatitis in obese individuals