Effects of inhaled budesonide on insulin sensitivity in nondiabetic patients with asthma and chronic obstructive pulmonary disease

Abstract

In the study reported here, investigators explored the following: (1) the effects of inhaled corticosteroid (ICS) therapy on insulin sensitivity (IS) (the Homeostatic Model Assessment-Insulin Resistance [HOMA-IR] Index, which has never been used before in nondiabetic patients with asthma and chronic obstructive pulmonary disease [COPD], was used in this investigation); and (2) differences and similarities between asthma and COPD groups. A total of 12 patients with asthma and 6 with COPD who were not previously treated with oral corticosteroids or ICSs were treated with budesonide, 400 mu g twice daily for 8 wk, via dry powder inhaler through the Aerolizer. Pretreatment and posttreatment values were recorded for forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), FFV1/FVC, C-reactive protein (CRP), blood glucose, serum insulin levels, area under the curve (AUC) for glucose and insulin in an oral glucose tolerance test (OGTT), and HOMA-IR Index. The trapezoid technique, the formula for HOMA-IR, and Wilkinson, Mann-Whitney U, and t tests were used. In the group of patients with asthma, posttreatment values for the HOMA-IR Index, glucose, and insulin at all time points during OGTT and AUC for glucose and AUC for insulin were not statistically different compared with pretreatment values. In patients with COPD who had been given ICS therapy, however, the second hour glucose level during OGTT increased significantly compared with pretreatment values (P=.46). Pretreatment and posttreatment second hour insulin values and posttreatment AUC for glucose were significantly higher in the COPD group than in the asthma group (P=.047, P=.044, and P=.031, respectively). A moderate positive correlation was noted between the percentage of difference in FFV1 and the change in HOMA-IR (pretreatment mean value of HOMA-IR +/- standard deviation [SD], 2.7 +/- 2.6) in asthmatic patients as the result of therapy (r=0.50, P=.138). Investigators concluded the following: (1) Differences in pathogenesis between asthma and COPD seem to offer the most plausible explanation for differences in carbohydrate metabolism achieved through ICS therapy; (2) the effect of an ICS on IS is associated not only with dose, treatment period, age, and body mass index (BMI) but also with the severity of initial mucosal inflammation; and (3) as a result of improvements in respiratory function noted after treatment had been given, IS was increased in asthmatic patients.