Inadequate glucose control in type 2 diabetes is associated with impaired lung function and systemic inflammation: a cross-sectional study.
Inadequate glucose control in type 2 diabetes is associated with impaired lung function and systemic inflammation: a cross-sectional study.
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DOI:
10.1186/1471-2466-10-38
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发表时间:
2010-07-26
影响因子:
3.1
通讯作者:
Casas A
中科院分区:
文献类型:
--
作者:
Dennis RJ;Maldonado D;Rojas MX;Aschner P;Rondón M;Charry L;Casas A
Inadequate glucose control may be simultaneously associated with inflammation and decreased lung function in type 2 diabetes. We evaluated if lung function is worse in patients with inadequate glucose control, and if inflammatory markers are simultaneously increased in these subjects. Subjects were selected at the Colombian Diabetes Association Center in Bogotá. Pulmonary function tests were performed and mean residual values were obtained for forced expiratory volume (FEV1), forced vital capacity (FVC) and FEV1/FVC, with predicted values based on those derived by Hankinson et al. for Mexican-Americans. Multiple least-squares regression was used to adjust for differences in known determinants of lung function. We measured blood levels of glycosylated hemoglobin (HBA1c), interleukin 6 (IL-6), tumor necrosis factor (TNF-α), fibrinogen, ferritin, and C-reactive protein (C-RP). 495 diabetic patients were studied, out of which 352 had inadequate control (HBA1c > 7%). After adjusting for known determinants of lung function, those with inadequate control had lower FEV1 (-75.4 mL, IC95%: -92, -59; P < 0.0001) and FVC (-121 mL, IC95%: -134, -108; P < 0,0001) mean residuals, and higher FEV1/FVC (0.013%, IC95%: 0.009, 0.018, P < 0.0001) residuals than those with adequate control, as well as increased levels of all inflammatory markers (P < 0.05), with the exception of IL-6. Subjects with type 2 diabetes and inadequate control had lower FVC and FEV1 than predicted and than those of subjects with adequate control. It is postulated that poorer pulmonary function may be associated with increased levels of inflammatory mediators.
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DOI:
10.1164/ajrccm.163.2.2006158
发表时间:
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影响因子:
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