Southern Adelaide Diabetes and Endocrine Services, Repatriation General Hospital, Daw Park, Adelaide 5041, Australia.
Rheumatology (Oxford). 2012 Jun;51(6):1112-9. doi: 10.1093/rheumatology/kes003. Epub 2012 Feb 12.
The aim of the study was to assess the effect of long-term prednisolone on fasting and post-glucose load glucose concentration in patients with inflammatory rheumatological disease. We hypothesized that prednisolone would predominantly increase post-glucose load glucose concentration and that fasting glucose would have poor sensitivity as a screening test for diabetes in patients receiving chronic prednisolone therapy.
In a cross-sectional study of subjects with inflammatory rheumatological disease but without known diabetes, 60 subjects [age = 70 (±10) years, 62% female] who were receiving chronic (>6 months) prednisolone [6.5 (±2.1) mg/day] (Group 1) and 58 controls [age = 70 (±11) years, 62% female] who had not received oral glucocorticoids for at least 6 months (Group 2) underwent an oral glucose tolerance test.
Fasting glucose was significantly lower [5.0 (±0.1) vs. 5.3 (±0.1) mmol/l, P = 0.02) and post-glucose load glucose concentration significantly higher [8.0 (±0.4) vs. 6.8 (±0.3) mmol/l, P = 0.02] in Group 1 than in Group 2. In a multiple regression analysis, glucocorticoid use (P = 0.004) and log CRP (P = 0.02) were independently associated with fasting glucose, while waist circumference (P = 0.01), but not glucocorticoid use, was independently associated with post-glucose load glucose concentration. A fasting glucose ≥5.6 mmol/l had 33 and 83% sensitivity for diabetes in Groups 1 and 2, respectively.
There is discordance between a reduced fasting and increased post-glucose load glucose concentration in rheumatological patients on long-term prednisolone. Therefore fasting glucose has poor sensitivity to screen for diabetes in prednisolone-treated patients. Treatment of prednisolone-induced hyperglycaemia should be directed at the postprandial period. Trial registration. Australian New Zealand Clinical Trials Registry, http://www.anzctr.org.au/, ACTRN12607000540415.
本研究旨在评估长期使用泼尼松龙对炎症性风湿性疾病患者空腹和葡萄糖负荷后血糖浓度的影响。我们假设泼尼松龙主要会增加葡萄糖负荷后的血糖浓度，并且在接受慢性泼尼松龙治疗的患者中，空腹血糖作为糖尿病筛查试验的敏感性较差。
在一项炎症性风湿性疾病患者（无已知糖尿病）的横断面研究中，60 名患者[年龄=70（±10）岁，62%为女性]正在接受慢性（>6 个月）泼尼松龙[6.5（±2.1）mg/天]（第 1 组），58 名对照者[年龄=70（±11）岁，62%为女性]在过去 6 个月内未接受口服糖皮质激素治疗（第 2 组），进行口服葡萄糖耐量试验。
第 1 组空腹血糖显著较低[5.0（±0.1）比 5.3（±0.1）mmol/l，P=0.02]，葡萄糖负荷后血糖浓度显著较高[8.0（±0.4）比 6.8（±0.3）mmol/l，P=0.02]。在多元回归分析中，糖皮质激素使用（P=0.004）和 log CRP（P=0.02）与空腹血糖独立相关，而腰围（P=0.01）但不是糖皮质激素使用与葡萄糖负荷后血糖浓度独立相关。空腹血糖≥5.6mmol/l在第 1 组和第 2 组中糖尿病的敏感性分别为 33%和 83%。
长期接受泼尼松龙治疗的风湿性疾病患者空腹血糖降低与葡萄糖负荷后血糖升高之间存在不一致性。因此，空腹血糖对筛查泼尼松龙治疗患者的糖尿病敏感性较差。应针对泼尼松龙引起的高血糖的餐后阶段进行治疗。试验注册。澳大利亚新西兰临床试验注册中心，http://www.anzctr.org.au/，ACTRN12607000540415。
