摘要
目的观察肾小球疾病患者糖皮质激素(GC)治疗所致的胰岛素抵抗(IR)的影响因素、临床表现、血糖恢复情况和防治。方法肾活检证实需用GC治疗、糖代谢和肾功能正常者43例,检测空腹血糖(FBG)、胰岛素、瘦素和肿瘤坏死因子α(TNFα)及常规实验室检查,同时检测口服82.5 g葡萄糖粉后2 h血糖(2 h BG)、胰岛素;应用泼尼松(0.8±0.11)mg.kg-1.d-1治疗8～13周后,重复检测上述指标。依据泼尼松治疗后FBG和2 h BG,将患者分为糖耐量正常组(NGT)20例和IR组23例,其中IR组再分为糖耐量异常组(IGT)12例和类固醇糖尿病(SD)组11例。IR者随访(15±4)个月至血糖恢复正常。结果①GC治疗前:NGT组FBG(4.2±0.9)mmol/L低于IR其他两组(5.3±0.9)mmol/L、(4.8±1.1)mmol/L(均P<0.05),泼尼松治疗后FBG与IR呈正相关(r=0.427～0.497,均P<0.005),用GC后各组各时相血糖明显升高,NGT组胰岛素分泌明显高于其他两组,SD组瘦素和TNFα水平明显高于其他两组,SD组服泼尼松后2 h胰岛素分泌明显低于服泼尼松前(均P<0.05)。②IGT组泼尼松用量减至0.5 mg.kg-1.d-1时,血糖恢复正常;SD组4例尿糖阳性患者,控制饮食并加拜唐苹(阿卡波糖)口服;1例出现多尿、多饮、多食和消瘦,用胰岛素控制血糖。结论GC所致的胰岛素抵抗主要是RI代偿性分泌不足,瘦素和TNFα起一定的作用。空腹血糖≤5.1 mmol/L或泼尼松0.5 mg.kg-1.d-1可降低GC所致胰岛素抵抗的发生率。
Objective To investigate the influencing factors of glucocorticoid-induced insulin resistance,clincal manifestation,blood glucose return,prevention and cure in renal glomerular disease. Methods Fasting blood glucose （FBG） ,insulin,serum leptin,tumor necrosis factor a（TNFa）, routine test and 2 hour blood glucose after taking orally 82.5 g glucose powder（2 h BG）,insulin were measured in 43 patients with renal glomerular disease who were confirmed by renal biopsy needing prednison （0.8±0.11）mg·kg^-1·d^-1 treated, had normal glycometabolism and renal function before and after taking prednisone for 8-13 weeks. The patients were divided into three groups：normal glucose tolerance （NGT） 46.5%（20 cases） , insulin resistance 53.5 % （23 cases） including：impaired glucose tolerance（IGT） 12 cases and steroid diabetes（SD） 11 eases by FBG and 2 h BG. The patients with insulin resistance were followed up until normal glycometabolism,for （15±4） months. Results OBefore prednisone treatment,FBG in NGT was lower than that in other two groups, （4.2 ± 0.9 ） mmol/L vs （ 5.3 ± 0.9） mmol/L and （4.8 ±1.1 ） mmol/L （all P G 0.05）, FBG was correlated with whether or not occurrencing IR after taking prednison （ r = 0. 427-0. 497, all P G 0. 005）. After prednisone treatment,blood glucose and insulin were higher in every group at each phase,insulin secreted in NGT was more than that in other two groups（ P〈0.05）,leptin and TNFa in SD group higher than that in other two groups （P 〈 0.05） ,2 h insulin secreting lower than before prednisone treatment（all P〈0.05）. ②No symptoms and signs in IGT occurred as decreased to prednisone 0.5mg·kg^-1·d^-1 ,blood glucose returned normal,but there were glucosuria in 4 eases controling drink and food, adding Glucobay（Acarbose） ;one ease suffered from diuresis, polydipsia, polyphagia and emaciated, treated by insulin. Conclusion The mechanism of steroid-induced IR is mainly due to deficiency in compensatory secretion o
出处
《临床荟萃》
CAS
北大核心
2007年第16期1144-1147,共4页
Clinical Focus
