Detection of glycemic abnormalities in adolescents with beta thalassemia using continuous glucose monitoring and oral glucose tolerance in adolescents and young adults with β-thalassemia major: Pilot study.
Detection of glycemic abnormalities in adolescents with beta thalassemia using continuous glucose monitoring and oral glucose tolerance in adolescents and young adults with β-thalassemia major: Pilot study.
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DOI：
10.4103/2230-8210.111647
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发表时间：
2013-05
影响因子：
--
通讯作者：
De Sanctis V
中科院分区：
文献类型：
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作者：
Soliman AT;Yasin M;El-Awwa A;De Sanctis V
据报道，重型β地中海贫血（BTM）患者存在胰岛素缺乏和抵抗。在早期检测血糖异常的不同方法中，使用连续血糖监测（CGM）尚未在这些青少年中进行彻底研究。采用动态血糖监测系统（CGMS）测定口服葡萄糖耐量（OGT）和72小时动态血糖浓度，计算稳态模式评价（HOMA），并对16例BTM青少年进行定量胰岛素敏感性检查指数（QUICKI）测定。16例BTM青少年（年龄19.75 ± 3岁）进行了调查。使用OGTT，（25%）有空腹血糖浓度（BG）受损（>5.6 mmol/L）。糖负荷后2 h，其中1例BG = 16.2mmol/L（糖尿病），2例为糖耐量减低（IGT）（BG > 7.8和<11.1mmol/L）。用CGMS监测餐后最大血糖，4例（25%）诊断为糖尿病（BG > 11.1mmol/L），9例（56%）诊断为IGT。HOMA和QUICKI分别显示水平<2.6（1.6 ± 0.8）和>0.33（0.36 ± 0.03），排除了这些青少年的显著胰岛素抵抗。β细胞功能（B%）与空腹血糖和2小时血糖呈显著负相关（r分别为-0.6和-0.48，P < 0.01）。空腹血清胰岛素和C肽浓度均与空腹血糖或铁蛋白水平无关。CGM期间的平均和最高血糖水平与空腹血糖（r分别为0.68和0.39，P < 0.01）和口服葡萄糖后2 h血糖（r分别为0.87和0.86，P < 0.001）显著相关。铁蛋白浓度与空腹血糖、OGTT 2 h血糖水平及CGM记录的平均血糖水平相关（r分别为0.52和0.43，P <0.01）。CGM已被证明是上级OGTT诊断血糖异常的青少年与BTM。β细胞功能缺陷而不是胰岛素抵抗似乎是这些异常的原因。
Both insulin deficiency and resistance are reported in patients with β-thalassemia major (BTM). The use of continuous blood glucose monitoring (CGM), among the different methods for early detection of glycemic abnormalities, has not been studied thoroughly in these adolescents. To assess the oralglucose tolerance (OGT) and 72-h continuous glucose concentration by the continuous glucose monitoring system (CGMS) and calculate homeostatic model assessment (HOMA), and the quantitative insulin sensitivity check index (QUICKI) was conducted in 16 adolescents with BTM who were receiving regular blood transfusions every 2-4 weeks and iron-chelation therapy since early childhood. Sixteen adolescents with BTM (age: 19.75 ± 3 years) were investigated. Using OGTT, (25%) had impaired fasting blood (plasma) glucose concentration (BG) (>5.6 mmol/L). 2-h after the glucose load, one of them had BG = 16.2 mmol/L (diabetic) and two had impaired glucose tolerance (IGT) (BG > 7.8 and <11.1 mmol/L). Monitoring the maximum (postprandial) BG using CGMS,4 adolescents were diagnosed with diabetes (25%) (BG >11.1 mmol/L) and 9 with IGT (56%). HOMA and QUICKI revealed levels <2.6 (1.6 ± 0.8) and >0.33 (0.36 ± 0.03), respectively, ruling out significant insulin resistance in these adolescents. There was a significant negative correlation between the β-cell function (B%) on one hand and the fasting and the 2-h BG (r=−0.6, and − 0.48, P < 0.01, respectively) on the other hand. Neither fasting serum insulin nor c-peptide concentrations were correlated with fasting BG or ferritin levels. The average and maximum blood glucose levels during CGM were significantly correlated with the fasting BG (r = 0.68 and 0.39, respectively, with P < 0.01) and with the BG at 2-hour after oral glucose intake (r = 0.87 and 0.86 respectively, with P < 0.001). Ferritin concentrations were correlated with the fasting BG and the 2-h blood glucose levels in the OGTT (r = 0.52, and r = 0.43, respectively, P < 0.01) as well as with the average BG recorded by CGM (r = 0.75, P < 0.01). CGM has proven to be superior to OGTT for the diagnosis of glycemic abnormalities in adolescents with BTM. Defective β-cell function rather than insulin resistance appeared to be the cause for these abnormalities.