Vigo A, Duncan B B, Schmidt M I, Couper D, Heiss G, Pankow J S, Ballantyne C M
Programa de Pós-Graduação em Epidemiologia, Faculdade de Medicina, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brasil.
Braz J Med Biol Res. 2007 Jul;40(7):933-41. doi: 10.1590/s0100-879x2006005000121.
To efficiently examine the association of glutamic acid decarboxylase antibody (GADA) positivity with the onset and progression of diabetes in middle-aged adults, we performed a case-cohort study representing the ~9-year experience of 10,275 Atherosclerosis Risk in Communities Study participants, initially aged 45-64 years. Antibodies to glutamic acid decarboxylase (GAD65) were measured by radioimmunoassay in 580 incident diabetes cases and 544 non-cases. The overall weighted prevalence of GADA positivity (>or=1 U/mL) was 7.3%. Baseline risk factors, with the exception of smoking and interleukin-6 (P <or= 0.02), were generally similar between GADA-positive and -negative individuals. GADA positivity did not predict incident diabetes in multiply adjusted (HR = 1.04; 95%CI = 0.55, 1.96) proportional hazard analyses. However, a small non-significant adjusted risk (HR = 1.29; 95%CI = 0.58, 2.88) was seen for those in the highest tertile (>or=2.38 U/mL) of positivity. GADA-positive and GADA-negative non-diabetic individuals had similar risk profiles for diabetes, with central obesity and elevated inflammation markers, aside from glucose, being the main predictors. Among diabetes cases at study's end, progression to insulin treatment increased monotonically as a function of baseline GADA level. Overall, being GADA positive increased risk of progression to insulin use almost 10 times (HR = 9.9; 95%CI = 3.4, 28.5). In conclusion, in initially non-diabetic middle-aged adults, GADA positivity did not increase diabetes risk, and the overall baseline profile of risk factors was similar for positive and negative individuals. Among middle-aged adults, with the possible exception of those with the highest GADA levels, autoimmune pathophysiology reflected by GADA may become clinically relevant only after diabetes onset.
为了有效研究中年成年人中谷氨酸脱羧酶抗体(GADA)阳性与糖尿病发病及进展之间的关联,我们进行了一项病例队列研究,该研究涵盖了社区动脉粥样硬化风险研究中10275名参与者约9年的情况,这些参与者初始年龄为45 - 64岁。通过放射免疫分析法在580例新发糖尿病病例和544例非糖尿病病例中检测了谷氨酸脱羧酶(GAD65)抗体。GADA阳性(≥1 U/mL)的总体加权患病率为7.3%。除吸烟和白细胞介素 - 6外(P≤0.02),GADA阳性和阴性个体之间的基线风险因素总体相似。在多因素调整的比例风险分析中,GADA阳性并不能预测新发糖尿病(HR = 1.04;95%CI = 0.55,1.96)。然而,对于阳性最高三分位数(≥2.38 U/mL)的个体,观察到一个小的、无统计学意义的调整后风险(HR = 1.29;95%CI = 0.58,2.88)。GADA阳性和GADA阴性的非糖尿病个体患糖尿病的风险特征相似,除血糖外,中心性肥胖和炎症标志物升高是主要预测因素。在研究结束时的糖尿病病例中,进展为胰岛素治疗的情况随基线GADA水平呈单调增加。总体而言,GADA阳性使进展为胰岛素使用的风险增加近10倍(HR = 9.9;95%CI = 3.4,28.5)。总之,在初始非糖尿病的中年成年人中,GADA阳性并未增加糖尿病风险,阳性和阴性个体的总体基线风险因素特征相似。在中年成年人中,除了可能GADA水平最高者外,GADA所反映的自身免疫病理生理学可能仅在糖尿病发病后才具有临床相关性。