Donahue Richard P, Stranges Saverio, Rejman Karol, Rafalson Lisa B, Dmochowski Jacek, Trevisan Maurizio
Department of Social and Preventive Medicine, School of Public Health and Health Professions, State University of New York at Buffalo, 3435 Main St., Farber Hall, Room 268 F, Buffalo, NY 14214, USA.
Diabetes Care. 2007 Jul;30(7):1724-9. doi: 10.2337/dc07-0040. Epub 2007 Apr 24.
We conducted a nested case-control investigation to examine whether elevated baseline concentrations of cystatin C predicted progression from normoglycemia to pre-diabetes over 6 years of follow-up from the Western New York Health Study.
In 2002-2004, 1,455 participants from the Western New York Health Study, who were free of type 2 diabetes and known cardiovascular disease at baseline (1996-2001), were reexamined. An incident case of pre-diabetes was defined as an individual with fasting glucose < 100 mg/dl at the baseline examination and > or = 100 and < or = 125 mg/dl at the follow-up examination, thereby eliminating individuals with prevalent pre-diabetics. All case patients (n = 91) were matched 1:3 to control participants based on sex, race/ethnicity, and year of study enrollment. All control subjects had fasting glucose levels < 100 mg/dl at both baseline and follow-up examinations. Cystatin C concentrations and the urinary albumin-to-creatinine ratio were measured from frozen (-196 degrees C) baseline blood and urine samples. Serum creatinine concentrations were available from the baseline examination only.
Multivariate conditional logistic regression analyses adjusted for age, baseline glucose level, homeostasis model assessment of insulin resistance, BMI, hypertension, estimated glomerular filtration rate, cigarette smoking, and alcohol use revealed a significantly increased risk of progression to pre-diabetes among those with elevated baseline concentrations of cystatin C (odds ratio 3.28 [95% CI 1.43-7.54]) (upper quintile versus the remainder). Results of secondary analyses that considered high-sensitivity C-reactive protein, interleukin-6, E-selectin, or soluble intercellular adhesion molecule-1 did not alter these results.
These results suggest that cystatin C was associated with a threefold excess risk of progression to pre-diabetes in this population.
我们开展了一项巢式病例对照研究，以检验在纽约西部健康研究中，随访6年期间，基线胱抑素C浓度升高是否可预测从血糖正常进展为糖尿病前期。
2002年至2004年，对纽约西部健康研究的1455名参与者进行了复查，这些参与者在基线期（1996年至2001年）无2型糖尿病和已知心血管疾病。糖尿病前期的发病病例定义为在基线检查时空腹血糖<100mg/dl，在随访检查时≥100且≤125mg/dl的个体，从而排除了患有糖尿病前期的个体。所有病例患者（n = 91）根据性别、种族/族裔和研究入组年份与对照参与者按1:3进行匹配。所有对照受试者在基线和随访检查时的空腹血糖水平均<100mg/dl。从冷冻（-196℃）的基线血液和尿液样本中测量胱抑素C浓度和尿白蛋白与肌酐比值。血清肌酐浓度仅可从基线检查中获得。
多因素条件逻辑回归分析对年龄、基线血糖水平、胰岛素抵抗的稳态模型评估、体重指数、高血压、估计肾小球滤过率、吸烟和饮酒进行了校正，结果显示，基线胱抑素C浓度升高的人群进展为糖尿病前期的风险显著增加（比值比3.28 [95%可信区间1.43 - 7.54]）（最高五分位数与其余人群相比）。考虑高敏C反应蛋白、白细胞介素-6、E选择素或可溶性细胞间黏附分子-1的二次分析结果未改变这些结果。
这些结果表明，在该人群中，胱抑素C与进展为糖尿病前期的风险增加三倍有关。
