The relation of markers of inflammation to the development of glucose disorders in the elderly - The cardiovascular health study

被引:429
作者
Barzilay, JI
Abraham, L
Heckbert, SR
Cushman, M
Kuller, LH
Resnick, HE
Tracy, RP
机构
[1] Kaiser Permanente Georgia, Div Endocrinol, Tucker, GA 30084 USA
[2] Emory Univ, Sch Med, Div Endocrinol, Atlanta, GA USA
[3] Univ Washington, Dept Biostat, Seattle, WA 98195 USA
[4] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA
[5] Univ Vermont, Dept Med, Coll Med, Colchester, VT USA
[6] Univ Vermont, Dept Pathol, Coll Med, Colchester, VT USA
[7] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA
[8] Medstar Res Inst, Washington, DC USA
关键词
D O I
10.2337/diabetes.50.10.2384
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Several studies suggest that inflammation plays a role in the pathogenesis of some glucose disorders in adults. We tested this hypothesis in a longitudinal cohort study of older individuals who had normal fasting glucose (FG) values at baseline. We compared the baseline levels of six inflammatory markers in participants who had developed glucose disorders at follow-up with those of participants whose FG remained normal at follow-up. Participants were members of the Cardiovascular Health Study, a prospective study of risk factors for cardiovascular disease in adults greater than or equal to 65 years. All 5,888 participants had baseline testing, including FG and markers of inflammation: white blood cell and platelet counts and albumin, fibrinogen, C-reactive protein (CRP), and factor VIIIc levels. At 3-4 years of follow-up, 4,481 (84.5%) of those who were alive had FG levels retested. Participants who developed diabetes (n = 45) had higher median levels of CRP at baseline than those who remained normoglycemic. On multivariate analysis, those with elevated CRP levels (75th percentile [2.86 mg/l] vs. 25th percentile [0.82 mg/l]) were 2.03 times (95% confidence intervals, 1.44-2.86) more likely to have diabetes on follow-up. Adjustment for confounders and other inflammatory markers did not appreciably change this finding. There was no relationship between the development of diabetes and other markers of inflammation. Inflammation, as measured by CRP levels, is associated with the development of diabetes in the elderly. Understanding the role of inflammation in the pathogenesis of glucose disorders in this age-group may lead to better classification and treatment of glucose disorders among them.
引用
收藏
页码:2384 / 2389
页数:6
相关论文
共 40 条
[1]   MECHANISMS OF PERSISTENT AIRWAY INFLAMMATION IN ASTHMA - A ROLE FOR T-CELLS AND T-CELL PRODUCTS [J].
BUSSE, WW ;
COFFMAN, RL ;
GELFAND, EW ;
KAY, AB ;
ROSENWASSER, LJ .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1995, 152 (01) :388-393
[2]  
Cabana VG, 1996, J LIPID RES, V37, P2662
[3]   An in vivo model for elucidation of the mechanism of tumor necrosis factor-α (TNF-α)-induced insulin resistance:: Evidence for differential regulation of insulin signaling by TNF-α [J].
Cheung, AT ;
Ree, D ;
Kolls, JK ;
Fuselier, J ;
Coy, DH ;
Bryer-Ash, M .
ENDOCRINOLOGY, 1998, 139 (12) :4928-4935
[4]  
CLAUSS A., 1957, ACTA HAEMATOL, V17, P237
[5]  
CUSHMAN M, 1995, CLIN CHEM, V41, P264
[6]   Factor VIII and other hemostasis variables are related to incident diabetes in adults - The Atherosclerosis Risk in Communities (ARIC) study [J].
Duncan, BB ;
Schmidt, MI ;
Offenbacher, S ;
Wu, KK ;
Savage, PJ ;
Heiss, G .
DIABETES CARE, 1999, 22 (05) :767-772
[7]   Chronic subclinical inflammation as part of the insulin resistance syndrome -: The Insulin Resistance Atherosclerosis Study (IRAS) [J].
Festa, A ;
D'Agostino, R ;
Howard, G ;
Mykkänen, L ;
Tracy, RP ;
Haffner, SM .
CIRCULATION, 2000, 102 (01) :42-47
[8]   Body mass index, diabetes, and C-reactive protein among US adults [J].
Ford, ES .
DIABETES CARE, 1999, 22 (12) :1971-1977
[9]  
Fried Linda P., 1991, Annals of Epidemiology, V1, P263
[10]   Association between C-reactive protein and features of the metabolic syndrome -: A population-based study [J].
Fröhlich, M ;
Imhof, A ;
Berg, G ;
Hutchinson, WL ;
Pepys, MB ;
Boeing, H ;
Muche, R ;
Brenner, H ;
Koenig, W .
DIABETES CARE, 2000, 23 (12) :1835-1839