Markers of inflammation and prediction of diabetes mellitus in adults (Atherosclerosis Risk in Communities study): a cohort study
Type 2 diabetes mellitus and atherosclerotic cardiovascular disease have common antecedents. Since markers of inflammation predict coronary heart disease and are raised in patients with type 2 diabetes, we investigated whether they predict whether people will develop type 2 diabetes. 12 330 men and...
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Veröffentlicht in: | The Lancet (British edition) 1999-05, Vol.353 (9165), p.1649-1652 |
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Sprache: | eng |
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Zusammenfassung: | Type 2 diabetes mellitus and atherosclerotic cardiovascular disease have common antecedents. Since markers of inflammation predict coronary heart disease and are raised in patients with type 2 diabetes, we investigated whether they predict whether people will develop type 2 diabetes.
12 330 men and women, aged 45–64 years, were followed up for a mean of 7 years. We analysed the association between different markers of acute inflammation and subsequent diagnosis of diabetes. In a subgroup of 610 individuals selected originally for an unrelated atherosclerosis case-control study, we also investigated diabetes associations with total sialic acid and orosomucoid, haptoglobin, and α
1-antitrypsin.
1335 individuals had a new diagnosis of diabetes. Adjusted odds ratios for developing diabetes for quartile extremes were 1·9 (95% CI 1·6–2·3) for raised white-cell count, 1·3 (1·0–1·5) for low serum albumin, and 1·2 (1·0–1·5) for raised fibrinogen. In the subgroup analysis, individuals with concentrations of orosomucoid and sialic acid of more than the median had odds ratios of 7·9 (2·6–23·7) and 3·7 (1·4–9·8), respectively. Adjustment for body-mass index and waist-to-hip ratio lessened the associations; those for white-cell count (1·5 [1·3–1·8]), orosomucoid (7·1 [2·1–23·7]), and sialic acid (2·8 [1·0–8·1]) remained significant.
Markers of inflammation are associated with the development of diabetes in middle-aged adults. Although autoimmunity may partly explain these associations, they probably reflect the pathogenesis of type 2 diabetes. |
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ISSN: | 0140-6736 1474-547X |
DOI: | 10.1016/S0140-6736(99)01046-6 |