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In-treatment HDL cholesterol levels and development of new diabetes mellitus in hypertensive patients: the LIFE study
Vise andre og tillknytning
2013 (engelsk)Inngår i: Diabetic Medicine, ISSN 0742-3071, E-ISSN 1464-5491, Vol. 30, nr 10, s. 1189-1197Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Aims Although hypertensive patients with low baseline HDL cholesterol levels have a higher incidence of diabetes mellitus, whether changing levels of HDL over time are more strongly related to the risk of new diabetes in hypertensive patients has not been examined.

Methods Incident diabetes mellitus was examined in relation to baseline and in-treatment HDL levels in 7485 hypertensive patients with no history of diabetes randomly assigned to losartan- or atenolol-based treatment.

Results During 4.71.2years follow-up, 520 patients (6.9%) developed new diabetes. In univariate Cox analyses, compared with the highest quartile of HDL levels (>1.78mmol/l), baseline and in-treatment HDL in the lowest quartile (<1.21mmol/l) identified patients with >5-fold and >9fold higher risks of new diabetes, respectively; patients with baseline or in-treatment HDL in the 2nd and 3rd quartiles had intermediate risk of diabetes. In multivariable Cox analyses, adjusting for randomized treatment, age, sex, race, prior anti-hypertensive therapy, baseline uric acid, serum creatinine and glucose entered as standard covariates, and in-treatment non-HDL cholesterol, Cornell product left ventricular hypertrophy, diastolic and systolic pressure, BMI, hydrochlorothiazide and statin use as time-varying covariates, the lowest quartile of in-treatment HDL remained associated with a nearly 9-fold increased risk of new diabetes (hazard ratio8.7, 95%CI 5.0-15.2), whereas the risk of new diabetes was significantly attenuated for baseline HDL <1.21mmol/l (hazard ratio3.9, 95%CI 2.8-5.4).

Conclusions Lower in-treatment HDL is more strongly associated with increased risk of new diabetes than baseline HDL level.

sted, utgiver, år, opplag, sider
2013. Vol. 30, nr 10, s. 1189-1197
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URN: urn:nbn:se:umu:diva-82616DOI: 10.1111/dme.12213ISI: 000325085300007Scopus ID: 2-s2.0-84884720694OAI: oai:DiVA.org:umu-82616DiVA, id: diva2:662699
Tilgjengelig fra: 2013-11-08 Laget: 2013-11-05 Sist oppdatert: 2023-03-24bibliografisk kontrollert

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