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Volume 19, Issue 3, Pages 147-154 (May 2005)


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Levels of plasma total adrenomedullin are related with two acute phase inflammatory reactants (fibrinogen and sialic acid) but not with markers of endothelial dysfunction in Type 1 diabetes: Adrenomedullin and vascular risk factors in Type 1 DM

M.T. García-Unzuetaa, J.R. Berrazuetab, C. Pesqueraa, S. Obayac, M.D. Fernándezc, C. Sedanod, J.A. AmadoaCorresponding Author Informationemail address

Received 12 May 2004; received in revised form 26 August 2004; accepted 31 August 2004.

Abstract 

Adrenomedullin (AM), an ubiquitous regulatory peptide with different actions, is known to be elevated in different clinical situations, including diabetes mellitus (DM), but its potential role in the pathogenesis of diabetic vascular complications is not clear. In the present study, we examined plasma total AM levels, and their association with different markers of endothelial dysfunction and with other established risk factors for cardiovascular diseases, in patients with Type 1 DM. We studied a total of 155 patients, 117 patients without any kind of vascular complications, 24 patients with retinopathy only, and 14 patients with retinopathy and microalbuminuria but normal renal function. None of them had clinical evidence of atherosclerotic disease. Compared with the control group (64 healthy participants), patients had raised fibrinogen, soluble E-selectin (sE-selectin), vascular cellular adhesion molecule (VCAM), angiotensin converting enzyme (ACE), and von Willebrand factor (vWf) (P<.001 in all cases), but plasma total AM, endothelin (ET), sialic acid, and homocysteine were not raised. In the diabetic group, AM levels correlated significantly with sialic acid (r=.16; P<.05), but a more significant correlation was found with fibrinogen (r=.30; P<.001). No correlation was found with the other parameters studied. In summary, plasma total AM levels seem to correlate with inflammatory markers but not with endothelial dysfunction markers in Type 1 diabetic patients without atherosclerotic disease.

a Endocrinology Service, Endocrine Unit, Hospital Universitario M. de Valdecilla, Valdecilla Street, Santander 39008, Spain

b Cardiology Service, Hospital Universitario M. de Valdecilla, University of Cantabria, Valdecilla Street, Santander 39008, Spain

c Clinical Biochemistry Service, Hospital Universitario M. de Valdecilla, University of Cantabria, Valdecilla Street, Santander 39008, Spain

d Haematology Service, Hospital Universitario M. de Valdecilla, University of Cantabria, Valdecilla Street, Santander 39008, Spain

Corresponding Author InformationCorresponding author. Tel.: +34 942 202514; fax: +34 942 201695

PII: S1056-8727(04)00094-7

doi:10.1016/j.jdiacomp.2004.08.002


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