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Carotid Atherosclerosis in Type 2 Diabetes Mellitus: Potential Role of Endothelin-1, Lipoperoxides, and ProstacyclinDepartment of Nuclear Medicine, endocrine Unit, Army Veterans Hospital, Athens, Greece.
Department of Nuclear Medicine, Army Veterans Hospital, Athens, Greece.
Department of Diabetic Unit, Army Veterans Hospital, Athens, Greece.
Department of Endocrine Unit, Army Veterans Hospital, Athens, Greece.
Royal Free and University College Medical School, University of London, England
Department of Endocrine Unit, Army Veterans Hospital, Athens, Greece.
Department of Pharmacy, University of Patras, Patras, Greece. Factors were studied that may initiate macroangiopathy or enhance or aggravate its patho genesis in patients with type 2 diabetes mellitus. A total of 151 diabetics were compared with healthy controls (n = 50); all patients and subjects were normotensive and without renal failure. Plasma endothelin-1 and free radical levels were measured. In addition, plasma prosta cyclin levels were assessed by assaying its stable, spontaneous, breakdown product 6-keto prostaglandin-F1a. Diabetics were divided into three groups: those with clinically evident macroangiopathy and those with early or without atherosclerosis (as determined by the carotid intima-media thickness. Plasma endothelin-1 levels were increased in all diabetics with atherosclerosis. Plasma free radical levels were increased in diabetics with macroan giopathy when compared with control subjects. The plasma levels of 6-keto-prostaglandin-F 1a were slightly, but significantly, decreased in the diabetics with macroangiopathy when compared with control subjects. The carotid intima-media thickness was significantly greater in diabetics without macroangiopathy when compared with the controls. Furthermore, the intima-media thickness increased significantly in this group of diabetics but not in the controls over a 30-month follow-up period. Several factors may contribute to atherogenesis in diabetics. These include increased plasma endothelin-1 and free radical levels as well as a defi ciency of prostacyclin. These factors may become targets for intervention as well as markers of disease progression.
Angiology, Vol. 53, No. 3,
279-285 (2002) |
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