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Hyperhomocysteinemia as Cardiovascular Risk Factor in Type 2 Diabetes Mellitus

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Cardiovascular Risk in Type 2 Diabetes Mellitus
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Abstract

Hyperhomocysteinemia has been associated to the development of cardiovascular disease, mainly premature atherosclerosis and thromboembolic disorders.

Experimental results indicate an involvement of hyperhomocysteinemia in endothelial dysfunction, lipid peroxidation, impaired synthesis of nitric oxide, and reduced expression of thrombomodulin.

Genetics defects leading to deficiencies of cystathionine beta synthase and methylene tetrahydrofolate reductase are responsible of increased plasma homocysteine in homozygotes.

Ageing, postmenopause, hypothyroidism, renal insufficiency, and reduction of plasma folate, account for non-genetic causes of hyperhomocysteinemia.

Increased plasma homocysteine have been recorded in both type 1 and type 2 diabetic subjects. Experimental evidence suggests that advanced glycation end products may act synergistically with homocysteine in the development of endothelial dysfunction. In general, diabetic patients with associated hyperhomocysteinemia showed higher levels of serum creatinine, and in type 2 diabetic subjects, multiple regression analysis has depicted albumin excretion rate as the parameter with strongest independent association with elevated plasma homocysteine. Patients with nephropathy and hyperhomocysteinemia were older and showed a more advanced stage of renal disease.

Succesful treatment of hyperhomocysteinemia is achieved with the oral administration of folate in association either to piridoxine, vitamin B12 and betaine. Higher doses of folate are required in patients with marked hyperhomocysteinemia and chronic renal failure.

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de Leiva, A. (2003). Hyperhomocysteinemia as Cardiovascular Risk Factor in Type 2 Diabetes Mellitus. In: Hâncu, N. (eds) Cardiovascular Risk in Type 2 Diabetes Mellitus. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59352-9_15

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  • DOI: https://doi.org/10.1007/978-3-642-59352-9_15

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-63946-3

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