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Hyperhomocysteinemia and Venous Thrombosis

Seminars in Hematology, 2007
It has been recognized, since the first description of the disease, that arterial and venous thrombosis are common in patients with homocysteinuria. Interest in the condition increased with reports from a large number of mainly retrospective studies showing that mildly elevated homocysteine levels are also associated with venous thromboembolism (VTE ...
Alex, Gatt, Michael, Makris
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Hyperhomocysteinemia and Atherothrombotic Disease

Seminars in Thrombosis and Hemostasis, 1998
Hyperhomocysteinemia is an independent risk factor for atherothrombotic disease. The mechanism by which homocysteine induces atherosclerosis and thrombosis is not fully understood. Data on arterial histology in humans with homocystinuria and mild hyperhomocysteinemia are limited.
S C, de Jong   +3 more
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Hyperhomocysteinemia After Kidney Transplantation

Transplantation Proceedings, 2011
To determine the prevalence of hyperhomocysteinemia (plasma homocysteine[Hcy] concentration≄15 μmol/L) and evaluate its correlation with allograft function.The study included 159 stable renal transplant recipients (104 men and 55 women). The prevalence and severity of hyperhomocysteinemia were compared in the transplant recipients vs 72 patients (48 ...
B, Einollahi   +6 more
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Hyperhomocysteinemia and thrombosis

Lipids, 2001
AbstractHomocysteine (Hcy) is a sulfhydryl amino acid derived from the metabolic conversion of methionine, which is dependent on vitamins (folic acid, B12, and B6) as cofactors or cosubstrates. In 1969, McCully first reported the presence of severe atherosclerotic lesions in patients with severe hyperhomocysteinemia and hypothesized the existence of a ...
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Hyperhomocysteinemia, inflammation and autoimmunity

Autoimmunity Reviews, 2007
Hyperhomocysteinemia is independently associated with the development of coronary, cerebral and peripheral vascular disease and deep-vein thrombosis in the general population. The evidence that cardiovascular involvement is particularly frequent and advanced in patients affected with several autoimmune diseases (AD), in which hyperhomocysteinemia ...
Lazzerini, P. E.   +6 more
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Hyperhomocysteinemia and Venous Thromboembolism

Seminars in Thrombosis and Hemostasis, 2006
Homocysteine (Hcy) is a sulfhydryl amino acid derived from the metabolic conversion of methionine, which is dependent on vitamins (folic acid, B12 and B6) as cofactors or cosubstrates. Severe hyperhomocysteinemia (homocystinuria), due to inherited metabolic defects of Hcy metabolism, is associated with very high risk of venous thromboembolism (VTE ...
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Hyperhomocysteinemia and Venous Thrombosis

The International Journal of Lower Extremity Wounds, 2002
Deep vein thrombosis (DVT) leads to venous ulcers in later life. Venous ulcers are the majority of chronic lower extremity wounds. Recent evidence suggests that hyperhomocysteinemia is an independent risk factor for venous thrombosis. Other evidence suggests that dietary supplementation with folic acids and vitamins helps to change hyper ...
Paul, Lee, Kailash, Prasad
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Hyperhomocysteinemia, Atherosclerosis and Thrombosis

Thrombosis and Haemostasis, 1999
SummaryHigh plasma levels of homocysteine are the results of the interplay between congenital and environmental factors. In the last two decades, a growing amount of interest has focused on mild-to-moderate hyperhomocysteinemia as a risk factor of thromboembolic diseases.
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Hyperhomocysteinemia and Immune Activation

Clinical Chemistry and Laboratory Medicine, 2003
Hyperhomocysteinemia is an established risk factor for atherosclerosis, thrombosis and other vascular diseases. Homocysteine auto-oxidation is considered to be crucially involved in the pathogenesis of these diseases. However, the question remains to be elucidated whether vitamin deficiency and homocysteine accumulation are causal for disease ...
Katharina, Schroecksnadel   +5 more
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[Hyperhomocysteinemia].

Casopis lekaru ceskych, 1996
Similarly as in other inborn metabolic diseases the cause of hyperhomocysteinaemia are interactions between genetically conditioned changes most frequently due to reduced cystathionine-beta synthase activities and negative factors of the external environment.
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