hyperhomocysteinemia


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hyperhomocysteinemia

(hī'pĕr-hō'mō-sis'tē-in-ē'mē-ă),
Condition with plasma levels of homocysteine higher than 12 μmol/L, associated with atherosclerosis, and with venous and arterial thrombosis, apparently by damaging endothelial cells. Acquired forms can be treated with vitamins B12 and B6 and with folate.

hyperhomocysteinemia

(hī″pĕr-hō″mō-sĭs-tē″ĭn-ēm'ē-ă) [″ + ″]
Elevated levels of homocysteine in the bloodstream. High levels of homocysteine are found in the blood of patients with homocystinuria. Mildly elevated levels are found in many persons who consume a Western diet.
References in periodicals archive ?
Several lines of evidence indicate that maternal hyperhomocysteinemia is an independent risk factor for CHD (Malik et al., 2017), and recent population studies in humans have indicated that folic acid supplementation before and/or during pregnancy can decrease CHD risk (Czeizel et al., 2015; Leirgul et al., 2015; Li et al., 2013).
Associated disorders include antiphospholipid syndrome, protein C deficiency, factor V mutation, arteriosclerosis, hyperhomocysteinemia, and hepatitis C.
Methionine being an essential amino acid is obtained from recycling it or from diet.7 Hyperhomocysteinemia (HHcy) is a well-known risk factor of atherosclerosis.8,11 It can promote all the factors which can lead to initiation of process of atherosclerosis including proliferation of vascular wall smooth muscle, and increasing oxidative stress.7,12 A number of studies have shown a positive association of coronary artery disease, stroke and venous thrombosis with increased plasma Hcy levels.13,14 Boushey et al.
(4) Thrombophilic study revealed hyperhomocysteinemia and methylenetetrahydrofolate reductase variants (C677T and A1298C).
To the Editor: Hyperhomocysteinemia (HHcy) is an important risk factor for atherothrombotic disease and venous thrombosis.[1] Normally, homocysteine (Hcy) is either remethylated to methionine (Met) by a Vitamin B12-dependent reaction or betaine as the methyl donor, or trans-sulfurated to cysteine through a pyridoxine-dependent reaction.
Genetic or nutritional deficiencies in folate/one-carbon metabolism lead to the hyperhomocysteinemia (HHcy) and are known to cause abnormalities in many organs, including the cardiovascular system and the brain [1].
Elevated homocysteine levels, hyperhomocysteinemia, increase the risk for metabolic syndrome and lead to endothelial dysfunction causing atherosclerosis as well as microinflammation [20, 21].
Here, we present a case of 18-year-old female with moyamoya disease with hyperhomocysteinemia.
In these regards, hyperhomocysteinemia (HHcy) has sprung into attention for its involvement in endothelial dysfunction [10].
Additionally, chronic maternal hyperhomocysteinemia may impair brain development and consequently the cognitive functions of the fetuses by the increase of neuronal vulnerability to excitotoxicity, oxidative stress and apoptosis [14,15].
Folate and vitamin B12 deficiency and hyperhomocysteinemia promote oxidative stress in adult type 2 diabetes.