Hyperhomocysteinemia and Thrombosis

Guba, Susan C.; Fonseca, Vivian; Fink, Louis M.

doi:10.1055/s-2007-994932

Cited by 49 publications

(26 citation statements)

References 128 publications

(275 reference statements)

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“…Plasma tCys was positively associated with age, sex, BMI, cholesterol, apolipoprotein B, tHcy, creatinine, and triglyceride levels. tCys was associated with plasma folate but had no association with vitamin B 12 or B 6 . Plasma tCys showed a significant negative relation to smoking.…”

Section: Determinants Of Tcysmentioning

confidence: 77%

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Plasma Total Cysteine as a Risk Factor for Vascular Disease

et al. 2001

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Background-Elevated plasma total homocysteine (tHcy) is a risk factor for cardiovascular disease. Although cysteine is structurally similar and metabolically linked to tHcy, its relation to the risk of cardiovascular disease has received little attention. We studied the relation between plasma total cysteine (tCys) levels and the risk of vascular disease in the coronary, cerebral, and peripheral vessels. Methods and Results-This case-control study included 750 patients with vascular disease and 800 age-and sex-matched control subjects recruited from 19 centers in 9 European countries. Conventional risk factors for cardiovascular disease were recorded. In addition, plasma levels of tCys, tHcy, folate, B 6 , B 12 , and creatinine were measured. Overall, a U-shaped relationship was observed between tCys and risk of vascular disease. With the middle range of 250 to 275 mol/L tCys used as the reference category, the adjusted risk of vascular disease at low (Յ225 mol/L) tCys levels was 2.1 (95% CI 1.2 to 3.6), and the risk at high (Ͼ300 mol/L) tCys levels was 1.6 (95% CI 1.1 to 2.3). Different shapes of the dose-response relationship were seen for the 3 vascular disease categories. The relation with peripheral vascular and cerebrovascular disease was U-shaped, whereas a weak positive relation was observed with coronary heart disease. Conclusions-Our data show a significant U-shaped relationship between tCys and cardiovascular disease after adjustment for tHcy, creatinine, and other cardiovascular disease risk factors.

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Section: Determinants Of Tcysmentioning

confidence: 77%

“…[1][2][3][4][5] A variety of mechanisms have been suggested for the vascular lesions associated with hyperhomocysteinemia, 6 and the redox property of the sulfhydryl group of homocysteine, leading to the formation of reactive oxygen species, 7,8 is believed to play a pivotal role.…”

mentioning

confidence: 99%

Plasma Total Cysteine as a Risk Factor for Vascular Disease

et al. 2001

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“…PBMCs were obtained from heparinized blood by gradient centrifugation in isopaque-Ficoll (Lymphoprep, Nycomed Pharma AS) within 45 minutes and were incubated in flat-bottomed 96-well trays (2ϫ10 6 /mL, 100 L per well, Costar, Corning Inc) in medium alone (RPMI-1640 medium [Sigma Chemical Co] containing 2 mmol/L L-glutamine, 100 U/mL penicillin, and 5% autologous serum) or with oxLDL (final concentration 100 g/mL). In some experiments, the cells were cultured in the presence or absence of 500 nmol/L 5-methyltetrahydrofolic acid (Sigma) in RPMI-1640 medium free of folic acid, vitamin B 12 , and pyridoxine (GIBCO-BRL Life Technologies) supplemented with 2 mmol/L L-glutamine, 100 U/mL penicillin, and 10% of autologous serum.…”

Section: Release Of Chemokines From Pbmcsmentioning

confidence: 99%

Folic Acid Treatment Reduces Chemokine Release From Peripheral Blood Mononuclear Cells in Hyperhomocysteinemic Subjects

Holven¹,

Aukrust²,

Holm³

et al. 2002

ATVB

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Abstract-Elevated plasma homocysteine concentration is an independent risk factor for cardiovascular disease. However, the mechanisms by which hyperhomocysteinemia induces vascular disease are uncertain. An early step in atherogenesis involves leukocyte migration into the arterial wall, a process regulated in part by chemokines. We hypothesized that homocysteine may exert its atherogenic effect in part through chemokine-mediated mechanisms, and in the present study, we examined the effects of folic acid supplementation for 6 weeks on chemokine levels in hyperhomocysteinemic individuals. Data showed the following: (1) Compared with control subjects, hyperhomocysteinemic subjects had elevated plasma levels of the CXC chemokines, epithelial neutrophil-activating peptide (ENA)-78 (PϽ0.05), and growth-regulated oncogene (GRO)␣ (Pϭ0.088), and homocysteine was significantly correlated with ENA-78 and GRO␣. (2) During folic acid treatment, normalization of homocysteine levels was accompanied by a marked reduction in oxidized low density lipoprotein-stimulated release of CXC chemokines (ie, GRO␣, ENA-78, and interleukin-8) and CC chemokines (ie, monocyte chemoattractant peptide-1 and RANTES) in peripheral blood mononuclear cells from these individuals. (3) The oxidized low density lipoprotein-induced release of ENA-78 from peripheral blood mononuclear cells from control subjects was significantly reduced when cells were incubated in the presence of folic acid. These data may suggest that homocysteine exerts atherogenic effects in part by enhancing chemokine responses in cells involved in atherogenesis and that folic acid supplementation may downregulate these inflammatory responses.

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“…In contrast, a common variant of the MTHFR gene, i.e. the MTHFR C677T polymorphism, appears in the heterozygous form in 30-40% and in the homozygous form in 10-13% of the general population of whites (126). This polymorphism results in a thermolabile variant of the MTHFR enzyme that has been shown to be associated with slightly or moderately elevated HC plasma concentrations.…”

Section: Hyperhomocysteinemia (Hhc)mentioning

confidence: 99%

Laboratory Investigation of Thrombophilia / LABORATORIJSKO ISPITIVANJE TROMBOFILIJA

Margetić¹

2014

Journal of Medical Biochemistry

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Summary: Laboratory investigation of thrombophilia is aimed at detecting the well-established hereditary and acquired causes of venous thromboembolism, including activated protein C resistance/factor V Leiden mutation, prothrombin G20210A mutation, deficiencies of the physiological anticoagulants antithrombin, protein C and protein S, the presence of antiphospholipid antibodies and increased plasma levels of homocysteine and coagulation factor VIII. In contrast, investigation of dysfibrinogenemia, a very rare thrombophilic risk factor, should only be considered in a patient with evidence of familial or recurrent thrombosis in the absence of all evaluated risk factors mentioned above. At this time, thrombophilia investigation is not recommended for other potential hereditary or acquired risk factors whose association with increased risk for thrombosis has not been proven sufficiently to date. In order to ensure clinical relevance of testing and to avoid any misinterpretation of results, laboratory investigation of thrombophilia should always be performed in accordance with the recommended guidelines on testing regarding the careful selection of patients, time of testing and assays and assay methods used. The aim of this review is to summarize the most important aspects on thrombophilia testing, including whom and when to test, what assays and assay methods to use and all other variables that should be considered when performing laboratory investigation of thrombophilia.Keywords: acquired risk factors, hereditary risk factors, laboratory investigation of thrombophilia, venous thromboembolism Sa`etak: Cilj laboratorijskog ispitivanja trombofilije je otkrivanje ve} ustanovljenih naslednih i ste~enih uzroka venskog tromboembolizma, me|u kojima su aktivirana rezistencija na protein C/mutacija faktora V Leiden, mutacija protrombina G20210A, deficijencija fiziolo{kih antikoagulanasa antitrombina, proteina C i proteina S, prisustvo antifosfolipidnih antitela i povi{enih nivoa homocisteina i faktora koagulacije VIII u plazmi. Nasuprot tome, ispitivanje disfibrinogenemije, veoma retkog faktora rizika za trombofiliju, treba uzeti u razmatranje samo kod pacijenata kod kojih postoje dokazi o porodi~noj ili rekurentnoj trombozi uz odsustvo svih navedenih faktora rizika. U ovom trenutku, ispitivanje trombofilije se ne preporu~uje za ostale potencijalne nasledne ili ste~ene faktore rizika, ~ija povezanost sa pove}anim rizikom za trombozu jo{ nije nedvosmisleno dokazana. Kako bi se obezbedila klini~ka relevantnost testiranja i izbeglo pogre{no tuma~enje rezultata, laboratorijsko ispitivanje trombofilije trebalo bi uvek vr{iti u skladu s preporukama za testiranje koje se odnose na pa`ljiv odabir pacijenata, vreme testiranja i testove i metode koji se koriste. Cilj ovog preglednog ~lanka je da se ukratko predstave najva`niji aspekti testiranja trombofilije, izme|u ostalog, koga i kada testirati, koje testove i metode upotrebiti i koje sve varijable treba uzeti u obzir prilikom laboratorijskog ispitivanja trombofilije.Klju~ne rije~i...

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Hyperhomocysteinemia and Thrombosis

Cited by 49 publications

References 128 publications

Plasma Total Cysteine as a Risk Factor for Vascular Disease

Plasma Total Cysteine as a Risk Factor for Vascular Disease

Folic Acid Treatment Reduces Chemokine Release From Peripheral Blood Mononuclear Cells in Hyperhomocysteinemic Subjects

Laboratory Investigation of Thrombophilia / LABORATORIJSKO ISPITIVANJE TROMBOFILIJA

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