Homocysteinemia, ischemic heart disease, and the carrier state for homocystinuria

Wilcken, D. E. L.; Reddy, S.; Gupta, Vatsala J.

doi:10.1016/0026-0495(83)90045-8

Cited by 122 publications

(39 citation statements)

References 17 publications

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“…Elevations in levels of serum homocysteine have been consistently demonstrated in patients with coronary and cerebrovascular disease, while discrete hyperhomocysteinaemia has been associated with increased risk for both myocardial infarction and stroke (Wilcken et al 1983 ;Ueland et al 1992 ;Boers, 1994). Although a variety of conditions may result in raised homocysteine, the link with vascular disease appears to remain constant.…”

Section: Identifying Genetically-determined Risk Factorsmentioning

confidence: 99%

Late-onset depressive disorders: a preventable variant of cerebrovascular disease?

Hickie¹,

Scott²

1998

Psychol. Med.

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The severe depressive disorders of late life are associated with high rates of medical morbidity and mortality, cognitive impairment, suicide, disability, complex treatment regimens, institutionalization and high costs to the community (Murphy, 1983; Murphy et al. 1988; Bruce & Leaf, 1989; NIH Consensus Development Panel, 1992; Alexopoulos et al. 1993a, b; Brodaty et al. 1993; Bruce et al. 1994; Forsell et al. 1994; Hickie et al. 1995; Blazer, 1996). Those disorders that are accompanied by cognitive impairment and/or concurrent medical morbidity have a particularly poor outcome (Bruce & Leaf, 1989; Alexopoulos et al. 1993b; Hickie et al. 1995, 1997a). Although psychosocial models of late-life depression place considerable importance on age-related psychological and social risk factors, those who survive into later life may actually be characterized by psychological resilience (Henderson, 1994; Blazer, 1997).Current aetiological research in late-life depression, therefore, places particular emphasis on the potential role of biological risk factors. The potential importance of vascular risk factors is receiving renewed attention and may provide opportunities for specific prevention and intervention strategies in high-risk populations. This emphasis on possible vascular risk factors, and the wider importance of vascular pathologies in late-life neuropsychiatric disorders, mirrors the emphasis of much earlier clinico-pathological studies (Binswanger, 1894; Alzheimer, 1895). The specific focus on the importance of small progressive changes within the subcortical white matter, as distinct from more discrete cortical infarcts (Olszewski, 1962), is now supported by the emerging neuroimaging literature and theoretical constructs in late-life depression (Krishnan, 1991, 1993; Hickie et al. 1996, 1997b; Krishnan et al. 1997).

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Section: Identifying Genetically-determined Risk Factorsmentioning

confidence: 99%

Late-onset depressive disorders: a preventable variant of cerebrovascular disease?

Hickie¹,

Scott²

1998

Psychol. Med.

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“…Once formed homocysteine is either transsulfurated by cystathionine-β-synthase or remethylated by methylene tetrahydrofolate reductase (10). Cystathionine-β-synthase is deficient totally in homocysteinuria and partially in its carrier state, leading to high levels of homocyteine (11). Methylene tetrahydrofolate reductase requires vitamins B6, B12 and folate as co-factors (10).…”

Section: Introductionmentioning

confidence: 99%

Hyperhomocysteinaemia in Sri Lankan patients with coronary artery disease

Mendis¹,

Ranatunga²,

Jayatilake

et al. 2011

Ceylon Med. J.

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Papers AbstractObjective To determine the association between hyperhomocysteinaemia and coronary artery disease (CAD) in a sample of Sri Lankans. Design A case control study. Setting Asiri Hospital, Kirula Road, Colombo 5, Sri Lanka. Subjects 105 patients with coronary artery disease and 112 controls. Method Fasting serum homocysteine levels were measured in 105 patients diagnosed as having CAD and in 112 unmatched controls. All patients admitted with clinical, electrocardiographical, biochemical or echocardiographical evidence of CAD were included in the study. Controls were selected from subjects admitted for health screening. Results 105 patients with CAD and 112 controls (unmatched for age and sex) were studied. A serum homocysteine level in excess of 18.2 µmol/l was considered high. Confounding effects of other conventional risk factors for CAD were controlled using multivariate logical regression analysis. Conclusion Hyperhomocysteinaemia is significantly associated with CAD. Multivariate logistic regression analysis indicated that the association between hyperhomocysteinaemia and CAD was confounded by other risk factors. However, statistical analysis revealed a significant independent association between hyperhomocysteinaemia and CAD (adjusted odds ratio = 2.881).

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Section: Introductionmentioning

confidence: 99%

“…However, partially impaired transsulfuration in heterozygotes for CBS deficiency is often not associated with elevated fasting plasma tHcy concentrations (26)(27)(28). When the transsulfuration pathway is stressed by an oral l -methionine load test, it is sometimes possible to differentiate between heterozygotes and controls by the higher postmethionine load plasma tHcy concentrations in the former group (27,28). In addition, changes in vitamin B-6 status do not affect fasting plasma tHcy concentrations (29,30), while high dose pyridoxine supplementation has been shown to attenuate the post-methionine load plasma tHcy concentrations (31,32).…”

Section: Introductionmentioning

confidence: 99%

The effect of a subnormal vitamin B-6 status on homocysteine metabolism.

Ubbink¹,

Merwe²,

Delport³

et al. 1996

J. Clin. Invest.

228

112

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Homocysteine, an atherogenic amino acid, is either remethylated to methionine or metabolized to cysteine by the transsulfuration pathway. The biochemical conversion of homocysteine to cysteine is dependent upon two consecutive, vitamin B-6-dependent reactions.To study the effect of a selective vitamin B-6 deficiency on transsulfuration, we performed oral methionine load tests on 22 vitamin B-6-deficient asthma patients treated with theophylline (a vitamin B-6 antagonist) and 24 age-and sex-matched controls with a normal vitamin B-6 status. Both groups had normal circulating vitamin B-12 and folate concentrations. Methionine loading resulted in significantly higher increases in circulating total homocyst(e)ine ( P Ͻ 0.01) and cystathionine ( P Ͻ 0.05) concentrations in vitamin B-6-deficient patients compared with controls. 6 wk of vitamin B-6 supplementation (20 mg/d) significantly ( P Ͻ 0.05) reduced post-methionine load increases in circulating total homocyst(e)ine concentrations in deficient subjects, but had no significant effect on the increase in total homocyst(e)ine concentrations in controls. The increases in post-methionine load circulating cystathionine concentrations were significantly ( P Ͻ 0.01) reduced in both groups after vitamin supplementation.It is concluded that a vitamin B-6 deficiency may contribute to impaired transsulfuration and an abnormal methionine load test, which is associated with premature vascular disease. ( J. Clin. Invest. 1996. 98:177-184.) Key words: folate • methionine • coronary heart disease • vitamin B-12 • cystathionine

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Homocysteinemia, ischemic heart disease, and the carrier state for homocystinuria

Cited by 122 publications

References 17 publications

Late-onset depressive disorders: a preventable variant of cerebrovascular disease?

Late-onset depressive disorders: a preventable variant of cerebrovascular disease?

Hyperhomocysteinaemia in Sri Lankan patients with coronary artery disease

The effect of a subnormal vitamin B-6 status on homocysteine metabolism.

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