Hyperhomocysteinaemia and multiple aneurysms

Homozygous homocystinuria, the most common genetic disorder of transulphuration, is associated with elevated plasma concentrations of homocystine, homocysteine, multiple clinical abnormalities and life-threatening thromboembolism. Several instances of vascular aneurysms have also been documented. More recently, an association between premature occlusive vascular disease and the heterozygous state has been proposed. We now report an unusual case in whom multiple aneurysms were associated with heterozygous homocystinuria.     

Hyperhomocysteinaemia in Sri Lankan patients with coronary artery disease

OBJECTIVE: 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 mumol/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).     

Hyperhomocysteinaemia: a risk factor for extracranial carotid artery atherosclerosis

Hyperhomocysteinemia arising from impaired methionine metabolism, and usually due to a deficiency of cystathionine ß-synthase is a significant and independent risk factor for symptomatic vascular disease. It is not known if hyperhomocysteinemia in apparently healthy asymptomatic subjects is associated with atherosclerosis and whether such a relationship is independent of conventional risk factors. The prevalence of asymptomatic extracranial carotid artery atherosclerosis was determined by duplex ultrasound examination in 25 obligate heterozygotes with respect for cystathionine ß-synthase deficiency (whose children were known to be homozygous for this genetic defect) and in 21 controls. Hyperhomocysteinemia was determined by a standard methionine-loading test and conventional risk factors were also recorded. Twelve of 25 obligate heterozygotes and 8 of 21 normal controls had evidence of extracranial carotid artery atherosclerosis. Hyperhomocysteinemia as a genetic trait was not a significant risk marker, but the actual homocysteine level was associated with an increased risk of carotid disease. After adjustment for the effects of other significant risk factors, the odds ratio of hyperhomocysteinemia for carotid disease was 1.038 per unit increase in homocysteine level (P=0.03). Hyperhomocysteinemia is a weak risk factor for asymptomatic extracranial carotid atherosclerosis and the relative risk associated with this genetic trait is less than that observed in a study of patients presenting with clinical manifestations of vascular disease.     

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