Hyperhomocyst(e)inemia induces multiorgan damage

Miller, Amanda; Mujumdar, Vibhas S.; Shek, Eugene W.; Guillot, J P; Angelo, Mike; Palmér, Lena; Tyagi, Suresh C.

doi:10.1007/s003800070030

Cited by 79 publications

(75 citation statements)

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“…In fact, a recent study reported that hyperhomocysteinemia markedly altered the activity of creatinine phosphokinases. 2 Therefore, one should be cautious in using CRc for evaluation of renal function during hyperhomocysteinemia. In a comparable study, McCully demonstrated the possible role of H(e) as an independent risk factor in cardiovascular diseases.…”

Section: Responsementioning

confidence: 99%

Why Does Elevated Plasma Homocysteine Result in Severe Microvascular Injury, but Not Glomerular Damage?

Rensma

Apperloo

Jong³

2003

Circulation

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Section: Responsementioning

confidence: 99%

Why Does Elevated Plasma Homocysteine Result in Severe Microvascular Injury, but Not Glomerular Damage?

Rensma

Apperloo

Jong³

2003

Circulation

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“…It has been suggested that unfiltered coffee increases plasma homocysteine concentrations in people with normal baseline concentrations. 2,4,5,11,12 Randomized clinical trials suggest that there is a homocysteine-raising effect of both filtered 13 and unfiltered coffee. 2 However, coffee intake in these studies was high (1 l per day) and at these levels of consumption, our results agree with the results of the above studies.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 Moreover, although homocysteine levels are lowered by the intake of folate, and vitamins B 6 and B 12 , elevated levels of homocysteine as well have been related with lifestyle habits, such as smoking and alcohol consumption. 1 A randomized clinical trial 3 and some population studies have suggested that a high intake of coffee is associated with raised concentrations of plasma homocysteine.…”

Section: Introductionmentioning

confidence: 99%

Erratum to: Patients with mild hypertensive heart disease and left ventricular outflow tract obstruction: treatment with angiotensin II antagonists

Panagiotakos

Pitsavos²,

Zampelas³

et al. 2004

Heart Vessels

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The aim of this work was to investigate the association between homocysteine levels and coffee consumption in a sample of cardiovascular disease-free men and women. From May 2001 to December 2002, we randomly enrolled 1514 men and 1528 women, stratified by age and gender, from the greater area of Athens. Blood samples were collected in the fasting state. Among other investigated factors, dietary habits (including coffee consumption in ml per day, adjusted for 28% caffeine containment) were evaluated using a validated food frequency questionnaire. Men consumed higher quantities of coffee compared with women (250 Ϯ 55 vs 150 Ϯ 60 ml/day, P ϭ 0.001), while homocysteine values were also higher in men than in women (14.5 Ϯ 6 vs 10.8 Ϯ 3.5 µmol/l, P ϭ 0.001). A doseresponse relationship of homocysteine levels with coffee consumption was observed (r ϭ 0.10, P ϭ 0.034). In particular, we found that homocysteine levels were 11.2 Ϯ 5 µmol/ l for no consumption, 11.7 Ϯ 7 µmol/l for Ͻ100 ml/day, 12.5 Ϯ 7µmol/l for 200-400 ml/day, and 12.7 Ϯ 4µmol/l for Ͼ500 ml/day consumption (P ϭ 0.018). The observed trend remained significant even after controlling for the interactions between coffee consumption with gender, smoking habits, physical activity status, and eating habits. However, the sole effect of the consumption of filtered coffee on homocysteine levels was significant only in those who consumed more than 500 ml/day (P ϭ 0.043). Although our findings cannot be evidence for causality, they can be the basis for hypotheses about the relation between homocysteine and coffee that can partially explain the mechanisms by which elevated homocysteine levels may influence coronary risk.

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“…69 Data from a recent animal study have demonstrated that experimentally induced hyperhomocysteinemia in rats causes endocardial endothelial cell apoptosis and may reduce capillary cell density. 70 Investigators also found structural damage to the aorta, kidney, and renal ureter, which suggests that homocysteineassociated endothelial/epithelial damage is possible in multiple organ systems. 70 C-reactive protein, on the other hand, is believed to be more of a marker than a cause of dysfunction.…”

Section: Risk Factors and Possible Pathogenic Mechanismsmentioning

confidence: 99%

“…70 Investigators also found structural damage to the aorta, kidney, and renal ureter, which suggests that homocysteineassociated endothelial/epithelial damage is possible in multiple organ systems. 70 C-reactive protein, on the other hand, is believed to be more of a marker than a cause of dysfunction. 69 Primary abnormalities of coagulation and platelet function are implicated in only a small percentage of strokes.…”

Section: Risk Factors and Possible Pathogenic Mechanismsmentioning

confidence: 99%

Pathophysiology and therapeutic targets for ischemic stroke

Levine

2004

Clin Cardiol

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Summary:The increased risk for stroke among those who have had a previous stroke or transient ischemic attack (TIA) and the tremendous burden of disability among stroke sufferers make both primary and secondary preventative strategies imperative. An understanding of the pathophysiology of stroke and TIA can help identify appropriate therapeutic targets. Stroke and Heart Disease Shared Pathology and Risk FactorsUnderlying atherosclerosis, which plays a significant role in both ischemic stroke and myocardial infarction (MI), is similar in both conditions. Despite this similarity, however, these two disease states are characterized by distinct differences in pathophysiology that go beyond the mere location of the thrombus. Coronary artery lesions tend to be more fibrotic than those found in the cerebral vasculature. 1, 2 Stroke patients are an extremely heterogeneous group compared with those who have had an MI. There is a variety of sources for the thrombus as well as numerous areas in which ischemic occlusion can occur. The evolution of the consequences of the ischemic event also differs in stroke and MI. Stroke pathology pursues a much longer course than MI, with secondary damage and metabolic sequelae occurring at times up to a month after the initial event. 3 The neurological complications and clinical manifestations following a stroke vary considerably as well, depending upon which areas of the brain were affected and to what degree. Patients may suffer from any combination of cognitive, motor, visual, sensory, language, speech, or mood deficits. Deficits can be discrete or global. Finally, despite the pervasive notion that stroke patients are at increased risk for acute MI, in up to 75% of stroke survivors a subsequent cardiovascular event could be another stroke. 4 However, both stroke and MI share many risk factors. Hypertension and diabetes mellitus are important modifiable risk factors for both stroke and heart failure. 5 In fact, cardiovascular disease, including stroke and heart disease, is the primary cause of death in persons with diabetes. 6 Hyperlipidemia is an accepted risk factor for coronary artery disease, and its contribution to ischemic stroke is also important. 7-10 Data from studies indicate that use of the beta-hydroxy-betamethylglutaryl-CoA reductase inhibitors or statins (cholesterol-lowering drugs) offers stroke protection and reduces the amount of carotid atheroma, although the mechanisms involved are unclear. [7][8][9][10] Lifestyle factors, such as obesity and smoking, and use of a number of chemical substances, including alcohol and both legal and illegal drugs, have been associated with cardiovascular disease in general and stroke in particular. 7,11,12 Some prescription medications have been associated with an increased incidence of stroke. In the past, early-generation oral contraceptives were found to increase stroke risk, 13 and controversy has surrounded hormone replacement therapy (HRT), with recent findings from the Hormone and Estrogen/progestin Replacement Study (HERS) a...

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Hyperhomocyst(e)inemia induces multiorgan damage

Cited by 79 publications

References 0 publications

Why Does Elevated Plasma Homocysteine Result in Severe Microvascular Injury, but Not Glomerular Damage?

Why Does Elevated Plasma Homocysteine Result in Severe Microvascular Injury, but Not Glomerular Damage?

Erratum to: Patients with mild hypertensive heart disease and left ventricular outflow tract obstruction: treatment with angiotensin II antagonists

Pathophysiology and therapeutic targets for ischemic stroke

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