Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperhomocysteinemia is currently regarded as an independent and modifiable risk factor for ischemic vascular diseases and thrombosis. We measured fasting plasma total homocysteine levels by HPLC with fluorescence detection in 30 patients presenting with acute coronary syndromes and 30 age and sex-matched control subjects. Demographic data, classical risk factors (systolic blood pressure, diabetes mellitus, smoking, ethanol intake, family history of ischaemic heart disease) and life-style habits were recorded. Lipid fractions including total cholesterol, triglycerides, HDL-cholesterol, total cholesterol/HDL-cholesterol ratio, serum creatinine, LDL-cholesterol and vitamins involved in the metabolism of homocysteine, folic acid and vitamin B12 were also assessed. Total fasting homocysteine concentrations were significantly higher in the patient group (12.2 +/- 1.01 micromol/l) than in the control subjects (7.05 +/- 0.36 micromol/l; p < 0.0001). Homocysteine correlated positively with age (r = 0.617; p < 0.01) and serum creatinine (r = 0.457; p < 0.01) in the patient group. Hyperhomocysteinemia was not associated with vitamin B12 or folate deficiency states. Vitamin B12 concentration was 273 +/- 16.4 ng/l in the control group and 284.3 +/- 32.2 ng/l in the patient group (p = NS). Serum folate concentration also was not significantly different between controls and patients; 7.57 +/- 0.58 microg/l and 8.05 +/- 0.72 microg/l, respectively. Since no significant difference was observed in the lipid parameters between patients and controls, the hyperhomocysteinemia in the patient group supports the view that homocysteine is an independent risk factor for cardiovascular diseases. Our results strongly suggest that elevated homocysteine levels are among the interacting factors in the complex, multifactorial pathophysiology of ischemic heart disease.
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PMID:Plasma homocysteine levels in acute coronary syndromes. 1073 56

The objectives of this study were to describe the distribution of serum levels of total homocysteine (HCys) in a sample of older patients consecutively admitted following acute ischemic cerebral stroke, as compared with healthy controls, and to test for possible relationships of HCys levels to some of the prevalent cardiovascular diseases in these stroke patients. One hundred and thirty-seven stroke patients and 132 healthy controls (age > or =60) participated in this study. HCys levels were determined by HPLC method with fluorescence detection. Correlates of HCys levels and clinical data were examined. The results showed that stroke patients (mean age 74.6+/-9.2) had higher HCys levels as compared with controls (13.8 and 9.8 respectively, p<0.001). Advanced age, male gender, absence of diabetes and a positive history of previous myocardial infarction were the factors associated with HCys levels higher than 10 mmol/L (Odds ratio 2.72, 2.54, 3.12, 3.55, respectively). We conclude that hyperhomocysteinemia is prevalent in older patients with acute ischemic stroke. Few factors associated with increased risk for hyperhomocysteinemia in these stroke patients were identified. The study supports earlier observations regarding elevated HCys levels in stroke patients and increased prevalence of associated cardiovascular disease.
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PMID:The relation of plasma total homocysteine levels to prevalent cardiovascular disease in older patients with ischemic stroke. 1074 32

The development of diabetic nephropathy shows marked variation among individuals. Not only hyperglycemia, but also genetic factors may contribute to the development of diabetic nephropathy. Methylenetetrahydrofolate reductase (MTHFR) is involved in remethylation of homocysteine to methionine. Decreased activity of MTHFR which can result in hyperhomocysteinemia may lead to cerebrovascular disease and coronary artery disease. Recently, a common C to T mutation at nucleotide position 677 of the MTHFR gene (MTHFR677CT) has been reported to be correlated with hyperhomocysteinemia and the severity of coronary artery disease as macroangiopathy. In the present study, we recruited 173 of Japanese type II diabetic patients with proliferative diabetic retinopathy who would be exposed to long-term hyperglycemia, and examined the contribution of the MTHFR gene polymorphism to the development of diabetic nephropathy as microangiopathy. The frequency of the mutated allele was 43.3% in patients with nephropathy (n = 105) versus 41.9% in those without nephropathy (n = 68). The genotype frequencies were +/+, 16.2%; +/-, 54.3%; -/-, 29.5% in patients with nephropathy versus +/+, 13.2%; +/-, 57.4%; -/-, 29.4% in those without nephropathy (+ indicates the presence of the mutation). The MTHFR genotype and allele frequencies were not significantly different between patients with and without nephropathy. Therefore, we conclude that the MTHFR gene polymorphism is not associated with the development of diabetic nephropathy in Japanese type II diabetic patients.
J Diabetes Complications
PMID:No association between MTHFR gene polymorphism and diabetic nephropathy in Japanese type II diabetic patients with proliferative diabetic retinopathy. 1076 3

Increasing age and male gender are unavoidable risk factors for peripheral arterial occlusive disease (PAOD). A number of studies have looked at classical risk factors for atherosclerosis, such as diabetes, hypertension, lipid abnormalities, and smoking, as well as some more recently identified associations, such as plasma fibrinogen levels, impaired glucose tolerance, and hyperhomocysteinemia. However, most "risk factors" are really associations. A causal relationship may only reasonably be firmly established if a prospective controlled study shows that removing the risk factor significantly alters the course of the disease, as with smoking. Smoking is probably the strongest risk factor for intermittent claudication (IC), but hyperhomocysteinemia also appears to be strongly associated with the development of PAOD. Moderate alcohol intake and regular physical exercise appear to have a protective effect. A genetic risk factor is suggested but not as yet confirmed. The magnitude of the association varies from odds ratios of 2 to 3 for smoking and diabetes. There is insufficient evidence for hyperhomocysteinemia, but the effect may be even greater. The association with hypertension and lipid abnormalities is surprisingly inconclusive.
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PMID:Predictors of early disease in the lower limbs. 1077 37

Hyperhomocysteinemia has been recognised as an independent risk factor for cardiovascular, cerebrovascular and peripheral artery disease. There is strong evidence suggesting that hyperhomocysteinemia accelerates the process of atherogenesis. Possible explanations for this will be shortly reviewed. Recently a growing interest has been focused on the association of hyperhomocysteinemia with diabetes mellitus and with chronic renal disease, including renal transplant recipients. Some clinical aspects of this occurrence, such as interactions with insulin, metformin, and cyclosporine and also with some vitamins, will be described. The issue of hyperhomocysteinemia in heart transplant patients will also be mentioned. Last of all, the interaction of homocysteine concentration with some beverages will be considered.
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PMID:Hyperhomocysteinemia as a risk factor for cardiovascular diseases. The association of hyperhomocysteinemia with diabetes mellitus and renal transplant recipients. 1085 May 96

Mild hyperhomocysteinemia has been considered a cardiovascular risk factor. However, recent prospective studies have not demonstrated that hyperhomocysteinemia or the underlying genetic defect on methylentetrahydrofolate reductase is associated with a higher risk of coronary or peripheral artery disease. We compared serum homocysteine, folate, and vitamin B(12) levels of patients with coronary and peripheral vascular disease with those of age- and sex-matched healthy individuals. Subjects taking multivitamins, with diabetes mellitus, or serum creatinine levels over 1.5 mg/dL were excluded from the study. Homocysteine was measured by fluorimetric high-performance liquid chromatography. Serum folate and vitamin B(12) levels were measured by an ion-capture method. We studied 32 patients with peripheral vascular disease (10 female), aged 69.6 +/- 11 y, 24 age- and sex-matched control subjects, 52 patients with coronary artery disease (7 female), aged 59.5 +/- 10.4 y, and 42 age- and sex-matched control subjects. Serum homocysteine levels were 11.7 +/- 7.4 and 9.3 +/- 4.5 micromol/L in vascular patients and in the control counterparts, respectively (not significant). The levels for coronary patients and the control counterparts were 9.0 +/- 3.9 and 8.6 +/- 3.6 micromol/L, respectively (not significant). Folate levels were 4.48 +/- 2.42 and 7.14 +/- 4.04 ng/mL in vascular patients and control subjects, respectively (P < 0.02); the levels in coronary patients and control counterparts were 5.15 +/- 1.9 and 6.59 +/- 2.49 ng/mL, respectively (P < 0.01). No differences in vitamin B(12) or tocopherol levels were observed between patients and control subjects. There were no differences in homocysteine levels, but lower serum folate levels were observed when comparing patients with atherosclerotic vascular disease and healthy control subjects.
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PMID:Low serum folate but normal homocysteine levels in patients with atherosclerotic vascular disease and matched healthy controls. 1086 99

All uremic patients have multiple risk factors for CAD including in many, the conditions that caused their ESRD--for example, diabetes and hypertension. conventional risk factors--for example, dyslipidemia and hyperhomocysteinemia. risk factors that are unique to uremia--for example, calcium and phosphate abnormalities. PD patients have particular risk with respect to their lipid status and hyperinsulinemia. Many of these risks are potentially modifiable, but evidence does not exist to assess the impact of treatment on clinical outcomes. Therefore, current decisions for therapy directed at risk factor modification must be made on an individual basis.
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PMID:Major and minor risk factors for cardiovascular disease in peritoneal dialysis. 1091 62

Cardiovascular disease is the leading cause of death in patients receiving dialysis. This is attributed in part to the shared risk factors of cardiovascular disease and end-stage renal disease. The risk factors for coronary artery disease include the classic cardiac risk factors of diabetes mellitus, hypertension, dyslipidemia, and smoking. Also in this population, hyperparathyroidism, hypoalbuminemia, hyperhomocysteinemia, elevated levels of apolipoprotein (a), and the type of dialysis membrane may play a role. Management begins with risk factor modification and medical therapy including aspirin, beta blockers, angiotensin converting enzyme (ACE) inhibitors, and lipid-lowering agents. Revascularization is often important, and coronary artery bypass grafting appears to be preferable to percutaneous transluminal coronary angioplasty. This is especially true for those with multivessel disease, impaired left ventricular function, severe symptoms, or ischemia. Congestive heart failure is another common problem in dialysis patients. The management includes correction of underlying abnormalities, optimal dialysis, and medical therapy. Data obtained from the general population indicate obvious benefits from ACE inhibitors and beta blockers, and these agents would be considered the therapies of choice. Erythropoetin is also an essential component of therapy, but the ideal hemoglobin concentration has yet to be determined. Peritoneal dialysis may be helpful in severe cases of heart failure. Pericarditis is seen in less than 10% of dialysis patients and is best diagnosed by clinical examination and echocardiography. Intensive dialysis is often the best initial therapy. Pericardiocentesis is reserved for the setting of pericardial tamponade, but a pericardial window is more definitive.
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PMID:Cardiac complications of end-stage renal disease. 1092 9

Endothelium-derived nitric oxide (EDNO) is a pivotal molecule in the regulation of vascular tone via the stimulation of vascular smooth muscle cell relaxation and concomitant vasodilation. In addition, EDNO exerts a number of other potent antiatherogenic effects, including inhibition of leukocyte-endothelial interactions, smooth muscle cell proliferation, and platelet aggregation. Endothelial vasodilator dysfunction has been observed in patients with CAD or coronary risk factors such as hypercholesterolemia, hyperhomocysteinemia, essential hypertension, diabetes mellitus, smoking, and aging. Most of these conditions are associated with increased oxidative stress, particularly increased production of superoxide radicals and elevated levels of oxidized LDL, both of which can attenuate the biological activity of EDNO. The levels of superoxide and oxidized LDL can be decreased by administering the small molecule antioxidants vitamins E and C. Vitamin C also spares intracellular thiols, which in turn can stabilize EDNO through the formation of biologically active S-nitrosothiols. Here we review the role that vitamins E and C and thiol compounds play in endothelium-dependent vasodilation. Understanding the mechanisms of the reversal of endothelial dysfunction by natural antioxidants will lead to successful therapeutic interventions of CAD and its clinical sequelae.
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PMID:The role of natural antioxidants in preserving the biological activity of endothelium-derived nitric oxide. 1094 22

Liver transplant recipients have an increased risk for cardiovascular disease because of a high incidence of obesity, arterial hypertension, diabetes mellitus, and hyperlipidemia. Hyperhomocysteinemia has been found to be an important risk factor for cardiovascular disease in large studies. Fasting serum levels of homocysteine were measured in 105 liver transplant recipients, and hyperhomocysteinemia was defined as a fasting serum homocysteine level greater than 13 micromol/L. Patients with versus without hyperhomocysteinemia were compared. The possible association of hyperhomocysteinemia with age, sex, cause of liver disease, time elapsed since liver transplantation, immunosuppressive therapy, folic acid level, liver function test results, renal function, and other cardiovascular risk factors was investigated. Patients with serum homocysteine levels greater than 15 micromol/L were treated with folic acid, 10 mg/d, and serum homocysteine levels were measured again 1 to 3 months later in 10 patients. Hyperhomocysteinemia was detected in 28 patients (27%). In univariate analysis, it was associated with hepatitis C virus infection, treatment with mycophenolate mofetil, and greater serum levels of alkaline phosphatase, gamma-glutamyl transpeptidase, urea, and creatinine. In multivariate analysis, only greater serum levels of creatinine (P =.006) were associated with hyperhomocysteinemia. Treatment with folic acid resulted in a decrease in fasting serum homocysteine levels in 9 of the 10 patients tested (P =.01). Hyperhomocystinemia, associated with renal dysfunction, is a frequent finding in liver transplant recipients. Treatment with folic acid may reduce fasting homocysteine levels.
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PMID:Hyperhomocysteinemia in liver transplant recipients: prevalence and multivariate analysis of predisposing factors. 1098 61


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