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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Accumulation of oxidized-matrix between the endothelium and myocytes is associated with endocardial endothelial (EE) dysfunction in diabetes and heart failure. High levels of circulating homocysteine (Hcy) have been demonstrated in diabetes mellitus (DM). These high levels of Hcy (hyperhomocysteinemia, HHcy) have a negative correlation with peroxisome proliferator activated receptor (PPAR) expression. Studies have demonstrated that Hcy decreases bioavailability of endothelial nitric oxide (eNO), generates nitrotyrosine, and activates latent matrix metalloproteinase (MMP), instigating EE dysfunction. PPAR ligands ameliorate endothelial dysfunction and DM. In addition Hcy competes with PPAR ligands. The understanding of molecular, cellular, and extracellular mechanisms by which Hcy amplifies DM will have therapeutic ramifications for diabetic cardiomyopathy.
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PMID:Role of nitric oxide in matrix remodeling in diabetes and heart failure. 1265 56

Cardiovascular, cerebrovascular and peripheral vascular diseases are the largest cause-specific reason for morbidity and mortality in end-stage renal disease (ESRD) patients. High prevalence of cardio- and cerebrovascular death may be explained by multiple factors present in patients with progressive renal disease, including hypertension, hyprelipidemia, hyperhomocysteinemia, diabetes mellitus, and hyperparathyroidism. Experimental studies have provided in vivo and in vitro data to support the notion that lipid abnormalities contribute to glomerular and interstitial injury of the renal parenchyma. Hypercholesterolemia and increased low-density lipoprotein (LDL) cholesterol are prevalent in patients with the nephrotic syndrome. Plasma high-density lipoprotein (HDL) cholesterol is decreased, and reverse cholesterol transport is impaired in hemodialysis (HD) and pre-ESRD patients. Chronic renal failure patients treated with HD have an increased prevalence of intermediate-density lipoprotein (IDL), and lipoprotein(a). The findings in the diabetic patients corresponded to those in non-diabetic patients with renal failure, but diabetic patients have higher apolipoprotein C-III and apolipoprotein E concentrations. Impaired lipid metabolism is common in patients receiving peritoneal dialysis (PD). In the most of the ESRD patients treated with peritoneal dialysis hypercholesterolemia and hypertriglyceridemia are found. Wide panels of therapeutic interventions aimed at correcting the lipid abnormalities that may develop in chronic renal patients, as well as in ESRD patients are currently available. Although some novel pharmacological agents are remarkably effective for returning the lipid abnormalities to normal, there is still no convincing evidence based on long-term prospective studies which clearly demonstrate a significant reduction in cardiovascular morbidity and mortality of ESRD patients. The therapeutic approaches, which may be considered, include mainly dietary and life-style modifications, selective use of some technical components of dialysis systems, and the judicious prescriptions of lipid-lowering drugs.
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PMID:[Lipoprotein disorders in chronic kidney failure, nephrotic syndrome and dialysis]. 1267 79

Cardiovascular (CV) disease in uremic patients is a major concern to the nephrologist because it represents the main cause of morbidity and mortality in chronic renal failure patients, both predialysis and while on dialysis therapy. CV mortality is 3 to 20 times higher in dialysis patients than in the general population at similar age. Of note, a high prevalence of CV comorbidity is already present at start of maintenance dialysis, and is predictive of subsequent mortality on dialysis. CV disease progresses over years prior to the onset of ESRD, because risk factors develop from the early stage of chronic renal insufficiency. However, CV disease may be prevented or attenuated in patients who benefit from early, regular care of CV risk factors. Mechanisms of uremic cardiopathy, the major cause of mortality in uremic patients, are multifactorial and their effects are cumulative. Risk factors for left ventricular hypertrophy are hypertension, anemia, fluid overload and arteriosclosis, all of which are amendable by therapy. Risk factors for accelerated atherosclerosis, responsible for ischemic cardiopathy and myocardial infarction, are both common factors (e.g., hypertension, tobacco smoking and diabetes) and factors more specific for the uremic state (e.g., dyslipidemia, hyperhomocysteinemia and oxidative stress), all of which also are amendable by proper therapy. As a result, mixed hypertensive and ischemic cardiomyopathy develops, ultimately leading to cardiac failure, together with accidents resulting from valvular and arterial calcifications (favored by calcium-phosphate disorders), and from occlusion of coronary, cerebral and peripheral arteries. Cardioprotective therapy thus has become a cornerstone in the management of chronic renal failure patients, in conjunction with renoprotective therapy. Cardioprotective strategy involves optimal treatment of hypertension, anemia, fluid overload, dyslipidemia, hyperhomocysteinemia and calcium-phosphate disorders, and smoking cessation. To achieve a maximal efficacy, such treatment has to be initiated as early as possible in the course of renal failure. Because of its complexity, the integrated combined nephrotective and cardioprotective therapy requires early and sustained guidance by a nephrologist throughout the whole predialysis period.
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PMID:[Cardioprotection: an essential component for predialysis chronic renal failure treatment]. 1272 13

Hyperhomocysteinemia is widely recognised as an emerging risk factor of endothelial dysfunction and vascular damage. In this study we wanted to verify if it, when associated to arterial hypertension--traditional risk factor--represents a higher added risk of organ damage during menopause, which is a condition connected to a higher incidence of cerebrovascular diseases. A survey of 30 postmenopausal women with similar characteristics (BMI, age, absence of relevant pathologies such as diabetes, metabolic disorders and absence of smoking) was selected (menopause had occurred from 12 to 16 months at the moment of observation). At the moment of the observation they had not gone through any continuous pharmacological therapy. They were subdivided into 3 groups: normotensive; hypertensive (with 2nd degree hypertension: mild to moderate) without organ damage; hypertensive with organ damage (TIA, ischaemic heart disease, etc.). The carotid IMT, measured with ultrasound method, was considered as an organ damage parameter. 43% of the patients had high levels of homocysteine (> 15 micromol/l), which are levels considered at risk in other surveys. The highest levels of homocysteine were recorded in hypertensive women with episodes of acute cerebrovascular damage (micromol/l = 24.3 +/- 8.9). In this group, a positive correlation (r = 0.7) was obtained between homocysteine levels and carotid IMT. The possible coexistence of hyperhomocysteinemia and arterial hypertension, even though without particularly high values for both of them, in menopause may represent a dangerous association responsible for a significant organ damage and, therefore, for acute cerebrovascular events.
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PMID:Hyperhomocysteinemia in menopausal hypertension: an added risk factor and a dangerous association for organ damage. 1272 36

Patients with end-stage renal disease face a particularly high risk of cardiovascular disease and total mortality. Part of their increased risk is due to a higher prevalence of established risk factors, such as arterial hypertension, diabetes, smoking, and anemia. Hypertension and diabetes have a very high prevalence in dialysis patients and play a major role in their high mortality and morbidity. Hyperparathyroidism, hyperhomocysteinemia and disordered lipid metabolism represent factors that are peculiarly altered by the uremic state. Inflammatory processes, high sympathetic activity, and the accumulation of an endogenous inhibitor of NO synthase (ADMA), have recently emerged as cardiovascular risk factors of paramount importance. Sleep apnea has been linked with nocturnal hypertension and could be implicated in the high prevalence of concentric hypertrophy of the left ventricle in these patients. Hypertension control, as well as appropriate treatment of anemia and cessation of smoking, constitutes a fundamental area of intervention in dialysis patients. It appears possible that, in the near future, control of chronic inflammatory processes of high sympathetic activity and endothelial dysfunction will further help to curb the exceedingly high cardiovascular mortality of patients on chronic dialysis treatment.
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PMID:Traditional and emerging cardiovascular risk factors in end-stage renal disease. 1275 78

Vascular dementia (VaD) is the second-most-common cause of dementia in the elderly, after Alzheimer's disease (AD). VaD is defined as loss of cognitive function resulting from ischemic, hypoperfusive, or hemorrhagic brain lesions due to cerebrovascular disease or cardiovascular pathology. Diagnosis requires the following criteria: cognitive loss, often predominantly subcortical; vascular brain lesions demonstrated by imaging; a temporal link between stroke and dementia; and exclusion of other causes of dementia. Poststroke VaD may be caused by large-vessel disease with multiple strokes (multiinfarct dementia) or by a single stroke (strategic stroke VaD). A common form is subcortical ischemic VaD caused by small-vessel occlusions with multiple lacunas and by hypoperfusive lesions resulting from stenosis of medullary arterioles, as in Binswanger's disease. Unlike with AD, in VaD, executive dysfunction is commonly seen, but memory impairment is mild or may not even be present. The cholinesterase inhibitors used for AD are also useful in VaD. Prevention strategies should focus on reduction of stroke and cardiovascular disease, with attention to control of risk factors such as hypertension, diabetes mellitus, hypercholesterolemia, and hyperhomocysteinemia.
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PMID:Vascular dementia: distinguishing characteristics, treatment, and prevention. 1280 86

Most cross-sectional and case-control studies indicate that an increased plasma total homocysteine (tHcy) level is an independent risk factor for coronary artery disease (CAD). However, this is still a controversial issue. Recently, it was reported that the level of tHcy is related to the extent and severity of CAD. This study was designed to investigate the relationship between plasma tHcy levels and the presence, extent, and severity of CAD. Three hundred and forty-one patients who underwent coronary angiography were included in the study. Of these patients, 195 had CAD and 146 had normal coronary arteries (control group). The mean tHcy level was found to be higher in patients with significant CAD (16.4 +/- 7.4 micromol/L vs 13.2 +/- 3.6 micromol/L, P < 0.001). This group also had a higher rate of hyperhomocysteinemia (HHcy) (22.6% vs 5.5%, P < 0.001). There were positive relationships between tHcy levels and male gender (P = 0.03, r = 0.16), smoking (P < 0.001, r = 0.19), hyperlipidemia (P = 0.006, r = 0.15), and hypertension (P < 0.001, r = 0.20). Using regression analysis HHcy was determined to be an independent risk factor for CAD (OR = 3.69, CI 95% 1.51-9.06, P = 0.004). However, HHcy was not an independent risk factor in patients with low cardiovascular risk profiles. There was no relationship between the level of tHcy and the severity, extent, and vessel scores of CAD. On the other hand, age and diabetes mellitus were related with all scores of CAD. In conclusion, although hyperhomocysteinemia is an independent risk factor for CAD in our region, it appears to be unrelated to the extent and severity of the disease.
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PMID:The effects of hyperhomocysteinemia on the presence, extent, and severity of coronary artery disease. 1282 3

Morbidity and mortality from diabetes mellitus remain high despite managing the traditional risk factors. Recent data imply that the pathophysiology of macrovascular and microvascular complications involve other factors. The metabolic syndrome precedes the onset of type 2 diabetes by many years. Early treatment of individuals with this syndrome might delay the onset of diabetes and its complications. Endothelial dysfunction, subclinical inflammation and impaired fibrinolysis may contribute to progression of macrovascular as well as microvascular complications. The roles of infection and hyperhomocysteinemia are less clear but may be significant. This review discusses the current knowledge on these "non-traditional" risk factors and therapies to improve them.
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PMID:Novel cardiovascular risk factors and macrovascular and microvascular complications of diabetes. 1286 62

Development of dementia depends on genetic susceptibility and on risk factors accessible to primary prevention. Among the latter, vascular risk factors are well defined: prevention of hyperhomocysteinemia, diabetes mellitus, hypercholesterolemia, and, to some extent, of arterial hypertension could avoid the cognitive decline of dementia. Estrogen replacement therapy, antiinflammatory drugs, alcohol, vitamin E and intellectual activities seem efficacious in term of primary prevention. When dementia is present, only vitamin E, selegiline and some antiinflammatory drugs have proved efficacy compared to placebo to slow the cognitive decline. Long-term effects of cholinesterase inhibitors need to be investigated in future trials.
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PMID:[Prevention of dementia: is it possible?]. 1286 24

Hyperhomocysteinemia is considered one of the emerging risk factors for the development of coronary artery disease (CAD). In order to know the prevalence of this metabolic disorder in a Mexican population with early CAD (< 50 years), we studied a group of these patients and compared the levels of homocysteine with a group of patients, paired by age and gender, without angiographic evidence of coronary atherosclerosis. Preliminary results show that the population with early CAD has more traditional risk factors, specially diabetes mellitus, and higher levels of homocysteine in plasma. Moreover there is a genetic factor with higher incidence of a TT homozygotic mutation of the MTHFR that increases homocysteine because of an altered folate metabolism.
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PMID:[Hyperhomocysteinemia as risk factor in a Mexican population]. 1296 56


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