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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A forty-two years old male underwent an aortic arch replacement for an emergency treatment of dissecting aortic aneurysm (DeBakey type I). Separate cardiopulmonary bypass was used with main arterial inflow cannula inserted to right femoral artery. After the operation, ischemia of the right lower extremity led to acute renal failure due to myonephropathic-metabolic syndrome. Peritoneal dialysis, hemodialysis, and continuous arterio-venous hemofiltration were performed. Renal failure improved gradually. At the diuretic phase serum calcium concentration began to rise. Inspite of large amount of fluid and furosemide injection it became higher and finally reached to 20 mg/dl level. Calcitonin injection (320 mu/day) was very effective. In 2 months after surgery serum creatinine and calcium concentrations went down to normal range. Abnormalities in calcium metabolism are frequent in rhabdomyolysis-induced acute renal failure. However, it is rare to encounter such a remarkable hypercalcemia as seen in this patient. When treating MNMS we should pay attention to the changes of serum calcium concentration.
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PMID:[Dissecting aortic aneurysm associated with myonephropathic-metabolic syndrome and hypercalcemia]. 202 21

This retrospective study of 279 embolectomies in 252 patients shows a mortality of 27%, and an amputation rate of 15% within the first month after the embolectomy. The mortality as well as the rate of amputations decreased through the first year. After this period the mortality was comparable to that of a normal population and the rate of amputation was negligible. The mortality rate as well as the number of amputations increased with increasing time-lag of the embolectomy. In addition, the rate of amputation increased with preexisting intermittent claudication. There was no significant difference in amputation rate between limbs with and without palpable pulsations in the groin on admission, but 8 out of 103 limbs without groin pulsations had successful major vascular reconstruction performed after failing embolectomy in contrast to none in the group where pulsations were present. In 28 patients the embolectomy was followed by impairment of renal function and 14 of these died. It is concluded that embolectomy must be performed as early as possible, vascular reconstruction must be considered if the embolectomy fails to revascularize the limb, preventive measures should be taken against renal failure, i.e. the myonephropathic-metabolic syndrome.
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PMID:Arterial embolism of the legs. A follow-up study of 252 patients. 406 15

Myonephropathic metabolic syndrome (MNMS) is a serious muscle reperfusion injury associated with acute renal failure. The exact pathogenesis of MNMS has not been fully elucidated, nor effective treatment, through the renal failure is thought to be a consequence of rhabdomyolysis. In the present study, the possible involvement of calpain in the lysis was investigated in a MNMS animal model employing a cell permeable calpain antagonist calpeptin. Male rabbits were subjected to bilateral hind leg ischaemia for 5 hours by clamping the distal aorta, followed by reperfusion for 3 hours. Blood pressure, plasma N-acethyl-beta-D-glucosaminidase (NAG) and the presence of myoglobinuria were serially determined. Blood pressure remained constant during the ischemic period but dropped by about 25% immediately after reperfusion. This was significantly attenuated by intraaortic administration of calpeptin. NAG gradually increased during ischemia and during reperfusion and this was also significantly reduced by calpeptin. Myoglobinuria appeared immediately after reperfusion, and was also attenuated by calpeptin. Calpeptin prevented lytic and degenerative changes of the hind leg muscles, determined by light and electron microscopy. Thus it is concluded that activation of calpain in skeletal muscle is an important etiologic factor of MNMS and that the occurrence of MNMS may be prevented by administration of a calpain antagonist.
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PMID:Involvement of calpain in myonephropathic metabolic syndrome (MNMS). 808 1

From January of 1987 to July of 1994, 83 patients with acute aortic dissection were treated at our institution. Of these, 7 patients (8%) sustained acute leg ischemia. Angiography showed that one patient had arterial occlusion at the abdominal aorta, three had occlusion at the right common iliac artery, and one had severe right common iliac artery stenosis. Four patients with acute type A dissection underwent emergency replacement of the aortic arch and/or ascending aorta. Three of them were discharged, but one patient died due to renal failure and multiple organ failure. In three patients with acute type B dissection, one with aortic rupture was successfully treated by replacement of the descending thoracic aorta; of the other two who received bypass operations for leg ischemia, one died due to myonephropathic metabolic syndrome and sepsis which were caused by a delay in surgery. In conclusion, emergency thoracic aortic repair should be performed in acute type A dissection with leg ischemia, whereas bypass operation for ischemic leg should be considered in patients of acute type B dissection with leg ischemia when they are not complicated with rupture or visceral ischemia.
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PMID:[Acute aortic dissection with leg ischemia]. 866 68

Mortality from coronary heart disease (CHD), stroke and end-stage renal failure are high in South Asian migrants in the UK. This is associated with high prevalence of diabetes and hypertension. These seem to be manifestations of a metabolic syndrome with insulin resistance (hyperinsulinaemia) and central obesity (based on high waist-to-hip ratio rather than on conventional measures of body mass index). This is associated with sedentary lifestyle, high serum triglycerides and low HDL-cholesterol. Mortality from stroke and end-stage renal failure are high in black migrants to the UK (both Caribbeans and West Africans). However, CHD mortality is low in this group. This pattern of mortality is associated with high prevalence of hypertension and diabetes. This group tends to be obese (particularly women) according to conventional measures of body mass index and to have hyperinsulinaemia, low serum triglycerides and high HDL-cholesterol. Conventional risk factors such as cigarette smoking and hypercholesterolaemia are less prevalent in ethnic minority populations in the United Kingdom and unlikely to explain the differences seen between groups, although each risk factor is likely to contribute to the variation in vascular disease within each group. There is difficulty in reconciling the results of migration studies (eg, from rural to urban environments) pointing to major environmental influences on the changes in cardiovascular risk factors with the consistent pattern of disease of ethnic groups across the world and in subsequent generations, suggesting a certain degree of genetic susceptibility. Important environment-gene interplays might be underlying some of these processes. The detection and management of hypertension and diabetes are still unsatisfactory in inner city areas and show variations by ethnic origin. Strategies for the control of CHD and stroke adopted in European countries directed mostly to white populations may be inappropriate for ethnic minority populations.
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PMID:Ethnicity and cardiovascular risk: variations in people of African ancestry and South Asian origin. 936 74

We review the progress in testing the thrifty phenotype hypothesis. Many human epidemiological studies both by ourselves and others have confirmed and extended the original observations on which the hypothesis was based. We are not aware of any contradictory findings and we emphasise the strength of the association between birth weight and the subsequent development of the metabolic syndrome. We have worked extensively experimentally to test the hypothesis in a rat model in which pregnant and/or lactating dams are fed a diet moderately restricted in proteins. The range of programming effects that we have discovered in this example of fetal and early postnatal growth restriction is listed and includes changes in hormone receptors, signalling molecules and regulatory enzymes. We have shown the model to develop diabetes, the metabolic syndrome and signs of premature renal failure. We summarise these and other similarities between the phenotype of this model and human Type 2 diabetes and the metabolic syndrome. The number of insults during early development which can lead to a similar outcome is discussed and the suggestion is made that the early life response to stress is limited in its flexibility with outcomes including ageing and decreased longevity. Our preliminary results indicate that some MODY genes could suggest pathways whereby the changes occur and that epigenetic changes during development are involved. We conclude that the way is now clear to discover early human markers of programming by early life growth restriction and to use these to devise strategies for the prevention of Type 2 diabetes.
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PMID:For debate: Fetal and early postnatal growth restriction lead to diabetes, the metabolic syndrome and renal failure. 1523 71

Hyperuricemia (HU) is present in 5-30% of the general population, although the prevalence is higher among some ethnic groups and seems to be increasing worldwide. Classically, chronic HU has been considered a risk factor for gout or lithiasis and is associated with alcoholism, obesity, hypertension, dyslipidemia, hyperglycemia/diabetes mellitus, renal failure and intake of certain drugs. HU is also associated with cardiovascular diseases such as hypertension, vascular disease, pre-eclampsia, pulmonary arterial hypertension, stroke, heart failure, ischemic heart disease and also metabolic syndrome, renal disease and increased mortality. It is uncertain if these associations are dependent or not, especially cardiovascular and renal diseases. Patients with chronic HU and also those with gout require both medical investigation for associated diseases or drugs as well as nutritional counseling and life-style changes. HU should alert physicians to possible complications.
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PMID:Primary prevention in rheumatology: the importance of hyperuricemia. 1512 Oct 34

About a third of new cases of renal failure in USA are attributed to hypertension despite controversy about the frequency and pathology of so called hypertensive nephrosclerosis. In spite of good documentation that obesity causes renal failure and in spite of the global epidemic of obesity this diagnosis does not feature on most renal failure registries. New documentation that progressive renal failure in hypertension is linked to insulin resistance and analysis of NHANES III data which shows a strong positive significant dose-response relationship between insulin resistance and chronic kidney disease strengthen the view that so called hypertensive nephrosclerosis may be linked more closely to obesity and insulin resistance than to blood pressure. The pathology of the kidney in hypertension has changed. Studies 50 years ago did not show segmental glomerulosclerosis, which has recently been shown to be the key lesion in hypertensive nephrosclerosis. Recent documentation that this is a major mechanism of progression in hypertension together with the fact that similar segmental glomerulosclerosis is the key lesion in obesity and the metabolic syndrome suggests that these factors are more important than hypertension in renal failure attributed to hypertensive nephrosclerosis.
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PMID:Hypothesis: obesity and the insulin resistance syndrome play a major role in end-stage renal failure attributed to hypertension and labelled 'hypertensive nephrosclerosis'. 1594 68

Homocysteine is an intermediate product in the methionine metabolism, which is catalysed by several enzymes with B2, B6, B12 vitamins and folic acid as cofactors. Moderate hyperhomocysteinemia, defined as total homocysteine concentration between 12 to 30 micromol/l, represents an independent risk factor for heart disease, vascular brain disease, phlebothrombosis and thromboembolic complications. It is related to placental abruptions, spina bifida and some neuropsychiatric disorders. Hyperhomocysteinemia is a metabolic syndrome based on interaction between genetic factors (most frequently 677C/T polymorphism of methylentetrahydrofolate reductase), diseases and demographic factors (smoking, aging, hormonal and nutritional factors). Moderate hyperhomocysteinemia occurs in about 20 to 30% of patients with clinical complications of atherosclerosis. Prospective and genetic studies have shown, that moderate hyperhomocysteinemia in healthy persons is only a weak predictor of cardiovascular diseases. Contrary to it, in patients with ischaemic heart disease, renal failure or diabetes mellitus and in thromboembolic disease, hyperhomocysteinemia represents a strong predictor of vascular morbidity and mortality. Toxic effects of hyperhomocysteinemia on the vascular wall can be explained by a chemical modification of lipoproteins and vascular structure, oxidative stress, endothelial dysfunction, inadequate endothelial cell regeneration, smooth muscle cell proliferation or by an accumulation of functionally non sufficient connective tissue. Also thrombogenic effects or an increased expression of cholesterol level controlling proteins and fatty acids in the liver can be considered. Treatment of hyperhomocysteinemia is based on the administration of pharmacological doses of folic acid, B6 and B12 vitamins, which can decrease total homocysteine concentration by 25 to 30%. Such decrease, which is in average 3 micromol/l, results in the decrease of relative risk of ischaemic heart disease by 11 to 16%, phlebothrombose by 25% and vascular brain diseases by 19 to 24%.
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PMID:[Consequences of moderate hyperhomocysteinemia in internal medicine]. 1530 62

Patients with end-stage renal disease have markedly increased risk for death from cardiovascular disease. Renal failure is associated with multiple metabolic and endocrinologic abnormalities, and these alterations are involved in advanced atherosclerosis and high cardiovascular risk. Increased insulin resistance index by homeostasis model assessment (HOMA-IR), a simple index of insulin resistance, was an independent predictor of cardiovascular mortality in nondiabetic patients on maintenance hemodialysis. Renal failure impairs lipoprotein metabolism leading to the atherogenic lipoprotein profile characterized by increased triglyceride-rich remnant lipoproteins such as intermediate-density lipoprotein, an independent factor of increased aortic stiffness. Non-high-density lipoprotein cholesterol, the sum of cholesterol of intermediate-density lipoprotein and other apoB-containing lipoproteins, is an independent factor associated with increased arterial thickness and a predictor of cardiovascular death in hemodialysis patients. The risk for cardiovascular death in hemodialysis patients is associated closely with hypertension and malnutrition, but not with obesity. The constellation of insulin resistance, dyslipidemia, hypertension, and malnutrition in renal failure suggests the presence of another type of metabolic syndrome promoting cardiovascular disease. In addition, vitamin D deficiency and abnormalities in calcium, phosphate, and parathyroid hormone levels increase the death risk from cardiovascular disease in renal failure. It is expected that treatment of these metabolic and endocrinologic alterations would improve the survival of patients with renal failure.
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PMID:Roles of metabolic and endocrinological alterations in atherosclerosis and cardiovascular disease in renal failure: another form of metabolic syndrome. 1549 Apr 3


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