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

To evaluate the risk factors for diabetes mellitus, I examined 2573 people (1851 males and 722 females) who received medical checkups more than twice at a health examination center in Tokyo during the period from 1976 through 1991. Diabetic patients were excluded at the beginning. The mean follow up duration was 5.2 years. A self-registering questionnaire was administered at the time of the health checkup. The standard of this study was the onset of diabetes mellitus or glucose intolerance (fasting blood sugar over 110 mg/dl). I compared two prognosis groups (a normal group and a diabetic group) in terms of age, examination findings and prevalence of health risks (lifestyle, stress and working form). I also assessed family history of diabetes and past history including hypertension, hepercholesterolemia and hyperuricemia. After assessing each variable, I employed Cox's proportional hazards model analysis. 1) Among the subjects, 296 persons (243/1851 [13.1%] males, and 53/722 [7.3%] females) were newly diagnosed with diabetes during the observation period. 2) The diabetic group had significant differences compared to the normal group in age, BMI (Body Mass Index), FBS (fasting blood sugar), smoking, drinking, eating no breakfast, dairy intake, hypertension, hypercholesterolemia, hyperuricemia, and family history by t-test and chi 2 test. 3) According to proportional hazards model analysis, FBS, age, family history, hypertension, smoking and BMI were selected as significant risk factors for diabetes in males. For females, breakfast, FBS, age, drinking and hypertension were selected. 4) Diabetes seemed to be related to fixed factors such as age, or genetic factors such as family history and FBS in males. For females, lifestyle, such as eating no breakfast and drinking habit played an important role.
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PMID:[Risk factors for diabetes mellitus evaluated by long-term observation]. 858 85

Clustering of elevated triglycerides, decreased high-density lipoprotein cholesterol (HDL-C), hyperuricemia, diabetes, and hypertension has been related to insulin resistance/high insulin levels and central and/or overall obesity. The extent to which these abnormalities cluster and whether hyperinsulinemia, central adiposity, and overall obesity each independently associate with this clustering were evaluated in 14,481 US whites and African-Americans 45 to 64 years of age. With the exception of hypertension, abnormalities rarely existed in isolated form. Clustering greatly exceeded chance association (P < .001). Although this clustering was greater in relative terms (ratio of observed to expected cluster frequency) in the lean and less centrally obese, it was greater in absolute terms (observed minus expected cluster frequency as a percent of total population) in the more centrally and more generally obese. The greatest excesses were found for clusters that included both hypertriglyceridemia and low HDL-C. Multiple logistic regression models showed strong and independent graded relationships of clusters with quintiles of fasting insulin (fifth quintile odds ratio, 10 to 54, P < .001) and to a lesser degree with quintiles of the waist to hip ratio (2.2 to 5.4, P < .001 for most) and of body mass index (1.6 to 4.5, P < .05 for most). In conclusion, all abnormalities cluster in excess of that predicted by chance, with clusters showing remarkable and graded independent associations with fasting hyperinsulinemia and to a lesser extent with central and overall obesity. Thus, a metabolic syndrome occurs in both lean and obese middle-aged US adults.
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PMID:Clustering of dyslipidemia, hyperuricemia, diabetes, and hypertension and its association with fasting insulin and central and overall obesity in a general population. Atherosclerosis Risk in Communities Study Investigators. 863 43

Secondary hyperlipoproteinemias are found in connection with other primary organic diseases. Typical examples are those seen with diabetes mellitus, liver and kidney diseases. In addition there are changes induced by hormonal dysfunctions such as hypothyroidism, by the use of oral contraceptives or in postmenopausal women. During pregnancy there is a physiological transient increase in lipoproteins. In addition to primary organic diseases there are a number of exogenous factors such as obesity, malnutrition and alcohol abuse causing hyperlipidemia. The relation between hypertension and hyperlipidemia described as familial dyslipidemic hypertension is less well known. Obesity, hypertension, dyslipidemia, hyperuricemia and impaired glucose tolerance are the basic conditions of the metabolic syndrome. Familial combined hyperlipidemia is a genetically determined, dyslipidemic syndrome with a high prevalence among patients with coronary artery disease and stroke. As there are some links between familial combined hyperlipidemia and secondary hyperlipoproteinemias, this disease entity is discussed together in this paper. Familial combined hyperlipidemia is metabolically, genetically and by this on a molecular level closely linked to familial dyslipidemic hypertension as well as the metabolic syndrome. The exact mechanism of this disease is currently unknown.
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PMID:[Secondary disorders of lipid metabolism, metabolic syndrome and familial combined hyperlipidemia]. 865 Sep 33

Because little is known about disordered metabolism of uric acid as a pathogenetic mechanism of renal damage in non-insulin-dependent diabetes mellitus (NIDDM) it was studied in 75 NIDDM and 48 IDDM patients. Clinical examination of the patients included evaluation of purin metabolism according to serum uric acid, diurnal urine excretion, uric acid clearance. Hyperuricemia occurred more frequently in NIDDM. Positive correlation was observed between hyperuricosuria and the severity of diabetic nephropathy which was more pronounced in IDDM.
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PMID:[Kidney lesions in non-insulin dependent diabetes mellitus]. 869 71

We report a 3 year survey concerning diabetes associated with hypertension in 260 diabetic patients at Ouagadougou. This association has been found in 29% of the cases. The patients were male subjects for 57% of them and seventy one more 50 years old. Other vascular risk factors have been observed: obesity (53%), smoking (15%), hyperuricemia (23%). Hypercholesterolemia and hypertriglyceridemia were observed respectively in 1% and 1.3% of the cases. Many complications arised during the survey: retinopathy in 51% of the patients, nephropathy for 35% and 12% with renal failure, macroangiopathy in 55% of the patients. The treatment was based on diuretics and calcic inhibitors. The results on the control of blood pressure were excellent but the high cost of this management is an important restrictive factor.
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PMID:[Arterial hypertension and diabetes in Ouagadougou (Burkina Faso)]. 876 55

The study purpose was to determine the following in a large sample of hospitalized patients: (1) the prevalence of hyperuricemia, (2) the association of hyperuricemia with other metabolic disorders, and (3) the factors independently predicting hyperuricemia. Five hundred adult patients (250 men and 250 women) were randomly selected from those admitted as inpatients over a period of 5 months. In all patients, body mass index (BMI), blood pressure, and serum glucose, lipid, creatinine, urea nitrogen, and urate concentrations were measured. The presence of diseases or use of medications known to affect serum urate levels were recorded. The mean level of serum urate was 5.6 mg/dL in the whole sample, 6.0 mg/dL in men and 5.3 mg/dL in women (P = .003, men v women). The prevalence of hyperuricemia was 27.6% (28.8% and 26.4% in men v women, P = nonsignificant). A definite or probable secondary hyperuricemia was found in 87.7% of the subjects. Hyperuricemia was rarely isolated (21%), whereas it was frequently associated with hypertension (60.1%), hyperlipidemia (31.2%), diabetes (28.3%), and obesity (21.7%). In 26.8% of the subjects, hyperuricemia was associated with two metabolic disorders, in 13.8% with three, and in 2.9% with four. Multiple metabolic disorders (three to four) were found in 16.7% of subjects with hyperuricemia. Serum urate levels progressively increased across a range of subjects from those without diabetes, hyperlipidemia, hypertension, or obesity to those with one, two, or a greater number of associated metabolic abnormalities. Multiple stepwise regression analysis showed that 43% of serum urate variability was explained by urea nitrogen levels, triglyceride levels, diuretic therapy, the inverse of creatinine (as an index linearly related to creatinine clearance), and BMI. These results indicate that in hospitalized subjects, hyperuricemia is (1) frequent, (2) a secondary phenomenon in most cases, and (3) frequently associated with other metabolic disorders. The major predictors of high serum urate levels are BMI, triglycerides, parameters of renal function, and use of diuretics. These variables explain a large proportion of serum urate variability.
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PMID:Serum uric acid and related factors in 500 hospitalized subjects. 896 92

Most of the primates, unlike other mammals, have mutations in urate oxidase gene and cannot catabolize urate in the bodies. In addition to the genetic defects, some human subjects have various abnormalities in urate metabolism. Urate metabolism abnormalities are classified into two categories, hyperuricemia and hypouricemia. Usually, the urate pool size of an adult male is about 1,200 mg, and 700 mg urate is produced daily. The production is balanced by the excretion of urate into urine (500 mg) and intestine (200 mg). If this balance is disturbed, either hyperuricemia or hypouricemia occurs. According to the mechanisms, hyperuricemia is classified into overproduction and underexcretion, and hypouricemia into underproduction and overexcretion. Overproduction of ruate is caused by PRPP synthetase superactivity, HPRT deficiency, leukemia and alcohol ingestion. Underexcretion of urate is caused by renal insufficiency and treatment by diuretics. Underproduction of urate is caused by xanthine dehydrogenase deficiency, purine nucleoside deficiency and allopurinol treatment. Overexcretion of urine is caused by familial renal hypouricemia, Fanconi's syndrome, diabetes mellitus and treatments with benzbromarone and probenecid. All of these conditions are classified, according to other aspects, into primary and secondary, and genetic and non-genetic abnormalities.
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PMID:[Abnormalities in urate metabolism: concept and classification]. 897 99

Characteristic feature of pathogenesis, epidemiology and laboratory findings in hyperuricemia of gouty patients are studied and reasonable treatments of gout in clinical medicine are discussed. Gout is characterized by repeated arthritis attacks on the metacarpophalangeal joint of the first toe or other small joints, especially overworked joints or those exposed to cold. The arthritis attack lasts for 3.5 days and then diminishes gradually. The intervals are shortened in patients under poor hyperuricemic control but tophi formation is less frequent. Complications in combination with hyperlipidemia, diabetes mellitus, obesity and hypertension, which are compatible to syndrome X, are frequent in gouty patients and are suspected of rapidly progressing to arteriosclerosis, such as ischemic heart diseases. Hyperuricemia consists of over-production and underexcretion, which can be diagnosed by the urate clearance test. Classification is valuable for surveying the underlying diseases of secondary hyperuricemia and treating gouty patients. Underexcretion was observed in 85% of gouty patients with hyperuricemia and even the mean urate clearance in the overproduction type was significantly lower than that of normal controls, suggesting that underexcretion is a fundamental phenomenon in all gouty patients. Treatments of complications as well as those of hyperuricemia with uricosuric agents are required for clinical treatment of gouty patients.
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PMID:[Characteristic features of gouty patients]. 897

A group of metabolic disorders including insulin resistance and hyperinsulinemia, impaired glucose tolerance, visceral obesity, hypertension, dyslipidemia, hyperuricemia, hypercoagulability and microalbuminuria determine the risk for the development of atherosclerosis, coronary artery disease and cerebral vascular disorders. Although available studies on the pathogenesis of the metabolic syndrome are equivocal, it is most frequently hypothesized that hereditary of insulin resistance leads to the remaining metabolic disorders including diabetes mellitus, atherosclerosis and coronary artery disease. Despite pathogenetic controversies, there are convincing arguments for the diagnosis of the metabolic syndrome and search for therapy improving insulin sensitivity and reducing hyperinsulinemia thus preventing the development of diabetes mellitus and coronary artery disease.
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PMID:[Insulin resistance and hyperinsulinemia--clinical aspects]. 899 30

It has been suggested that impaired fibrinolytic-coagulation system, such as increased concentration of inhibitors to fibrinolysis or activators to coagulations, occasionally may play a role in the development of atherosclerotic vascular disease. In this study, we aimed to elucidate the relationship of serum lipids to fibrinolytic-coagulation system. The subjects studied were 190 outpatients at Kyorin University Hospital, 108 of whom were mostly hypertension, diabetes mellitus and hyperuricemia (Control), 59 of whom were coronary heart disease (CHD), 25 of whom were cerebrovascular disease (CVD). Blood samples were measured the levels of blood coagulation factors VII (F-VII) and X (F-X), and plasminogen activator inhibitor-1 (PAI-1) in these subjects, together with the concentrations of serum lipids. The serum levels of F-X was significantly higher in CHD subjects than in controls (111 +/- 19% vs 101 +/- 22%, p < 0.05). However, there was a no significant difference of F-VII among three groups. And we found that the levels of serum lipids, especially serum triglycerides showed a significant positive correlation between the concentrations of F-VII (r = 0.343, p < 0.01) and F-X (r = 0.513, p < 0.01), and PAI-1 (r = 0.528, p < 0.001) in CHD and CVD subjects. For this reason, 156 bank employee subjects were also admitted to this study (Bank employees). In bank employee subjects, the serum levels of triglycerides also showed a significant positive correlation with the levels of F-VII (r = 0.321, p < 0.001), F-X (r = 0.254, p < 0.001) and PAI-1 (r = 0.420, p < 0.001). These data suggest that serum lipids, particularly triglycerides have a close relationship with thrombogenesis as evidenced by activated F-VII and F-X in the extrinsic coagulation system and also by elevated PAI-1 activities in fibrinolysis. Therefore, when we try to prevent the patients from CHD or treat them, we ought pay attentions not only to serum cholesterol or LDL-cholesterol for their atherogenic actions, but also to triglycerides because of their close correlation with extrinsic coagulation system and anti-fibrinolytic activities. The reduction of fibrinolytic capacity due to increased plasma levels of F-VII, X and PAI-1 may have importance in atherosclerotic vascular disease, particularly in patients with hypertriglyceridemia.
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PMID:Serum triglycerides and blood coagulation factors VII and X, and plasminogen activator inhibitor-1. 922 31


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