Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, we have measured plasma glucose and insulin levels at fasting and following an oral glucose load (75g) in 39 non-diabetic subjects (22 untreated hypertensive, 17 normotensive subjects). We also assessed plasma cholesterol (Ch), triglyceride (TG) levels and Na(+)-K(+)-pump activity in the membranes of their erythrocytes. Overall, hypertensive subjects have hypercholesterol, hypertriglyceride, glucose intolerance and hyperinsulinemia. These changes accorded with Syndrome X proposed by Reaven. In multivariant analysis, after correcting for age, BMI, diastolic pressure (DBP) was positively related to fasting, 1/2h insulin and insulin area under cure (AUC) (P < 0.05). Both systolic pressure (SBP) and DBP were negatively correlated to Na(+)-K(+)-pump (P < 0.01, 0.001), while Na(+)-K(+)-pump was negatively fasting, 1/2h, 1h, 2h insulin levels and insulin AUC (P < 0.05, 0.05, 0.01, 0.01, respectively). These results showed that insulin may affect Na(+)-K(+)-pump activity to develop hypertension independent of age and obese. We also postulated that insulin resistance was causal in the syndrome X, also one of factors developing coronary artery disease.
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PMID:[Insulin resistance and hypertension]. 780 25

A 60-year-old man was admitted to the Kyushu University Hospital because of poor glycemic control of diabetes mellitus. Although he had been treated with glicrazide and nifedipine for his diabetes and hypertension, the controls of the diseases were unsatisfactory. Plasma triglyceride level was 186 mg/dl. Furthermore, extreme insulin resistance was found by measuring glucose infusion rate with an euglycemic hyperinsulinemic clamp method. These findings were compatible to those seen in syndrome X. After admission, diet therapy of 1,800 Cal was started and his metabolic disorders such as hyperglycemia, hyperlipidemia, and hypertension were all improved. Moreover, euglycemic hyperinsulinemic clamp study also revealed a decreased insulin resistance after diet therapy. Our experience from the case suggested that insulin resistance may closely related with the metabolic disorders of the disease "syndrome X".
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PMID:[A case of syndrome X whose hyperglycemia, hyperlipidemia and hypertension were improved as accompanying with decreased insulin resistance]. 785 34

Metformin is a biguanide antidiabetic medication, that has been in use for over 30 years. Its mechanism of action, unknown until a few years ago, is now linked to an improved peripheral sensitivity to insulin, through a stimulated tissue glucose uptake by a transporter linked system. Interest in metformin has been revived by the recent observation of a specific activity of this agent on some of the major traits of the so called 'polymetabolic syndrome' (or 'syndrome X'), characterized by: insulin resistance, hypertriglyceridemia, hypertension and reduced fibrinolytic activity. Metformin, in studies examining one or more of these, has been shown, possibly through its peripheral insulin sensitizing mechanism, to correct most of the major symptoms characterizing this insulin resistance syndrome. Metformin, similarly to the other biguanide phenformin, has been rated as potentially dangerous, because of the possible induction of lactic acidosis, in some cases with a fatal outcome. Metformin is, however, associated with a very low incidence of lactic acidosis because, differently from phenformin, it does not undergo liver metabolism and, as a consequence, there are no high-risk groups, displaying an impaired metabolic handling. In this review, in addition to an overall evaluation of the more recent data on the mechanism of action and clinical use of metformin, a detailed clinical analysis of all published cases of lactic acidosis is provided. These data indicate that the risk in metformin use is negligible, provided that care is taken when prescribing the drug to patients with suspected clinical risks of lactic acidosis.
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PMID:Re-evaluation of a biguanide, metformin: mechanism of action and tolerability. 786 18

Recent epidemiologic studies in the United Kingdom have led to the hypothesis that adverse nutritional experiences in utero have a powerful influence on the development of degenerative diseases in adulthood. Poor fetal growth as measured by weight, length, head, chest, and abdominal circumferences is a strong predictor of hypertension, diabetes, hyperlipidemia, alteration in clotting factors, Syndrome X,* and mortality from cardiovascular and chronic obstructive airways disease. The theory of fetal origins of adult disease proposes that early defects in the development, structure, and function of organs lead to a programmed susceptibility, which interacts with later diet and environmental stresses to cause overt disease many decades after the original insult.
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PMID:Maternal and fetal determinants of adult diseases. 789 83

Obesity frequently clusters with hypertension, hyperlipidemia, non-insulin-dependent diabetes mellitus, and ischemic heart disease with hyperinsulinemia as syndrome X. Although central obesity has been recognized to have a strong genetic component, few candidate genes have been studied in this disorder. After a recently described association between the apolipoprotein-D (Apo-D) gene polymorphism and non-insulin-dependent diabetes mellitus by our group, we have now looked at a TaqI polymorphism of the Apo-D gene in two other components of syndrome X, namely obesity and hyperinsulinemia. Apo-D genotype differences were found between obese subjects (n = 57) and slim controls (n = 57; P = 0.006). Furthermore, in the obese group an association was found between the Apo-D genotype and fasting insulin (P < 0.001). Preliminary evidence, therefore, suggests that the TaqI Apo-D polymorphism can be used as a genetic marker for obesity and several components of syndrome X.
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PMID:Apolipoprotein-D polymorphism: a genetic marker for obesity and hyperinsulinemia. 791 35

The relationship of dyslipidemia, particularly hypercholesterolemia to coronary heart disease is now well established. Although ischemic heart disease and stroke share many of the same risk factors, the relationship of cholesterol to stroke remains controversial. The 6-year and 12-year follow-up of the MRFIT study showed that elevated cholesterol significantly increased the risk for fatal nonhemorrhagic stroke. Atkins found no evidence that lowering plasma cholesterol influenced the incidence of fatal or nonfatal stroke and regression analysis showed no statistical association between the magnitude of cholesterol reduction and the risk for fatal stroke. We cannot preclude the possibility that more effective cholesterol lowering over a longer period of time might be effective. Hypertension is the most powerful risk factor for stroke. The San Antonio Heart Study reported a clustering of cardiovascular risk factors in individuals who developed hypertension during an eight-year follow-up period (higher levels of BP, fasting TC and LDLC, TG, glucose and insulin, and BMI, less favourable fat deposition, and lower HDL). Insulin resistance may be the unifying factor that results in those phenomena, the so-called syndrome X. The important factor underlying syndrome X may be central or visceral obesity, suggesting that maintenance or attainment of ideal weight would be a powerful preventive factor against both CHD and nonhemorrhagic stroke. There is evidence from the Treatment of Mild Hypertension Study that nutritional/hygienic measures can reduce the syndrome X risk factors and hence the risk of coronary heart disease and stroke.
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PMID:Dyslipidemia and metabolic factors in the genesis of heart attack and stroke. 791 92

The aim of this study is to try to evaluate the relationship between arterial hypertension and ischemic heart disease (IHD) in the light of the physiopathologic response pattern to the dipyridamole echocardiography test (DET) in hypertensive patients, in pharmacologic washout, without any electrocardiographic ST segment depression during exercise tests or at rest. Sixty patients affected by mild to moderate asymptomatic essential arterial hypertension were studied: the subjects had a sitting diastolic blood pressure > or = 95 < or = 114 mmHg; there were 38 men and 22 women with a mean age of 49.8 +/- 7.6 years (range twenty-nine to sixty-eight). All patients had undergone high-dose DET (0.84 mg/kg in ten minutes). No patients developed side effects or asynergy in cardiac contractility during the test. In the absence of any significant coronary artery obstruction assessed angiographically, 18 patients (30%) showed ST segment depression > 1.0 mV during DET, sometimes with the presence of ventricular and/or supraventricular extrasystoles. In this group of patients the left ventricular mass index (LVMI) and duration of hypertension (in months) were higher as compared with those of the other 42 patients (respectively: 160.2 +/- 5.1 vs 129.2 +/- 9.2 g/m2, P < 0.02; and 30 +/- 4.8 vs 9 +/- 5.4 months, P < 0.007). In conclusion it is reasonable to speculate from these data that the ischemic-like" dipyridamole-induced ST segment depression, like that shown by patients affected by Syndrome X, might involve a worse prognosis in hypertensive patients. This may be because of increased coronary resistance due to structural modification or anatomic background.
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PMID:Hypertension and ischemic heart disease. Role of dipyridamole echocardiography test. 797 8

Several studies have shown evidence of the key role of the endothelium in modulating the tone of epicardial coronary vessels, in the different manifestations of coronary artery disease. Recently, the role of endothelium-dependent vasodilation has been focused, because clinical observations have suggested that myocardial ischemia might be caused or aggravated by inappropriate vasoconstriction of resistance vessels. An abnormal endothelium-dependent vasodilation, either of epicardial and of coronary microvasculature, has been documented in patients with syndrome X and in patients with history of hypertension and left ventricular hypertrophy. Vasoconstriction of the small coronary vessels is probably the mechanism underlying the impaired increase of coronary blood flow during atrial pacing and the wide variations of the ischemic threshold in some patients with chronic stable angina. In patients with variant angina, the endothelial function seems abnormal only in the conductance vessels. It is likely that the endothelial dysfunction of the small coronary arteries be present in many clinical situations in which a discrepancy between a mild atherosclerosis of epicardial coronary artery and signs of ischemia exists, as it has been observed early after successful angioplasty and after coronary artery reperfusion during acute myocardial infarction.
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PMID:[Endothelial dysfunction in ischemic syndromes]. 802 14

The review summarizes data about interconnection between atherosclerosis and diabetes mellitus. Special attention is paid to their joint developmental factors such as hyperinsulinemia and insulin resistance. It is shown that hyperinsulinemia may form an independent risk factor. At the same time both factors can lead (during both diabetes mellitus and atherosclerosis) to changes in lipid metabolism and development of atheroms. Mechanisms of the development of insulin resistance and hyperinsulinemia are analyzed. The so-called syndrome X is described in detail. It is characterized by a triad of changes: insulin resistance and hyperinsulinemia, changes in lipid metabolism and hypertension. Some methods of treatment of insulin resistance and hyperinsulinemia during atherosclerosis and diabetes mellitus are described.
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PMID:[Pathogenesis of atherosclerosis in diabetes mellitus. The role of insulin resistance and hyperinsulinemia]. 804 24

Due to high uric acid clearance, which occurs prior to puberty, hyperuricosuria rather than hyperuricemia may be the only clue to diagnosis of purine overproduction in children who have enzymatic defects or who develop the condition in the course of treatment of malignancies. The probable inclusion of hyperuricemia as a part of syndrome X associated with insulin resistance may help in understanding its clinical associations, including coronary artery disease. Gout, hypertension, and lead often go together; thus, perhaps we should check for lead toxicity routinely in this setting. Asymptomatic joints of patients with gout contain monosodium urate crystals, and research on the factors that determine the occurrence of clinical inflammation in this setting continues as an area of current interest. Coating of the crystals by different proteins may modify their inflammatory potential and may be an important modulating mechanism.
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PMID:Hyperuricemia and gout. 806 19


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