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)

Turner syndrome afflicts approximately 50 per 100,000 females and is characterized by retarded growth, gonadal dysgenesis, and infertility. Much attention has been focused on growth and growth promoting therapies, while less is known about the natural course of the syndrome, especially in adulthood. We undertook this study to assess the incidence of diseases relevant in the study of Turner syndrome. The study period was from January 1, 1984 to December 31, 1993, and the study base was all women living in Denmark during the study period. We used data from the Danish Cytogenetic Central Register and the Danish National Registry of Patients to assess morbidity. This study supports several earlier studies reporting increased morbidity and confirms results of a recent study on cancer in Turner syndrome. Women with Turner syndrome seem to have an increased incidence of fractures, osteoporotic fractures in adulthood, and non-osteoporotic fractures in childhood. Furthermore, diabetes mellitus, both NIDDM and IDDM, was found with a markedly increased incidence in Turner syndrome, as well as ischemic heart disease, hypertension, and stroke. The risk of cancer, except cancer of the large bowel, does not seem to be elevated in Turner syndrome. Our data suggest that patients with Turner syndrome are extraordinarily prone to abnormalities constituting the metabolic syndrome (e.g., hypertension, dyslipidaemia, NIDDM, obesity, hyperinsulinemia and hyperuricemia). The present data may help to explain the decreased life span found in patients with Turner syndrome.
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PMID:Morbidity in Turner syndrome. 947 75

The reduction of coronary mortality is not as large as one would expect from the observed blood pressure lowering in trials of antihypertensive medications. This is not surprising; hypertension is a complex disease where the high blood pressure is only one of numerous coronary risk factors. Sympathetic overactivity in hypertension, independent of the blood pressure, may be conducive to premature atherosclerosis by inducing insulin resistance and dyslipidemia. Through its trophic effect on blood vessels, sympathetic overactivity potentiates vasoconstriction. This, in turn, accelerates hypertension and the metabolic syndrome. The hypertrophy of small coronary arterioles decreases the coronary reserve and enhances coronary spasms. Tachycardia, which is due to increased sympathetic tone and a decreased parasympathetic tone, favors arrhythmias and sudden death in congestive heart failure and hypertension. Increased hematocrit is frequently found in male patients with hypertension, and high hematocrit is a predictor of coronary heart disease/thrombosis. The increase of hematocrit is in part due to an alpha adrenergic postcapillary venoconstriction. Enhanced sympathetic drive, insulin resistance and dyslipidemia have been demonstrated also in congestive heart failure, but the clinical importance of these findings is not fully understood.
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PMID:Clinical consequences of the autonomic imbalance in hypertension and congestive heart failure. 954 Jan 30

Cardiovascular risk factors were compared between 126 people with non-insulin-dependent diabetes mellitus (NIDDM) and 530 non-diabetics (controls), in a random sample of people (Chinese, Malays, and Asian Indians) aged 40-69 years from the general population of Singapore. Data were adjusted for age and ethnicity. For both genders, people with NIDDM had higher mean body mass indices, waist-hip ratios and abdominal diameters. They also had a higher prevalence of hypertension, higher mean levels of fasting serum triglyceride, slightly lower mean levels of serum high-density-lipoprotein cholesterol, and higher mean levels of plasma plasminogen activator inhibitor-1 and tissue plasminogen activator (antigen). These factors are components of syndrome X (metabolic syndrome) and increase the risk of atherosclerosis and thrombosis. In contrast, there were no important differences for cigarette smoking, serum total and low-density-lipoprotein cholesterol, serum apolipoproteins A1 and B, plasma factor VIIc and plasma prothrombin fragment 1 + 2. Females with NIDDM, but not males, had a higher mean serum fibrinogen level than non-diabetics, which could explain why NIDDM has a greater cardiovascular effect in females than males. Serum lipoprotein(a) concentrations were lower in people with NIDDM. Mean levels of serum ferritin, a pro-oxidant, were higher in people with NIDDM than controls, but there were no important differences for plasma vitamins A, C and E, and serum selenium, which are anti-oxidants.
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PMID:Cardiovascular risk factors in non-insulin-dependent diabetics compared to non-diabetic controls: a population-based survey among Asians in Singapore. 954 28

Microalbuminuria is associated with increased morbidity and early mortality in non-insulin-dependent diabetes mellitus (NIDDM), mostly due to cardiovascular disease. This association may be due to a higher prevalence of known cardiovascular risk factors in those with microalbuminuria. We examined the relationship of microalbuminuria to components of the metabolic syndrome in 98 NIDDM patients with elevated urinary albumin excretion rate (UAER) (> 10.5 micrograms/min) (high UAER) and 102 normoalbuminuric NIDDM patients. Patients with high UAER were older than normoalbuminuric patients (P < 0.05), but they did not differ with respect to duration of diabetes, total cholesterol, body mass index (BMI) or the prevalence of smoking. A total of 58 (60%) patients with elevated UAER had two or more of hypertension, ischaemic heart disease (IHD), hypertriglyceridaemia and obesity compared with 41 (40%) in the normoalbuminuric group, (P < 0.05). Only nine (9.2%) high UAER patients had none of the above risk factors compared with 26 (25.5%) in the normoalbuminuric group (P < 0.01). The prevalence of hypertension (blood pressure (BP) > 160/95) was significantly higher in high UAER patients; 61/98 (62%) versus 39/102 (38%) in normoalbuminuric group, (P < 0.05). Elevated UAER was also associated with a higher risk of macrovascular disease (P < 0.01). The high UAER group included 50 Caucasian, 30 Asian and 18 Afro-Caribbean. The three groups did not differ with respect to total cholesterol, glycosylated haemoglobin (HbA1c) or prevalence of smoking. Asians had a lower BMI, a lower BP and a lower prevalence of peripheral vascular disease (PVD), but had a higher serum triglyceride (P < 0.01 for all) compared with Caucasian. Patients of Afro-Caribbean origin had a lower prevalence of IHD (0%) compared with both Asians (16%) and Caucasians (22%). Elevated UAER in NIDDM is closely associated with components of the metabolic syndrome and an increased risk of IHD and PVD. There are however, significant ethnic differences in this association.
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PMID:Relationship of elevated urinary albumin excretion to components of the metabolic syndrome in non-insulin-dependent diabetes mellitus. 959 78

Hypertension which is part of the metabolic syndrome has frequently a family background. The authors investigated therefore indicators of insulin sensitivity by the method of a hyperinsulinaemic euglycaemic clamp in the offspring of hypertensive probands. In conjunction with the increased interest in the role of muscles in influencing insulin sensitivity the authors were also interested in serum amino acid levels. They examined a group of 15 healthy offspring of hypertonic subjects (PHT) and compared them with a group of 18 healthy volunteers without a family-history of hypertension. PHT had as compared with controls a higher systolic pressure (117 +/- 7.2 mm Hg vs. 106.1 +/- 11.7 mm Hg p < 0.01). In the clamp examination in PHT significantly lower indexes of tissue insulin sensitivity were recorded, SI (46.51 +/- 11.8% vs. 54.3 +/- 7.79%, p = 0.02) and ISI (6.6 +/- 3.99 vs. 9.88 +/- 5.05, p < 0.01). In the PHT group were, in addition to the different ratio of some branched chain amino acids and tyrosine, also relations between indicators of insulin sensitivity and arginine. It is thus obvious that signs of reduced insulin sensitivity are present in PHT already in the preclinical stage. Relations between the altered insulin sensitivity and arginine, the precursor of nitrogen oxide, apparent only in PHT could be a stimulus for seeking associations with endothelial damage described in insulin resistant conditions.
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PMID:[Relation between serum amino acids and insulin sensitivity (results of a clamp study in offspring of hypertensive patients]. 960 33

Decreased insulin sensitivity is associated with diabetes mellitus, ischemic heart disease, and hypertension, both independently and in association as what is called the metabolic syndrome. Although the negative effects of obesity, sedentary lifestyles, and high-fat diets on insulin sensitivity are well established, the influence of type and quantity of dietary carbohydrate is more controversial. This study aimed to assess the acute (24 h) effects of a high-sucrose compared with a high-starch diet on insulin sensitivity and to identify changes in blood metabolites that might lead to altered insulin sensitivity. Eight healthy adults consumed high-sucrose or high-starch diets (50% of dietary energy) in a randomized, crossover trial. Insulin sensitivity was assessed by a short insulin tolerance test the following morning. No differences were detected in insulin sensitivity, either for glucose metabolism [Kitt(glucose) (the rate constant for the decline in blood glucose concentrations) for sucrose diet = 3.86%/min, for starch diet = 3.72%/min; pooled SEM = 0.23] or for lipid metabolism [Kitt(NEFA) (the rate constant for the decline in blood fatty acid concentrations) for sucrose diet = 12.9%/min, for starch diet = 11.4%/min; pooled SEM = 1.18]. Profiles for blood glucose and serum insulin concentrations revealed higher peaks and lower troughs with the high-sucrose diet whereas area under the curve for glucose was higher with the high-starch diet (6780 +/- 245 mmol x L/min) than with the high-sucrose diet (6290 +/- 283 mmol x L/min) (P < 0.001). Plasma fatty acid concentrations showed a late postprandial rise with the sucrose-rich diet relative to the starch-rich diet, which was mirrored with a fractionally later peak in triacylglycerol concentrations.
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PMID:Acute effects on insulin sensitivity and diurnal metabolic profiles of a high-sucrose compared with a high-starch diet. 1007 50

According to the actual knowledge obesity is a serious, nutrition-dependent pathology with a high number of consequences. Endocrine sequence of obesity such as PCO-HAIR-syndrome (polycystic ovarian syndrome, hyperandrogenemia-insulin-resistance) with its cycle disorders and sterility are beginning already in adolescent and women of young reproductive age. With ageing more serious risks such as non-insulin dependent diabetes mellitus (NIDDM), arteriosclerosis followed by coronary disease, stroke and hypertension, metabolic syndrome and a higher prevalence of malignant diseases will appear. Based on these five risks obesity should be treated early when therapeutic strategies are more successful than in older ages. The definition of a diagnosis and the beginning of a weight reduction programme combined with intense motivating treatment as well as medical and psychotherapeutic guidance is an important preventive contribution.
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PMID:[Obesity--significance in adolescence and for reproduction]. 962 28

Obesity may either be unspecific as indicated by an increased body mass index (BMI) or due to an abnormal fat-distribution as indicated by an increased waist-to-hip ratio (WHR). The latter is frequently associated with deteriorations of glucose tolerance, hypertriglyceridaemia and hypertension (the metabolic syndrome), a syndrome which is among the strongest risk factors of ischemic heart disease. It is important to note that visceral obesity is a frequent feature of the polycystic ovary syndrome. Also, weight gain after menopause is often associated with a particular increase of the WHR. Obesity as indicated by an increased BMI (> 30 kg/m2) is a weak but easily detectable risk marker of venous thrombotic disease. This risk needs to be considered in clinical practice since obesity was shown to enhance the power of precipitating risk factors of venous disease such as pregnancy, surgery or estrogen treatment.
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PMID:[Obesity and thrombotic vascular diseases]. 962 33

Increased sympathetic tone is found in about 30% of patients with hypertension. This abnormality is closely associated with the metabolic syndrome of dyslipidaemia and hyperinsulinaemia. In this short review we discuss the mechanisms by which sympathetic over-activity could cause the metabolic syndrome. Sympathetic stimulation enhances cardiac and vascular hypertrophy. Left ventricular hypertrophy is a strong predictor of poor cardiovascular outcomes. Hypertrophy of resistance vessels accelerates hypertension, whereas hypertrophy of smaller coronary vessels limits coronary reserve and increases tendency for coronary spasms. Epidemiologically, high haematocrit is associated with hypertension and is recognized as an independent coronary risk factor. Sympathetic stimulation increases haematocrit through an increase of post-capillary vascular resistance. Sympathetic over-activity is also associated with platelet activation which may further add to the risk of coronary thrombosis in neurogenic hypertension. Tachycardia, which is due to increased sympathetic and deceased parasympathetic tone, is a hallmark of neurogenic hypertension. Fast heart rate is a strong predictor of coronary events and sudden death. The mechanisms by which tachycardia increases the cardiovascular risk are outlined.
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PMID:Effect of sympathetic overactivity on cardiovascular prognosis in hypertension. 965 30

Recent studies in Europe, North America, and the developing world have shown that low birth weight and other indices of abnormal fetal growth in babies born at term are linked with a higher prevalence of glucose intolerance and NIDDM in adult life. Reduced fetal growth is also associated with a higher prevalence of the metabolic syndrome (in particular, hypertension and vascular disease) and with insulin resistance in adult life. Because birth size is determined largely by nongenetic factors, these findings have led to the "fetal origins" hypothesis, which proposes that fetal adaptations to an adverse intrauterine environment that reduces fetal growth program lifelong physiological changes. These changes in turn predispose to diabetes and the metabolic syndrome. The mechanisms are unknown, but evidence from animal studies and preliminary human evidence suggests that adverse events in early life may influence the neuroendocrine development of the fetus. This results in long-term alterations in the setpoint of several major hormonal axes, including an increase in adrenal glucocorticoid secretion. These hormonal alterations may contribute to the predisposition to diabetes and the metabolic syndrome in people who were small at birth.
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PMID:Birth weight and the future development of diabetes. A review of the evidence. 970 43


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