Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this investigation was to evaluate the benefits and the potential risks of a very low calorie protein-diet in obese patients with metabolic abnormalities and at increased cardiovascular risk. To this end, the 420 kcal diet (with 50% of energy as protein) was administered for 10 days to 10 grossly obese subjects with glucose intolerance, hyperlipemia, arterial hypertension, ischemic cardiopathy and thrombotic risk related to high levels of fibrinogen factor VIII and reduced fibrinolytic activity. Weights loss averaged 360 g/day with a mean protein loss of 17 g/day occurring essentially during the very early phase of the diet. There was a rapid normalisation of blood pressure, plasma lipids and glycaemia. With the exception of a slightly negative potassium balance other ion remained in balance. There was no change in electrocardiogram, in parameters of blood coagulation or in hepatic and renal function. There was only a moderate increase in ketonaemia and plasma urate. It appears therefore, that an 8 to 10 day very low calorie protein-diet is well tolerated even in obese patients with increased cardiovascular risk, and that it corrects of several metabolic abnormalities without alteration in cardiac, hepatic or renal function.
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PMID:[Evaluation of tolerance of a modified protein diet in obese subjects]. 665 61

The value of hyperuricemia as a risk factor for cardiovascular mortality was investigated in 3195 men and 3160 women aged 40-69 years in Finland. Hyperuricemia was associated with obesity, impaired glucose tolerance, hypertension and history of heart disease. The total mortality of hyperuricemic men and women in 5 years was significantly higher than the mortality of normouricemics. Cardiovascular mortality was not higher in hyperuricemics than in normouricemics. However, in hyperuricemic women without known heart disease cardiovascular mortality was significantly increased in the follow-up period between 5 and 12 years. Total and cardiovascular mortality rates were significantly higher in hyperuricemic men with known heart disease than in corresponding normouricemic men. A rise of serum uric acid may be secondary to more advanced atherosclerosis. Thus, hyperuricemia may be associated with more advanced heart disease and it is not an independent cause of cardiovascular diseases.
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PMID:Hyperuricemia as a risk factor for cardiovascular mortality. 696 92

As part of a study of risk factors for glucose intolerance and heart disease in Australian Aborigines and persons of European descent, we elicited the prevalence of food habits that may be associated with high fat and high salt intakes. Interview data were gathered from population-based samples in country towns and visitors to an Aboriginal health service in a state capital city, all in southeastern Australia. Among persons aged 13 years and over, the frequency of eating takeaway food as a meal was categorised as monthly or less, weekly, more than once per week, and daily or more often. The prevalence of eating such meals was higher among city Aborigines than those living in the country town; the prevalence was lowest among the country-town Europeans (chi 2 = 184, 6 df, P < 0.001). The prevalence of adding salt during cooking and food consumption was higher among Aborigines compared with Europeans. Among country-town Aboriginal males aged 35 or under, 25 of 40 (63 per cent) added salt to cooked food 'most of the time', compared with 66 of 185 (36 per cent) Europeans (chi 2 = 9.8, P = 0.002). Among Aboriginal females, 47 of 64 (64 per cent) were in the highest category of salt use, compared with 35 of 190 (18 per cent) of Europeans (chi 2 = 66.3, P < 0.001). About one-third of country-town Aboriginal males used dripping to fry food, but in the other ethnicity, gender and location groups, vegetable oil was the most frequent choice. The main differences in food habits were associated with ethnicity, rather than location.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Food habits in Aborigines and persons of European descent of southeastern Australia. 820 12

The purpose of this study was to investigate the prevalence of hypercholesterolemia among subjects having diabetes and glucose intolerance, according to the guidelines of the National Cholesterol Education Program (Adult Treatment Panel II, ATP II). This survey consisted of 2090 subjects (856 men, 1234 women) aged 30 years or more from the Sun-Ming district of Kaohsiung city. Glucose tolerance status was ascertained for both medical history and a 75-g oral glucose tolerance test according to World Health Organization criteria. Frequency of elevated total cholesterol in female subjects with abnormal glucose tolerance is significantly greater than in those with normal glucose tolerance (NGT). However, only male subjects with undiagnosed NIDDM (UDDM) had a statistically higher rate of hypercholesterolemia than those with NGT. Of UDDM individuals, 68% have total cholesterol level between 200 and 239 mg/dl and two or more risk factors for heart disease or evidence of coronary heart disease or total cholesterol > or = 240 mg/dl or high-density lipoprotein (HDL) cholesterol < or = 35 mg/dl. Such individuals should have their low-density lipoprotein (LDL) cholesterol measured. Using the ATP II, LDL cholesterol levels warranting dietary treatment for hypercholesterolemia would be expected in 76% of UDDM. Due to the high prevalence of coronary heart disease in diabetic patients, investigation of blood lipid levels and coronary heart disease risk factors should be routine in these patients, and treatment strategies should include management of lipid disorders and the many other risk factors. A high frequency of dyslipidemia was found among UDDM group in our study. Early detection of undiagnosed diabetic patients is also very important in decreasing the prevalence of coronary heart disease.
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PMID:Hypercholesterolemia in undiagnosed non-insulin-dependent diabetes in southern Taiwan. 868 43

Pediatric lung transplantation is becoming more common, and with increasing experience there is increasing success. The most common indications for considering lung transplantation are cystic fibrosis, pulmonary vascular disease (usually due to congenital heart disease), and fibrotic lung disease. The contraindications and complications are similar to adult transplant patients, although post-transplant lymphoproliferative disease and airway complications may occur more frequently. The patients with cystic fibrosis face additional obstacles to the success of transplantation: airway colonization with Gram-negative organisms, pancreatic insufficiency, glucose intolerance, and osteoporosis. The survival for children is comparable to adults, reaching about 65% at 1 year, and 69% at 2 years.
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PMID:Pediatric lung transplantation. 918 31

Increasing attention is being paid to disturbances in glucose metabolism as key explanatory factors for the development of coronary artery disease. We studied the prevalence of impaired glucose tolerance and non-insulin-dependent diabetes and the levels of plasma insulin after an oral glucose tolerance test in 99 men with heart disease but without a history of diabetes referred to coronary arteriography; we also compared the outcome with a matched control group (n = 116). The severity of atherosclerosis in coronary angiograms was evaluated according to glucose tolerance status. Among the 99 patients with coronary artery disease, 37.4% had an abnormal oral glucose tolerance test result, whereas only 18.1% of the control group had an abnormal result (p < 0.01). Moreover, patients with heart disease and normal glucose tolerance were hyperinsulinemic compared with the control group (p < 0.01). By analysis of variance no statistically significant difference in severity of coronary atherosclerosis on coronary angiograms was found. In conclusion, we demonstrated frequent disturbances in glucose metabolism indicating insulin resistance in patients with ischemic heart disease without a history of diabetes, but we could not demonstrate a relation between these disturbances and degree of coronary atherosclerosis.
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PMID:Glucose tolerance status and severity of coronary artery disease in men referred to coronary arteriography. 920 Mar 89

The number of Americans with diabetes mellitus has increased 50% since 1983 to 16 million. An interesting and startling factor is that only half of these diabetics are aware they have the disease. Diabetes mellitus can lead to blindness, heart disease, stroke, nerve damage, kidney failure, and periodontal disease. It is the fourth leading cause of death in the United States. A metabolic disorder affecting insulin metabolism and associated blood glucose intolerance regulation, diabetes may be classified by the following categories: type I-insulin dependent diabetes mellitus which is commonly found in children and adolescents and type II-non-insulin-dependent or adult-onset diabetes which occurs in patients over forty and is associated with obesity. The dental hygienist's role in education, prevention, and therapeutics has expanded to detection and recognition of oral manifestations of diabetes. The dental hygienist may be the first to recognize the presence of the disease. This article aims to acquaint the dental hygienist with the clinical picture of a dental patient with diabetes mellitus.
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PMID:A dental hygiene perspective in the detection of diabetes mellitus. 959 74

Friedreich's ataxia is an autosomal recessive neuro-degenerative disorder involving both central and peripheral nervous system. Patients also show a systemic clinical picture presenting heart disease and diabetes mellitus or glucose intolerance. The disease is caused by mutations in the FRDA gene mapped on chromosome 9q13. The product of the gene is frataxin, an 18 kDa soluble mitochondrial protein with 210 amino acids. Crystal structure suggests a new, not previously reported, protein fold. The most frequent mutation is the expansion of a GAA trinucleotide repeat located within the first intron of the gene, and represents 98% of the mutations. Point mutations are described in compound heterozygous subjects with one expanded allele. A two-step model of GAA normal alleles towards premutation alleles, which might generate further full expanded mutations in the population with Indo-European ancestry, has been postulated. Clinical phenotype is variable and an inverse correlation with the GAA expansion size has been observed. Analysis of the GAA triplet is a strong molecular tool for clinical diagnosis, genetic counselling and prenatal diagnosis. Friedreich's ataxia patho-genesis is not solved yet. Substantial data from organism models, such the S. cerevisae yeast and more recently conditioned knock-outs in mouse, and studies in heart biopsies and fibroblast cultures from patients suggest an important role of mitochondrial iron in the development of the disease. Iron is accumulated in the mitochondrial matrix of both the yeast frataxin deficient mutant and the patient fibroblasts. It has been postulated that iron-induced oxygen radical affects the oxidative phosphorylation in frataxin deficiency states favouring the disease pathology. A second hypothesis postulates a direct role of frataxin in the mitochondrial energy activation and oxidative phosphorylation. Iron chelator drugs and antioxidant drugs have been postulated for Friedreich's treatment. No results from clinical trials are available yet, but idebenone, a short-chain quinone, seems to reduce the size of hypertrophic cardiomyopathy and levels of oxidative stress molecules in patients.
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PMID:Friedreich's ataxia and frataxin: molecular genetics, evolution and pathogenesis (Review). 1135 Dec 69

Intrauterine growth retardation (IUGR) increases the risk of developing glucose intolerance and cardiovascular disease in adulthood. Fetal exposure to excess glucocorticoids may contribute to IUGR. Despite the importance of glucose supply for fetal growth, studies on glucose transporter expression in IUGR are few. Two glucose transporters, GLUT1 and GLUT3, are expressed in placenta. In rodent placenta, GLUT1 is replaced by GLUT3 during late gestation. We examined placental GLUT protein expression in 21-day pregnant rats administered dexamethasone (DEX) from day 15 of gestation via osmotic minipump (at doses of 100 or 200 microg/kg body wt. per day). A dose-dependent decline in placental and fetal weight occurred in the DEX groups at day 21. Placental GLUT3 protein expression increased dose-dependently in the DEX groups (by 1.3-fold (n.s) and 2.3-fold (P<0.01), respectively). GLUT1 protein expression also increased dose-dependently in the DEX groups (by 1.6-fold (P<0.05) and 1.9-fold (P<0.01), respectively). In the DEX-treated groups, altered GLUT protein expression occurred in the absence of altered peroxisome proliferator-activated receptor-gamma (PPAR-gamma) protein expression in day 21 placenta; however, PPAR-gamma protein expression in day 21 fetal hearts was greatly suppressed. We conclude that increased placental GLUT1 protein expression may reflect an attempt to increase placental or fetal glucose supply to attenuate the effect of excessive exposure to glucocorticoids to diminish fetal growth, whereas suppression of cardiac PPAR-gamma expression during cardiac development may contribute to the increased risk of developing heart disease found in people of below average birthweight.
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PMID:Enhanced placental GLUT1 and GLUT3 expression in dexamethasone-induced fetal growth retardation. 1173

Gastroenteropancreatic (GEP) neoplasms originate from any of the various cell types belonging to the neuroendocrine system. A general characteristic of GEP endocrine tumours is that the vast majority produce and secrete a multitude of peptide hormones and amines. Many patients with malignant metastasising tumours present clinical symptoms related to hormone hyperproduction. These include the so-called carcinoid syndrome, characterised by flushing, diarrhoea, wheezing and right heart disease, which is predominantly associated with the serotonin- and tachykinins-producing carcinoids of the midgut. Several types of syndrome associated with GEP endocrine tumors are caused by overproduction of a specific hormone. For instance, the well-known Zollinger-Ellison syndrome is gastrin-mediated. The so-called 'insulinoma syndrome' depends on excessive production of insulin and proinsulin, resulting in hypoglycemia. The 'glucagonoma syndrome' is characterised by necrolytic migratory erythema, diabetes and diarrhoea. The Verner-Morrison syndrome, which is brought about by high circulating levels of vasointestinal peptide (VIP). produces severe secretory diarrhoea. Finally the 'somatostatinoma syndrome' involves gallbladder dysfunction and gallstones, diarrhoea with or without steatorrhea, and impaired glucose tolerance. The biochemical diagnosis of endocrine digestive tumors is based on general and specific markers. The best general markers are chromogranin A (CgA) and pancreatic polypeptide (PP). Specific markers for endocrine tumors include insulin, gastrin, glucagon, vaso intestinal polypeptide (VIP), somatostatin and the primary cathabolic product of serotonin, 5-hydroxyndoleacetic acid (5-HIAA). Localisation procedures commonly applied, in the diagnosis of endocrine tumours include ultrasound (US), computed tomography (CT) and somatostatin receptor scintigraphy (SRS).
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PMID:Epidemiology, clinical features and diagnosis of gastroenteropancreatic endocrine tumours. 1176 60


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