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)

Several studies have reported high levels of oestrogens--especially oestradiol--in plasma in men surviving an acute myocardial infarction (AMI). We have measured plasma levels of the two major oestrogens, oestrone and oestradiol, for three days during the acute AMI and at three months after discharge. Patients admitted to a coronary care unit with ischaemic heart disease without proof of an infarction and patients without evidence of heart disease served as controls. We found significantly higher oestrone levels during the acute infarction than at three months afterwards and also higher than in men without AMI. Men who died shortly after admission had grossly elevated plasma oestrone concentrations. As oestrone levels were correlated to excretion of catecholamines and cardiac enzyme levels in plasma and as circulating levels of oestrone are influenced by ACTH, the hyperoestronaemia may reflect stress-induced increased adrenocortical activity. Plasma oestradiol concentrations in men with AMI decreased significantly during the first three days after admission. In men given no medication oestradiol concentrations did not differ significantly from those in the control groups. Three months after the infarction, the median plasma oestradiol (but not oestrone) concentrations were significantly elevated, but not if only data from men given no medication were considered.
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PMID:Variability in plasma oestrogen concentrations in men with a myocardial infarction. 207 57

Secondary hypertrophic cardiomyopathy (HCM) was diagnosed in 55 newborns and infants without heart disease. The 17 newborn infants of diabetic mothers, 23 infants given ACTH treatment for infantile spasms, 9 ventilated premature infants or babies with bronchopulmonary dysplasia and 6 infants with different underlying diseases comprising this group underwent 2-dimensional echocardiography. In almost all cases echocardiographic evidence of HCM resolved after removal of the exogenous or endogenous causative factor. Myocardial effects of several substances are known and their pathophysiological mechanisms are discussed. Since HCM may precede systemic disease or may often be the first pointer to a triggering agent, further diagnostic procedures are always indicated. Hence, the diagnosis of primary HCM should be made by exclusion.
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PMID:[Secondary myocardial hypertrophy in newborn infants and infants without congenital heart defect]. 285 96

Cigarette smoking alters the pattern of endogenous steroid levels. We examined this phenomenon in two separate male groups. Group A consisted of 189 dyslipidemic men participating in the Helsinki Heart Study and group B of 100 men including patients with heart disease and healthy controls. The subjects in the latter group underwent ACTH-testing. In group A, smokers had significantly higher basal androstenedione and dehydroepiandrosterone sulfate (DHEAS) levels and androstenedione/cortisol ratios than nonsmokers. Mean concentrations of cortisol, dehydroepiandrosterone (DHEA), androstanediol glucuronide, testosterone, and sex-hormone binding globulin (SHBG) did not differ between smokers and nonsmokers. In group B, smokers had lower high density lipoprotein (HDL)-cholesterol and apolipoprotein AI and higher triglyceride levels than nonsmokers. Basal androstenedione and ACTH stimulated androstenedione and DHEA concentrations were higher in smokers. No significant differences were found in basal insulin, SHBG, estrone, estradiol, testosterone, free testosterone, and dihydrotestosterone concentrations between smokers and nonsmokers. These results suggest that smoking decreases the activity of either 21- or 11 beta-hydroxylase in the adrenal cortex, which results in increased secretion of adrenal androgens.
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PMID:Cigarette smoking is associated with elevated adrenal androgen response to adrenocorticotropin. 866 73

Woman 75-year-old treated 30 years for syndrome of acromegaly refused pituitary surgery and irradiation. Five years and nine months before death she had a colon carcinoma successfully removed. Multinodular hyperfunctional goitre was treated with carbimazole. For six last years of life corticosteroids were given as a replacement therapy. Her cause of death was the heart failure due to acromegalic heart disease. In autopsy a large intrasellar and extrasellar pituitary adenoma without rests of nonneoplastic tissue was found. Nevertheless the target peripheral endocrine glands except ovaries, were not atrophic. A multinodular goitre and diffuse adrenocortical hyperplasia were revealed. Histology, and immunohistochemistry demonstrated that mot neoplastic cells were producing GH and ACTH, dispersly Prl, scattered cells were positive for beta-subunit of FSH, LH, TSH. Electron microscopy proved most of the cells to be densely granulated. We classify the adenoma according to the newly proposed WHO pituitary tumours classification (1) as plurihormonal, hyperfunctional, extrasellar, typical adenoma from densely granulated cells. We conclude that in plurihormonal adenomas with dominant (in the case referred acromegalic) symptomatology the additional hormonal production should be monitored as a possible source of important complications.
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PMID:[Multihormonal and multifunctional hypophyseal adenoma and the acromegaly syndrome]. 1104 8

Obesity, a principal risk factor for the development of diabetes mellitus, heart disease, and hypertension, is a growing and serious health problem all over the world. Leptin is a weight-reducing hormone produced by adipose tissue, which decreases food intake via hypothalamic leptin receptors (Ob-Rb) and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. Protein tyrosine phosphatase 1B (PTP1B) negatively regulates leptin signaling by dephosphorylating JAK2, and the increased activity of PTP1B is implicated in the pathogenesis of obesity. Hence, inhibition of PTP1B may help prevent and reduce obesity. In this study, we revealed that phenethyl isothiocyanate (PEITC), a naturally occurring isothiocyanate in certain cruciferous vegetables, potently inhibits recombinant PTP1B by binding to the reactive cysteinyl thiol. Moreover, we found that PEITC causes the ligand-independent phosphorylation of Ob-Rb, JAK2, and STAT3 by inhibiting cellular PTP1B in differentiated human SH-SY5Y neuronal cells. PEITC treatment also induced nuclear accumulation of phosphorylated STAT3, resulting in enhanced anorexigenic POMC expression and suppressed orexigenic NPY/AGRP expression. We demonstrated that oral administration of PEITC to mice significantly reduces food intake, and stimulates hypothalamic leptin signaling. Our results suggest that PEITC might help prevent and improve obesity.
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PMID:Phenethyl isothiocyanate activates leptin signaling and decreases food intake. 3038 68