Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Endocrine and neurological diseases are rare causes of arterial hypertension in childhood. They represent less than 5% of all cases of secondary hypertension. Inflammatory, traumatic, and tumorous disorders of the central nervous system rarely result in chronic hypertension but may frequently be associated with acute hypertensive crisis. The most important hypertensinogenic endocrine diseases are the catecholamine producing tumors pheochromocytoma and neuroblastoma and disorders of the adrenal cortex such as Cushing's syndrome, hyperaldosteronism, 11-hydroxylase deficiency and other mineralocorticoid excess syndromes. Renin producing tumors, hyperthyroidism and hyperparathyroidism are rare causes of hypertension in children. Neurogenic and endocrine forms of hypertension have contributed considerably to a better understanding of the pathophysiology of blood pressure regulation. They are of particular interest to the pediatrician since specific therapy may be available.
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PMID:[Endocrine and neurogenic hypertension in childhood]. 666 53

During the past 10 years we experienced 234 patients with atrial fibrillation of whom 94 patients (40.2%) showed a paroxysmal form. Underlying diseases of these 94 patients were hypertension and/or coronary heart disease in 51 (54.3%), rheumatic valvular disease in 3 (3.2%), hyperthyroidism in 2 (2.1%), and miscellaneous diseases in 15 patients (16.0%). Idiopathic atrial fibrillation was found in the remaining 23 patients (24.5%). Frequency of paroxysm was variable. paroxysm occurred only once or twice in 35 patients (37.2%) and more than 21 times in 20 patients (21.3%). Duration of a single paroxysm ranged from less than 24 hours in 49 patients (52.1%) to more than 15 days in 7 patients (7.4%). Atrial fibrillation became permanent in 19 (25.3%) of 75 patients who had been observed for a period of more than 1 year.
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PMID:Clinical features of paroxysmal atrial fibrillation. An observation of 94 patients. 723 May 14

An angiotensin II antagonist, [sacrosine1, isoleucine8] angiotensin II, was infused into thyrotoxic patients. Blood pressure was monitored before and during the infusions to investigate whether the renin-angiotensin-aldosterone system was involved in the maintenance of blood pressure in normotensive and hypertensive thyrotoxic patients. Five out of 17 normotensive patients with hyperthyroidism showed more than a 10 mmHg decrease in mean blood pressure in response to the infusion (responders), while the remaining 12 patients showed no substantial change in blood pressure (non-responders). The infusion caused little change in blood pressure in 8 hyperthyroid patients with systolic hypertension. The mean levels of serum thyroxine, triiodothyronine, plasma renin activity and plasma aldosterone concentration in the normotensive responders were significantly higher than the values in the normotensive non-responders. There were no significant differences in these laboratory values between the hypertensive patients and the normotensive non-responders except that serum triiodothyronine levels were significantly higher in the hypertensive patients. The present study indicates that increased activity of the renin-angiotensin-aldosterone system is involved in the maintenance of blood pressure in most normotensive patients with severe hyperthyroidism, while hypertension in patients with hyperthyroidism is not angiotensin II dependent.
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PMID:Blood pressure response to an angiotensin II antagonist in thyrotoxic patients with and without high blood pressure. 740 85

The purpose of this retrospective study was to elucidate 1) which subgroups are prone to have ischemic cerebrovascular disease (CVD) among patients with atrial fibrillation (Af), 2) vulnerable period of CVD after the diagnosis of chronic Af and 3) the clinical efficacy of antiplatelet therapy in chronic nonvalvular Af patients. During 9 years, a total of 479 patients included 124 cases with paroxysmal Af, 30 cases with paroxysmal Af initially which later changed to chronic Af and 325 cases with chronic Af were enrolled. Among these 355 cases with chronic Af, 57 cases had valvular heart disease (VHD). The results were as follows: 1) The high risk subgroups (incidence rate/100 person-years is more than 6) were chronic Af with VHD or hypertension. The low risk subgroups (less than 2) were paroxysmal Af under 60 years of age, chronic Af with mitral valve prolapse syndrome or with hyperthyroidism. 2) There was no vulnerable period for occurrence of CVD during 9 years' follow-up from the onset of Af. 3) No significant difference in the incidence of CVD was seen in the groups with antiplatelet therapy and without.
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PMID:[Ischemic cerebrovascular disease in patients with atrial fibrillation]. 750 May 53

Since their initial description in 1957, the interferons (IFNs) have been increasingly used to treat a wide array of diseases. Acute adverse effects, i.e. 'flu-like' syndromes, hypo- or hypertension, tachycardia, headache, myalgias and gastrointestinal disorders, occur within the first hour or day after starting treatment. They are seldom treatment-limiting and are easily manageable. Sub-acute and chronic effects develop after several days, usually within 2 and 4 weeks of therapy. The most typical is neurological toxicity, including fatigue/asthenia, and behavioural and cognitive changes. Such symptoms may seriously impair quality of life and result in treatment discontinuation. Seizures have seldom been described. Other infrequent central nervous system adverse effects include vertigo, cramp and oculomotor nerve paralysis. Distal paraesthesias and peripheral neuropathy have been reported. IFN-associated autoimmunity is quite rare but a matter of concern. Biological or clinical manifestations usually require several months to become apparent. Autoantibodies have been shown to develop in most patients but have been inconsistently associated with clinical symptoms of systemic lupus erythematosus, rheumatoid-like arthritis and thyroiditis. Both hypo- and hyperthyroidism have been described but are usually reversible. Other infrequent autoimmune reactions include diabetes, pemphigus and worsening of multiple sclerosis. Although several patients present with a pre-existing autoimmune disorder, no predisposing factor has been clearly established. While hypotension and tachycardia are the most frequent acute cardiovascular complications, a few additional cases of cardiac arrhythmias and myocardial ischaemia have been reported after a short course or several weeks of treatment. These latter complications do not appear to be dose-dependent or age-related. Isolated cases of congestive heart failure have also been described. Mild proteinuria has been observed in 15 to 25% of patients, but acute renal toxicity is uncommon. A transient rise in serum aminotransferase levels is frequently noted during the first stage of therapy, especially in patients receiving the highest dosages. Direct hepatotoxicity is extremely rare. Autoimmune hepatitis, which is ill-diagnosed as chronic viral hepatitis, and de novo induction of autoimmune hepatitis, account for the majority of liver diseases. Haematotoxicity is relatively common but mild to moderate, and develops gradually during the first weeks of treatment. Neutropenia is the most common haematological toxicity, but is usually not dose-limiting and resolves rapidly upon drug discontinuation. Myelosuppression, autoimmune and immune allergic haemolytic anaemias and thrombocytopenias have seldom been described. Cutaneous adverse effects comprised nonspecific erythema and hair loss and, less frequently, vasculitis, local ulcerations at the site of injection and exacerbation of psoriasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical toxicity of the interferons. 751 63

beta-Adrenoceptor antagonists such as propranolol and atenolol ameliorate the symptoms of human hyperthyroidism. We wished to define whether the cardiac changes of hyperthyroidism are attenuated by treatment with the beta-adrenoceptor antagonist atenolol. Rats were treated with triiodothyronine (T3) [1 mg/kg/day subcutaneously (s.c.) for 14 days] together with oral atenolol (100 mg/day on days 8-14); physiological parameters, inotropic and chronotropic responses in isolated cardiac tissues to compounds that increase intracellular cyclic AMP, and ventricular beta 1- and beta 2-adrenoceptors were measured. Administration of T3 produced marked hyperthyroidism, leading to increased metabolism, cardiac hypertrophy, tachycardia, hypertension, marked decrease in or loss of positive inotropic responses to calcium chloride, norepinephrine (NE), forskolin, and theophylline and increased ventricular beta 1- and beta 2-adrenoceptor density. Atenolol treatment of hyperthyroid rats attenuated the increases in heart rate (HR), rectal temperature, and O2 consumption but did not alter cardiac hypertrophy, hypertension, decreased positive inotropic responses or increased beta-adrenoceptor density. We conclude that beta-adrenoceptor antagonists produce only limited changes in hyperthyroidism-induced cardiovascular responses; furthermore, beta-adrenoceptor antagonists are unlikely to attenuate the cardiovascular risk factors of hyperthyroidism.
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PMID:Beta-adrenoceptor antagonism and the hyperthyroid rat heart. 752 70

The two isomers of the positive inotropic compound EMD 53998, (+)EMD 57033 and (-)EMD 57439, possess selective calcium sensitizing and phosphodiesterase (PDE) inhibitory properties, respectively. We measured the pharmacological responses to both enantiomers in isolated rat cardiac and vascular tissues and in muscles from severely failing human hearts. We also measured positive inotropic and chronotropic responses to EMD 57033 in cardiac tissues from rats with thyroid dysfunction, diabetes, or hypertension. Both compounds increased force of contraction in isolated rat cardiac tissues, although the ventricular response to EMD 57439 was only approximately 10% that of calcium chloride. Forskolin pretreatment potentiated responses to both compounds in atria but only to EMD 57439 in ventricles. Hyperthyroidism increased ventricular responses to EMD 57033 relative to calcium chloride; hypothyroidism and diabetes decreased these responses. Ventricular responses were unchanged in hypertensive rats. Both enantiomers produced positive inotropy in human isolated right atrial trabeculae, although the maximal increases were only 14% (EMD 57033) and 26% (EMD 57439) that of calcium chloride. In rat thoracic aortic rings, both enantiomers produced relaxation; the responses due to EMD 57033 were endothelium dependent. Thus, calcium sensitization produces positive inotropy and vascular relaxation in rats. Positive chronotropic responses to EMD 57033 are most likely due to PDE inhibition. The limited inotropic response in severely failing human myocardium, together with possible vasorelaxation, may provide cardiac support in heart failure without an excessive increase in cardiac O2 demand.
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PMID:Calcium sensitization as a positive inotropic mechanism in diseased rat and human heart. 752 44

Eighty patients with benign intracranial hypertension (BIH) (76 females, 4 males, age range 15-54 years) were studied. Endocrine changes (pregnancy-17, obesity-16, dysmenorrhea-15, hyperthyroidism-7, etc.) were the most common cause of BIH (72.5%-58 from 80). Besides general sings of intracranial hypertension (papilledema-80, headache-76, nausea-47, dizziness-43, obnubilations-39), 36 (45%) patients had visual problems. After treatment complete recovery took place in 48 patients, non-significant residual changes persisted in 16 patients, main symptoms of BIH persisted in 16 patients. Papilledema regressed completely in 52 patients, post-papilledematous discoloration of optic disks or optic atrophy were discovered in 12 patients.
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PMID:[The syndrome of benign intracranial hypertension]. 757 31

Pituitary adenomas are frequently encountered, benign intracranial tumours. Clinically classified according to their capacity to produce and secrete hormones, pituitary tumours are diagnosed from the clinical manifestations and biochemical findings of specific pituitary hormone overproduction or of impaired pituitary function due to pressure on normal pituitary cells, the pituitary stalk or the hypothalamus. Additionally, the tumour may result in neurological manifestations due to its effect as an intracranial space-occupying lesion. Pituitary adenomas may present acutely with pituitary apoplexy after intrapituitary haemorrhage or infarction. The subsequent hypofunction of the pituitary with concomitant neurological sequelae of an expanding intracranial mass are often associated with excruciating headache, diplopia and visual field defects. Gradually developing neurological deficits or secondary endocrine failure over several years may precede the recognition of non-secretory tumours (30-40% of pituitary adenomas) as well as some of the hormone-producing adenomas, especially when they expand beyond the confines of the sella turcica. Asymptomatic masses occur in the pituitary in 5-27% of unselected autopsy series. About 10-20% of pituitaries imaged as part of a brain study contain lesions 'consistent with a pituitary adenoma', with about half being pituitary adenomas ('incidentalomas'). Many advocate screening such cases for a wide spectrum of pituitary function abnormalities. Clinical judgement should be utilized to determine the extent of the work-up and the frequency of follow-up. Acromegaly, a clinical syndrome caused by excess growth hormone secretion, accounts for one-sixth of resected pituitary tumours. This disorder leads to chronic progressive disability and a shortened life span, with approximately 50% of untreated acromegalic patients experiencing premature death. The prevalence of acromegaly has been estimated to range from 50 to 70 per million, with the age of diagnosis usually between the third and fifth decades. Conditions associated with acromegaly include glucose intolerance, diabetes mellitus, lipid abnormalities, cholelithiasis, goitre, and hyperthyroidism, respiratory complications, hypertension, cardiovascular disease, and calcium metabolism abnormalities. An association between acromegaly and cancer, especially of the colon, is now recognized. Epidemiological series have indicated that cancer of the colon, breast and other types of malignancy are a cause of death with increased frequency in acromegalics compared with expected rates. Hypopituitary symptoms secondary to the mass effect of macroadenomas in acromegalic patients are common. Among premenopausal women, menstrual irregularities and galactorrhoea have been reported in 40-70%, while more than half of the men complain of impotence and decreased libido.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and differential diagnosis of pituitary tumours with emphasis on acromegaly. 762 86

Fifteen per cent of cerebrovascular accidents have a cardiac origin, two thirds of which are due to atrial fibrillation (AF). The Framingham study showed the risk of an ischaemic cerebral event to be increased by 5.6 in AF unrelated to rheumatic heart disease and by 17.5 when AF is associated with valvular heart disease. The risk of embolism is higher in elderly subjects and in those with underlying cardiac disease. Other high risk conditions include hypertension, diabetes, hyperthyroidism and cases with echocardiographic changes: left atrial dilatation, pre-thrombotic state or intra-atrial thrombus, atheroma of the ascending aorta. This stratification of risk should be taken into account when deciding on treatment. Conscious of the importance of the risk of embolism in AF, several authors have undertaken, over the last few years, randomised studies of the prevention of thromboembolic complications of AF: the AFASAK, BAATAF, SPAF and SPINAF trials. All showed the unquestionable efficacy of warfarin, even at low doses, at the price of a haemorrhagic risk of less than 2% per year for severe haemorrhages. A more recent study (SPAF II) confirmed the value of aspirin at the dosage of 325 mg/day which would seem to be a good alternative to anticoagulant therapy when this is contraindicated, although aspirin is less effective. The indications for anticoagulant therapy have become clearer since the publication of these results. Anticoagulant therapy is essential in permanent AF whether or not associated with rheumatic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Thromboembolic complications of arrhythmia due to atrial fibrillation]. 778 20


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