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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen acromegalic patients underwent echocardiography, phonocardiography, stress electrocardiography with Thallium perfusion scanning and gated radioisotope left ventricular angiocardiograms. Abnormalities consisting of increased echo left ventricular mass index, low velocity of circumferential fiber shortening or elevated pre-ejection period to left ventricular ejection time ratio were found in six patients with coexistent hypertension or coronary disease. Concentric left ventricular hypertrophy was also found in three patients with no known etiology other than acromegaly of greater than thirteen years' duration or with fasting growth hormone concentrations greater than 100 ng/ml. One of these three also had left ventricular dysfunction. Neither hypertrophy nor ventricular dysfunction was found in other acromegalics with shorter duration of disease or lower growth hormone concentrations or with normal growth hormone concentrations after therapy. A high prevalence of coronary artery and hypertensive heart disease is associated with acromegaly. A few patients with acromegaly have a specific, potentially reversible cardiomyopathy probably related to prolonged acromegaly or very high growth hormone concentrations.
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PMID:Cardiac size and function in acromegaly. 14 34

The renin-angiotensin-aldosterone system in patients with acromegaly was evaluated by infusing [sarcosine1, isoleucine8]angiotensin II, a competitive angiotensin II antagonist, into five acromegalic patients with hypertension and three normotensive acromegalics. The drug was infused at a rate of 600 ng/kg . min for 30 min, 1 h after iv injection of 40 mg furosemide. In addition, before the infusion, plasma samples were obtained for determination of PRA and plasma aldosterone concentration. A significant pressor response to [sarcosine1, isoleucine8]angiotensin II was observed in all eight patients. Preinfusion PRA and plasma aldosterone concentration were significantly lower than in normal controls. It is concluded that in acromegaly, the renin-angiotensin-aldosterone system is suppressed and that this system is probably not involved in maintenance of the high blood pressure observed in some acromegalic patients.
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PMID:Blood pressure response to an angiotensin II antagonist in patients with acromegaly. 42 97

The behaviour of the renin-angiotensin-aldosterone system was evaluated in 16 acromegalic patients, of whom 7 were hypertensive. The patients were studied in basal conditions, after suppression with 9alpha-fluorohydrocortisone, and after stimulation with furosemide. Baseline and after furosemide PRA were significantly lower in acromegalic hypertensive patients than in the normotensive group. Mean urinary aldosterone excretion was found at the upper limits of the normal range; it was occasionally elevated, but the values were not satistically different in the two groups. There was a suppression after 9 alpha fluorohydrocortisone in both groups, though it did not reached the 50%. These data show that there is a disorder of the renin-angiotensin-aldosterone system in acromegalic subjects. This defective regulation is sometimes similar to that present in primary aldosteronism. In fact in two patients a typical phlebographic and scintigraphic picture of primary aldosteronism has been found; surgery, performed in both patients, revealed a large cortical adenoma in one case and a macronodular hyperplasia in the second case. However, the relationship between this adrenal abnormalities and hypertension in acromegaly are not yet completely clarified.
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PMID:Plasma renin activity and urinary aldosterone in acromegaly. 48 12

Echocardiography was used to evaluate cardiac anatomy and function in 25 patients with accromegaly. Eighty per cent of the patients (20 of 25) had abnormal echocardiograms including 13 patients without other signs or symptoms of cardiac involvement. The most common abnormality was increased left ventricular mass with concentric left ventricular wall thickening, which was found in 64 per cent (16 of 25) of the patients. Increased left ventricular transverse dimension at end diastole was found in 36 per cent (nine of 25) of the patients. Other echocardiographic abnormalities found included left atrial or aortic root enlargement (three patients), disproportionate septal thickening (one patient) and depressed left ventricular ejection fraction (three patients). Since five of the patients with increased left ventricular mass had no history of hypertension or hyperthyroidism, the increased mass cannot be ascribed solely to these conditions commonly associated with acromegaly. Furthermore, the degree of cardiac hypertrophy showed no significant correlation with pre- or post-treatment growth hormone levels, or with known duration of acromegaly prior to treatment. Thus, although the pathophysiology and significance of cardiac abnormalities in acromegalic patients is not yeat fully understood, echocardiography does provide a sensitive tool for detecting such abnormalities before they are otherwise apparent.
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PMID:Echocardiographic assessment of cardiac anatomy and function in acromegalic patients. 50 95

Examination of the cardiovascular apparatus (cv) of 25 acromegalic patients revealed an increased incidence of cardiovascular pathology as against normal individuals. Acromegalic patients with arterial hypertension (AH) show a twice higher incidence of ischemic cardiopathy, cardiomegaly with obvious or latent cardiac failure, arrhythmias, which frequently lead to death. The uncertain pathogeny of cardiomyopathy implied: hypoxia due to heart hypertrophy (over 500 g and increased cross-section of the fibre to over 26/mu), adrenergic deficiency resulting from increased protein synthesis and decrease in thyrosine, a precursor of myocardic cathecolamines. The increased incidence of coronary pathology is favoured in acromegalic patients by diabetes, hyperlipoproteinemia, low endogenous heparin, increased ureic acid and platelet adhesivity. Hypophysectomy by hypophysolysis (20 cases) brings relief and cures cardiovascular pathology, reduces AH, corrects the coronary risk factors, cures hypophyseal diabetes. The existence of AH and cardiovascular pathology is an indication for surgical treatment in evolutive acromegaly.
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PMID:Cardiovascular pathology in acromegaly and some effects of the 90 yttrium implant in the hypophysis. 69 1

Acromegaloidism is a condition which resembles acromegaly by its clinical manifestations but is not due to pituitary or hypothalamic dysfunction. Twenty patients were diagnosed as having this disorder and the results from studying growth hormone (GH) responses in 15 patients (11 women and four men) were included in this report. Clinical manifestations closely resembled those of acromegalics, including history of progressive changes, acral enlargement, visual disturbances, abnormal visual fields in four patients, and sella turcica enlargement in two patients. The glucose tolerance test (GTT) was abnormal in 12/15 patients, 13/15 were > 10 percent obese, 8/15 had hypertension, 7/15 had large-statured relatives, but lactorrhea was absent in all patients. The mean serum GH concentration was 2.2 ng/ml, which suppressed to 0.6 ng/ml during the GTT; increased to 24 ng/ml during hypoglycemia; and increased to 10.3 ng/ml after L-dopa ingestion. Other pituitary hormones (LH, FSH, TSH, prolactin), the metyrapone test, 24-hour random and nocturnal sleeping GH concentrations were normal. These GH values and responses helped to differentiate acromegaloidism from treated and untreated acromegaly. The pathogenesis of acromegaloidism was not determined, but somatomedin studies may prove helpful in further defining this disorder.
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PMID:Pituitary function and growth hormone dynamics in acromegaloidism. 73 19

Lung function has been assessed by spirometry, body plethysmography, flow volume loops and single breath transfer factor in thirty patients with acromegaly. Having excluded eight patients with kyphosis and/or clinical or radiological evidence of pulmonary venous hypertension we have found a significant correlation between duration of acromegaly and lung size as assessed by total lung capacity. Excluding the same eight patients we have found evidence of small airways narrowing in eight patients, seven of these eight had had acromegaly for nine years or longer, and the duration of acromegaly was significantly longer in the patients with small airways narrowing than in those without. In the absence of other recognized causes it is possible that small airways narrowing in acromegaly is caused either by the increased whole blood volume with pulmonary vascular engorgement, or by increase in size of the soft tissues of the small conducting airways. Six of the eight patients with kyphosis and/or pulmonary venous hypertension also had evidence of small airways narrowing. Thus fourteen of the thirty patients with acromegaly had small airways narrowing. Five men had evidence of extra thoracic airway narrowing and in four the duration of acromegaly was ten years or longer. We conclude that the increase in total lung capacity, the incidence of small airways narrowing and the incidence of upper airway narrowing are all related to the duration of acromegaly. It seems that once duration exceeds eight years patients are very likely to develop abnormalities of lung function either primarily from the effects of acromegaly on the airways and lung or secondarily from the associated cardiovascular and thoracic skeletal abnormalities. It seems probable that the small airways and upper airway narrowing contribute to the morbidity and mortality of this disease. This study provides further evidence that acromegaly should be treated early.
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PMID:Lung function in acromegaly. 75 Oct 89

A 40-year-old patient with a ten-year history of acromegaly had persistent disease despite prior treatment with conventional pituitary radiotherapy and two transsphenoidal hypophysectomies. Initial evaluation showed characteristic acromegalic features, hypertension, amenorrhea, inappropriate diaphoresis, and poorly controlled diabetes mellitus despite isophane insulin suspension daily. Growth-hormone levels were high and did not suppress with glucose load. Treatment with bromocriptine was associated with prompt improvement in glucose intolerance, with elimination of insulin requirement within 72 hours of institutions of this therapy. Blood pressure normalized; inappropriate diaphoresis disappeared. Within three months ovulatory menses were noted to resume for the first time in ten years. There was progressive improvement in the soft-tissue changes of acromegaly. The growth-hormone levels fell within three hours after the first dose of bromocryptine and remained suppressed throughout her six-month course of therapy.
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PMID:Complete remission of acromegaly with medical treatment. 76 12

1. In 29 patients with acromegaly, plasma renin activity and growth hormone were measured during fasting and recumbency on free diet. Exchangeable sodium was measured in all cases and expressed as a percentage of the expected value on the basis of lean body mass. 2. Twenty-two control subjects without evidence of cardiovascular, renal or endocrine disease were studied in the same way. 3. There was a significant increase in exchangeable sodium and suppression of plasma renin activity in the acromegalic patients in comparison with control subjects. 4. There was a significant positive correlation between exchangeable sodium and plasma growth hormone. 5. Hypertensive acromegalic patients (diastolic blood pressure larger than or equal to 100 mmHg) tend to have a lower (although not significantly so) exchangeable sodium than normotensive subjects. 6. We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly.
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PMID:An investigation into the pathogenesis of hypertension in acromegaly. 87 24

The effect of chronic administration of growth hormone (GH) to osteoporotic patients was studied using the techniques of total body neutron activation analysis, whole body counting, calcium tracer kinetics, photon absorptiometry, quantitative microradiography, and urinary hydroxyproline. Two dosage schedules were utilized for six months each: 2 units daily and 0.2 w3/4 units of GH daily (where W represents body weight expressed in kg). The lower dosage (2 units) did not produce any appreciable change in the indices studied. Following the higher dose, no evidence of any anabolic effect was apparent in most patients (i.e., no increase in total body levels of Ca, Na, K, P, or Cl). Increases were noted in the urinary calcium excretion rate and in the urinary hydroxyproline excretion. Bone mineral content decreased. The bone biopsies displayed an increase in bone formation and resorption surfaces in response to treatment, but these changes were not statistically significant. It may be concluded that under the conditions of this study, GH administration did not result in an increment in skeletal mass. Several side effects that are characteristic of acromegaly were observed, including hyperglycemia, hypertension, arthralgia, and the carpal tunnel syndrome. Because of the lack of demonstrated benefit and the associated complications of therapy, GH administration does not appear to be of value in the treatment of osteoporosis.
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PMID:Effects of growth hormone in osteoporosis. 99 24


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