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

Experience in the management of 100 cases of acromegaly is described. Three quarters of these had been referred directly to the endocrine clinic at the Middlesex Hospital. The remainder were referred from the Royal Post-graduate Hospital because they were thought unsuitable for yttrium implantation. The patients were studied by clinical assessment of severity, by measurement of basal growth hormone levels on three separate mornings, and by a review of possible complications. Particular attention was paid to diabetes, hypertension, cardiomegaly, respiratory, vascular and skeletal changes as well as visual field defect. Aggressive treatment was recommended in 77 patients. It was not recommended in the remainder on account of age, intercurrent illness or the apparent mildness of the condition. Fifty-nine patients were treated by trans-sphenoidal hypophysectomy. In 46 of the 59 patients the mean basal growth hormone level has been reduced to 5 ng/ml or less. In 39 this followed operation, in five operation and subsequent X-ray therapy and in two operation and the continuing effect of previously implanted yttrium. Of these 46 patients in whom the growth hormone level has been reduced to normal, 26 do not show any deficiency of anterior pituitary trophic hormones, 13 have gonadotrophin defect (in eight of these it was present before the operation) and seven require full replacement therapy. One patient died at home six weeks after the operation from a pulmonary embolus. There was one case of CSF rhinorrhoea which stopped spontaneously and three of acute frontal sinusitis. Trans-sphenoidal hypophysectomy is shown to be an effective means of treating acromegaly. If the basal level of growth hormone is not reduced to normal by six weeks after operation, it is recommended that a course of X-ray therapy should be given. This does not apply if irradiation has been used before operation.
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PMID:The treatment of acromegaly with special reference to trans-sphenoidal hypophysectomy. 115 91

In a genetically hypertension-prone (S) strain of rats it was observed previously that males generally developed hypertension more rapidly on a high salt diet than did females although final pressure ultimately were similar in both sexes. A genetic study had shown that there was no sex-linkage involved in setting blood pressure levels, so it was thought that the gonads might be involved. In the present work, castration of males had no effect on blood pressure but in the females it caused a rise in pressure that could not be distinguished from that in males, both on a high and low salt diet. Castration resulted in greater growth in females than in controls, whereas it had the opposite effect in males. It was speculated that these changes were due to influences on pituitary growth hormone with castration increasing the net output of growth hormone (or enhancing receptor sensitivity to it) in the female and the opposite in the male. From the work of others, there are some data compatible with such an interpretation. Experimentally, growth hormone will induce hypertension in rats. Therefore, it is conceivable that growth hormone is involved in the increment in hypertension observed in these castrate females. Because the effect on blood pressure was observed in castrate females on both high and low NaCl diets, it was considered unlikely that the blood pressure effect was simply due to increased NaCl intake in the food associated with greater growth. It was suggested that this rise in blood pressure with cessation of ovarian function might bear on the unsettled question of "menopausal" hypertension in women: in the genetically susceptible individual an increase in growth hormone associated with declining ovarian funtion in the menopause could provide the stimulus for the appearance of hypertension some years earlier than would otherwise have been the case.
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PMID:Role of the gonads in hypertension-prone rats. 116 74

This summary of management of pill patients covers contraindications, individualizing pill formulations for normal women, and for diabetics, hypertensives, hyperlipidemics and those with personal or familial history of thrombophebitic or vascular disorders. The estrogen or progestagen balance of a pill can be selected to suit the individual. All patients beginning oral contraception should have pelvic exam, breast exam, cervical smear, fasting blood glucose, hematology and SMA-12, repeated in 3 months and yearly thereafter. Normally the pill causes transitory deterioration in glucose tolerance, increased growth hormone, a permanent change in insulin response, effects that are irreversible in 20% of users. Prediabetics should be given sequentials; diabetics should be followed weekly or monthly during oral contraception. Severe hypertension occurs in about 1% of pill users, but the risk is 4 times higher in women who had hypertension in pregnancy. Patients with increased personal or familial risk should be checked every 3 months and pills stopped immediately if blood pressure exceeds 150/100. In pill users cholesterol and free fatty acids remain normal, but lipoproteins, lecithins and triglycerides increase after 6 weeks to a plateau by 6-18 months, in proportion to estrogen dose. Since patients normally only discover hyperlipidemia after a clinical event such as xanthoma or vascular accident, those with related familial or personal history should have blood lipid studies every 3 months, and be given a progestagen only pill. Adolescents who are at high risk of pregnancy should receive progestagen or sequential pills, if their growth, bone age, hypothalamic function and reproductive organs are mature. The risk of idiopathic or posttraumatic thromboembolism is 3-9 times higher in pill users than in the normal population, but the only way of testing for risk in an individual is to do a detailed series of coagulation tests. Those predisposed should be given progestagen only or low dose pills.
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PMID:[Program of surveillance of patients under oral contraceptives]. 122 Jan 2

Of hormones secreted by the pituitary, a direct effect on cardiac metabolism and function is exerted only by growth hormone (GH). Its chronic overproduction in adulthood leads to acromegaly. The main cardiovascular manifestations of acromegaly are hypertension and cardiac hypertrophy. The paper summarizes the results of clinical research into the "acromegalic heart" in an internationally unique group of 78 patients with acromegaly on long-term follow-up. Both clinical findings and experimental data available in the literature indicate that cardiac hypertrophy is due to a direct effect of GH on the myocardium. Hypertension occurs in 50% of patients, has the nature of volume hypertension and exerts only an additive effect on the development of left ventricular hypertrophy. Once GH overproduction has been eliminated, cardiac hypertrophy and hypertension can be reversed to a certain stage, a finding highlighting the necessity of instituting treatment of acromegaly as early and as vigorous as possible.
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PMID:Heart in pituitary diseases. 130 50

The angiotensin converting enzyme (ACE) is a key component of the renin angiotensin system that contributes to the regulation of blood pressure (BP). Recent demonstration of linkage between the ACE locus and elevated BP in a rat model of hypertension has further emphasized ACE as a candidate gene in human hypertension. We report the localization of the ACE gene on the genetic map of chromosome 17, and identify an extremely polymorphic marker at the human growth hormone (hGH) locus which shows no recombination with ACE. We have found no evidence to support linkage between the ACE locus and hypertension, which suggests that mutations at the ACE locus do not commonly contribute to the pathogenesis of hypertension in our test population.
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PMID:Absence of linkage between the angiotensin converting enzyme locus and human essential hypertension. 133 66

The effect of treatment of hypertension with nifedipine on plasma renin activity, blood serum level of aldosterone in the course of renin test, and cortisol and growth hormone concentrations after stimulation with insulin hypoglycemia was followed during two weeks of treatment in 40 patients with essential hypertension. No significant differences in the secretion of the hormones studied, as compared to the patients with the normal arterial blood pressure, were found. After nifedipine treatment no significant changes in the secretion of aldosterone, cortisol and growth hormone were observed despite a significant fall in the arterial blood pressure while there was a moderate stimulatory effect on renin secretion. The results obtained indicate that nifedipine has only small effect on the hormonal system of patients with essential hypertension.
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PMID:[Effect of nifedipine treatment on the renin-aldosterone system and secretion of cortisol and growth hormone in patients with essential hypertension]. 136 91

We used color-Doppler echocardiography in an investigation of cardiac morphology and function to verify the cardiac anatomic and functional changes in acromegalic patients with or without hypertension and hyperlipemic states. Fifteen patients with growth hormone-secreting pituitary adenoma (mean age: 47.9 years) and 15 healthy control subjects were studied. We measured serum growth hormone (GH), somatomedin-C, cholesterol, triglyceride levels and carried out echocardiographic studies of the following cardiac morpho-functional parameters: left ventricular diameter, volume, mass and wall systolic stress. Serum GH and somatomedin-C levels were significantly higher in acromegalic patients than in controls (p < 0.001 and p < 0.001 respectively). Echocardiography evidenced increased left ventricular mass (60% of the acromegalic patients; p < 0.05) and increased wall systolic stress (53.3%; p < 0.05). Color-Doppler analysis evidenced abnormal diastolic function in 8 acromegalic patients (p < 0.001). We thus conclude that the most characteristic feature of acromegalic heart disease is left ventricular involvement, diastolic dysfunction, increased left ventricular mass or wall systolic stress. The pathogenesis is most probably multifactorial: essential hypertension, associated with slow and progressive evolution of heart disease, appears to be a determining factor.
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PMID:[Acromegalic cardiopathy: a morphofunctional study with color-Doppler echocardiography]. 145 53

Intrauterine growth retardation (IUGR) is an important cause of small stature in children presenting to paediatric endocrinologists. IUGR has to be differentiated from familial ('constitutional') short stature, where the growth deficit is genetically determined and/or induced by smallness of the mother (maternal constraint). Intrinsic fetal anomalies such as chromosomal abnormalities, primary growth failure syndromes, congenital infections and congenital anomalies are of equal importance with maternal disorders, in particular chronic use of alcohol, tobacco and narcotics, and pregnancy complications like hypertension and pre-eclampsia, in causing fetal growth retardation. The relative importance of placental abnormalities and environmental factors (with the exception of malnutrition) appears to be small. Some catch-up growth of children with IUGR has been observed in about 70% of all cases during the first year of life. Many IUGR children show major or minor birth defects which may be predisposing factors or may also coexist because of common underlying factors producing both small stature and structural anomalies. Since in most children with IUGR adult heights to be expected are below the population range, growth hormone treatment has been tried for many years, but the data available from the literature are not encouraging to date and need to be re-evaluated in controlled long-term trials.
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PMID:Intrauterine growth retardation and familial short stature. 152 54

The microcirculation was measured by nail-fold capillary video microscopy in 21 patients (12 men, 9 women; mean age 54.7 [29-74] years) with acromegaly. Levels of growth hormone (12.0-71.7 microU/ml) and of somatomedin C (2.4-10.5 IU/ml) were elevated in 10 patients, despite preceding treatment. Eleven patients had an increase in myocardial thickness and nine had impairment of left ventricular function, although only slight in most. Left ventricular hypertrophy was demonstrable even in the absence of hypertension. No patient had evidence of coronary heart disease. Nail-fold capillary video microscopy (capillary density, torque index, reactive hyperaemia, epidermal blood flow) failed to distinguish between successfully treated patients and those with persistently elevated growth hormone concentrations or disease duration of over 5 years. There was no evidence of inadequate capillary blood flow as a cause of abnormal function in hypertrophied organs.
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PMID:[Cardiac function and the skin microcirculation in acromegaly]. 153 57

A case of anaplastic astrocytoma following radiotherapy for growth hormone secreting pituitary adenoma is presented with a review of the literature. A 43 year old female was admitted with the signs of acromegaly and hypertension. An eosinophilic pituitary adenoma was subtotally removed by transsphenoidal approach, and followed by 60 Gy irradiation using a 2 x 2 cm lateral opposed field. Fourteen years later at the age of 57, she suffered from headache, recent-memory disturbance and uncinate fits. CT scan and MRI disclosed ring-like enhanced mass lesion in the left temporal lobe, corresponding to the previous irradiated field. 18F-FDG PET showed hypermetabolism at the lesion. Left frontotemporal craniotomy was performed, and a reddish gray gelatinous tumor containing necrotic center and cyst was partially removed. Histologically, the tumor consisted of hypercellular astrocytic cells with perivascular pseudorosette. Coagulation necrosis at the center of the tumor, and hyalinosis and fibrosis of the blood vessels in and around the tumor, which might have been caused by the antecedent radiotherapy, were recognized. Postoperative radio- and chemotherapy were given, however, she expired 13 months after the operation. Seven cases, including ours, of malignant glioma following radiotherapy for pituitary adenoma were reported in the literature. A total dose of irradiation varies from 45 to 95 Gy with a mean of 50 Gy. The period of latency before tumor occurrence ranges from 5 to 22 years with a mean of 10 years. The differentiation of radiation-induced gliomas from radionecrosis of the brain is also discussed.
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PMID:[Anaplastic astrocytoma 14 years after radiotherapy for pituitary adenoma]. 157 77


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