UMLS:C0020538 - FACTA Search

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Cushing's syndrome during pregnancy is most often caused by an adrenal cortical tumour; it is a rare event which bears poor foetal and maternal prognoses. We report 3 cases of adrenal cortex carcinoma diagnosed during pregnancy (after 24, 27 and 28 weeks respectively of amenorrhea) and revealed by local tumoral signs in 2 cases and by pulmonary embolism in the third. Because hair growth was moderate and weight gain as well as high blood pressure had mistakenly been attributed to the pregnant state, these clinical features of hypercortisolism has only lately been related to tumoral secretion. The hypercortisolic state was firmly established by comparing the patients' urinary cortisol levels (677, 941 and 2,167 micrograms/day) and 20-hour salivary cortisol levels (9.9, 15 and 25.3 micrograms/ml) with values obtained in women at the same stage (88 +/- 11.4 micrograms/day and 2.31 +/- 0.25 micrograms/ml). The aetiological diagnosis was made by the finding of a highly increased salivary testosterone levels (50, 34 and 95 pg/ml; normal = 8.6 +/- 4 pg/ml), and by magnetic resonance imaging which showed unilateral adrenal masses of 3, 8 and 20 cm in diameter respectively. These 3 cases illustrate the difficulty of the clinical diagnosis of hypercortisolism during pregnancy. Assessment of the unbound steroids and magnetic resonance imaging are the most useful methods for an early diagnosis, thus preventing the severe complications which may otherwise reveal this rare pathological condition.
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PMID:[Cushing syndrome during pregnancy. New diagnostic methods used in 3 cases of adrenal cortex carcinoma]. 129 77

Cushing's syndrome with pregnancy is rare, and only about 60 cases have been reported. In the recent 4 years, 3 cases were diagnosed in Chang Gang Memorial Hospital. They presented with serious maternal complications early in the second month of pregnancy, including hypertension, proteinuria and lower leg edema. Unfortunately it was not diagnosed until the 20th week of pregnancy. They had the same hormone profile as other Cushing's syndrome patients who were not pregnant. Under the supportive treatment they had outcomes of two premature deliveries and one still birth. Just after delivery all patients received left adrenalectomy and pathology showed adenoma. All of them had good recovery courses. According to the literature, early treatment (surgical operation, medical treatment, or irradiation) could decrease maternal morbidity and fetal loss rate.
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PMID:[Cushing's syndrome with pregnancy. Report of three cases]. 129 59

A 57-year-old obese woman with hypertension, diabetes mellitus, osteoporosis, and a 40-year history of secondary amenorrhea was diagnosed with corticotropin-dependent Cushing's syndrome. Dynamic endocrine testing and radiological evaluation did not reveal definitively the source of the excess corticotropin. Bilateral adrenalectomy was performed with resolution of the signs and symptoms of hypercortisolism. Four years later, the patient was noted to have rising serum corticotropin levels and an enlarging pituitary mass; hyperprolactinemia also was documented. A diagnosis of Nelson-Salassa syndrome was made, and she underwent a transsphenoidal adenomectomy. A histological examination of the specimen revealed two distinct, albeit contiguous, adenomas: a corticotroph adenoma and a lactotroph adenoma. Postoperatively, the serum prolactin and corticotropin levels decreased significantly. Although the stalk section effect resulting from compression by a pituitary adenoma can raise serum prolactin levels, a concurrent lactotroph adenoma should be considered in patients with nonfunctional or functional pituitary adenomas of other types associated with significantly elevated prolactin levels. The mechanisms underlying simultaneous adrenocorticotropic hormone and prolactin excess are discussed.
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PMID:Coexisting corticotroph and lactotroph adenomas: case report with reference to the relationship of corticotropin and prolactin excess. 131 62

The most common ectopic production of a pituitary hormone is the one of ACTH leading to Cushing's syndrome. Ectopic ACTH-hypersecretion is the cause of Cushing's syndrome in 10-15% of all cases. The ACTH-secreting tumours are often oat-cell carcinomas of the lung, less frequently pancreatic cancers, hypernephromas, or C-cell carcinomas of the thyroid. Some of these tumours may be benign or semi-benign as the rare carcinoid tumours and cause great problems in the differential diagnosis of ACTH-dependent hypercortisolism. Out of 173 of our patients with Cushing's syndrome observed in the last 12 years 21 were caused by ectopic ACTH-production. Of these 21 patients 13 have a small cell carcinoma of the lung. The ectopic ACTH-syndrome often has typical clinical features caused by the levels of ACTH and cortisol leading to hypocalcemic alkalosis with muscle weakness and wasting, carbohydrate intolerance, and hypertension with oedema. The survival time in many of these patients is not long enough to allow them to develop typical signs of Cushing's syndrome though they are often highly pigmented. These patients are easily diagnosed. However, patients with small tumours which do not cause very elevated ACTH-levels and who have the more typical clinical signs of full-blown Cushing's syndrome are difficult to recognize. For the differential diagnosis of ACTH-dependent Cushing's syndrome the corticotropin-releasing hormone (CRH) stimulation test and dexamethasone suppression test with high doses are helpful. In special cases the venous sampling procedure for ACTH-measurements is necessary, also CT or NMR is helpful. Ectopic CRH-production is a rare cause of ACTH-dependent Cushing's syndrome. Patients with ectopic CRH-production and consecutive ACTH-hypersecretion from the pituitary have not been studied extensively. There are especially no well documented results of the use of the CRH-stimulation test in vivo in this group of patients with Cushing's syndrome. On the other hand, in the documented cases, not only CRH-, but also ACTH-production was found in the tumours. So far, this rare cause of ACTH-dependent Cushing's syndrome has to be excluded or confirmed by the measurement of endogenous CRH-levels. But until now we have not been able to detect one single case of ectopic CRH-production using a sensitive homologous CRH-radioimmunoassay over a period of more than 8 years in which we have seen nearly 120 newly diagnosed patients with ACTH-dependent Cushing's syndrome. Only in the plasma and tumour tissue of two patients of other groups have we found high CRH-levels.
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PMID:Ectopic production of ACTH and corticotropin-releasing hormone (CRH). 132 73

Cyclosporine is a specially useful immunosuppressor agent in children subjected to renal transplantation, minimizing the deleterious effect of steroids on growth and the development of Cushing syndrome. However, side effects which require close supervision are well known, including liver, kidney and central nervous system toxicity. Seizures, cerebellar ataxia, aphasia, paresthesia and behavioral disorders are characteristic of the latter. Hypertension and hypomagnesemia have been identified as risk factors. In contrast to nephrotoxicity, CNS toxicity is not related to plasma levels of cyclosporine. In this paper 2 patients, 10 and 11 year old, manifesting cyclosporine neurotoxicity after renal transplant, are reported.
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PMID:[Neurotoxicity caused by cyclosporin A in renal transplantation in children]. 134 84

Glucocorticoid (GC) excess (Cushing's syndrome) is associated with hypertension in at least 70% of patients (in our series 89/130), independently of the subtype (pituitary or adrenal) and the duration, but not of the age of the patients. Cardiovascular damage is quite frequent in hypertensives, but is sometimes also present in normotensives. The mortality of patients with Cushing's syndrome is four times that of the general population when matched for age and sex, and much of this excess mortality is caused by cardiovascular disease. Hypertension remits in most of the patients after successful treatment, but may persist in some. Hypertension also occurs in 20% of patients treated with GC orally. The type of hypertension is independent of salt uptake, can not be controlled by spironolactone but is inhibited by a GC antagonist such as RU486. Experimentally-induced hypertension with oral cortisol (F) is associated with a rise in cardiac output, a fall in calculated total peripheral resistance, an increased forearm vascular responsiveness to exogenous norepinephrine, but no change in overall sympathetic tone, or in norepinephrine reuptake. The increased pressor responsiveness is probably due to local postsynaptic effector mechanisms in the resistance vessels, which could be important in phasic increases in neuronally mediated constrictor responses. Both in patients with Cushing's syndrome and in those on chronic GC treatment, the circadian blood pressure variations are absent or reversed. This may contribute to the deleterious effects of the GC excess on blood vessels. The vascular effects of the GC may be mediated by the activation of specific cardiovascular receptors, by modulating vascular transport systems, or by altered catecholamine or prostaglandin metabolism. GC may also act as mineralocorticoids (MC): in fact type 1 MC receptors are unable, in vitro, to distinguish between aldosterone and cortisol. The specificity-conferring mechanism of typical target organs for MC (e.g. kidney)--is thought to be due to the action of local 11-beta-hydroxysteroid dehydrogenase, which converts F to biologically inactive cortisone (E). When the activity of the enzyme is impaired (syndrome of apparent MC excess, liquorice or carbenoxolone administration), F acts as a MC and MC-hypertension with hypokalemia occurs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Glucocorticoid-dependent hypertension. 139 Feb 89

The mechanisms of hypertension during primary hyperaldosteronism and Cushing's syndrome are not completely understood. An enhanced vascular sensitivity to noradrenaline has been described in both situations. Neuropeptide Y (NPY) induces direct vasoconstriction and potentiates the action of noradrenaline. Sodium retention and dexamethasone have been shown to increase circulating NPY levels in animals and the expression of NPY in neuroendocrine cells. In order to determine if NPY could be involved in the enhanced vascular sensitivity to noradrenaline associated with adrenocortical hyperactivity, we measured plasma NPY in patients with Cushing's syndrome (n = 26) and primary hyperaldosteronism (n = 15) and compared it with that of hypertensive patients with pheochromocytomas (n = 13) or essential hypertension (n = 51) and with normotensive controls (n = 47). The concentration of NPY-Like immunoreactivity (NPY-Li) (mean +/- S.E.) in controls was 39.6 +/- 3.0 pg/ml. Elevated concentrations were found in 77% of the samples collected from pheochromocytoma patients (1180.4 +/- 394.0 pg/ml). NPY-Li levels in patients with essential hypertension (35.0 +/- 2.6 pg/ml), primary hyperaldosteronism (31.3 +/- 3.9 pg/ml) and Cushing's syndrome (33.1 +/- 4.8 pg/ml) were not different from that of controls. NPY-Li levels in hypertensive and normotensive patients with Cushing's syndrome were similar (38.5 +/- 7.5 vs 24.2 +/- 3.7 pg/ml). No correlation was found between the NPY-Li level and the mean blood pressure at the time of sampling. Our results suggest that NPY is unlikely to be involved in the pathogenesis of hypertension associated with primary hyperaldosteronism and Cushing's syndrome.
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PMID:Plasma concentration of neuropeptide Y in patients with adrenal hypertension. 147 6

The antiprogestin RU 486 converts the early pregnant uterus by increasing the sensitivity of the myometrium to prostaglandin (PG). These effects of antiprogestin have resulted in the development of nonsurgical procedures to abort embryos based on a combination of RU 486 and different PG-analogues administered vaginally or intramuscularly. RU 486 also has a softening effect on the cervix which may be used as pretreatment in second and third trimester abortions. The effects, mode of action, dangers, and the many other postulated clinical implications (like breast cancer, meningioma, ectopic pregnancy, fetal death in utero, induction of labour, initiation and promotion of lactation, endometrial or ovarian cancers, leukemia, Cushing's syndrome, uterine adenomyosis, acute uremia, leiomyosarcoma, hypertension, etc.) are discussed.
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PMID:[Mifepristone (RU 486)]. 151 99

Adrenal tumors are usually diagnosed by clinical symptoms of hormone excess. The increasing use of ultrasound and computed tomography results in the detection of a substantial number of incidentally discovered adrenal tumors. Most of these tumors are nonfunctional adrenocortical adenomas, but a few cases of subclinical cortisol production in "incidentalomas" have been reported. We investigated prospectively the prevalence of autonomous cortisol production in 68 patients (44 females and 24 males, aged 25-90 yr) with adrenal incidentalomas at our institution. As a screening procedure all patients with incidentalomas underwent an overnight dexamethasone suppression test (1 mg). Patients who failed to suppress serum cortisol below 140 nmol/L (5 micrograms/dL) underwent more comprehensive studies (prolonged dexamethasone suppression test, determination of the diurnal rhythm of cortisol secretion in saliva, and CRH stimulation test). Eight patients (12% of all patients with incidentalomas; 5 females and 3 males, aged 25-71 yr) were finally identified as having cortisol-producing tumors, and the findings in these patients were compared with those of overt Cushing's syndrome in 8 patients (8 females, aged 26-50 yr) suffering from cortisol-producing adrenal adenomas. The tumor size of patients with cortisol-producing incidentalomas ranged from 2-5 cm. No specific signs and symptoms of hypercortisolism were present, but arterial hypertension (seven of eight subjects), diffuse obesity (four of eight subjects), and noninsulin-dependent diabetes mellitus (NIDDM; two of eight subjects) were frequently observed. Baseline cortisol levels were in the normal to upper normal range, whereas baseline ACTH levels were suppressed in five of the eight patients. In none of the patients was serum cortisol suppressible by low dose or high dose dexamethasone. The ACTH and cortisol responses to CRH were normal in two, blunted in one, and suppressed in four patients. Unilateral adrenalectomy was performed in seven patients and resulted in temporary adrenal insufficiency in four of them. After surgery, improvement of arterial hypertension, a permanent weight loss in obese subjects, and a better metabolic control of NIDDM were noted in the majority of patients. The following conclusions were reached. Incidentally diagnosed adrenal tumors with pathological cortisol secretion in otherwise clinically asymptomatic patients are more frequently observed than previously assumed. Adrenocortical insufficiency is a major risk in these patients after adrenalectomy. After surgery, hypertension, obesity, and NIDDM may improve. Patients with asymptomatic adrenal incidentalomas, therefore, should be screened for cortisol production by means of an overnight dexamethasone suppression test.
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PMID:Preclinical Cushing's syndrome in adrenal "incidentalomas": comparison with adrenal Cushing's syndrome. 151 73

To assess the cardiac characteristics and postoperative courses in patients with Cushing's syndrome, electrocardiography and echocardiography were performed to study 12 consecutive, unselected patients, and results were compared with those of essential hypertension and primary aldosteronism. Eleven patients had hypertension and 7 had diabetes mellitus. Before adrenalectomy, common electrocardiographic abnormalities consisted of high-voltage QRS complexes (10 patients) and negative T waves (7 patients). Echocardiograms showed left ventricular hypertrophy in 9 patients, and all the patients had evidence of asymmetric septal hypertrophy. In patients with left ventricular hypertrophy, the thickness of the interventricular septum ranged from 16 to 32 mm, whereas the ratio of the thickness of interventricular septum to that of the posterior wall ranged from 1.33 to 2.67. The interventricular septum in Cushing's syndrome was extremely thicker and asymmetric septal hypertrophy occurred more often than essential hypertension and primary aldosteronism. Nine patients could be followed up after operation. In these patients abnormal electrocardiographic findings had normalized, the thickness of interventricular septum had decreased and asymmetric septal hypertrophy had disappeared except in 1 patient. The reason why left ventricular hypertrophy in Cushing's syndrome is severe is still unknown. Because left ventricular hypertrophy is more severe and the frequency of asymmetric septal hypertrophy much greater in Cushing's syndrome than in essential and other secondary hypertension, it is thought that not only increased aortic pressure but excessive plasma cortisol may be etiologic factors in the progression of left ventricular hypertrophy in Cushing's syndrome.
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PMID:Cardiac characteristics and postoperative courses in Cushing's syndrome. 153 96

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