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

Pregnancy and Cushing's syndrome are seldom found together (40 cases in the literature), since hyperadrenocorticism is often responsible for anovulation by gonadotropin suppression. We report the case of a 25-year old para II woman whose pregnancy was complicated by diabetes and arterial hypertension at 31 weeks and who received the conventional treatments (special diet, insulin therapy, pindolol). Caesarean section, motivated by premature rupture of the membranes, was performed at 37 weeks, delivering a healthy infant. The diagnosis of hypercortisolism with low ACTH level was made post partum. An adrenal tumour (the most frequent cause of Cushing's syndrome occurring during pregnancy) was removed after pre-operative treatment with ketoconazole, and endocrine functions returned to normal.
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PMID:[Adrenal adenoma disclosing after delivery]. 209 25

The role of a high CRH level in normal pregnancy remains unknown. Therefore we evaluated the concentrations of CRH and the related hormones in patients with pregnancy-induced hypertension. Fourteen women with pregnancy-induced hypertension, aged 20-39, at 30-39 gestational week, were investigated. The control group consisted of 20 healthy pregnant women matched according to gestational age. Plasma CRH beta-endorphin-like immunoreactivity, cortisol, and human placental lactogen were measured by radioimmunoassay, ACTH by an immunoradiometric method. It was found that in hypertensive patients the mean CRH concentration was significantly higher (4257 +/- 840 (SEM) ng/l) than that in healthy pregnant women (1083 +/- 227 ng/l, p less than 0.001). The concentration of ACTH, however, was only slightly higher 65.0 +/- 6.0 vs 50.7 +/- 2.5 ng/l p less than 0.025, whereas the differences in beta-endorphin, cortisol and human placental lactogen were not significant. In both groups there was no correlation between the CRH level and those of the related hormones. In healthy pregnant women the CRH level closely correlated with gestational age (r = 0.76, p less than 0.001), whereas in patients with hypertension no such correlation was present (r = 0.29). We assume that the marked enhancement of plasma CRH in pregnancy-induced hypertension is probably caused by its decreased breakdown in ischemic placental tissue, but its increased synthesis in the placenta and its indirect counterregulatory hypotensive role must also be considered.
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PMID:Enhancement of plasma corticotropin-releasing hormone in pregnancy-induced hypertension. 214 45

The short- and long-term outcome and special problems of 24 children with infantile spasms and tuberous sclerosis (TS) was studied. The diagnosis of TS is frequently missed: white spots on the skin have to be carefully looked for. In the present study, these spots were always found, and calcifications or hypodense areas of the brain were revealed by CT scans before one year of age. In addition to epilepsy, manifestations of TS included: giant cell astrocytoma, iridic heterotopia, cardiac rhabdomyoma, brain cysts, polycystic kidneys with severe arterial hypertension, retinal phakomas, angiofibroma and white spots on the skin. Long-term outcome was poor. None of the children had normal intelligence and all but one had epilepsy, which was often intractable. Behavioural problems were common. The prognosis, in terms of later intelligence, epilepsy and behavioural problems, was worse than in those with 'idiopathic' infantile spasms or in those with simultaneous neurological disorders. An early diagnosis of TS in patients with infantile spasms clarifies the prognosis and avoids some of the hazards of ACTH therapy. TS children have a high relapse rate after ACTH therapy, so prolonged courses may be indicated.
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PMID:Tuberous sclerosis and infantile spasms. 215 40

Beta-endorphin (B-Ep), ACTH plasma levels and cortisol serum levels have been evaluated by RIA, in 27 patients suffering from essential blood hypertension and in 20 healthy control subjects. The study was repeated in the hypertensive group after clonidine treatment for 15 days. B-Ep plasma levels were normal in the I stage of hypertension and did not show any significant difference in relation to the severity and duration of hypertension. ACTH and cortisol circulating levels in the hypertensive patients were in normal range. The increase of B-Ep plasma levels in the II and III stage of the hypertension is not modified by the reduction of blood pressure values; therefore it is unlikely linked to the elevated blood pressure, but probably to the vascular complications. Moreover, the results obtained after clonidine treatment seem to exclude that the hypotensive action of the drug is mediated by increment of B-Ep circulating levels.
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PMID:[Plasma levels of beta-endorphin and ACTH and serum levels of cortisol in different stages of arterial hypertension before and after clonidine therapy]. 216 79

A genetic male with 17 alpha-hydroxylase deficiency is described. The patient, raised as a female, was seen at 17 yr of age for impuberism. She presented all the features of the classical severe form of the disease: complete female phenotype; hypertension; hypokalemia; elevated levels of plasma progesterone, 11-deoxycorticosterone, corticosterone (B), and ACTH; and suppression of renin and aldosterone production. Levels of 17-hydroxyprogesterone, 17-hydroxypregnenolone, and all androgens were barely detectable. Hormone steroid patterns were determined in basal conditions and after acute ACTH stimulation in the parents and the two unaffected brothers in order to identify the heterozygotes. Subtle abnormalities in B and aldosterone secretion were observed in the male members of the family. On the basis of an increased ratio of B to aldosterone the two brothers were assumed to be heterozygotes. The mother had normal basal and stimulated levels of B, deoxycorticosterone, and aldosterone. In the parents and two brothers the progesterone responses to ACTH were exaggerated. The most striking finding in the father and both brothers was the observation of increased basal plasma 17-hydroxyprogesterone, unresponsive to ACTH stimulation, suggesting a partial Leydig cell 17,20-lyase deficiency in the male heterozygotes of this family. This study shows that a short ACTH test can help to identify the heterozygotes in affected families, but the abnormalities found are more heterogeneous than previously suggested.
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PMID:A case of male pseudohermaphroditism due to 17 alpha-hydroxylase deficiency and hormonal profiles in the nuclear family. 216 72

This study investigated the ability of two diuretics, amiloride and frusemide, to prevent the development of ACTH induced hypertension in conscious sheep. Infusion of amiloride (20 mg/day) or frusemide (50 mg/day) for three days into normotensive sheep did not have any significant effects on blood pressure. Amiloride blocked ACTH-induced hypertension and the sodium retention and hypokalemia which is usually associated with ACTH administration. Frusemide failed to completely block the hypertension and potassium loss, however it blocked the transient initial urinary sodium retention associated with ACTH-induced hypertension. As frusemide failed to completely block the hypertension it is unlikely that the amiloride effect is due primarily to effects on urinary Na excretion. It is possible that amiloride is exerting its antihypertensive effects by blocking sodium channels.
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PMID:Amiloride blocks the onset of ACTH-induced hypertension in the sheep. 217 63

Age-related increase of vascular resistance determines blood pressure (BP) level in normotensive and hypertensive people. Maintenance of normotension in old age is connected with a decrease of the cardiac output. Increased cardiac output is considered to be an important factor of arterial hypertension in old age. Disturbances in renin-angiotensin-aldosterone and hypophyseal-adrenal systems are observed with advanced age and their degree increases in arterial hypertension. Variability of BP within normal range is closely connected with plasma aldosterone and cortisol concentrations. BP level and increased cardiac output are related to increased plasma ACTH and vasopressin concentrations in hypertensive subjects.
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PMID:[Hormonal mechanisms in the regulation of arterial pressure and its hemodynamic structure in old age]. 217 88

A unique case of 17 alpha-hydroxylase deficiency with steroid-responsive primary hyperaldosteronism is reported. Initially the patient was misdiagnosed as testicular feminization for 16 years and was thought to have typical primary hyperaldosteronism for 5 years. However, careful detailed endocrine studies showed markedly elevated progesterone, deoxycorticosterone, and 18-hydroxycorticosterone values with low levels of 17-hydroxyprogesterone, 11-deoxycortisol, testosterone, and DHEA-Sulfate. In contrast to the suppressed aldosterone levels that are found in 17 alpha-hydroxylase deficiency, this patient's aldosterone levels were inappropriately elevated before and after ACTH stimulation. Use of glucocorticoid replacement resolved the patient's symptoms and completely corrected the hypokalemia and hypertension. In summary, recognition of 17 alpha-hydroxylase deficiency with steroid-responsive primary hyperaldosteronism is important because hypertension, hypokalemia, and symptoms respond to steroid replacement.
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PMID:17 alpha-hydroxylase deficiency masquerading as primary hyperaldosteronism. 226 76

A case of a 29 year old man with typical picture of Cushing's syndrome is presented: pronounced hypodynamics, diabetes mellitus, hypertension, transitory psychic disorders, severe hypokalemia, metabolic alkalosis, hypercorticism, disturbed 24 h rhythm of cortisol secretion, high serum ACTH level. The treatment with steroidogenesis blockers (Metyrapone, o,p'DDD) led to a limited improvement. The well expressed organic changes in the cardiovascular and respiratory systems and pulmonary thromboembolism led to a fatal outcome. The post mortem examination revealed a pancreatic tumor 30/30 mm in size (histologically carcinoid) and enlarged hypophyseal gland with oxyphil cell hyperplasia. The electron microscopic examination found secretory granules in the pancreatic tumor cells. Concurrent ectopic secretion of ACTH by the oxyphil tumor cells is discussed.
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PMID:[Cushing's syndrome resulting from ectopic hormonal secretion]. 228 96

Selective renal phlebography, phlebotonometry, selective analysis of the blood from the renal veins and vena cava inferior for the activity of plasma renin, catecholamines, prostaglandins E2, pO2 and pCO2, peripheral blood analysis for levels of progesterone, androstendione, testosterone, ACTH, ACTH-tolerance test, orchidometry, ejaculate microscopy, evaluation of seminal plasma testosterone, trochanter index and parameters of sexual maturation were performed during the treatment of 70 patients with left varicocele. Based on the results the authors concluded that not only the left testicle, but the left adrenal was involved in the course of organic renal venous hypertension. A significant feedback correlation was revealed between the peripheral blood progesterone and the left kidney venous pressure (r = -0.50, p less than 0.01) and between the peripheral blood progesterone and the number of motile spermatozoa in the ejaculate (r = -0.31, p less than 0.05). Pathogenesis of organic renal venous hypertension and spermatogenesis failure were supplemented by the conclusion that the left adrenal central vein was the first to involve into the compensation of venous hypertension. Retrograde alterations in the direction of the blood flow in the left adrenal central vein resulted in the abnormal stimulation of steroidogenesis in the cortical layer. The excessive production of antiandrogenic steroid hormones by the left adrenal gland was a cause of spermatogenesis damage in both testicles. The blockage of the left adrenal androgenic hormones of the hypothalamo-hypophyseal system can deteriorate the process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The role of the functional interrelation of the adrenals and testes in the pathogenesis of sterility in patients with left-sided varicocele]. 236 17


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