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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

Spontaneous canine hyperadrenocorticism is a disorder caused by the excessive production of cortisol by the adrenal cortex. Without treatment, hyperadrenocorticism is generally progressive with an unfavorable prognosis. Many factors, however, influence prognosis, including rate of progression, severity, and underlying cause. In untreated hyperadrenocorticism, death may result from metastasis of an adrenocortical carcinoma, growth of a pituitary tumor, or most commonly from complications associated with sustained hypercortisolism itself such as hypertension, cardiovascular disease, thromboembolism, glucose intolerance, and increased susceptibility to infection. This chapter will discuss the origin, diagnosis and, in some cases, treatment of the many complications associated with hyperadrenocorticism in the dog.
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PMID:Concurrent illness and complications associated with canine hyperadrenocorticism. 213 75

Pregnancy is a rare occurrence in women with Cushing's syndrome. Amenorrhea or oligomenorrhea occurs in about 75% of premenopausal women with Cushing's syndrome as a result of suppression of gonadotrophin secretion primarily by excess glucocorticoids. We have reviewed pregnancies in women with Cushing's syndrome (63 cases from the literature and four cases of our own). Since pregnant women without Cushing's syndrome develop some features of Cushing's syndrome, such as hypertension, hyperglycemia, and striae, a high index of clinical suspicion must be maintained to prevent delay in diagnosis. The physiologic changes in adrenocorticosteroid metabolism during pregnancy further complicate the diagnosis. Maternal and fetal risks increase markedly when pregnancy does occur in women with hypercortisolism. However, the wide spectrum of severity of the disease mandates an individualized approach to the therapy in each case.
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PMID:Cushing's syndrome and pregnancy. 240 45

We studied the hormonal background of the fluid derangements and arterial hypertension associated with adrenocorticotrophic hormone (ACTH) treatment for infantile spasms in ten infants aged 5-22 months. They received a 6 week course of (carboxymethyl-cellulose-)ACTH: 80 IU at 0800 hours daily in weeks 1-3, then tapering, and termination at the end of week 6. The infants showed large, variable increases in 24 h urine cortisol during treatment. The mean plasma cortisol concentration (24 h after ACTH injection) was not significantly increased, but was correlated with the relative dose of ACTH. The mean plasma aldosterone concentration decreased. No significant change occurred in plasma renin activity (PRA), or in the concentrations of renin substrate (RS) or arginine vasopressin (AVP). Seven infants developed arterial hypertension, which was severe in three. This severe hypertension was associated with the highest relative ACTH doses and the highest plasma RS and cortisol concentrations. In the group as a whole, systolic blood pressure correlated with plasma RS and cortisol concentrations, but not with the other parameters. At the end of treatment urine and plasma cortisol dropped below the pretreatment levels and stayed low for greater than 2 weeks. There was a sharp peak in PRA and plasma aldosterone concentration, and a decrease in plasma RS. Plasma AVP levels dropped markedly. The mean body weight increased sharply and urine flow decreased. Mean plasma electrolyte levels remained unaltered. The danger at termination of ACTH treatment appears to be associated with a sudden transition from hypercortisolism to hypocortisolism, activation of the renin-angiotensin-aldosterone axis, and suppression of AVP secretion.
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PMID:Hormonal background of the hypertension and fluid derangements associated with adrenocorticotrophic hormone treatment of infants. 255 92

The secondary, nonrenal forms of hypertension principally include pheochromocytoma, hyperaldosteronism, hypercortisolism, iatrogenic hypertension following medication, and hypertension related to overindulgence. Other very rare secondary forms of hypertension will not be considered here. Pheochromocytoma is the most dangerous of all the forms of hypertension. Diagnosis of the underlying cause of endocrine-derived hypertension is achieved by hormone analysis. Due to the small size of endocrine tumors, their exact localization can often not be established by sonography, such that CT or MR are the examinations of choice. Scintigrams are only necessary in special cases. For tumor localization in Cushing's disease, hormone measurements from the petrosal sinus are occasionally required. Medication, and above all, continual alcohol consumption, play an increasing role in the etiology of hypertension.
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PMID:[Diagnosis of extrarenal, secondary forms of hypertension]. 269 54

Amelioration or cure of hypertension, hypercortisolism, diarrhea with steatorrhea, and massive proteinuria resulted from excision of a pheochromocytoma that contained immunoreactive ACTH, VIP, and somatostatin. Ectopic ACTH production by the tumor was clearly the cause of the hypercortisolism, and the possible involvement of VIP and somatostatin in the diarrhea and steatorrhea was considered. The response to tumor removal suggested that the mesangioproliferative glomerulonephritis shown on renal biopsy was also a paraneoplastic phenomenon.
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PMID:Hypercortisolism, diarrhea with steatorrhea, and massive proteinuria due to pheochromocytoma. 286 63

A young male patient demonstrated unusual features of Cushing's syndrome, atrial myxomas and freckled skin pigmentation. At 4.5 years of age he presented with intermittent swelling of his face and abdomen associated with weight gain and mild hypertension. A left atrial myxoma, suspected from routine physical examination, was surgically removed at 6.1 years of age. The initial mild symptoms clinically thought to be due to Cushing's syndrome, persisted intermittently without any consistent biochemical abnormality. At 10 years of age height velocity decreased and at 12 years early osteoporosis was observed radiologically. Repeated dexamethasone tests revealed a paradoxical increase in cortisol and corticotrophin from normal basal levels. Further investigation showed a cyclical pattern of hypercortisolism. The removal of a pituitary microadenoma failed to correct the features of Cushing's syndrome or prevent intermittent hypercortisolism. At 15.3 years a second left atrial myxoma was removed. This was followed by bilateral adrenalectomy. Histologically the features were consistent with primary pigmented nodular adrenocortical disease. This is the first patient described with cyclical Cushing's syndrome as part of this unusual complex of disorders.
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PMID:Cyclical Cushing's syndrome presenting as short stature in a boy with recurrent atrial myxomas and freckled skin pigmentation. 316 6

Cushing's syndrome in childhood is generally recognized by classical features such as truncal obesity, striae, easy bruising, moon facies, hypertension and growth retardation. Exceptionally, Cushing's syndrome has been reported to present as growth failure alone. We diagnosed transient hypercortisolism in 6 children who had poor growth as their only presenting abnormality. The 6 children all had integrated concentrations of cortisols (IC-F) (14.1 +/- 1.7 micrograms/dl; mean +/- 1 SD) which exceeded the IC-F in healthy children and adults (5.7 +/- 1.5 micrograms/dl; P less than 0.001). The IC-F of these 6 index cases overlapped the range of IC-F in patients with pathologically proven Cushing's syndrome (20.2 +/- 4.7 micrograms/dl). Four of the 6 patients were treated with human growth hormone for 8 months and showed a marked improvement in their growth rates. Four patients have entered puberty and are growing at normal rates. Three of the 6 children had normal repeat IC-Fs, subsequently, at a time they had normal growth rates. In 1-1/2 to 3 years of follow-up, none of the patients developed any other stigmata of Cushing's syndrome. We conclude that transient hypercortisolism, documented by the IC-F, may cause growth failure without other symptoms of Cushing's syndrome. Growth hormone therapy may improve the growth rate of these children at the time of their poor growth.
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PMID:Growth impairment due to transient hypercortisolism. 346 64

Among the many potential causes of secondary hypertension are renal parenchymal disease, occlusive renal arterial disease, adrenocortical abnormalities, and pheochromocytoma. Renovascular hypertension can result from either renal parenchymal or occlusive renal arterial disease. Laboratory testing can help in identification and differentiation. Parenchymal diseases usually modify the urine substantially without producing urographic abnormalities, while occlusive arterial lesions produce urographic abnormalities but the urine remains normal. The diagnosis of renal occlusive arterial disease is best defined by arteriography. The only definite criterion for the existence of hypertension of renal origin is cure by either nephrectomy or renal revascularization. Adrenocortical causes of hypertension include enzymatic deficiencies, Cushing's syndrome, and primary aldosteronism. In enzymatic deficiencies, the physical findings provide the most important clues to the type of enzyme deficiency involved. In Cushing's syndrome, accurate determination of the cause of the hypercortisolism is important in terms of choice and success of treatment. The diagnosis of primary aldosteronism rests primarily on the demonstration of nonsuppressible aldosterone excretion rate during salt loading; the presence of inappropriate kaliuresis and/or suppressed plasma renin activity provides corroborative evidence of primary aldosteronism, but the absence of either or both does not preclude the diagnosis. Pheochromocytoma, although rare, is a serious and potentially fatal cause of hypertension. Definitive diagnosis depends on laboratory test results, and the tumor is usually localized by computed tomography.
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PMID:Secondary hypertension. A streamlined approach to diagnosis. 372 9

The case is presented of a male patient hospitalized for severe arterial hypertension determined by chronic constitutional hyperadrenalism. Splanchnic-sympathectomy was performed, associated to medullar sclerosis of the left adrenal with 40% sodium salicylate (genetic chemical surgery). The results after 3 years were good, both clinically and paraclinically. The constitutional background was normo-hypoadrenergic and the ecologic balance of the patient became normal after surgery.
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PMID:[Severe arterial hypertension due to chronic constitutional hyperadrenalism. Splanchnic sympathectomy and left adrenal medulla sclerosis with 40 percent sodium salicylate (result after 3 years--genetic chemosurgery)]. 622 Apr 31


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