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

A patient with suspected exogenous hyperadrenocorticism and hypertension was treated with cessation of steroids, a low-sodium diet, and moderate doses of diuretics. Hypertension persisted, and severe dehydration and hyponatremia developed, but all responded to normal saline administered intravenously. The concurrence of (1) hypoadrenocorticism and its attendant fluid and electrolyte disturbances, (2) the use of diuretics, and (3) an intact renin-angiotensin system was responsible for the exaggerated and seemingly paradoxical responses. Selection of diuretics should be made cautiously and careful patient monitoring is imperative when compromised adrenocortical function is suspected.
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PMID:Unusual blood pressure response in a patient with secondary adrenocortical insufficiency. 743 55

Cushing's syndrome, an unusual group of disorders characterized by hypercortisolism, must be considered in the differential diagnosis of such common clinical problems as hirsutism, menstrual irregularity, hypertension, diabetes mellitus, and obesity. Its distinct forms--pituitary-dependent Cushing's syndrome (Cushing's disease), adrenal tumor and ectopic ACTH syndrome--must be identified correctly so that specific therapy can be administered. In the majority of cases, use of a relatively simple diagnostic sequence will provide accurate and rapid diagnosis. However, in our experience with more than 60 patients, diagnostic difficulties may arise from a variety of conditions (e.g., drug interference, alcohol ingestion, and depression). In addition, unusual circumstances, such as unexpected responses to dexamethasone, may complicate the diagnosis. Our approach to these problems is illustrated through a report of seven cases, and we emphasize that the proper management of Cushing's syndrome mandates a thorough marshalling of all the available data.
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PMID:Cushing's syndrome: problems in diagnosis. 745 63

Pheochromocytoma was diagnosed in 4 dogs with pituitary-dependent hyperadrenocorticism and 2 dogs with hyperadrenocorticism caused by adrenocortical tumor. All dogs were examined initially because of clinical signs associated with hyperadrenocorticism. Pheochromocytoma was suspected in 2 dogs with pituitary-dependent hyperadrenocorticism that had ultrasonographic evidence of an adrenal gland mass, and in 1 dog suspected to have hyperadrenocorticism associated with an adrenocortical tumor after complications (systemic hypertension, cardiac arrhythmias) developed during induction of anesthesia. Pheochromocytoma was an unexpected finding at necropsy in the remaining 3 dogs. Two dogs collapsed suddenly and died before diagnostic tests could be performed; the other dog died during anesthesia for cobalt teletherapy of a pituitary macroadenoma. Hypertension, most notable during digital manipulation of the affected adrenal gland, developed during anesthesia and surgery in 3 dogs that underwent exploratory celiotomy.
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PMID:Pheochromocytoma and hyperadrenocorticism in dogs: six cases (1982-1992). 762 33

The authors describe the unusual case of a 52-year-old man with Cushing's syndrome caused by bilateral pigmented micronodular adrenal hyperplasia. The only features of hypercortisolism were hypertension and severe symptomatic osteopenia with vertebral, rib, and scapular fractures. Four years after bilateral adrenalectomy, the bone density had increased slightly, but the patient remained osteopenic and continued to have vertebral compression fractures. This case report emphasizes the importance of an indepth search for secondary causes of osteoporosis, including evaluation of adrenal function in patients who have unexplained osteoporosis. Early diagnosis and treatment is imperative to prevent severe bone loss and associated skeletal morbidity.
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PMID:Severe symptomatic osteopenia in a man with pigmented micronodular adrenal hyperplasia. 764 84

A case of adrenocorticotropic hormone independent bilateral adrenocortical macronodular hyperplasia (AIMAH) is reported. A 59 year old male was admitted to hospital because of hypertension. Subsequently, hypercortisolism, low plasma adrenocorticotropic hormone (ACTH), loss of diurnal rhythm of ACTH, lack of suppression with high dose dexamethasone were found and bilateral adrenal enlargement was detected by abdominal computerized tomography and adrenal scintigraphy. Bilateral total adrenalectomy was performed under a diagnosis of bilateral adrenal hyperplasia associated with Cushing's syndrome. Both adrenal glands were enlarged in size and weight. Bulging nodules were found at the cut section. Microscopically, a variegated histologic pattern including trabecular, adenoid and zona glomerulosa-like (ZG-like) structures was revealed in the nodules. Immunohistochemical examination disclosed positive staining of cytochrome P-450 17 alpha, negative of 3 beta-HSD in the ZG-like structure. Ultrastructurally, the cells composing the ZG-like structure were similar to those of the ZG in normal adrenal cortex. The authors agree that AIMAH is one of the entities causing Cushing's syndrome, and advise pathologists to keep this disorder in mind when they examine the adrenals in Cushing's syndrome.
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PMID:Adrenocorticotropic hormone-independent bilateral macronodular adrenocortical hyperplasia associated with Cushing's syndrome. 778 95

Glucocorticoids mainly act through binding to cytosolic receptors that translocate to the nucleus after ligand binding, and dimerize to affect gene transcription in multiple fashions. The liganded receptors may interact with DNA at specific glucocorticoid responsive-elements, may physically hinder the ability of other transcription-regulating proteins to interact with their own DNA response-elements, and may form intranuclear complexes with the transcription factor c-jun, thus changing the number of c-jun/c-fos heterodimers that bind at AP-1 sites. By these, and perhaps other, mechanisms, physiologic concentrations of glucocorticoids regulate normal tissue metabolism, and supraphysiologic concentrations cause Cushing's syndrome. Cushing's syndrome leaves virtually no body tissue untouched. Left untreated, it results in progressive adiposity, myopathy, dermopathy (atrophy, stria, purpura, and hirsutism), psychopathy, glucose intolerance, hypercholesterolemia, hypertension, atherosclerosis, immunosuppression, and, ultimately, death. The physiology underlying each of these effects of hypercortisolism has been reviewed. The differences in the presentation of Cushing's syndrome in children and adults have also been discussed. The goal of the clinician must be to identify individuals with Cushing's syndrome as early in the course of the disease as possible so as to avoid the devastating complications that result from prolonged hypercortisolism. In patients for whom screening tests are equivocal, or only intermittently elevated, it may be necessary to re-evaluate the patient over time to establish that the patient has hypercortisolism. Some clinical guidelines for which patients to screen for hypercortisolism have been presented. Once hypercortisolism is established, patients with mild hypercortisolism (urine free cortisol less than four-fold above the upper limit of normal) should undergo tests to differentiate true Cushing's syndrome from a pseudo-Cushing state.
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PMID:Glucocorticoid action and the clinical features of Cushing's syndrome. 780 50

Familial glucocorticoid resistance (FGR) is a rare hereditary disorder characterized by hypercortisolism and the absence of stigmata of Cushing's syndrome. The inability of glucocorticoids to exert their effects on target tissues is compensated for by increases in circulating corticotropin (ACTH) and cortisol, the former causing excess secretion of both adrenal androgens and adrenal steroid-biosynthesis intermediates with salt-retaining activity. There is considerable variability in the clinical presentations of FGR ranging from asymptomatic, to isolated chronic fatigue and to hypertension with or without hypokalemic alkalosis or to hyperandrogenism, or both. In women, hyperandrogenism can result in acne, hirsutism, menstrual irregularities, oligoanovulation, and infertility; in men it may lead to infertility and in children to precocious puberty. The reported molecular defects in FGR, such as point mutations and a microdeletion of the glucocorticoid receptor (GR) gene, cause partial resistance by, respectively, compromising the function of the GR or decreasing its intracellular concentration in glucocorticoid target tissues. Complete glucocorticoid resistance is believed to be incompatible with life in humans. Hence, the glucocorticoid resistance cases reported have been partial and of variable degree. The extreme variability in the clinical manifestations of the disorder can, additionally, be explained by differing sensitivity of target tissues to mineralocorticoids or androgens or both, and perhaps by different biochemical defects of the glucocorticoid receptor, causing selective resistance of certain glucocorticoid responses in specific tissues. Isolated tissue-resistance from a somatic mutation of the GR in a corticotropinoma from a patient with Nelson's syndrome was also found, suggesting that this may be a mechanism of tumorigenesis. There is additional evidence that defects of GR function can appear surreptitiously in a variety of clinical conditions, suggesting that glucocorticoid resistance in humans may be involved in the pathogenesis and/or clinical picture of a plethora of disease states, of which FGR is the archetype.
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PMID:Glucocorticosteroid resistance in humans. Elucidation of the molecular mechanisms and implications for pathophysiology. 782 90

Adrenalectomy for adrenal tumor was performed on 25 patients at Kushiro municipal general hospital between 1982 and 1993. There were 17 women and 8 men aged 34 to 66 (mean 52.7) years. Clinical diagnoses were pheochromocytoma (6), Cushing's syndrome (8), primary aldosteronism (4), incidentaloma (7). Pathological diagnoses were pheochromocytoma (6), cortical adenoma (17), hyperplasia with hypercortisolism (1), schwannoma (1). Angiography and venous sampling were unuseful for clinical identification of adrenal tumor. After removal of the tumor, glucose-intolerance disappeared in 4 of 6 cases with pheochromocytoma and one of 7 cases with incidentaloma, mental aberration was improved in 2 of 8 cases with Cushing's syndrome, and hypertension was improved in 4 of 7 cases with incidentaloma. Since clinical symptoms (hypertension and glucose-intolerance) were improved postoperatively in 4 of 7 cases with incidentaloma, adrenalectomy is recommended for incidentaloma. Transabdominal approach was suitable for pheochromocytoma and bilateral adrenal tumor, but postoperative recovery was slow. In our experience, pleural injury was found in 40% of translumbar approach. Four laparoscopic operations were performed recently, this procedure gave most fast postoperative recovery to compare with other approach.
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PMID:[Clinical study of 25 cases with adrenal tumor--comparison between transabdominal, translumbar, laparoscopic approach]. 802 40

A 38 year old woman and her first cousin, a 41 year old man, presented both with hypertension, hypokalemia, hyperaldosteronism, and low plasma renin activity in our Hospital. In both patients, plasma and urine aldosterone were constantly above the normal range, even on a high NaCl diet (250 mEq/day), while the plasma aldosterone response to postural changes was normal. In the female patient abdominal ultrasonic scan, CT scan, MRI, and adrenal gland phlebography were normal, but blood from the left adrenal vein contained 1002 pg/ml of aldosterone, versus 91 pg/ml in the contralateral one. Interestingly, the secretion of cortisol was also lateralized (plasma cortisol levels being of 28.8 mcg% in the left, 2.3 mcg% in the right adrenal gland), although neither clinical nor laboratory signs of hypercortisolism were present. Spironolactone treatment (100 mg/daily) completely reversed the syndrome of mineralocorticoid excess. After 2 years, patient has normal blood pressure and serum K+ levels.
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PMID:Unilateral adrenal hypersecretion of both aldosterone and cortisol in two first cousins with a syndrome of mineralocorticoid excess but without signs of hypercortisolism. 805 32

To investigate whether chronic endogenous hypercortisolism might alter adrenomedullary phenylethanolamine N-methyltransferase activity, we measured epinephrine/norepinephrine (E/NE) ratios in the adrenal venous blood of 8 patients undergoing surgery for Cushing's syndrome and in 12 control subjects undergoing surgery for left kidney diseases. To investigate the adrenomedullary secretory activity in Cushing's syndrome, we measured basal E plasma levels in 24 patients and 32 age- and sex-matched normal control subjects, and we evaluated the adrenomedullary response to glucagon in 9 patients and in 22 age- and sex-matched normal subjects. Last, to clarify whether chronic endogenous hypercortisolism might modify E plasma levels through a modification of E metabolism, we measured the E MCR in four patients and four age-matched controls. Mean (+/- SEM) E/NE ratio in adrenal venous blood was similar in patients with Cushing's syndrome (4.61 +/- 0.78) and in the control group (4.71 +/- 0.74). Mean (+/- SEM) basal plasma E was significantly lower in patients with Cushing's syndrome (98.2 +/- 10.9 vs. 184 +/- 25.1 pmol/L, P < 0.01) than in the control group. Similarly, plasma NE also was reduced (0.75 +/- 0.09 vs. 1.10 +/- 0.07 nmol/L, P < 0.01). In patients with Cushing's syndrome the E response to glucagon was significantly reduced (P < 0.01). E MCR was almost identical in patients with Cushing's syndrome (1.48 +/- 0.10 L/min.m2) and in control subjects (1.51 +/- 0.10 L/min.m2). Our data demonstrate that: 1) chronic endogenous hypercortisolism is not able to change adrenomedullary phenylethanolamine N-methyltransferase activity and therefore the quality of adrenomedullary secretion; and 2) chronic endogenous hypercortisolism causes a decrease in basal and stimulated adrenomedullary activity without altering E MCR significantly. Therefore the adrenal medulla does not seem to play a pathogenetic role in the hypertension of Cushing's syndrome.
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PMID:Adrenal medulla secretion in Cushing's syndrome. 820 Sep 34


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