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

Endocrine hypertension secondary to disorders of the adrenal glands is uncommon, but by no means rare. The importance of correct biochemical diagnosis and subsequent localization of the responsible lesion(s) lie in the fact that many of these syndromes occur in younger patients, may exhibit familial patterns of inheritance and are frequently amenable to surgical cure. The radiopharmaceuticals (131)1-6 beta-iodomethyl-19-norcholesterol (NP-59), a marker of adrenocortical cholesterol uptake, and (131)1- and (123)1-metaiodobenzylguanidine (MIBG), a norepinephrine (NE) analog and marker of energy-dependent NE storage vesicle accumulation, can be shown to accurately localize adrenal cortex and sympathoadrenal dysfunction, respectively. In Cushing's syndrome (CS) not only does the pattern of NP-59 uptake depict the adrenal dysfunction and its pathophysiologic basis, but the level of NP-59 accumulation reflects the degree of adrenocortical hyperfunction. Adrenocorticotrophin-independent CS is uniformly and accurately localized, especially in bilateral cortical nodular hyperplasia where even high resolution computed tomography (CT) may fail to depict the often subtle, asymmetric anatomic abnormalities. Dexamethasone suppression NP-59 adrenal scintigraphy has been shown to be highly sensitive and specific, and exceeds the efficacy of CT in the differentiation of adenoma and bilateral hyperplasia in primary aldosteronism. MIBG is useful as a sympathoadrenal imaging agent whose clinical utility has been demonstrated in the localization of pheochromocytoma, especially as a modality to screen the body for multiple and extraadrenal, recurrent, or metastatic lesions. Moreover, the extent of metastatic involvement from neuroblastoma can also be accurately depicted using MIBG. In this review we will examine the role of adrenal scintigraphy in the characterization of hypersecretory disorders of the adrenal cortex, medulla, and related conditions that produce hypertension as part of their symptom(s) complex. This approach, which is complementary to other anatomical modalities of imaging, can be used to advantage in the localization of functioning cortical and medulla adrenal diseases and other neoplasms of adrenergic origin.
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PMID:Scintigraphic studies in adrenal hypertension. 265 11

The adrenal glands produce glucocorticoids (approximately 25 mg cortisol/day), mineralocorticoids (approximately 100 micrograms aldosterone/day) and androgens (e.g. dehydroepiandrosterone = DHEA approximately 10 mg/day) in their cortex and catecholamines in their medulla. Excessive cortisol production leads to Cushing's syndrome. In approximately 2/3 of the cases this is due to ACTH oversecretion most often from a pituitary adenoma and can be cured by removal of this adenoma. Cushing's syndrome caused by an adrenal adenoma, carcinoma or bilateral nodular adrenal hyperplasia is treated by adrenal surgery. Nelson's syndrome consists of hyperpigmentation of the skin and an often aggressively growing pituitary adenoma which secretes excessive amounts of ACTH. Treatment is surgical. Conn's syndrome (primary hyperaldosteronism) is due to aldosterone hypersecretion most often from an adrenal adenoma (therapy: unilateral adrenalectomy), more seldom from bilaterally hyperplastic adrenals (therapy: spironolactone). Excessive adrenal androgen secretion is found in the adrenogenital syndrome in which defective cortisol biosynthesis leads to ACTH oversecretion and ACTH-stimulated overproduction of cortisol precursors, some of which are androgens. Treatment consists of glucocorticoids which suppress the ACTH oversecretion. Pheochromocytomas produce excessive amounts of catecholamines and cause hypertension which can be persistent as well as episodic. Therapy consists of adrenalectomy. Malignant tumors of the adrenals have a poor prognosis. Incidentally found adrenal masses ("incidentalomas") are observed at regular intervals if they are small and should be surgically removed if they have a tendency to grow or are large (greater than or equal to 5 cm phi).
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PMID:[Normal and pathologic endocrinology of the adrenal glands]. 268 Oct 84

The simultaneous occurrence of renovascular hypertension and an adrenocortical adenoma is a rare entity. The case of a 64-year-old woman who underwent an aortorenal bypass graft for renovascular hypertension requiring a multidrug antihypertensive regimen is presented. Persistently elevated blood pressures in the postoperative period prompted further workup for other causes of hypertension. Laboratory evaluation showed hyperaldosteronism and hyporeninemia despite enalapril administration. Abdominal computerized tomography (CT) revealed a left adrenal mass which, on surgical removal, was found to be a cortical adenoma. Subsequently, her antihypertensive therapy has been reduced to a single agent. Previous authors have described only four patients with malignant hypertension who had the rare clinical combination of renal artery stenosis and an aldosteronoma. This case reemphasizes the critical need for a thorough search for other surgically correctable lesions in those patients who remain severely hypertensive after the "definitive" operation.
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PMID:The simultaneous occurrence of renal artery stenosis and an aldosteronoma in a patient with hypertension. 268 7

During the last 7 years, operation was performed for 94 cases of adrenal tumor in our series, of which 14 were incidentally found by abdominal computed tomography or echography. They included 9 cases of pheochromocytoma, 1 of Cushing's syndrome, 3 of ganglioneuroma and 1 of cortical adenoma. Five of 9 pheochromocytoma cases were devoid of hypertension, but all 9 cases had abnormally high levels of urinary catecholamines and/or their metabolites. The 4-year autopsy series of Japan (1980-1983) included about 153,000 cases. Except the metastatic tumors, the following lesions were incidentally found in the adrenal gland: 310 of cortical adenoma, 153 of cortical hyperplasia, 39 of pheochromocytoma and 17 cases of neurogenic tumors. Some of the cortical adenomas are presumed to be more than 1 cm in diameter. So, they are expected to be found incidentally, more frequently in the future. Surgery is not necessary for most of them, except for functioning tumors. Most of the pheochromocytomas are presumed to be hormonally active, and should be treated surgically. It is probable that these functioning tumors had been missed clinically, especially in the elderly persons. Neurogenic tumors and myelolipomas may be left in place, when malignancy can be ruled out.
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PMID:[Adrenal incidentaloma--report of 14 operated cases and analysis of 4-year autopsy series of Japan]. 269 80

Authors report here an interesting case of a woman who has been treated for essential hypertension for 12 years. Beside the hypertension, an extreme virilization appeared. A large adenoma, originated from the left adrenal gland have been explored behind the clinical picture. After surgical removal of the adenoma, adrenocortical hormones decreased to the normal levels. Systemic blood pressure decreased considerably the virilisation showed gradual involution. The correct treatment of the patient was a decade late, resulting in the development of encephalopathic syndromes.
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PMID:[Essential hypertension caused by a virilizing adrenal tumor]. 272 34

One must consider the 17-DOS as a biosynthetic pathway with multiple regulatory factors. ACTH is its dominant regulator but in the absence of ACTH and in conditions where plasma renin activity is increased, this biosynthetic pathway maintains its sensitivity to exogenous ACTH. Suppression of the renin system delays the general recovery of aldosterone after the removal of an aldosterone producing adenoma but not of the 17-DOS: a pattern also showed after the removal of a DOC-producing adenoma. In addition to the possible role of the renin system there remain inexplicable situations in its regulation that cannot be explained by ACTH and renin. Our studies suggest that a non-renin, non-ACTH factor may influence the basal production of these steroids, and by its reduction, permits deviation of steroid substrate to cortisol production. This sequence may be operative in the "stress syndrome". Finally, one of the more interesting phenomenonologic patients who has been observed is a young male who has the biochemical findings and clinical signs of DOC excess with hypertension, hyperplasia, suppression of aldosterone and the RAS, and normal cortisol levels. All the 17-DOS are elevated and both adrenal veins have high concentrations. He represents excessive stimulation of this pathway by putative 17-deoxy regulator excess. The renin system is suppressed and ACTH levels are normal. Treatment with suppressive doses of glucocorticoid hormones diminishes the elevated 17-DOS and cortisol and ameliorates blood pressure. In summary, there seems to occur in clinical disorders and contrived experimental settings, suggestions that a non-renin, non-ACTH factor can regulate the 17-DOS, absence can explain some of the unusual conditions described (Fig. 1). The 17-DOS, while a vestigial pathway, may still cause disease, and provide clues to central organization of the adreno-cortical response to injury, stress, and disease.
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PMID:The regulation of the 17-deoxy steroids in man. 275 48

Unilateral adrenalectomy was performed in 32 patients with primary hyperaldosteronism due to tumour of the adrenal gland and with arterial hypertension (AH) of various degree of severity. Stable normalization of AH occurred in 14 patients and in 18 its course improved. The results of a retrospective analysis of a hypotensive effect, the morphological picture of the removed adrenal and the findings of clinico-biochemical and instrumental study made it possible to establish preoperatively the diagnostic criteria for the identification of two tumorous forms of primary hyperaldosteronism: aldosterone-producing adenoma proper and the tumorous form of adrenocortical hyperplasia. They have different pathogenesis and postadrenalectomy hypotensive effect.
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PMID:[Clinico-morphologic characteristics of 2 tumor forms of primary hyperaldosteronism]. 277 Jan 98

A 48-year-old man was admitted for treatment of Cushing's syndrome due to right adrenal adenoma, associated with chronic renal failure (CRF) with a blood urea nitrogen level of 64.2 and serum creatinine level of 3.9 mg/dl. After removal of the adrenal adenoma, the CRF deteriorated with progressive symptoms of anorexia, vomiting and hypertension, and the patient was placed on hemodialysis. Prior to adrenalectomy, the 17 OHCS and 17 KGS in the urine were not so high. However, the urinary 17 KS was high with an elevated 11-oxy fraction. In comparison with 2 patients suffering from adrenal Cushing's syndrome with normal renal function, there were no large accumulated quantities of glucuronic conjugated and unconjugated metabolites in the plasma of the CRF Cushing's syndrome, with confirmation ascribable to the radioimmunoassayable cross-reactivity of the cortisol antiserum used in the radioimmunoassay kit. In the Cushing's syndrome with CRF, almost all the cortisol, which was hypersecreted from the adenoma, was presumed to be converted to the 11-oxy fraction of 17 KS, possibly by activation of hepatic enzymes.
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PMID:Cortisol and its metabolites in the plasma and urine in Cushing's syndrome with chronic renal failure (CRF), compared to Cushing's syndrome without CRF. 279 94

150 patients dying from renal cell carcinoma are studied in order to reveal the background disease, incidence and character of the nephrosclerosis and the possible morphogenetic link between nephrosclerosis and carcinoma. Renal cell carcinoma is found to develop in 82.7% of cases in the kidneys with signs of nephrosclerosis. The diffuse nephrosclerosis developing in connection with the hypertension disease, atherosclerosis, diabetes mellitus, chronic pyelonephritis, nephrolithiasis is the most important. Proliferation of the canaliculi epithelium with the appearance of undifferentiated cells are regularly found in the nephrosclerotic areas. The disturbance of the epithelium differentiation is followed by the development of dysplasia the phenotypical variants of which are similar to those of renal cell carcinoma. Adenomas are found in 11.3% of cases of renal cell carcinoma which may originate from the adenomas developing against the background of nephrosclerosis.
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PMID:[Background and precancerous processes in renal cell carcinoma]. 280 41

A 47-year-old female presented with hypertension, hypokalaemia, low plasma renin, high plasma aldosterone and was found to have a left adrenal tumour 4 cm in diameter by computerized tomography. Detailed biochemical studies showed high plasma levels of 11-deoxycorticosterone and corticosterone in addition to aldosterone and 18-hydroxycorticosterone. Basal 11-deoxycorticosterone levels were particularly high. Corticosterone, 18-hydroxycorticosterone and aldosterone concentrations were abnormally sensitive to infusions of ACTH and angiotensin II. Plasma cortisol and assays for sex hormones were normal although there was evidence that cortisol derived from the neoplasm. At operation a well-differentiated adrenocortical carcinoma weighing 50 g (56 X 30 X 36 mm) was removed. There was no evidence of metastases following surgery. Adrenal function returned to normal. Review of the literature suggests that adrenocortical carcinoma should be suspected in patients who otherwise have typical features of Conn's syndrome, but whose tumours are more than 3 cm in diameter. Measurement of steroids such as 11-deoxycorticosterone in addition to aldosterone is recommended since abnormally high values may also help to distinguish between hyperaldosteronism due to adenoma and carcinoma. Previously reported cases of isolated aldosterone production by a carcinoma cannot be substantiated.
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PMID:Hypermineralocorticoidism due to adrenal carcinoma: plasma corticosteroids and their response to ACTH and angiotensin II. 282 95


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