Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary aldosteronism-characterized by hypertension, hypokalemia and metabolic alkalosis--is caused by benign adenomata or bilateral adrenal hyperplasia in most cases. Aldosterone producing carcinomata of the adrenal cortex are very rare tumors. As the histological classification is difficult, the diagnosis is often drawn from tumor size, very high levels of plasma aldosterone, severe hypokalemia and malignant behaviour. The prognosis is very poor: Overall median and 5 year survival rate from diagnosis of adrenocortical carcinoma are 14 months and 24%.
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PMID:[Malignant aldosteronoma in the differential diagnosis of Conn syndrome]. 321 80

The sonograms of 26 patients (19 adults and seven children) with pathologically proven diagnoses of primary adrenocortical carcinoma were evaluated. Clinical corroboration was obtained in all cases. The size of the lesions ranged from 3 to 22 cm. The five smaller lesions (3-6 cm) showed a homogeneous echo pattern, similar to renal cortical echogenicity. The 21 larger lesions varied in echo texture, having a heterogeneous appearance with focal or scattered echopenic or echogenic zones representing areas of tumor necrosis, hemorrhage, and/or, rarely (19%), calcification. Even the largest lesions were fairly well delineated, often with a lobulated border. Few (7/26 or 27%) showed a surrounding echogenic thin capsulelike rim. All five small lesions showed clinical evidence of endocrine activity. Larger lesions were hormonally active less often (9/21 or 43%). Twelve patients (46%) showed no sign of endocrine activity and presented with symptoms such as fever, weight loss, abdominal discomfort, abdominal mass, hematuria, and hypertension. In the pediatric and adolescent age group (0-16 years), all tumors were hormonally active, while only seven (37%) of tumors in the adult population (17-69 years) were hormonally active. Unfortunately no echo pattern was characteristic enough to allow differentiation of adrenal adenoma from carcinoma. Smaller lesions are more likely to be benign, and larger lesions with areas of necrosis, hemorrhage, and calcification are more likely to be malignant.
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PMID:Primary adrenocortical carcinoma: sonographic evaluation with clinical and pathologic correlation in 26 patients. 355 25

The effect of o, p'-DDD on a functioning adrenocortical carcinoma is described. A 52-year-old woman, who had a huge adrenocortical carcinoma and pulmonary metastasis, was treated by a low-dose administration of o, p'-DDD, which reduced the tumor size. The excretion of urinary 17-OHCS was decreased, whereas plasma cortisol was not decreased but rather increased. This was considered to be caused that o, p'-DDD functioned as a cytotoxic factor which did not improve the states of hyperkalemia, hyperglycemia and hypertension. This suggested that monitoring to measure multiple steroids in addition to plasma cortisol and urinary 17-OHCS was useful for recognizing the general conditions of patients with adrenocortical carcinoma receiving o, p'-DDD therapy.
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PMID:Significant regression of the tumor combined with the high level of plasma cortisol by low-dose administration of O, p'-DDD in a case with Cushing's syndrome caused by adrenocortical carcinoma. 356 3

An adrenocortical carcinoma (15.5 g) secreting excessive amounts of steroids with weak mineralocorticoid activity in a 25-year-old woman was studied with particular reference to its in vivo and in vitro secretions of steroids. Severe hypertension, occasional low serum potassium and suppressed PRA were the major clinical findings, and were improved with removal of the tumor. In the preoperative stage, plasma levels of 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone, corticosterone and 18-hydroxycorticosterone were all increased. However, the plasma level of aldosterone was repeatedly normal. Although plasma levels of pregnenolone, 17-hydroxypregnenolone, progesterone and 17-hydroxyprogesterone were very high, those of other late step steroids, i.e. 11-deoxycortisol, cortisol, dehydroepiandrosterone, androstenedione and testosterone were almost normal. From these findings, a major etiological role of weak mineralocorticoids such as 11-deoxycorticosterone, 18-hydroxycorticosterone and corticosterone in her hypertension was suggested. Pregnenolone and 17-hydroxypregnenolone in tumor tissue were increased, but 11-deoxycorticosterone, corticosterone, aldosterone, cortisol and adrenal androgens such as dehydroepiandrosterone, androstenedione and testosterone were below normal or low normal. In vitro production of 11-deoxycorticosterone, aldosterone or cortisol by the tumor tissue slices was very low and scarcely responded to synthetic ACTH.
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PMID:An adrenocortical tumor secreting weak mineralocorticoids. 360 14

Adrenocortical carcinoma is a rare disorder that can be revealed by an isolated syndrome of mineralocorticoid excess. In a retrospective study of 137 patients referred to our hypertension clinic in the past 10 years for primary aldosteronism, four cases of adrenocortical carcinoma were identified. The clinical presentation of these patients was similar to that of patients with Conn's adenoma, but preoperatively, malignant tumoral primary aldosteronism was suspected because of profound hypokalemia, marked elevation in plasma aldosterone levels, and enlarged size and weight of an heterogenous adrenal tumor with internal calcifications. Malignancy was confirmed by the histologic features. No prognostic criteria could be established and two patients died despite specific surgery, which was performed in all cases. More recent developments in the use of mitotane led to the addition of adrenocorticolytic therapy in the remaining two patients, who are still alive at the time of this report.
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PMID:Isolated clinical syndrome of primary aldosteronism in four patients with adrenocortical carcinoma. 367 52

This report deals with the follow-up diagnostic evaluation of 18 patients previously treated for adrenal cortical carcinoma. The role of computed tomography is emphasized. Nine patients had adrenalectomy and the other 9 had adrenalectomy and ipsilateral nephrectomy. The left kidney and adrenal were removed in 8 patients. The patients were evaluated for 2-59 months with an average follow-up of 16 months. Of the 13 patients (72%) who had recurrent or metastatic disease, 8 experienced local recurrence in the adrenal fossa, 2 of whom had associated renal involvement. The recurrence was seen in 5 patients in the left and in 3 patients in the right side. Metastases occurred in the lung (7 patients), liver (3 patients), peritoneum (2 patients), paraaortic lymph nodes (3 patients), and bone (1 patient). At the time of the discovery of recurrence or metastases, 5 patients presented with lung metastases found on chest x-rays, 3 had recurrent Cushing's syndrome or hypertension, 3 had abdominal pain, 1 had weight loss, and 1 was asymptomatic.
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PMID:Computed tomography after adrenalectomy in adrenal cortical carcinoma. 407 56

Although secondary hyperaldosteronism due to renal vein thrombosis may occur as a result of renal cell carcinoma or adrenal cortical carcinoma, primary hyperaldosteronism is rarely associated with the latter. This paper describes a patient with adrenal cortical carcinoma who presented with the clinical features of primary hyperaldosteronism 1 year after hypertension had been diagnosed; intravenous pyelography had not been done then. Drug therapy was ineffective, and the patient died 10 weeks after presentation.
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PMID:Adrenal cortical carcinoma: an unusual cause of hyperaldosteronism. 635 90

Adrenal cortical carcinoma may present solely with a syndrome of mineralocorticoid excess. Primary aldosteronism, resulting from adrenal carcinoma, is unusual and has only been reported rarely. A review of the literature revealed 19 cases with marked hypertension and hypokalemia, resulting from mineralocorticoid excess produced by adrenal cortical carcinoma. We report an additional case that supports the hypothesis that adrenal carcinoma may mimic hyperaldosteronism. Extensive assay of adrenal function will demonstrate the presence of biologically inactive steroids, suggesting the presence of adrenal cortical carcinoma.
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PMID:Mineralocorticoid excess secondary to adrenal cortical carcinoma. 649 89

The clinical and pathologic features of three cases of surgically removed myelolipoma of the adrenal gland are presented. As with 18 previously reported cases, the lesions were found in obese, middle-aged persons; two of three had chronic, systemic disease (vasculitis and lymphoma, sustained hypertension). The only symptom possibly attributable to the neoplasm was nonspecific abdominal pain, and each lesion was identified by inferior renal displacement on intravenous urography. As computed tomography becomes widely available, the authors expect more myelolipomas to be detected that require surgical exploration, since there are no satisfactory, specific radiographic criteria to differentiate adrenal myelolipoma from adrenocortical carcinoma.
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PMID:Myelolipoma: an unusual surgical lesion of the adrenal gland. 705 29

A 51-year-old female was thought to have Conn's syndrome because she had hypertension, hypokalaemia and low plasma renin activity. The cause was not aldosterone excess, but there was an adrenal cortical carcinoma producing 11-deoxycorticosterone (DOC) in extremely large quantities, with ineffective 11 beta-steroid hydroxylation. Plasma and urinary aldosterone levels were within the normal range. Blood levels of other steroids including those on the pathways of formation of glucocorticoids and sex steroids were unaffected. The tumor was cultured in vitro and shown by high performance liquid chromatography (HPLC) to produce predominantly DOC from tritiated pregnenolone, with no detectable aldosterone, in agreement with the in vivo results.
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PMID:Hypermineralocorticism without excessive aldosterone secretion: an adrenal carcinoma producing deoxycorticosterone. 713 66


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