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)

Four post-menopausal women had Cushing's syndrome due to adrenal cortical carcinomas. Comprehensive analyses of blood and urinary steroids showed that although the steroid profiles differed between patients, the pattern in each patient remained almost constant as the disease progressed, or remitted due to therapy. Elevations of serum testosterone and oestradiol were commensurate with the extent of virilisation, and the urinary output of aldosterone was associated with the severity of hypertension. A new finding was that all had substantially increased urinary free deoxycorticosterone. Complete surgical removal of the primary tumours was impossible but when most of the tumour tissue was removed, full clinical and biochemical remissions were obtained for a short time in 2 patients. One patient obtained a clinical and biochemical remission from op'DDD. In another patient the drug caused reduction both in blood pressure and in urinary aldosterone excretion, but there were unpleasant side effects. A third patient could not tolerate op'DDD. Metyrapone therapy produced neither clinical nor biochemical improvement in 3 patients. The mean duration of survival was 17 months after the first symptoms and 10 months from the date of operation. Despite advances in drug therapy, adrenal cortical carcinoma remains a lethal disease. Biochemical screening of multiple steroids offers a means of early diagnosis and disease monitoring. Extensive surgical removal of the tumour offers the best chance of a clinical and biochemical remission.
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PMID:Cushing's syndrome due to adrenocortical carcinoma - a comphrensive clinical and biochemical study of patients treated by surgery and chemotherapy. 22 56

Adrenal cortical carcinoma in a 4 1/4-month-old girl was treated by surgery in combination with actinomycin D, cyclophosphamide, and 5-fluorouracil given daily for 5 days every third week for 13 1/2 months. Postoperative hypertension and raised 24-hour 17-hydroxy- and 21-oxosteroids suggested residual microscopical tumour activity. These findings resolved during chemotherapy. The patient is alive and well 22 months after completing chemotherapy. Adrenal cortical carcinoma may rarely mimic neuroblastoma or nephroblastoma when the tumour is not clinically secretory.
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PMID:Unusual case of adrenal cortical carcinoma in a female infant. 64 50

We have reported tissue distribution studies in rats and dogs with a new adrenal imaging agent. 131I-6beta-iodomethyl-19-nor-cholesterol (NP-59). This agent concentrated five times higher in the adrenal cortex than 131I-19-iodocholesterol without increased concentration in non-adrenal tissues. We now report in 34 patients, the findings on scintigraphy with NP-59 compared with angiograms and/or adrenal vein hormone levels and histopathology, including 13 patients with hypercortisolism, 12 with primary aldosteronism, 2 with low renin hypertension, 5 with catecholamine excess, 1 with a liver metastasis from an aldosterone producing adrenal cortical carcinoma, and 1 with anaplastic adrenal cortical carcinoma. NP-59 adrenal cortical uptake was more rapid and intense and background activity was less prominent, allowing earlier and more definite interpretation of images than was possible with 131I-19-iodocholesterol.
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PMID:A new and superior adrenal imaging agent, 131I-6beta-iodomethyl-19-nor-cholesterol (NP-59): evaluation in humans. 88 97

This is a report of a rare and unusual case of adrenal pathology. A patient presented with clinical and biological signs of primary aldosteronism and computed body tomography scan led to our suspecting the presence of a left adrenocortical carcinoma. The in vitro studies performed on the resected tumour showed very low synthesis of mineralocorticoids and glucocorticoids. The patient could not be reexamined until 15 months later, when he still suffered hypertension; another tomography scan revealed a mass on the right adrenal gland. The studies performed on this second tumour confirmed the diagnosis of Conn's adenoma: active in vitro biosynthesis of 18-hydroxy-corticosterone and aldosterone from exogenous tritiated precursors.
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PMID:Concurrent adrenocortical carcinoma and Conn's adenoma in a man with primary hyperaldosteronism. In vivo and in vitro studies. 152 66

A 24-year-old man visited our hospital complaining of hypertension and headache. Endocrinological findings revealed no abnormalities except for a slight decrease in serum adrenocorticotropic hormone (ACTH), a slight increase in urine 17-ketosteroid (17-KS), and a marked increase in serum pregnenolone. Computed tomography and magnetic resonance imaging revealed a 3 x 3 cm mass in the right adrenal area and I131-aldosterol scintigraphy demonstrated a high absorption of the isotope in the right adrenal area. Vena cavography suggested a 2 x 2 cm tumor thrombus originating in the right adrenal. Under the diagnosis of the right adrenocortical carcinoma, adrenalectomy and removal of the tumor thrombus were performed. Both serum pregnenolone and urine 17-KS returned to the normal level within a week after the operation and blood pressure was well controlled without any medication 3 months after the operation. Thus, the tumor seemed to be endocrinologically active.
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PMID:[Adrenocortical carcinoma: report of a case]. 164 74

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

Adrenocortical carcinoma (ACC), a very rare tumor in children in the United States, is apparently more common among Brazilian children. We reviewed the medical records of 40 children whose disease was diagnosed between 1966 and 1987. There were 12 boys and 28 girls; their median age was 3.9 years (range, 1 day to 15.7 years). Virilization was the most common clinical sign (37 of 40); other signs included abdominal mass, deepened voice, plethora, hypertension, seizures (seven patients) and, rarely, weight loss (two patients). The median time between first signs or symptoms and diagnosis was 1.4 years (range, 3 days to 5 years). Four of 33 tumors were classified as benign according to the Weiss, van Slooten, or Hough systems (tumor tissue was unavailable for seven patients). Tumors were completely resected in 26 of 38 patients; of those, 17 are in continuous complete remission, five relapsed, and four have been lost to follow-up. One patient, who had local recurrence, has been in a third complete remission for 18+ months after tumor resection and chemotherapy (cisplatin and etoposide). Of the remaining 14 patients, 11 died of progressive disease, the diagnosis was confirmed at autopsy in two, and one has been lost to follow-up. Univariate analysis disclosed that age greater than or equal to 3.5 years at diagnosis, interval of greater than or equal to 6 months between first symptoms and diagnosis, tumor weight greater than 100 g, tumor size greater than 200 cm3, and high levels of urinary 17-ketosteroids (17-KS) and 17-hydroxycorticosteroids (17-OH) were associated with an unfavorable outcome. Multivariate analysis disclosed that only a tumor size greater than 200 cm3 independently identifies those patients with an unfavorable prognosis. Among the variables known before surgery, age, and the interval between first symptoms and diagnosis were important predictors of outcome. Our data suggest that some children with ACC and certain clinical characteristics are at high risk of primary treatment failure and, therefore, are good candidates for investigational adjuvant therapy.
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PMID:Adrenocortical carcinoma in children: a study of 40 cases. 229 12

Ketoconazole, an oral antimycotic agent, is known to have a potent inhibitory effect on adrenal steroid production. It was given at a dose of 1200 mg/day to a 52-year-old female patient with a virilizing adrenocortical carcinoma in order to achieve better metabolic control pre-operatively. Together with a rapid normalisation of hypertension and hyperglycemia, a dramatic fall was noticed in serum and urinary adrenal steroids after a few days. Levels of total testosterone (20 nmol/l), androstenedione (greater than 35 nmol/l) and DHEA-sulphate (greater than 28 nmol/l) fell to normal levels in 6 days. By contrast, levels of 17-OH-progesterone (30 nmol/l) and progesterone (2.45 nmol/l) increased slightly, indicating inhibition of adrenal 17,20-lyase. Cortisol (620 nmol/l at 08.00 h) fell to very low levels (50 nmol/l) on day 6 of the trial. We conclude that ketoconazole is very effective in suppression of adrenal tumoural steroidogenesis and merits consideration in pre-operative use. We warn against dangerous hypoadrenalism which seems to occur earlier in tumoural than in normal adrenal metabolism.
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PMID:Use of ketoconazole in the treatment of a virilizing adrenocortical carcinoma. 277 22

We report a 45-year-old female with left adrenocortical carcinoma resulting in Cushing syndrome. She visited the 3rd Department of Internal Medicine, Kanazawa University Hospital with complaints of moon face, amenorrhea and hypertension. A diagnosis of left adrenal tumor with Cushing syndrome was made and she was transferred to our clinic. Left thoracoabdominal adrenalectomy was performed. The histologic report was compatible with adrenocortical carcinoma with no invasion into adjunctive tissues. She is now on endocrinologic study and is being administered 1,1-dichloro-2-[o-chlorophenyl]-2[p-chlorophenyl] ethane. There is no evidence of local recurrence or remote metastasis.
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PMID:[Adrenocortical carcinoma with Cushing syndrome: report of a case]. 280 88

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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