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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A man of 38 years of age was found to have a type I endocrine polyadenomatosis in 1969. He was operated upon for removal of tumor of the islets of Langerhans with lymph gland metastases, and the head of the pancreas was removed. This was followed at a later date by ablation of two parathyroid adenomas. A clinically silent adenoma of the left adrenal was not removed and a silent and enclosed pituitary tumore was discovered. There were no clinical or hormonal signs of progression of the pancreatic tumor ten years later, but hypertension and behavioural disorders had developed. Catecholamine levels were normal. Selective blood aldosterone levels were just within significant values. A massive increase in prolactin secretion (more than 100 times the normal) was noted. This could be reduced by bromocriptine, and the possible role of prolactin in the behavioural disorders present is discussed.
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PMID:[Prolactin adenoma and Wermer's syndrome. A 10-year follow-up of a case with two parathyroid tumors, as adrenal adenoma, and a malignant pancreatic tumor (author's transl)]. 4 60

A case of a feminizing adrenocortical tumor associated with Cushing's syndrome in a 29 year old male is presented. The ultrastructural features are compared with adrenal tumors secreting aldosterone, glucocorticoids of androgens. As in adrenal carcinomas, this tumor demonstrates nuclear pleomorphism with enlarged nucleoli and nuclear pseudoinclusions. The cytoplasmic organelles show some parallels between feminizing and androgen-secreting adrenal tumors. Different types of mitochondria occur with varying amounts of smooth endoplasmic reticulum. Numerous microbodies are present. Histological and ultrastructural signs indicating probably malignancy are discussed and it is noted that most of the feminizing adrenal tumors are carcinomata. Neither local recurrence nor distant metastases have yet been detected in this case, two years after excision of the tumor.
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PMID:Feminizing adrenocortical tumor. Histological and ultrastructural study. 20 8

Results of using radioisotopic visualization of the adrenal glands together with the hormonal profile determination ACTH, renin, aldosterone, cortisol) for the diagnosis of the adrenal gland affections are presented. Parameters of the scintigraphic appearance of the affected adrenal cortex were developed to distinguish six types of scintigraphic patterns of the adrenal gland, which were the most frequent. Clinical analysis of the results of the examination of patients indicated Conn's disease in 24 patients (it was verified during the operation), 12 had unilateral corticosteroma of the adrenal gland, 8 suffered from residual adrenal gland tissue, and 2 had metastases of malignant tumours of the adrenal glands. Accumulation of radiopharmaceutical preparations into the corpus luteum was revealed in one case.
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PMID:[Clinical value of radionuclide imaging in the diagnosis of the adrenal cortex lesions]. 22 89

Metastases to the adrenal glands are common in patients with cancer, but among those affected, hyperreninemic hypoaldosteronism is noted very rarely. A case of hyperreninemic hypoaldosteronism secondary to metastatic hepatocellular carcinoma is reported. Laboratory data revealed selective aldosterone deficiency with hyperreninemia. Biopsy documented replacement of the adrenal glands with metastatic hepatocellular carcinoma. A review of the literature disclosed that the present case was an extremely rare one of its kind.
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PMID:Hyperreninemic hypoaldosteronism due to hepatocellular carcinoma metastatic to the adrenal gland. 185 Mar 33

CT is the imaging procedure of choice for the detection of most suspected adrenal masses. But except for some patients with acute adrenal hemorrhage or fat-containing myelolipoma, the precise histologic nature of an adrenal mass is not apparent from the CT image. MIBG radionuclide scanning is useful in some patients with pheochromocytoma, whereas bilateral adrenal venous sampling for hormone assay is necessary for correct lateralization in some patients with a small aldosterone-producing adenoma. The potential value of MR imaging in the characterization of adrenal masses, especially to distinguish benign adrenal cortical adenomas from metastatic disease, is now under investigation. Currently percutaneous aspiration biopsy is still necessary to make this distinction in patients with an adrenal mass and a known extra-adrenal primary neoplasm.
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PMID:Overview of adrenal imaging/adrenal CT. 269 71

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

The aim of this study is to report on Aminoglutethimide-induced hormonal modifications in advanced breast cancer. Estradiol (E2), Testosterone (T), Dehydroepiandrosterone sulphate (DHEA(s] and Aldosterone (A) were determined before, and once every two weeks during treatment with Aminoglutethimide plus Hydrocortisone in 13 menopausal women with advanced breast cancer. The patients were selected either for their E2 and P4-receptor-positive in the original tumor or in metastases or by presenting objective clinical improvement to prior endocrine treatment. On the basis of the response to treatment the patients may be classified in two groups: 1) responders (n = 7) and 2) non-responders. No significant modifications of T concentrations were obtained in group 1 until after the first 8 months of treatment. One spontaneous menopausal patient with a T basal value of 0.80 ng/ml was evaluated during 12 months of treatment. From month 8, T diminished to values below 0.30 ng/ml, indicating a direct action of Aminoglutethimide, hydrocortisone or both drugs on ovarian steroidogenesis. The results obtained from the remaining hormonal parameters, evaluated in all the cases beginning from the second week of treatment, remained unchanged throughout the entire period of study. They were as follows: 1) E2 diminished with respect to basal values between 36 and 60%, thus confirming Aminoglutethimide inhibitory effect upon peripheral aromatization; 2) DHEA(s) diminished between 80 and 90%, indicating an adrenal inhibition due to the combined effect of both drugs, and 3) Aldosterone diminished to values between 80 and 110 pg/ml, these values being within the normal lower range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preliminary study of hormone determinations during aminoglutethimide therapy for advanced breast cancer. 623 71

In the present study two patients with aldosterone-producing adrenal carcinomas are reported. The clinical features were characterized by hypertension and severe hypokalemia with muscular weakness, flaccid paralysis of arms and legs, diarrhea and polyuria. In both cases excessively high plasma aldosterone levels and suppressed plasma renin activity were found. In contrast to most other cases with aldosterone-secreting tumours plasma cortisol, urinary free cortisol excretion, 17-hydroxy- and 17-ketosteroids were in the normal range. There was no clinical evidence of oversecretion of sex hormones. After adrenalectomy blood pressure and serum potassium normalized and the clinical symptoms disappeared. Plasma aldosterone and urinary aldosterone secretion returned to normal, while plasma renin activity remained low. Three and a half and 6 months later primary aldosteronism and the associated clinical symptoms reappeared due to hormonally active metastases. After introducing the antitumour drug o,p'-DDD in patient 1 aldosterone secretion normalized and the clinical status of the patient markedly improved. However, 10 months after diagnosis the patient died due to a haemorrhage from a liver metastasis. In patient 2 tumour-invaded regional lymph nodes were surgically removed with only minor changes in the hormone pattern.
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PMID:Primary aldosteronism due to adrenal carcinomas. 637 76

Hypertension may be a prominent and sometimes the dominant expression of tumours of the adrenal cortex as demonstrated in a personal series of 9 cases and in comparable series in the literature. It is therefore important, despite their relatively low incidence, to recognise adrenal cortical tumours as the cause of hypertension. The present study was undertaken to show that this diagnosis is relatively easy. The simplest indicators are:--the change in body electrolytes with hypokalaemia and hyper-kaliuria is practically constant and should prompt a hormonal investigation to demonstrate increases adrenal secretion of mineralocorticoids;--there is also a high incidence, despite the variable profiles of plasma and urinary corticosteroids, of paradoxical lowering of plasma aldosterone in parallel with normal or low PRA which does not react to orthostatism. These two preliminary investigations are the prelude and invitation to the measurement of other mineralocorticoids, especially desoxycorticosterone secondary to a relative block of 11-betahydroxylation from what other in vivo and in vitro studies have shown. Repeated monitoring of the preceding investigations is important for the post-operative follow-up and diagnosis of recurrences or metastases.
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PMID:[Hypertension in malignant tumors of the adrenal cortex. A review of clinical, biological and hormonal features]. 662 10

Evaluation for hypertension revealed a hypernephroma in two patients and increased plasma renin concentrations (PRC) of 2.8 and 3.1 GU . 10(-4)/ml, respectively. In one of the patients, bilateral renal venous catheterization showed lateralization of PRC toward the tumor side in the ratio 10:3. She had secondary hyperaldosteronism with a plasma aldosterone concentration (PAC) of 738 pmol/l, and hypokalemia with a serum potassium level of 3.0 mmol/l. In the other patient, who had malignant hypertension, PAC was not measured but serum potassium was subnormal (3.3 mmol/l). After nephrectomy, blood pressure (BP), PRC and serum potassium returned to normal in both as did PAC in one of the patients. At regular follow-ups through one year after nephrectomy, BP, PRC, PAC and serum potassium remained normal and metastases were not discovered. The increased incidence of hypernephroma in hypertensive patients underscores the importance of acknowledging this possibility during evaluation for hypertension.
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PMID:Hypernephroma and hypertension. Two case reports. 701 Sep 27


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