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At least 649 records · Page 36Linked to original sources
PubMed1975

Dissociation of in vivo and in vitro "autonomy" in human adrenocortical tumour.

The diagnosis of Cushing's syndrome due to "autonomous adrenocortical tumour" has been established in a patient by appropriate examinations (especially dexamethasone suppression test, ACTH stimulation test, ACTH measurement by radioimmunoassay). Isolated cells have been prepared from a piece of the tumour by a trypsin technique so that the action of ACTH on steriodogenesis in these cells could be studied in vitro. Basal production of corticosteroids by the isolated tumour cells was low (0.3 mu plus or minus 0.04/2 h/10-5 cells). Addition of ACTH induced a dose-dependent stimulation of corticosteroid production. The tumour cells appeared to be unable to produce corticosteroids in the absence of ACTH; maximal production was rather low (1.38 mu plus or minus 0.07/2 h/10-5 cells). A possible explanation for the discrepancies between endocrine function tests and the results of the in vitro studies is given.

Adrenal Cortex Hormones↗
PubMed1977

Metabolic regulation and relationship of endogenous protein kinase activity and steroidogenesis in isolated adrenocortical carcinoma cells of the rat.

In the adrenocortical carcinoma cell, in contrast to normal isolated adrenal cells, 10 to 50 muunits of ACTH do not raise the level of adenosine cyclic 3':5'-monophosphate (cyclic AMP), protein kinase activity, and steroidogenesis. This indicates a lesion in the tumor adenylate cyclase system. Two-tenths to 10 mM cyclic AMP and guanosine cyclic 3':5'-monophosphate (cyclic GMP) which stimulate steroidogenesis in a normal cell, activate protein kinase activity in a concentration-response manner without any detectable rise in steroidogenesis in the adrenocortical carcinoma cell. Cycloheximide and actinomycin D do not inhibit the stimulation of the phosphorylation. These results suggest that the tumor cyclic nucleotide-dependent protein kinase activity is unrelated to steroidogenesis and is also not under the transcriptional or translational control steps. Curiously, muM concentrations of cyclic AMP, in contrast to cyclic GMP, stimulate protein kinase activity. In a normal cell, both cyclic AMP and cyclic GMP, in this concentration range, stimulate protein kinase without an increase in steroidogenesis. It is therefore proposed that, in contrast to the normal cell, there is an additional defect in cyclic GMP-dependent protein kinase.

Adenylyl Cyclases↗
PubMed1981

[Diagnosis and therapy of hormonally active cancer of the adrenal cortex. Study of 5 cases].

Adrenocortical carcinomas are very rare tumors. The diagnosis and therapeutic results in 5 female patients are reported. In 4 cases the tumor displayed biochemical and clinical features of Cushing's syndrome, while one was an adrenocortical carcinoma with hypersecretion of aldosterone only. The mean age was 53.6 +/- 8.2 years. In all four cases with Cushing's syndrome the diagnosis was established by measurement of urinary free cortisol extraction rates and excretion rates of 17-ketogenic steroids (mean 1794.5 +/- 1968 micrograms/24 h for free cortisol and 50.5 +/- 24.9 mg/24 h for 17-ketogenic steroids), while the excretion of 17-OH-steroids was in the normal range in one case with hypercortisolism. The patient with mineralocorticoid excess showed markedly elevated plasma aldosterone levels (840 pg/ml) and undetectable plasma renin activity (less than 0.2 ng/ml/3 h), but normal urinary excretion rates of 17-hydroxy- and 17-ketosteroids. The adrenal lesions were localized by intravenous pyelography or sonography and by angiographic procedures, while radioscanning by 131I-cholesterol showed no uptake of activity. Unilateral adrenalectomy was performed in four cases. After appearance of hormonally active metastases o,p'DDD was administered as an antitumor agent in 3 patients. Two of these patients died 10 and 25 months after surgery. One patient with multiple lung metastases is still alive, with a postoperative course of more than 80 months.

Adrenal Cortex Hormones↗
PubMed1975

Primary aldosteronism. A study in contrasts.

Two patient with primary aldosteronism, one with a solitary adrenal adenoma and the other with bilateral nodular hyperplasia, are described. Both patients showed the classic features of primary aldosteronism in electrolyte and hormone patterns, but there were important differences in the biochemistry of their excised adrenal tissue. In addition, the injection of plasma from the patient with bilateral adrenal hyperplasia into the sheep's transplanted adrenal gland elicited a definite aldosterone secretory response, but there was no aldosterone response to the injection of plasma from the patient with a solitary adrenal adenoma. The findings support the hypothesis that an extra-adrenal stimulus may contribute to the pathogenesis of bilateral adrenal hyperplasia.

Adenoma↗