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PubMed1989

Use of ketoconazole in the treatment of a virilizing adrenocortical carcinoma.

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.

Adrenal Cortex Hormones↗
PubMed1998

Diagnosis and treatment of adrenal tumours: a review of 35 years' experience.

OBJECTIVE: To review and analyse clinical data on the diagnosis and management of patients with adrenal masses. PATIENTS AND METHODS: Patients admitted with adrenal masses between 1960 and 1995 were reviewed. The series comprised 116 males (mean age 41.4 years, SD 10.5, range 3-77) and 95 females (mean 36.9 years, SD 11.6, range 1-62); eight patients were < 14 years old and the overall mean (SD) age was 39.4 (12.8) years. The diagnosis was based on symptoms, signs, hormone levels and imaging studies. All tumours were confirmed by surgery, and pathology and results of analysis assessed statistically. RESULTS: Over the last 35 years, the incidence of adrenal tumours was 1.7% of all patients admitted with genitourological diseases or 9.7% of patients with genitourinary tumours at our institution. The prevalence of adrenal tumours in males and females was similar but Cushing's syndrome was 3.1 times more frequent in females than in males and phaeochromocytoma 1.9 times more frequent in males than females. Most patients with adrenal tumour were aged 30-50 years. Of 211 adrenal tumours, 151 (72%) were functional, with a prevalence of benign tumour, and 60 (28%) were nonfunctional, with 35% malignant. There were 78 'incidentalomas' which included 18 functional tumours. Overall, 210 tumours were removed and one was explored. Correlation analysis between tumour size and character or hormone levels showed that size was significantly positively correlated with tumour character (r = 0.4010, P < 0.001), but there was no relationship between tumour size and hormonal levels. The postoperative complication rate was 3.3% and the mortality 0.5%. CONCLUSIONS: Based on this analysis we recommend that computed tomography is the first method used to define and localize the adrenal masses, that hormone levels should be determined in symptomatic or asymptomatic patients with adrenal masses, and that functional adrenal tumours and solid incidentalomas of any size should be removed surgically.

Adolescent↗
PubMed1987

Pluripotent steroidogenesis and ultrastructure in adrenocortical adenomas causing Cushing's syndrome.

Adrenal vein catheterization data from 2 patients with adrenocortical adenomas causing Cushing's syndrome are presented and the electron-microscopic features of one of the tumors are described. Based on the catheterization data both tumors produced all three classes of adrenal steroids (mineralocorticoids, glucocorticoids and sex steroids). Electron-microscopic examination of the tumor cells suggested an origin from the zona fasciculata. If one accepts the theory of a common cellular origin of adrenal tumors, then the pattern of steroidogenesis would indicate that the postulated original 'stem' cell retains the potential of secreting all classes of adrenocortical steroids. The clinical presentation of such tumors would thus reflect the hypersecretion of one of the steroid classes relative to the others.

Adenoma↗
PubMed2005

Steroid profile in an adrenocortical carcinoma producing aldosterone.

We report a rare case of primary aldosteronism due to an adrenocortical carcinoma. A 61-year-old woman with a history of hypertension and hypokalemia was referred for evaluation of a 4.2 cm measuring adrenal mass without secondary signs of malignancy. Endocrinological testing was consistent with primary aldosteronism. The patient underwent surgical resection of the adrenal mass; histology revealed an adrenocortical carcinoma. Postoperatively blood pressure, serum potassium, and aldosterone returned to normal. Four months after adrenalectomy, the patient presented again with hypokalemic hypertension and was found to have metastatic disease. Endocrinological investigation revealed primary aldosteronism and subclinical autonomous glucocorticoid hypersecretion. Careful hormonal investigation should be obtained in patients with adrenal masses causing excessive aldosterone secretion. In uncertain cases of primary aldosteronism, we would suggest to measure 18-hydroxycortisol levels, as excessive amounts may indicate adrenocortical carcinoma.

Adrenal Cortex Hormones↗
PubMed1984

[Value of hormonal markers in the detection and therapeutic surveillance of malignant adrenal cortical carcinoma].

The value of hormonal markers in the diagnosis and early and late surveillance of adrenocortical carcinoma was assessed in a series of 10 cases and from a review of the literature. Although hormonal investigation with measurement of precursors, performed whenever there is the least clinical suspicion of ACC, is of certain diagnostic value, the possibilities of postoperative controls have not yet been fully exploited: the results are difficult to interpret because of possible interference due to the secretion of the controlateral adrenal; plasma renin activity is rarely assessed in the late postoperative period. A general strategy of investigation and surveillance is proposed.

Adrenal Cortex Hormones↗
PubMed2003

N-terminal proopiomelanocortin acts as a mitogen in adrenocortical tumor cells and decreases adrenal steroidogenesis.

There is evidence that proopiomelanocortin (POMC)-derived peptides other than ACTH are involved in pituitary-dependent adrenal growth. We have synthesized the human N-terminal POMC fragment 1-28-POMC with the disulfide bridges in the correct position between cysteine residues 2-24 and 8-20 and studied the activity of these peptides in adrenocortical tumor cells in vitro. 1-28-POMC stimulated cell proliferation in human NCI-h295 and mouse Y-1 adrenal cancer cell lines and also in primary cultures of bovine adrenocortical cells in a concentration-dependent manner. 1-28-POMC led to rapid activation of the MAPKs extracellular signal-regulated kinases-1 and -2, but not c-Jun N-terminal kinase and p38, pathways. Steroid hormone production (cortisol, 17-hydroxyprogesterone, and dehydroepiandrosterone sulfate) in NCI-h295 cells was decreased by 1-28-POMC in a concentration-dependent fashion. However, protein levels of important regulators of steroidogenesis [steroidogenic factor-1, DAX-1 (dosage-sensitive sex reversal-adrenal hypoplasia congenita critical region on the X-chromosome 1), steroidogenic acute regulatory protein, and cytochrome P450 side-chain cleavage enzyme] remained unaffected by 1-28-POMC treatment. Our results provide evidence that synthetic 1-28-POMC induces adrenal tumor cell proliferation, inhibits adrenal steroidogenesis, and mediates its action by signaling via the extracellular signal-regulated kinase pathway. The distinct roles of 1-28-POMC and ACTH in the regulation of adrenal growth and steroidogenesis suggest that the adrenal cortex is under the dual opposing control of fragments from the same mother peptide POMC.

17-alpha-Hydroxyprogesterone↗
PubMed1983

Ultrastructural and biochemical studies in human adrenocortical adenomas associated with primary aldosteronism.

Correlation between ultrastructural features and adrenal steroid hormone contents was studied in two human adrenocortical adenomas associated with primary aldosteronism. In two adrenocortical adenoma cells, large numbers of lipid droplets were characteristically observed in the cytoplasm, these lipid droplets were closely related to the endoplasmic reticula or mitochondria. On the other hand, biochemically, in two adrenocortical adenomas, aldosterone and progesterone were higher than those in the normal parts of the same adrenal glands. Whereas, dehydroepiandrosterone was less than that in the normal parts of the same adrenal glands. From these data, the functional aspects in adrenocortical adenomas associated with primary aldosteronism are discussed.

Adenoma↗
PubMed2001

Scintigraphic patterns of adrenocortical carcinoma: morpho-functional correlates.

OBJECTIVE: Adrenocortical scintigraphy has demonstrated clinical utility in the morpho-functional characterization of adrenal tumors. The aim of this study was to identify possible relationships between the scintigraphic pattern and endocrine and/or morphological data in a series of adrenocortical carcinomas. DESIGN AND METHODS: Twenty-one patients with adrenocortical carcinoma (11 nonfunctioning and 10 hormone-secreting) were investigated with 75Se-methyl-nor-cholesterol scintigraphy. Clinical, hormonal, radiological, and pathological data were analyzed. RESULTS: The adrenal mass showed no radiocholesterol uptake in 18 cases (11 nonfunctioning and 7 functioning lesions). Contralateral normal adrenal gland was visualized in all patients with nonfunctioning tumors, whereas classic bilateral nonvisualization was observed in the 7 cases with hyperfunctioning masses. Three patients with cortisol-producing carcinomas showed radiotracer uptake by the mass, without visualization of the contralateral gland. At histology, the tumors were shown to be undifferentiated adrenocortical carcinomas; they had an aggressive clinical behavior. CONCLUSIONS: Radiocholesterol scintigraphy has an important role in diagnosing adrenocortical carcinomas, which typically are not visualized. However, 30% of hypersecreting adrenocortical carcinomas show an atypical increased tracer uptake, not predictive of the biochemical and histological features of the tumor.

Adolescent↗
PubMed1992

Corticoid production by four dogs with hyperfunctioning adrenocortical tumours during treatment with mitotane (o,p'-DDD).

In two dogs with hyperadrenocorticism due to an adrenocortical tumour, treatment with o,p'-DDD was started. Their hormonal response was monitored by measurements of the urinary corticoid/creatinine ratio. In one dog, two courses of 10 days treatment with o,p'-DDD were ineffective, whereas in the other dog the urinary corticoids decreased to very low levels after only six days of treatment, and corticosteroid supplementation had to be started. Two other dogs received o,p'-DDD according to a protocol used for the treatment of pituitary-dependent hyperadrenocorticism which aims at the complete destruction of the adrenal cortices, with substitution for the induced hyperadrenocorticism. Both dogs made a good recovery and their urinary corticoid/creatinine ratio decreased to within the reference range. In one of them the tumour had decreased considerably in size by five weeks after the start of the treatment.

Adenoma↗
PubMed2000

Management approaches to adrenal incidentalomas. A view from Ann Arbor, Michigan.

Adrenal masses are discovered incidentally in 1 to 3% of abdominal CT scans performed for investigation of nonadrenal-related abdominal complaints. Although most incidentally discovered masses are clinically silent, 10% are hormone-secreting and are associated with subtle symptoms of hormone excess. The major concern is the possibility that such a mass is malignant and requires surgical intervention. Benign adrenal cortical adenomas are 60 times more common than primary adrenal cortical carcinomas, which are rare, and many of the lesions that are malignant are metastatic from extra-adrenal neoplasms. Size is a significant factor in determining the probability that the lesion is benign or malignant, and there is concensus that most benign lesions are smaller than 3 cm, whereas most malignant lesions are larger than 6 cm. Uncertainty remains, however, as to the potential malignant character of masses measuring 3 to 6 cm; thus, size alone is insufficient for determining if an incidentally-found adrenal mass is benign or malignant, and information obtained from other diagnostic techniques, such as CT, MR imaging, and adrenal scintigraphy with 131I 6 beta-iodomethylnorcholesterol, should be considered. Fine needle biopsy of an adrenal mass is not recommended unless there is strong suspicion that the mass is metastatic from an extra-adrenal neoplasm.

Adenoma↗
PubMed1993

Acute thrombocytopenic purpura in an infant with Cushing's syndrome: a case report.

This paper describes the case of a female child who presented with severe thrombocytopenia and Cushing's syndrome. The underlying cause was found to be an adrenal cortical adenoma, removal of which was followed by complete recovery of both conditions. The pathogenesis of both presenting features in relation to the adrenal tumor is discussed.

Adenoma↗
PubMed1983

Multiple thoracotomy combined with chemotherapy in metastatic adrenal cortical carcinoma: a case report and review of the literature.

A case is reported in which multiple bilateral pulmonary metastasectomies for metastatic adrenal cortical carcinoma were performed and which resulted in an unusually long survival of over 25 years from the first thoracotomy and over 28 years from removal of the primary adrenal cortical carcinoma. The patient is alive and free of tumor as of the latest follow-up. We believe this is the longest survival after pulmonary metastasectomy for carcinoma published to date.

Adolescent↗
PubMed1998

Smad3 is involved in the intracellular signaling pathways that mediate the inhibitory effects of transforming growth factor-beta on StAR expression.

Transforming growth factor betas (TGFbetas) constitute a family of dimeric proteins that regulate growth and differentiation of many cell types. TGFbeta1 is also a potent autocrine regulator of adrenocortical steroidogenesis. We have recently shown that in primary cultures of bovine fasciculo-reticularis cells, the main target of TGFbeta is the steroidogenic acute relay protein (StAR), a key protein necessary for intramitochondrial cholesterol transport. Here, we show that StAR expression is also inhibited by TGFbeta1 in the human adrenocortical carcinoma cell line NCI-H295R. This inhibitory effect is mediated by Smad proteins. Indeed, we found that overexpression of wild-type Smad3 inhibited endogenous StAR mRNA expression while overexpression of a dominant negative Smad3 protein reversed the inhibitory effect of TGFbeta1 on StAR mRNA expression. Taken together, these results demonstrate that the Smad3 protein is involved in TGFbeta-dependent regulation of steroidogenesis.

Adrenal Cortex↗
PubMed1981

An improved basal medium for Y-1 mouse adrenal cortex tumor cells in culture. 2. Stability of steroidogenic pathway and chromosome number.

Y-1 cells were passaged weekly for 6 wk in MACT IV medium without a period of adaptation to this basal medium that requires 1% dialyzed fetal bovine serum as a supplement. The steroid pathway and chromosome number, reported earlier for this cell line under culture conditions that used much higher concentrations of nondialyzed sera, remained stable despite dialysis and reduction of the fetal bovine serum to 1%.

Adrenal Cortex Hormones↗
PubMed2005

Adrenocortical carcinoma producing 11-deoxycorticosterone: a rare cause of mineralocorticoid hypertension.

A 37-yr-old man presented with the classic signs of mineralocorticoid excess hypertension and hypokalemia. The cause was not aldosterone excess, but elevation of plasma 11-deoxycorticosterone (DOC). Computed tomography (CT) scans showed a large right adrenal mass without signs of metastatic disease. The tumor was removed by open laparotomy, and histology revealed an adrenocortical carcinoma. Two yr after diagnosis, the patient is in good general condition and there is no sign of recurrence or metastatic disease, despite the large tumor size. DOC producing adrenocortical carcinomas causing mineralocorticoid hypertension are very rare, so far only 10 cases have been described in the literature.

Adrenal Cortex Hormones↗