Cases reported "Adrenal Cortex Neoplasms"

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1/12. A patient with preclinical Cushing's syndrome and excessive DHEA-S secretion having unilateral adrenal carcinoma and contralateral adenoma.

    We report a case of preclinical Cushing's syndrome in a 54-year-old male associated with bilateral adrenocortical tumours. Physical findings and general laboratory data were unremarkable except for mild hypertension (158/90 mmHg) and impaired glucose tolerance. Endocrinological evaluation revealed the presence of autonomous cortisol secretion including unsuppressible serum cortisol by 8 mg dexamethasone test (11 microg/dl), high serum DHEA-S (3580 ng/ml, normal: 400-3500) and increased urinary 17-KS excretion (31.0-35.8 mg/day, normal: 5.8-21.3). CT scan demonstrated the presence of tumours in both adrenals and bilateral adrenalectomy was subsequently performed. Histological examination of the resected specimens revealed an adrenocortical carcinoma on the right side and an adenoma on the left side with noticeable cortical atrophy in non-neoplastic adrenals. Immunohistochemical study of steroidogenic enzymes demonstrated that all the steroidogenic enzymes involved in cortisol biosynthesis were expressed in both right and left adrenal tumours. Enzymatic activities of 21, 17alpha, 18, 11beta-hydroxylases were detected in both right and left adrenals except for the absence of 11beta-hydroxylase activity in the left adrenal adenoma. Results of in vitro tissue steroidogenesis examined in short-term tissue culture of the specimens revealed no significant differences between carcinoma and adenoma in cortisol production, but the production of adrenal androgens in carcinoma was significantly higher than that in adenoma, which may indicate the importance of evaluating adrenal androgen levels in patients with adrenocortical neoplasms.
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2/12. Glucocorticoid-dependency on GH secretion and tumor growth in a GH-producing pituitary adenoma with Cushing's syndrome.

    We report a rare case of a 40-year-old woman with Cushing's syndrome and acromegaly. At the age of 28 she was diagnosed with Cushing's syndrome due to a left adrenal tumor concomitant with a GH-producing pituitary tumor. Before adrenal surgery her basal GH levels were extremely high and CT scanning revealed a high-density mass in the sella turcica. A 28 g left adrenocortical adenoma was removed by adrenalectomy. During the four months after the adrenalectomy, basal GH levels dramatically decreased and the high-density mass detected by CT scanning had disappeared but the basal GH levels and IGF-1 had not been normalized. She gradually became acromegalic in the twelve years after the adrenalectomy. At the age of 40 CT scanning showed reappearance of the pituitary tumor. In order to examine the glucocorticoid dependency on GH secretion, we compared the GH secretion in a series of endocrinological tests before and after oral 8 mg dexamethasone administration for 7 days. There was no difference between before and after dexamethasone administration in the GH secreting pattern, but basal GH levels were apparently increased after dexamethasone treatment. Transsphenoidal surgery was done and pathological examination showed a GH-producing pituitary adenoma. in vitro, dexamethasone increased GH secretion from the cultured GH-producing adenoma cells in a dose-dependent manner. In this case, both GH secretion and pituitary tumor growth seemed to be dependent on glucocorticoid.
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3/12. food-dependent androgen and cortisol secretion by a gastric inhibitory polypeptide-receptor expressive adrenocortical adenoma leading to hirsutism and subclinical Cushing's syndrome: in vivo and in vitro studies.

    Aberrant gastric inhibitory polypeptide (GIP) receptor expression in bilaterally hyperplastic adrenals or unilateral adrenal adenomas is a rare form of adrenal hyperfunction. So far, only few cases have been described. In all these cases, cortisol was the predominant steroid released in a food-dependent manner, leading to the development of non-ACTH-dependent Cushing's syndrome. In the present study, we describe a novel case of a GIP receptor-expressive adrenocortical adenomatous nodule, detected incidentally by computed tomography scanning in a 41-yr-old lady with hirsutism but no clinical signs of Cushing's syndrome, on physical examination. Hormonal investigations in morning fasting samples showed slightly elevated androgen levels, low-normal baseline cortisol, normal suppression of cortisol after dexamethasone administration, and ACTH levels that were not suppressed and did stimulate after CRH administration. The elevated urinary free cortisol excretion, in conjunction with an atypical cortisol diurnal rhythm, raised the possibility of an aberrant stimulation of cortisol production by the adrenal tumor. Further studies demonstrated food-dependent secretion of cortisol, which was abolished by prior octreotide administration. Notably, substantial amounts of adrenal androgens were also secreted after food consumption. Removal of the tumor resulted in undetectable cortisol and androgen levels that did not respond to food consumption. Histological examination of the excised tumor revealed an adrenocortical adenomatous nodule originating from the inner zona reticularis, consisting mainly of compact cells. A steroidogenic secretory pattern, indicating the concomitant release of adrenal androgens and cortisol, was also observed in vitro from tumor cells cultured in the presence of GIP. The in vitro secretory response to GIP was higher for the adrenal androgen DHEA, compared with cortisol. The expression of the GIP receptor in tumor cells, but not in the adjacent normal adrenal, was demonstrated by RT-PCR), using specific oligonucleotide probes for this receptor. In summary, we describe a patient with a GIP-expressive cortisol and androgen oversecreting adrenocortical nodule with the unusual presentation of hirsutism and not the typical clinical signs of Cushing's syndrome. It is of note that food intake in this patient provoked a substantial increase in both adrenal androgen and cortisol levels that, together with the histological appearance of this nodule, was compatible with a zona reticularis-derived tumor. Thus, aberrant expression of the GIP receptor does not exclusively involve cells of a zona fasciculata phenotype, as previously reported, but may also occur in other types of differentiated adrenocortical cells.
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4/12. Characterization of a newly established cell line derived from human adrenocortical carcinoma.

    BACKGROUND: ACT-1, a new cell line of human adrenocortical carcinoma, has been established and successfully maintained in culture. This study examined the biological characteristics of the cells. methods: The tumor cells were isolated from a surgical specimen of the tumor thrombus and cultured in monolayer. RESULTS: Histologically, the primary tumor was composed of a solid proliferation of large polygonal cells. A part of the atrophic adrenal cortex remained at the periphery of the tumor. The cultured ACT-1 cells were spindle-shaped in morphology and grew exponentially with an approximate population doubling time of 24 h. A chromosomal analysis revealed a modal number of 61 with consistent structural abnormalities of add(3)(q11), add(9)(p11), and add(16)(ql1). The expression of 3beta-hydroxysteroid dehydrogenase was observed in the ACT-1 cells as well as in normal human adrenal glands. Conclusions: The ACT-1 cell line provides a reproducible model system which gives good insight into the oncogenesis of adrenocortical carcinoma.
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5/12. Effects of serotonin and vasopressin on cortisol production from an adrenocortical tumor causing subclinical Cushing's syndrome.

    In dexamethasone-suppressed healthy volunteers, the serotonin4 (5-HT4) receptor agonist cisapride and lysine vasopressin [LVP, an analog of arginine vasopressin (AVP)] have no influence on plasma cortisol levels (PCL). In contrast, cisapride and AVP have been shown to stimulate cortisol secretion in patients with adrenal tumor or bilateral adrenal hyperplasia and Cushing's syndrome. In this report, we describe a case of adrenocortical adenoma causing subclinical Cushing's syndrome. cisapride and terlipressin, a precursor of LVP, both induced an increase in PCL reaching 88% and 100%, respectively, without any significant variation of plasma ACTH levels. in vitro experiments were conducted to investigate the effects of 5-HT and AVP on cortisol production from cultured tumor cells and normal adrenocortical cells. 5-HT and AVP both induced a dose-dependent increase in cortisol production from cultured tumor cells. Comparison of the data obtained with tumor and normal cells, respectively, showed that 5-HT was more efficient to stimulate steroidogenesis in adenomatous than normal cells. Concurrently, the efficacy and potency of AVP were both higher in tumor than normal cells. Collectively, these results show that the abnormal in vivo responses of the adrenocortical adenoma to cisapride and LVP could be ascribed to an increased sensitivity of the tumor tissue to 5-HT and AVP. The data also suggest that the adrenocortical tumor overexpressed eutopic 5-HT4 and V1 receptors.
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6/12. Non-functioning adrenocortical adenoma in culture. Quantitative and morphological observations.

    This report describes the morphological responses of unstimulated and stimulated non-functioning adrenocortical adenoma in culture. The removed adrenocortical adenoma was composed mainly of clear-type cells and partially had a small area of cholesterol granuloma. These adenoma cells had many lipid droplets and round to long rod-shaped mitochondria with tubular or tubulo-lamellar cristae which were similar to those in Cushing's adenoma. The non-functioning adrenocortical adenoma cells which were incubated in vitro under ACTH (10 mIU/ml) and angiotensin ii (10(-6) M/ml) stimulation, were examined by phase contrast microscopy, transmission and scanning electron microscopy, and the content of cortisol and aldosterone in the culture medium was measured by radioimmunoassay. As a result of exposure of ACTH, the cultured cells revealed the retraction response and production of cortisol and aldosterone. After administration of ACTH for many days, the cultured cells showed characteristic changes in sER and mitochondria. The sER were markedly developed and packed tightly into a network of dilated tubules. mitochondria were larger and more numerous than in the unstimulated cells. The mitochondria appeared to be entwined by the tubules of the sER. Lipid droplets decreased in number.
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7/12. Hypermineralocorticism without excessive aldosterone secretion: an adrenal carcinoma producing deoxycorticosterone.

    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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8/12. Vasopressin-responsive adrenocortical tumor in a mild Cushing's syndrome: in vivo and in vitro studies.

    We report a case of a Cushing's syndrome caused by an autonomously secreting unilateral adrenocortical tumor, characterized by a clinically and biologically mild hypercortisolemic state and an unusual response pattern to vasopressin. Laboratory tests showed normal early morning plasma cortisol and 24-h urinary cortisol excretion, but lack of nycthemeral variations and suppressed plasma ACTH. Urinary cortisol excretion was not suppressed by either the low dose or the high dose dexamethasone test. Injection of lysine vasopressin, (10 IU, im) induced a marked increase in plasma cortisol, without an elevation of plasma ACTH. Computed tomography scan revealed an adrenocortical mass of the left gland with a contralateral atrophic gland. Removal of the tumor led to complete remission of Cushing's symptoms. in vitro studies were then performed to investigate the effect of arginine vasopressin (AVP) on calcium mobilization in cultured tumor cells using a microfluorimetric technique. Application of AVP in the vicinity of the cells induced a rapid and marked increase in the intracellular calcium concentration. Preincubation of the cells with the V1 vasopressin receptor antagonist [d(CH2)5,Tyr(OMe)2]AVP totally suppressed the AVP-induced stimulation of intracellular calcium concentration. reverse transcription followed by polymerase chain reaction of tumor ribonucleic acid with specific oligonucleotides amplified high levels of V1 receptor signal compared with normal adrenocortical ribonucleic acid. Specific oligonucleotides for the V2 or V3 receptors amplified only a faint signal. This is the first report describing a mild case of Cushing's syndrome caused by an AVP-sensitive cortisol-producing adenoma. The direct effect of AVP on cultured tumor cells was mediated through the V1 type of vasopressin receptor, similar to that previously characterized in normal human fasciculata cells, suggesting that the tumor expressed an eutopic V1 AVP receptor and exhibited overresponsiveness to AVP.
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9/12. Chromosomal aberrations in two adrenocortical tumors, one with a rearrangement at 11p15.

    Adrenocortical tumors are detected with increasing frequency, but symptomatic cases with excessive hormone production are rare. We investigated cytogenetically one benign aldosterone-producing tumor (Conn Syndrome)(case 1) and one malignant cortisol-producing tumor (cushing syndrome)(case 2). radioimmunoassay of cell culture supernatant of case 2 detected cortisol secretion during 2 months in culture. flow cytometry of spill-out cells from case 2 showed a bimodal pattern (dna Index 1.0, 1.4). Case 1 revealed a marker chromosome in 4/25 cells analyzed; the marker was a long acrocentric partially derived from chromosome 2,der(2q). In case 2, a cytogenetic harvest was achieved after prolonged culture time (6 weeks) and a marker chromosome, add(11)(p15), was detected in 16/22 cells. A breakpoint of 11p13, as well as loss of heterozygosity of alleles on 11p15, has been reported in the literature for other malignant adrenocortical cancers.
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10/12. Double adenomas with different pathological and hormonal features in the left adrenal gland of a patient with Cushing's syndrome.

    We report a 52-year-old women with Cushing's syndrome who presented with two adenomas in the left adrenal gland. One tumour appeared dark brown and the other appeared yellow on the cut surface. The non-neoplastic adrenal demonstrated marked cortical atrophy. Upon histological examination, the brown tumour was found to be composed of both compact and clear cells. In contrast, the yellow tumour was composed of clear cells associated with pseudoglandular formation and marked degeneration. Immunohistochemical studies demonstrated positive immunostaining of cytochrome P-450 specific for 17 alpha-hydroxylation (P-450c17) in the brown but not the yellow tumour. Other steroidogenic enzymes except for dehydroepiandrosterone sulphotransferase were detected in both tumours. The biochemical activities of 21-hydroxylase, 17-hydroxylase and 11 beta-hydroxylase in the brown tumour (6.10 nmol/mg protein/4 minutes, 1.87 nmol/mg protein/2 minutes and 5.71 mumol 11-OHCS formed/g protein/10 minutes, respectively) were much greater than those in the yellow tumour. Gel-supported three-dimensional native-state primary culture of the tumours demonstrated a much higher concentration of cortisol in the culture medium for the brown tumour (5750 nmol/l on 4th day). vimentin expression was detected in both tumours but cytokeratin expression was detected only in the yellow tumour. The Ki67 labelling index in the brown tumour was greater than that in the yellow tumour. These results indicated that these two adenomas had different biological characteristics and the brown tumour was primarily involved in over-production of cortisol in this patient. When analysing unilateral multiple adrenocortical lesions, approaches using immunohistochemical studies for steroidogenic enzymes, enzyme activity assays and cell culture can help to define the steroidogenesis of individual adrenocortical lesions.
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