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1/43. recurrence of adrenal aldosterone-producing adenoma.

    Conn's syndrome (adrenal aldosterone-producing adenoma) and bilateral adrenal hyperplasia are the most common causes of primary aldosteronism. The treatment of choice for patients with aldosterone-producing adenoma is unilateral total adrenalectomy. recurrence after adequate surgery is exceptional. We present a patient with recurrence of an aldosterone-producing adenoma in the right adrenal gland 9 years after adenomectomy of a aldosterone-producing adenoma in the same adrenal gland. We conclude that adenomectomy is not an adequate therapy for patients with adrenal aldosterone-producing adenoma.
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2/43. Cushing's syndrome caused by Ewing's sarcoma secreting corticotropin releasing factor-like peptide.

    Procedures were carried out in a 12-year-old girl to relate Ewing's sarcoma of the left tibia with Cushing's syndrome. Computed tomography revealed a normal pituitary and hypothalamus but bilateral adrenal hyperplasia without focal enlargement, thus readily excluding hypothalamic-pituitary-adrenal tumor. Negative results from a high-dose dexamethasone suppression test do not support pituitary-dependent Cushing's disease. Ewing's sarcoma was diagnosed on tibial biopsy. The regression of the physical and biochemical findings of Cushing's syndrome subsequent to amputation of the left lower leg strongly suggests ectopic Cushing's syndrome caused by Ewing's sarcoma. Immunohistochemical studies of the resected bone were negative for corticotropin but positive for corticotropin releasing factor-like peptide. We conclude that this is the first reported case of ectopic Cushing's syndrome in a child that is caused by Ewing's sarcoma secreting corticotropin releasing factor-like peptide.
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3/43. [18F]fluoro-2-deoxy-D-glucose ([18F]FDG) positron emission tomography imaging of thymic carcinoid tumor presenting with recurrent Cushing's syndrome.

    We report a case of a young woman with Cushing's syndrome (CS), in whom although endocrine investigations and negative pituitary imaging were suggestive of ectopic ACTH secretion, the results of inferior petrosal sinus (IPS) sampling after coricotropin-releasing hormone (CRH) stimulation were suggestive of pituitary acth hypersecretion. (111)In-labelled octreotide and high-resolution computer tomography (CT) revealed a lesion possibly responsible for the ACTH source in the thymus. thymectomy confirmed concomitant ectopic CRH and probable ACTH production by a thymic neuroendocrine carcinoma. After an 8-year remission period the patient developed a clinical and biochemical relapse. A high-resolution computed tomography (CT) scan of the thorax showed a 2-cm nodule in the thymic bed, which was positive on a [(18)F]fluoro-2-deoxy-D-glucose ([(18)F]FDG) positron emission tomography (PET) scan. However, a repeated thymectomy did not result in remission. A repeat [(18)F]FDG PET study showed persistent disease in the thymic bed and also uptake in the adrenals. The patient underwent bilateral adrenalectomy, which resulted in clinical remission. A further [(18)F]FDG PET scan 8 months later showed no progression of the thymic tumor and confirmed complete excision of the adrenals. This is a rare case of concomitant CRH and ACTH secretion from a thymic carcinoid tumor; the case illustrates the usefulness of functional imaging with [(18)F]FDG PET in the diagnosis, management and follow-up of neuroendocrine tumors.
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4/43. Ectopic adrenocorticotropic hormone-syndrome in medullary carcinoma of the thyroid: a retrospective analysis and review of the literature.

    Cushing's syndrome (CS) in medullary thyroid carcinoma (MTC) is rare. Only 50 cases have been reported. We report 10 cases of MTC with ectopic adrenocorticotropic hormone (ACTH)-dependent syndrome (EAS), analyzed retrospectively. Among 1640 patients with MTC, 13 developed EAS (0.7%). In 10 patients CS could unequivoqually be related to MTC (0.6%). CS was always clinically obvious. It revealed MTC in 3 cases and followed diagnosis by an average of 34.5 months in the others. Metastases were often present at diagnosis. immunohistochemistry with ACTH antibodies was positive in one case. diagnosis of ectopic CS was established according to clinical and biologic features, and absence of corticotropic adenoma as well as parallel evolution between tumor and CS. Therapy was medical and surgical: anticortisolic drugs alone or in association with somatostatin analogue, somatostatin analogue alone, and bilateral adrenalectomy. Eight patients died within 2 to 30 months, 4 of hypercortisolism complications (3 peritonitis and 1 hypokalaemia), 4 of MTC progression. EAS is a rare complication of MTC. The prognosis is poor because of frequency of metastasis at diagnosis. Persistent hypercortisolism can, by itself, lead to death, and has to be treated specifically.
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5/43. Ectopic adrenocorticotrophic hormone production and neoplasm.

    Three patients presented with severe hypokalaemic, hypochloraemic alkalosis, muscle weakness and later cutaneoud pigmentation. There were few signs of Cushing's syndrome. Two had bronchial and one pancreatic neoplasm. plasma cortisol and urinary steroid metabolites were extremely elevated and synacthen stimulation showed significant adrenal capacity even with adrenal metastases. Aminoglutethamide reduced plasma cortisol in two patients.
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6/43. Primary aldosteronism due to a malignant ovarian tumor.

    A case of a young woman with the syndrome of primary aldosteronism and malignant ovarian tumor is reported. Hormone studies revealed extremely high urinary aldosterone, undetectable plasma renin activity, elevated plasma 17beta estradiol and testosterone, and low plasma FSH and LH. plasma cortisol and urinary 17-hydroxycorticoids were at the upper normal limits. autopsy disclosed an ovarian tumor, histologically an arrhenoblastoma, with polymorphic aspects. The adrenal glands grossly were normal. aldosterone was found by the double radioisotopic technique in the neoplastic tissue.
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7/43. Gastric carcinoid with ectopic production of ACTH and beta-msh.

    A 51-year-old woman with typical Cushing's syndrome of about 9 years duration was shown to have a gastric carcinoid tumor. plasma levels of ACTH and cortisol were elevated and lacked the normal diurnal rhythm. Urinary excretion of steroids was unaffected by the administration of either metyrapone or dexamethasone. Fluctuation in urinary steroid excretion, as well as transient hypokalemic alkalosis and glycosuria suggested periodic hormonogenesis. The extirpated gastric carcinoid was shown to contain immunoreactive ACTH and beta-msh. However, the biologic ACTH activity was undetectable by in vivo steroidogenic assay. By gel filtration, it was demonstrated that both tumor and plasma ACTH was predominately "big" ACTH. Although postoperatively she developed hypoadrenocorticism severe enough to require ACTH treatment, her pituitary-adrenal function was gradually restored. This is the first documented case of ectopic ACTH syndrome caused by gastric carcinoid in which successful cure was achieved by surgery.
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8/43. Cushing's disease in a child with lymphosarcoma and acute leukemia.

    A 6-year-old girl with lymphosarcoma developed Cushing's syndrome. Suppression-stimulation studies verified adrenal hyperfunction secondary to bilateral adrenocortical hyperplasia, and the course suggested the possibility of "ectopic ACTH" production by the neoplasm as the etiology.
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9/43. Fine structure of adrenal cortex in ectopic ACTH syndrome.

    A 49-year-old man with pancreatic adenocarcinoma, suggestive of islet cell origin, showed clinical and biochemical features of ectopic ACTH syndrome and underwent bilateral adrenalectomy. light microscopy revealed adrenocortical compact cell hyperplasia and lipid depletion. The zona glomerulosa was detected in small foci and fasciculata cells extended up to the capsule. Electron microscopy disclosed enlargement of adrenocortical cells, massive SER accumulation, RER increase, lipid depletion, prominence of the golgi apparatus and development of complex interdigitations between closely apposed cell membranes. These changes were attributed to the stimulative effect of ACTH discharged from the non-pituitary tumor. mitochondria exhibited enlargement, pleomorphism and cavitation. Most of the adrenocortical cells contained mitochondria with vesicular cristae--a characteristic feature of fasciculata cells. In a few cells, under the capsule, some mitochondria possessed lamellar cristae. Gradual transformation to the vesicular type was, however, apparent indicating that mitochondria are not rigidly constant structures.
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keywords = adrenal cortex, adrenal, cortex
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10/43. Ectopic ACTH, prostatic oat cell carcinoma, and marked hypernatremia.

    Locally recurrent, poorly differentiated carcinoma of the prostate was associated with hypokalemic alkalosis, marked hypernatremia, diabetes mellitus of recent onset, and hyperosmolar syndrome. These findings, with mild hypertension, in the absence of clinical features of Cushing's syndrome, suggested an ectopic ACTH syndrome. plasma ACTH and cortisol levels were markedly elevated, and failed to suppress in response to either low or high-dose dexamethazone administration. The patient's condition deteriorated rapidly. autopsy findings included carcinoma extensively infiltrating the prostate with extension to the urinary bladder, and metastases confined to the pelvic nodes and soft tissues. The adrenal glands weighed 23 g and showed diffuse hyperplasia. Extract of the prostatic tumor was analyzed for ACTH and showed approximately 40 times normal plasma levels (or about 4,010 pg/g of tissue); ultrastructural features showed secretory granules consistent with ACTH content of the tumor cells. Such cells were positive when stained for ACTH by peroxidase-tagged immunochemical methods. The case fulfills all established criteria for relating excess corticosteroid production and nonpituitary tumors.
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