Cases reported "Cushing Syndrome"

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1/68. An ACTH-producing pituitary carcinoma developing Cushing's disease.

    An autopsy case of an ACTH-producing pituitary carcinoma in a 59-year-old man who developed Cushing's disease is reported. The surgically removed pituitary tumor was diagnosed as chromophobe adenoma, however, pulmonary metastases appeared 2 years after the operation. autopsy revealed a residual pituitary tumor in the sella turcica with systemic metastases to the lungs, liver, pulmonary lymph nodes, hypothalamus, dura mater, and the subarachnoid space of the midbrain and spinal cord. immunohistochemistry revealed ACTH positivity in the tumor cells. Further immunohistochemical study showed positive high expression of Ki-67 in the tumor removed at surgery as well as in the autopsied tumor. Ki-67 labeling index provided valuable information about the invasive and proliferative potential compared to noninvasive benign pituitary adenoma.
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keywords = sella turcica, turcica, sella
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2/68. Inefficiency of the anticoagulant therapy in the regression of the radiation-induced optic neuropathy in Cushing's disease.

    radiation-induced optic neuropathy is a rare complication (prevalence less than 1%) following radiotherapy of the sellar region. However, the vasculopathy in Cushing's disease predisposes to radiation-induced injury. We report the case of a 24-year-old man with Cushing's disease since he was 16. The hormonal study including bilateral inferior petrosal sinus catheterization diagnosed a pituitary right lesion, but imagiology was always negative. He underwent a transsphenoidal microadenomectomy and the pathological study showed the presence of corticotrophic hyperplasia but no adenoma. Secondary hypothyroidism and hypogonadism as well as permanent diabetes insipidus were diagnosed and because the patient was not cured he underwent a second transsphenoidal total hypophysectomy. After that and because he was still hypercortisolemic, pituitary external irradiation was given in a total dose of 6000 rad. Six months later he developed progressive bilateral visual loss. Cerebral MR revealed focal enhancement of the enlarged optic nerves and chiasm, associated with demyelination areas of the posterior visual pathways. Treatment was tried first with high doses of corticosteroids and later with anticoagulants-heparin EV. 1000 U/h during 7 days followed by warfarin, but unsuccessfully, probably because the patient was already amaurotic at the beginning of the last treatment.
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ranking = 0.050402833295461
keywords = sella
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3/68. Supra- and extrasellar pituitary microadenoma as a cause of Cushing's disease.

    There has been accumulating evidence that pituitary adenomas which cause Cushing's disease are located not only in sella turcica but also in various extrasellar and intracranial regions. We describe a case of Cushing's disease caused by a supra- and extrasellar ACTH-producing microadenoma, which originated in the anterior pituitary and extended upward without connecting to the stalk. The pituitary microadenoma was identified and removed by transsphenoidal microsurgery. After the surgery the patient experienced complete remission. This type of pituitary microadenoma is considered to be rare, but in order to accomplish successful surgical treatment, it is necessary to consider that pituitary adenomas which cause Cushing's disease may be located in such an unusual position.
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ranking = 1.3024169997728
keywords = sella turcica, turcica, sella
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4/68. Extrapituitary parasellar microadenoma in Cushing's disease.

    Negative sellar exploration (despite the results of endocrine evaluation indicating Cushing's disease), the high incidence of failure of total hypophysectomy, and remission of Cushing's syndrome after unsuccessful hypophysectomy and sellar irradiation suggest that the etiology of refractory Cushing's disease, in some patients, lies near the sella but not in the pituitary gland. We present 5 patients, out of 626 who received surgery for Cushing's disease, in whom an ACTH-secreting extrapituitary parasellar adenoma was identified: 2 after unsuccessful total hypophysectomy for the treatment of refractory Cushing's disease, 2 after unsuccessful hemihypophysectomy (the first, 2 yr before treatment at the NIH for Nelson's syndrome; and the second, with recurrent Cushing's disease 5 yr after negative transsphenoidal exploration), and 1 with a preoperative diagnosis of an intraclival microadenoma, which was cured by resection of the tumor. In all cases, an extrapituitary parasellar microadenoma was confirmed unequivocally as the cause of the disease, by negative pathology of the resected pituitary gland (patients 1, 2, 3, and 5), and/or the remission of the disease after selective resection of the extrasellar adenoma (patients 3, 4, and 5). Three of 5 patients had a partial empty sella. These patients support the thesis that ACTH-secreting tumors can arise exclusively from remnants of Rathke's pouch, rather than from the adenohypophysis (anterior lobe or pars tuberalis of the pituitary gland) and can be a cause of Cushing's disease. In the sixth presented case, an extrapituitary tumor was suspected at surgery after negative pituitary exploration, but serial sections of the hemihypophysectomy specimen revealed a microscopic focus of tumor at the margin of the resected gland. This case demonstrates the importance of negative pituitary histology to establish the presence of an extrapituitary parasellar tumor as an exclusive source of ACTH, and it supports the value of clinical outcome to establish the diagnosis with selective adenomectomy of an extrapituitary parasellar tumor. In patients with negative pituitary magnetic resonance imaging, especially in the presence of a partial empty sella, the diagnostic and surgical approach in Cushing's disease should consider the identification and resection of extrapituitary parasellar adenoma, which can avoid total hypophysectomy, as was possible in 3 of our 5 patients.
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ranking = 0.75604249943192
keywords = sella
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5/68. Cushing's disease in a 7-month-old girl due to a tumor producing adrenocorticotropic hormone and thyreotropin-secreting hormone.

    We present the case of a 7-month-old baby with Cushing's disease due to an adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma combined with cells producing thyreotropin-secreting hormone (TSH). In MRI scans, a contrast-enhancing lesion was seen inside the pituitary fossa, and it extended into the suprasellar region. On the assumption of a pituitary adenoma, surgery was performed. Corresponding with biochemical findings, histopathological evaluation revealed an ACTH- and TSH-producing tumor. Genetic analysis did not demonstrate an alteration at codon 201 (Arg) and 227 (Glu). To our knowledge, this is the first case described in a child of this age.
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keywords = sella
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6/68. Cushing's syndrome due to an ectopic ACTH-secreting pituitary tumour mimicking occult paraneoplastic ectopic ACTH production.

    A 32-year-old man presenting with typical features of Cushing's syndrome showed baseline cortisol and ACTH values indicating ACTH-dependent disease. Dynamic function tests (dexamethasone, corticotropin releasing hormone (CRH), desmopressin), were suggestive of paraneoplastic ectopic ACTH production. However, inferior petrosal sinus (IPS) ACTH sampling demonstrated a maximum baseline central (363 pmol/l)-peripheral (19 pmol/l) ACTH gradient of 19.1 for the right IPS, conventionally suggestive of Cushing's disease. However, again, IPS ACTH level did not increase after CRH stimulation. magnetic resonance imaging, while showing no evidence of an intrasellar tumour, revealed an 1.5 x 1.0 cm mass in the left sphenoid sinus which was initially interpreted as most probably being a mucosal polyp. After neurosurgical removal of the tumour, transient secondary adrenal insufficiency was present. The structure and immunostaining characteristics of the tumour demonstrated an ACTH cell adenoma of the pituitary. Ectopic ACTH-secreting pituitary adenomas may cause significant difficulties in differential diagnosis, localisation and appropriate therapy. Thus, although these tumours are rare, they should be included in the list of possible causes of ACTH-dependent Cushing's syndrome.
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ranking = 0.050402833295461
keywords = sella
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7/68. 'Gangliocytomas' of the pituitary: a heterogeneous group of lesions with differing histogenesis.

    Hamartomatous or neoplastic ganglion cells in the sella turcica are an unusual cause of symptoms. They have been reported in association with a functioning or nonfunctioning pituitary adenoma, with pituitary cell hyperplasia, and occasionally as masses unassociated with an adenoma, again with variable endocrinologic findings. Fewer than 50 cases of intrasellar ganglion cell lesions have been reported in the literature, only six of them associated with Cushing's syndrome. We describe the clinicopathologic features of another eight patients, three of whom presented with acromegaly, four with apparently nonfunctioning adenohypophyseal masses, and one with Cushing's syndrome. On histology, six of them were found to have sparsely granulated growth hormone (GH)-producing adenomas with ganglion cell areas, one appeared to have a gangliocytoma not associated with an adenoma, whereas the eighth had a ganglion cell lesion in the posterior pituitary. The morphologic and immunohistochemical findings suggest that the ganglion cell component of seven of these tumors has resulted from neuronal differentiation in a GH-producing adenoma, despite the lack of demonstrable adenoma in one case. A true sellar "gangliocytoma" or hamartoma of ectopic hypothalamic-type neurons appears to be a rarer explanation for the presence of ganglion cells in a pituitary biopsy.
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ranking = 1.1008056665909
keywords = sella turcica, turcica, sella
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8/68. From macroprolactinoma to concomitant ACTH-PRL hypersecretion with Cushing's disease.

    Multiple pituitary hormone hypersecretions have been already described, but the combination of PRL and ACTH excess is rare. This report deals with a 42-yr-old woman affected by macroprolactinoma (PRL 12,720 microg/l, huge tumor with extrasellar extension at imaging). After one year on dopaminergic treatment causing PRL normalization and tumor shrinkage, she developed hypercortisolism (UFC 1,000 microg/24 h, ACTH 200 ng/l). Cushing's disease was diagnosed. After neurosurgery (at immunocytochemistry mixed ACTH-PRL adenoma was shown) hypercortisolism remitted, whereas pathological hyperprolactinemia with tumor remnant in cavernous sinus persisted and hypopituitarism developed. The patient reported seems atypical for the following reasons: 1) the concomitant PRL and ACTH hypersecretions; 2) the clinical presentation with hypercortisolism following hyperprolactinemia; 3) the surgical cure of hypercortisolism with persisting hyperprolactinemia.
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ranking = 0.050402833295461
keywords = sella
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9/68. 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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keywords = sella turcica, turcica, sella
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10/68. Cushing's syndrome caused by ectopic corticotropin secretion by multiple peripheral pulmonary carcinoids and tumorlets of carcinoid type.

    Multiple peripheral pulmonary carcinoid tumors or their smaller counterparts (tumorlets of carcinoid type) are the most unusual form of carcinoids as a cause of ectopic corticotropin syndrome. Only three case reports were found in the literature. We describe a 35 year-old female patient with ectopic corticotropin secretion due to multiple peripheral pulmonary carcinoid tumors and tumorlets. A high-dose dexamethasone suppression test result led to the diagnosis of Cushing's disease in our case. But no tumor was identified on sella imaging and bilateral inferior petrosal sinus sampling was non-diagnostic. Computed tomography of the lungs revealed multiple acinar-nodular parenchymal infiltrations confined to the left lung. Corticotropin-dependent hypercortisolism persisted after bilateral adrenalectomy. A second operation was necessary to remove the hyperplastic adrenal remnants. Meanwhile, computed tomography findings of the thorax were unchanged. We decided to explore these nodules by open lung biopsy. During the procedure multiple nodules ranging 12 to 3 mm in diameter scattered throughout the left lung were observed and left pneumonectomy was performed. Histopathological diagnosis was multiple peripheral carcinoid tumors and tumorlets of carcinoid type showing positive immunostaining with corticotropin. This observation emphasizes a rare form of carcinoids as a cause of ectopic corticotropin secretion and its unusual response to high dose dexamethasone suppression test.
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keywords = sella
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