Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cushing's syndrome, caused by ectopic ACTH production during Zollinger-Ellison syndrome, raises difficult therapeutic problems. We report a case of clinical and biological efficacy of long acting somatostatin (SMS) in this condition. In a short term study with 200 micrograms SMS bid, symptoms of hypercorticism disappeared while cortisol and ACTH serum concentrations fell below the normal values. Longterm treatment was instituted with 50 micrograms SMS bid. Excellent clinical efficacy as well as normal cortisol and ACTH serum concentrations were maintained during the nine month follow up. Lipotrophic hormone (LPH) serum concentration remained raised. No decrease in size of hepatic metastases was observed. Long acting somatostatin analogues may be useful in endocrine paraneoplastic syndromes.
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PMID:Long acting somatostatin treatment of paraneoplastic Cushing's syndrome in a case of Zollinger-Ellison syndrome. 289 23

A 41-year-old man presented with Cushing's syndrome and the biochemical features of ectopic ACTH production. Investigation revealed mediastinal metastases from a medullary carcinoma of the thyroid. The peripheral plasma contained grossly elevated levels of bombesin-like immunoreactivity (irBombesin) as well as calcitonin; blood sampling via a venous catheter confirmed a gradient of irBombesin, but not of ACTH, in the mediastinal vein draining the tumour. On extraction the tumour contained a bombesin-like peptide, but not vasopressin or corticotrophin releasing factor and only very low levels of ACTH; immunohistochemical studies showed positive immunostaining for bombesin and calcitonin but none for ACTH or CRF. No ACTH was released from dispersed tumour cells in vitro. However an extract of the tumour stimulated ACTH release in vitro from perifused dispersed rat anterior pituitary cells. This is the first reported case of Cushing's syndrome due to ectopic production of a bombesin-like peptide, causing excessive pituitary ACTH secretion.
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PMID:Pituitary ACTH dependent Cushing's syndrome due to ectopic production of a bombesin-like peptide by a medullary carcinoma of the thyroid. 298 8

We report the history, laboratory and histological findings in a man who presented with Cushing's disease. Despite removal of the primary pituitary tumour, his disease progressed and after bilateral adrenalectomy, he became pigmented and plasma ACTH levels remained elevated. He had further pituitary surgery and radiotherapy, to relieve compression of the optic chiasma. Plasma ACTH levels remained elevated. He developed liver, bone and lymph gland metastases and after an acute paraparesis due to spinal metastases he died. Immunoperoxidase staining techniques demonstrated ACTH in the pituitary recurrence and metastases. The combination of bone, liver and lymph node metastases has not previously been reported, nor has ACTH been reported before in metastases from a primary intrasellar tumour.
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PMID:An intrasellar pituitary tumour producing metastases in liver, bone and lymph glands and demonstration of ACTH in the metastatic deposits. 300 76

In some instances, tumors can produce signs and symptoms at a distance from the tumor or its metastases. These are defined as paraneoplastic syndrome or humoral syndrome associated with neoplasms. Paraneoplastic syndromes can arise from circulating substances secreted by tumors. The most well-recognized and frequent concomitant of neoplasms is the production of hormones by nonendocrine tumors. These are usually called ectopic hormone-producing tumors and bring about clinically endocrinologic manifestations secondary to hormone excess in patients with nonendocrine tumors. Paraneoplastic endocrine syndromes frequently observed are Cushing's syndrome due to ectopic production of ACTH, SIADH due to ectopic production of ADH, hyper-calcemia, hypoglycemia and so on. In order to establish a paraneoplastic etiology for alteration in hormone production, evidence that the hormone is produced by the tumor must be proved. Paraneoplastic endocrine syndromes should be distinguished from hormone production by benign cells, hormone production by a malignancy of an endocrine organ or alterations in hormone production being due to infiltration into the endocrine organ by a primary tumor. The treatment of ectopic endocrine syndromes should be directed primarily at the tumor. Because the course of this type of syndrome usually runs parallel to the course of the underlying tumor, the ectopically produced hormone can be a useful monitoring marker of the disease.
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PMID:[Paraneoplastic endocrine syndromes]. 301 95

Pituitary carcinoma is defined as a malignant pituitary tumour associated with blood- or lymph-borne metastases. Cushing's disease is frequently present in patients with this condition. After adrenalectomy for Cushing's disease, a 37-year-old man developed Nelson's syndrome resulting from a pituitary carcinoma with metastases to the spinal cord, cauda equina, heart, liver, and pancreas. The primary tumour and its metastases showed immunocytochemical staining for ACTH, beta-lipotrophin, and variably for beta-endorphin and alpha-melanocyte stimulating hormone (alpha-MSH). A coincidental glioblastoma was also present. Nine cases of Cushing's disease associated with pituitary carcinoma, including the present patient, are documented in the literature. The case reported is only the second in which immunohistochemical staining of the primary pituitary tumour and its metastases was performed, and the first in which ACTH-related peptides, in addition to ACTH itself, were demonstrated in the carcinoma cells.
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PMID:Pituitary pro-opiomelanocortin-cell carcinoma occurring in conjunction with a glioblastoma in a patient with Cushing's disease and subsequent Nelson's syndrome. 302 76

A patient with metastatic islet cell carcinoma demonstrated multiple clinical syndromes simultaneously with secretion of ACTH, gastrin, glucagon, and serotonin. Hepatic arterial embolization resulted in an initial decrease in all secretory products, which was sustained for glucagon and serotonin. Recrudescence of the Cushings and Zollinger-Ellison syndrome was managed by surgical extirpation of the primary tumor and regional metastases as well as bilateral adrenalectomy. Electron microscopy and immunocytochemistry of the primary tumor and the metastatic lesions revealed the presence of multiple types of granules within single cells and, different patterns of secretory profiles in different tumor sites.
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PMID:Metastatic islet cell tumor with ACTH, gastrin, and glucagon secretion. Clinical and pathologic studies with multiple therapies. 303 1

A case is described of a patient with a small-cell prostatic carcinoma containing immunoreactive CRH, in conjunction with ACTH-dependent Cushing's syndrome. The serum concentrations of CRH, ACTH, beta-endorphin and calcitonin were all found to be above normal. Post-mortem examination revealed a prostatic tumour with multiple metastases, and a diffuse hyperplasia of pituitary corticotropic cells and adrenal cortical cells. In sections of the primary prostatic tumour, immunoreactive cells were demonstrable with antisera raised against human CRH, TSH, calcitonin and somatostatin, but not with antisera against ACTH or beta-endorphin. By radioimmunoassay the CRH-like material could also be demonstrated in extract of the prostatic tumour and the material from both plasma and tumour extract eluted at the position of human CRH on gel chromatography (Sephadex G-75). These findings provide support for the interpretation that the patient's Cushing's syndrome was due to a CRH-producing prostatic tumour. Finally, the origin and the clinical significance of the neuroendocrine cells in the prostatic carcinoma is discussed.
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PMID:Carcinoma of the prostate with Cushing's syndrome. A case report with histochemical and chemical demonstration of immunoreactive corticotropin-releasing hormone in plasma and tumoral tissue. 326 36

Neuroendocrine tumours of upper gastrointestinal tract fall into two main categories. First carcinoid tumours of the stomach and duodenum and secondly endocrine pancreatic tumours. The endocrine tumours of the gastric mucosa include two main types, so called ECL-oma of the corpus and fundic region and gastrin producing carcinoids or hyperplasia of the antrum and duodenum. The endocrine tumours of pancreas include entopically secreting insulinomas, glucagonomas, somatostatinomas, PP-omas, and ectopically secreting tumours, such as gastrinomas and tumours producing ACTH, GHRH, and calcitonin. The diagnosis of a neuroendocrine tumour of the upper gastrointestinal tract is based on the recognition of certain clinical syndromes and the determination of certain humoral products. A broad battery of radioimmunological assays for determination of different peptides is mandatory for the diagnosis and follow up of these patients. The diagnosis is also based on histological and immunocytochemical investigation of tissue specimens obtained at operation or by biopsy. Ultrasound investigation is the best non-invasive technique to detect metastases from neuroendocrine gut and pancreatic tumours, but angiography might unveil metastases down to a size of less than 5 mm. Surgery is still the primary treatment procedure but other treatments are needed because many patients have metastases already at the time of diagnosis. Chemotherapy with streptozocin combined with 5-fluorouracil or adriamycin and human leucocyte interferon has demonstrated objective response rate of about 70%. The new somatostatin analogue SMS 201-995 is an important adjunct in controlling clinical symptoms in patients with neuroendocrine gut and pancreatic tumours. A combination of different treatment procedures is needed for long-term management of these patients.
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PMID:Neuroendocrine tumours of the upper gastrointestinal tract and pancreas. 329 22

Two cases of a rare neuroendocrine skin tumour (Merkel cell carcinoma) are reported. The tumour affects mainly old women and men. It has a great tendency to metastasize to lymph nodes and distant sites. The primary treatment is surgical but radiotherapy has an important role to play. Merkel cell tumours are capable of producing NSE and have also been documented to secrete calcitonin and ACTH. Difficulties in histological diagnosis are frequent. The definitive diagnosis can only be made by electron microscopic examination.
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PMID:Merkel cell tumour of the skin. 370 Dec 4

A 28 year old man presented with partial hypopituitarism and signs of a pituitary tumour. A chromophobe adenoma was partially removed by right frontal craniotomy. Seven years later complete hypopituitarism and hyperprolactinaemia were documented, at which time there was no evidence of tumour recurrence of CT scan. The patient was treated with bromocriptine but the pituitary tumour redeveloped a year later. Nine years after the original operation the first metastasis was demonstrated together with very high prolactin levels. The intracranial metastasis, and the pituitary tumour were removed at a second craniotomy following which the prolactin concentration fell. Further metastases developed subsequently and the patient died 12 years after the initial diagnosis. At autopsy multiple metastases were found in the brain, tumour cells were present in the subarachnoid space and in cerebral veins. The pituitary tumour and secondaries were shown by immunocytochemistry to contain prolactin but not ACTH or growth hormone. This appears to be the third well documented case of a metastasizing, prolactin secreting pituitary tumour.
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PMID:Multiple intracranial metastases from a prolactin secreting pituitary tumour. 397 26


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