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

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

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 tumors of the thymus bear many similarities to "carcinoids" and "oat-cell carcinomas" in other organs, and are clinicopathologically distinct from thymomas, thymic seminomas, and other primary tumors of this gland. They are associated with Cushing's syndrome or multiple endocrine neoplasia in 35% of cases, and are often locally aggressive. Approximately 30-40% of patients have distant metastases of their tumors that ultimately result in fatality, since the response of thymic neuroendocrine neoplasms to irradiation and chemotherapy is poor. Ultrastructural studies and immunohistochemical stains for chromogranin, protein gene product 9.5, and synaptophysin are effective tools for the diagnosis of thymic carcinoid and oat-cell carcinoma.
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PMID:Neuroendocrine neoplasms of the thymus. 329 Aug 67

Twenty-five patients affected by adrenal glands pathology underwent CT and MRI: 6 non-functioning adenomas, 2 Cushing's adenomas, 2 Conn's adenomas, 6 metastases, 3 cysts, 2 carcinomas (Cushing's syndrome), 1 lymphoma and 3 pheochromocytomas. Diagnosis was subsequently confirmed either at surgery, or autopsy, or with needle biopsy. In all cases normal adrenal glands and pathological lesions were showed by MRI. T1 signal intensity and mass diameter were compared with T2 signal intensity, represented by the intensity ratio between the adrenal mass vs normal hepatic parenchyma. MRI signal intensity, usually high in case of malignancy and low in adenomas, shows a mean value which is much wider than that referred to mass diameter evaluation (carcinoma is larger than adenoma); for this reason those findings have proved to be insufficiently accurate for adrenal tissue characterization, even for the evaluation of cysts and pheochromocytomas. In the same cases CT showed higher accuracy.
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PMID:[MR tomography in adrenal pathology. Preliminary report on 25 histologically controlled cases]. 337 95

Over a 2 year period, 63 of 1,459 patients examined by computerized tomography were found to have adrenal masses. In 19 patients (1.3 percent of patients examined and 30 percent of patients with adrenal masses), they were unexpected and did not give rise to symptoms or signs. Three patients were explored. Two of the patients had adrenocortical adenomas and a third, a ganglioneuroma. Adrenal function tests were performed in 14 patients and showed evidence of Cushing's syndrome in 1 patients and revealed no abnormalities in 13. The lesions in 10 of 11 nonsurgical patients followed by computerized tomography for 11 to 36 months showed no change. One lesion became significantly smaller. In a review of 988 autopsy reports, grossly visible adrenal masses were present in 73 patients (7.3 percent), including 19 adrenocortical adenomas (1.9 percent) and 50 metastases (5 percent). We conclude that serendipitous adrenal masses are usually small, nonfunctioning, and benign, the most common lesion being adrenocortical adenoma. A protocol has been suggested for management to identify the minority of patients with functioning or malignant lesions and to avoid unnecessary surgery in the others who have benign disease.
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PMID:Serendipitous adrenal masses: prevalence, significance, and management. 401 56

This report deals with the follow-up diagnostic evaluation of 18 patients previously treated for adrenal cortical carcinoma. The role of computed tomography is emphasized. Nine patients had adrenalectomy and the other 9 had adrenalectomy and ipsilateral nephrectomy. The left kidney and adrenal were removed in 8 patients. The patients were evaluated for 2-59 months with an average follow-up of 16 months. Of the 13 patients (72%) who had recurrent or metastatic disease, 8 experienced local recurrence in the adrenal fossa, 2 of whom had associated renal involvement. The recurrence was seen in 5 patients in the left and in 3 patients in the right side. Metastases occurred in the lung (7 patients), liver (3 patients), peritoneum (2 patients), paraaortic lymph nodes (3 patients), and bone (1 patient). At the time of the discovery of recurrence or metastases, 5 patients presented with lung metastases found on chest x-rays, 3 had recurrent Cushing's syndrome or hypertension, 3 had abdominal pain, 1 had weight loss, and 1 was asymptomatic.
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PMID:Computed tomography after adrenalectomy in adrenal cortical carcinoma. 407 56

We describe a woman with metastatic small cell carcinoma of the lung who presented with pituitary apoplexy and hyperprolactinemia. Within seventeen months she developed florid Cushing's syndrome with anasarca, hyperpigmentation, hypertension with marked hypercortisolemia (not suppressible with 8 mg dexamethasone), elevated serum ACTH, hypokalemic metabolic alkalosis, and multiple hepatic metastases. This picture suggested the presence of ectopic ACTH syndrome. She died 26 months after the episode of pituitary apoplexy. Primary small cell carcinoma of the lung was diagnosed post-mortem. Metastases were present in the left lung, regional lymph nodes, heart, liver, bone marrow, sphenoid bone, anterior pituitary and pituitary capsule. Posterior pituitary was normal. There was no evidence of pituitary hyperplasia, of adenoma or of primary pituitary carcinoma. The results suggest the presence of a primary ACTH-producing small cell carcinoma of the lung that metastasized to the parasellar sphenoid bone and then extended to the anterior pituitary and dura to mimic a primary intrasellar cause of pituitary apoplexy and Cushing's syndrome. The case demonstrates how difficult it may be to diagnose the etiology of Cushing's syndrome and it emphasizes a unique variation in the presentation of small cell carcinoma of the lung.
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PMID:Metastatic small cell carcinoma of the lung presenting as pituitary apoplexy and Cushing's syndrome. 608 26

In the present study, the effects of o,p'-DDD on plasma levels of pregnenolone, 17 alpha-hydroxypregnenolone, progesterone, 17 alpha-hydroxyprogesterone, 11-deoxycorticosterone, deoxycortisol, corticosterone, cortisol, androstenedione and testosterone were studied in 6 patients with adrenal carcinoma (3 with Cushing's syndrome, 2 with adrenogenital syndrome, one without clinical manifestation) and 6 with Cushing's disease. Plasma levels of these steroids were decreased in all of the patients with adrenal carcinoma. The decrement of progesterone and 17 alpha-hydroxyprogesterone was greater than that of pregnenolone and 17 alpha-hydroxypregnenolone. These results indicate that o,p'-DDD inhibits both cholesterol cleavage enzyme and 3 beta-hydroxysteroid dehydrogenase coupled with delta 5 to 4 isomerase system. Plasma levels of pregnenolone and 17 alpha-hydroxypregnenolone showed a twofold increase on the 7th day after consecutive administrations of o,p'-DDD in patients with Cushing's disease. Plasma levels of cortisol were decreased to normal one month after continuous o,p'-DDD treatment. Urinary 17-OHCS and 17-KS have been decreased out of proportion to the decrease in plasma cortisol in the first week of o,p'-DDD treatment. Such a disparity suggests that o,p'-DDD might affect the extra-adrenal metabolism of cortisol. However, no evidence was found for the inhibition of hepatic C17-20lyase and glucuronyl transferase. Regression of pulmonary metastases was observed in one case with Cushing's syndrome due to adrenal carcinoma, suggesting that o,p'-DDD causes necrosis of the metastatic adrenal carcinoma. A remission of the disease was obtained in one patient with Cushing's disease after 6 months of continuous o,p'-DDD treatment. The usefulness of o,p'-DDD for the treatment of adrenal carcinoma with metastases and Cushing's disease was confirmed.
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PMID:[The effects of o,p'-DDD on human adrenal steroid synthesis]. 609 74


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