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)

The case of a 52-year-old woman with acromegaly, diabetes insipidus, and visual impairment caused by a metastatic growth hormone-releasing hormone (GRH)-produced pancreatic tumor is reported. Serum growth hormone (GH) and somatomedin C levels were elevated to 14 ng/ml (normal < 5 ng/ml), and 3.20 U/ml (normal < 1.88 U/ml), respectively. Paradoxical increases were observed in GH levels after glucose tolerance and thyrotropin-releasing hormone-stimulation tests. Biopsy of a pituitary tumor observed on computerized tomography scans and magnetic resonance studies revealed a metastatic cancer. When circulating GRH levels were measured, a marked increase in plasma GRH (1145 pg/ml; normal < 4-1 pg/ml) was observed. The patient died of cachexia due to metastases. Postmortem examination revealed that a primary tumor, a malignant endocrine lesion, was present in the pancreas, with metastatic tumors in the pituitary, lung, liver, and adrenal glands. Synthesis and production of GRH by the tumor was demonstrated by Northern blotting and immunohistochemical analysis. The pituitary gland showed hyperplastic, but not adenomatous changes. The authors stress the importance of both exploration for an ectopic source of GRH and the search for a GH-producing pituitary adenoma when unusual signs and symptoms are seen in patients with acromegaly.
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PMID:Acromegaly, diabetes insipidus, and visual loss caused by metastatic growth hormone-releasing hormone-producing malignant pancreatic endocrine tumor in the pituitary gland. Case report. 767 23

A 34-year-old male developed multiple intracranial and intraspinal metastases from an invasive ACTH secreting pituitary adenoma. He was initially admitted to our hospital complaining of visual loss 10 years ago, presenting a pituitary tumor with suprasellar extension. At first, transsphenoidal surgery was performed, and histological finding was pituitary apoplexy. He developed recurrence of the tumor 2 times. At the second, third and fourth operation, the histological finding was an ACTH secreting pituitary adenoma with atypia. Metastases within the central-nervous system of pituitary adenoma is a rare entity and only 21 cases have been published. A review of previously published cases follows.
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PMID:[ACTH producing pituitary adenoma with multiple intracranial metastases and spinal dissemination]. 770 Apr 93

Mice bearing retinoblastoma susceptibility gene (RB) germ-line mutations almost invariably develop pituitary neoplasms. We therefore tested 17 patients with pituitary tumors for loss of heterozygosity (LOH) using an RB sequence polymorphism and 5 polymorphic microsatellite markers surrounding the RB gene on the long arm of chromosome 13. In all of the 13 malignant or highly invasive pituitary tumor cases, and in 4 of their respective metastases, a RB allele was lost. In contrast, no LOH at the RB locus was detected in 4 benign pituitary adenoma cases. Three invasive tumors also lost a portion of 13q, which included D13s137, D13s133, and D13s118 telomeric and centromeric to RB, respectively. Immunohistochemical analysis, however, revealed the presence of RB protein in tumors with LOH and the RB locus. Therefore, although inactivation of RB may play a role in the development of invasive pituitary adenomas and carcinomas in mice, another tumor suppressor gene on 13q is likely involved in human pituitary tumor progression. LOH of 13q markers may also be of predictive value in determining the biological behavior of pituitary macroadenomas and their progression to invasiveness and frank malignancy.
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PMID:Frequent loss of heterozygosity at the retinoblastoma susceptibility gene (RB) locus in aggressive pituitary tumors: evidence for a chromosome 13 tumor suppressor gene other than RB. 2886 62

The cases of two elderly women treated for temporal hemianopsia due to a large pituitary mass with suprasellar extension are presented. In both cases, the clinical picture, without diabetes insipidus and cranial nerve paralysis, as well the neuroimaging and endocrinological investigation showing hypopituitarism, were suggestive of a non-secreting pituitary adenoma. In the first patient malignant tissue was unexpectedly encountered during transsphenoidal surgery. Anatomopathological investigation confirmed the presence of a metastasis of a breast carcinoma for which she had been treated 17 years earlier. In the second patient, a preoperative chest X-ray before transsphenoidal surgery revealed an asymptomatic bronchial tumour. Subsequently a squamous cell carcinoma with a metastasis in the pituitary was confirmed. These two cases illustrate the fact that a pituitary metastasis can closely mimic a pituitary adenoma. Even in the absence of suggestive symptoms such as diabetes insipidus and/or cranial nerve paralysis the possibility of metastatic disease in the differential diagnosis of a pituitary mass should always be considered.
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PMID:Pituitary metastasis mimicking a pituitary adenoma. A description of two cases. 772 37

Only 12 cases of pituitary tumors that metastasized within the central nervous system have been reported. A further case is presented in which the histology of the multiple dural metastases remained identical to that of the original tumor, a pituitary adenoma. The authors discuss management of these rare lesions that appear histologically benign.
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PMID:Multiple dural metastases from a pituitary adenoma. Case report. 793 1

The aim of this retrospective study was to assess the contribution of thallium-201 single-photon emission tomography (SPET) in the detection and differential diagnosis of brain tumours. In 90 patients 201Tl SPET was performed because of clinical or radiological suspicion of tumoral invasion, completed by technetium-99m hexamethylpropylene amine oxime and 99mTc-sestamibi SPET in some patients. For all tumours, diagnosis was based on biopsy or autopsy. Other diagnoses were made only after clinical and radiological follow-up for at least 6 months. Histologically tumours consisted of astrocytoma stage I or II (number of patients, n = 6), astrocytoma stage III (n = 8), glioblastoma multiforme (n = 14) and oligodendroglioma (n = 3), brain metastasis (n = 14), lymphoma (n = 3), meningioma (n = 3), pituitary adenoma (n = 2), pineal tumour (n = 1), colloid cyst (n = 1) and craniopharyngioma (n = 1). False-negative studies included pineal tumour (n = 1), colloid cyst (n = 1), craniopharyngioma (n = 1), astrocytomas stage I or II (n = 6) and stage III (n = 3), oligodendroglioma (n = 2) and metastasis in the brain stem (n = 1). Additional metastases approximately < 1.5 cm were not detected in two patients and 201Tl SPET underestimated tumoral extent in one patient suffering from glioblastoma multiforme (n = 1). A false-positive study was obtained in a patient with skull metastasis (n = 1). All 15 patients who were finally shown to suffer from ischaemic infarction had a normal SPET study 9-28 days after the onset of symptomatology. Of five patients with haemorrhagic infarction, studied within 2 weeks, four were false-positive. Of six patients with intracranial haemorrhage, studied 9-39 days later, one showed focal 201Tl accumulation. Two further false-positive studies consisted of angioma and epidural haematoma. Finally, SPET studies were normal in six patients with definite diagnosis of (reactive) gliosis (n = 3), Binswanger's encephalopathy (n = 1), postinfectious encephalopathy (n = 1) and multiple sclerosis (n = 1). In the patient population presented, sensitivity of 201Tl SPET for supratentorial brain tumours was 71.7% and specificity was 80.9%. Clinical information and control SPET studies in combination with early, 30-min and 3- to 4-h delayed imaging may be expected to improve on these figures. On the other hand it seems that, in addition to tumoral histology, the presence of tumours in the fossa posterior and small volumes contribute to the occurrence of false-negative 201Tl SPET studies.
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PMID:Sensitivity and specificity of thallium-201 single-photon emission tomography in the functional detection and differential diagnosis of brain tumours. 795 48

In pediatric patients, endogenous Cushing syndrome is an infrequent condition almost always due to one of two conditions. 1) Adrenal gland tumors account for 70% of Cushing syndromes in young pediatric patients. They cause rapidly progressive hypercorticism not due to increased ACTH production (elevated plasma and urine cortisol levels, very low ACTH and LPH levels unchanged by dexamethasone, metyrapone or CRH). Imaging techniques determine the side and spread of the tumor and look for metastases. Following surgical removal, patients with indicators of malignant disease (tumor weight above 30 g, extracapsular spread or metastases, independently from pathological data) are given op'DDD. 2) Cushing disease occurs in peripubertal patients and causes overweight with delayed statural gain. ACTH production is increased (positive dexamethasone suppression test and provocative metopirone and CRH tests) as a result of a pituitary adenoma which should be looked for by magnetic resonance imaging and whose removal ensures recovery in 50% of cases. Other therapeutic tools include op'DDD, radiation to the pituitary, and bilateral adrenalectomy as the last resort given the high risk of post-adrenalectomy pituitary tumor (50% of pediatric patients). Other causes are exceedingly rare: primary nodular hyperplasia of the adrenal glands and production of ACTH by a nonpituitary tumor. Corticosteroid treatment is the most common cause of Cushing syndrome in children.
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PMID:[Cushing syndrome in children]. 823 97

Pituitary tumors rarely metastasize outside the central nervous system. Of the more than 100 reported TSH-secreting adenomas, we now describe the first carcinoma. A 40-yr-old woman had transsphenoidal surgery for a large TSH-secreting pituitary adenoma in 1984. She had increased thyroid hormone levels with a TSH that varied from 16-31 microU/mL, and an unusually high alpha-subunit that ranged from 125-150 ng/mL. Because of residual tumor, she had a left craniotomy in 1985 followed by radiation. Despite these therapies, she had a residual tumor that remained stable until January 1989 when her tumor nearly doubled in size. She received radiation therapy and octreotide with marked diminution of the tumor and clinical improvement. In August 1989, she presented with leg weakness, and magnetic resonance imaging revealed a large sacral mass. A biopsy confirmed that the sacral mass was a metastasis from the pituitary tumor. Due to additional metastases in the lung, she received 5-fluorouracil, cytoxan, and adriamycin, with marked decrease in her lesions. Further substantiation of the metastatic pituitary tumor was made when the patient returned in December 1989 with a pleural effusion containing pituitary tumor cells. Of all the reported cases of TSH-secreting adenomas, this case had the highest alpha-subunit portending future metastases. Furthermore, the apparent response to octreotide and response to chemotherapy are encouraging and suggest that new therapies should be explored. Finally, since TSH-secreting adenomas tend to be more invasive than other pituitary tumors, this case underscores the need for early diagnosis and aggressive treatment of these tumors.
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PMID:Thyrotropin-secreting pituitary carcinoma. 843 99

Plasma levels of chromogranin A (CgA) were measured by ELISA in 22 patients with pheochromocytoma (18 non-metastatic, 3 metastatic, and 1 mixed neuroendocrine-neural tumor), 9 patients with primary hyperparathyroidism, and 9 patients with pituitary adenoma. The plasma levels of CgA were compared with norepinephrine, epinephrine, parathyroid hormone and pituitary hormones, i.e., growth hormone and prolactin. In pheochromocytoma, CgA in preoperative plasma of the patients without metastasis was 228 +/- 38 U/L (mean +/- SEM) and significantly higher than healthy controls (30 +/- 11 U/L, n = 40). Plasma CgA was decreased after removal of the tumors (28 +/- 6.0 U/L), except in three patients with metastatic pheochromocytoma and a mixed neuroendocrine neural tumor. The concentration of CgA in the patients with non-metastatic pheochromocytoma was significantly correlated with that of plasma norepinephrine (P < 0.005, r = 0.68) and urinary norepinephrine (P < 0.05, r = 0.65), but not with that of epinephrine. There was an exceptional case in which CgA was extremely high, but the CA level was normal. This tumor was a highly malignant pheochromocytoma with extensive metastases composed of small tumor cells which were occasionally positive for tyrosine hydroxylase immunohistochemically. These cells were considered to be poorly differentiated tumor cells and synthesized a very small amount of norepinephrine. Plasma levels of the patients with primary hyperparathyroidism and the patients with pituitary adenoma were 44 +/- 4 U/L and 48 +/- 8 U/L, respectively. Only one patient with a growth hormone-producing pituitary adenoma had a high level of CgA. Plasma CgA is a useful tumor marker for pheochromocytoma, even for malignant pheochromocytoma without elevated CA level, but not for hyperparathyroidism, or pituitary adenoma.
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PMID:Plasma chromogranin A in pheochromocytoma, primary hyperparathyroidism and pituitary adenoma in comparison with catecholamine, parathyroid hormone and pituitary hormones. 922 69

Pediatric central nervous system neoplasms include a spectrum of both glial and nonglial tumors that differ significantly in location and biological behavior from those of adults. Brain tumors in infants and children most often arise from central neuroepithelial tissue, whereas a significant number of adult tumors arise from central nervous system coverings (e.g., meningioma), adjacent tissue (e.g., pituitary adenoma), or metastases. Most adult brain tumors are supratentorial malignant gliomas, whereas the most common malignant pediatric brain tumor is the cerebellar primitive neuroectodermal tumor (medulloblastoma). This article reviews neuropathological characteristics of the more common pediatric brain tumors. Entities, such as the brainstem glioma, and less common neoplasms like the desmoplastic infantile ganglioglioma and the central nervous system atypical teratoid/rhabdoid tumor are reviewed because they occur almost exclusively in children. Known cytogenetic and molecular characteristics of childhood brain tumors are also reviewed.
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PMID:Neuropathology of pediatric brain tumors. 944 21


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