Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumors from 42 surgically resected pituitaries and from 13 autopsy cases were studied immunohistochemically with polyclonal antisera to 7 anterior pituitary hormones and with a newly developed monoclonal antibody directed against human chromogranin for evaluation of the distribution of chromogranin in normal and neoplastic pituitaries. In addition, a prospective study was done for assessment of the prevalence, morphology, and endocrine cell types of pituitary tumors in 100 autopsy subjects. When these 55 pituitary adenomas were examined with monoclonal antibody (LK2H10) directed against human chromogranin, selective staining of normal adenohypophyseal cell types and pituitary tumors was observed. Most null-cell adenomas (12/14) were positive for chromogranin, whereas all prolactin (PRL)-producing adenomas (19/19) were negative. Growth hormone (GH) adenomas were focally positive (9/9). All oncocytomas (2/2), 1 thyrotropin (TSH) adenoma, and a follicle-stimulating hormone/luteinizing hormone adenoma were positive for chromogranin. One or more adenomas were present in 14% of the autopsy cases. The tumors occurred most frequently in patients in the fifth through the seventh decades of life. Immunohistochemical staining of 13 adenomas revealed 1 TSH, 1 ACTH, and 4 PRL-producing tumors, whereas 7 other tumors, which were null-cell or undifferentiated adenomas, failed to stain for any of the seven principle pituitary hormones. These results indicate that antibody LK2H10 to human chromogranin is useful in the immunohistochemical characterization of pituitary adenomas. Incidental pituitary microadenomas from autopsy-derived pituitaries most commonly produce PRL, or they belong to the null-cell or undifferentiated tumor group.
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PMID:Pituitary adenomas. An immunohistochemical study of hormone production and chromogranin localization. 608 68

Double tumors were found in the anterior and posterior lobes of pituitary gland at autopsy in a patient who presented with progressive deterioration of mental status. The chromophobe adenoma of anterior lobe consisted of a mixture of non-immunoreactive hormone containing cells and a few prolactin (PRL) and growth hormone (GH) cells in the mid portion whereas the periphery of the tumor contained immunoreactive cells for PRL, GH, thyroid-stimulating hormone (TSH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). A microscopic focus of granular cell myoblastoma (GCM) was found in the posterior lobe. Differentiation of tumor cells into anterior pituitary cells and GCM is discussed.
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PMID:Double tumors of anterior and posterior pituitary gland. 626 28

The follicular structures present in the human pituitary gland were studied, at the light-microscopic level, using histochemical and immunocytochemical techniques. The antisera applied in the peroxidase-antiperoxidase procedure were anti-hFSH beta, anti-hLH beta, anti-hPRL, anti-hGH, anti-hTSH beta, anti-hLPH beta, anti-pACTH, and anti-hACTH. In the 10 normal pituitaries examined, follicles were always found in the three areas of the adenohypophysis. The wall of the pars distalis follicles showed the seven immunoreactive cell types studied, while follicle-stimulating hormone (FSH) and luteinizing hormone (LH) cells were the only ones present in the wall of the pars tuberalis follicles. Most of the cell types studied were also present in the wall of the intermediate area follicles, but these follicles had characteristics not found in the other two areas. They were very large, with frequent interconnections forming a three-dimensional network of anastomotic cavities, and the colloid had different histochemical affinity. None of the hormones studied could be detected by immunocytochemistry within the follicular colloid. Three of the ten pituitary adenomas examined showed numerous follicular structures. Some of the follicles in the adenomatous pituitaries were similar to those found in the normal adenohypophysis, but there were also follicles filled with only traces of colloid and numerous blood cells in the cavity, and follicles filled with neoformed connective tissue. In one of these cases, FSH/LH immunoreactive adenoma cells were seen in the wall of the follicles. The results obtained suggest that the finding of pituitary adenomas with follicular structures is not uncommon and that the follicles originate from the tumor cells. In addition, the follicles seem to have several functional stages, explaining the finding of different types of follicular formation.
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PMID:Constitution and behavior of follicular structures in the human anterior pituitary gland. 632 78

Forty women with hyperprolactinemia with and without radiologic evidence of prolactin-secreting pituitary adenoma were prospectively treated with bromocriptine. On the basis of tomographic studies, the patients were divided into either a microadenoma group (N = 19) or no adenoma group (N = 21). Both groups had similar distributions as to obstetric history, menstrual abnormalities, levels of baseline serum luteinizing hormone, follicle-stimulating hormone, and thyrotropin. Patients in the adenoma group had significantly higher (p less than 0.001) baseline serum prolactin levels (173 +/- 4.4 ng/ml) than those of patients without adenoma (61.1 +/- 4.5 ng/ml). Patients without an adenoma required significantly less bromocriptine (5 to 7.5 mg) (p less than 0.005) to normalize serum prolactin or establish a pregnancy than did those who had an adenoma (5 to 20 mg). Similarly, patients with adenoma resumed ovulatory cycles (8.7 +/- 1.2 versus 5.7 +/- 0.06 weeks), had their galactorrhea disappear (11.3 +/- 2.1 versus 5.6 +/- 1.1 weeks), and become pregnant (16.2 +/- 2.5 versus 9.8 +/- 1.5 weeks) in a significantly longer time (p less than 0.01) than did those who had no adenomas. There was no significant difference in the pregnancy rate between the groups, and the overall rate was 86% of 28 patients desiring pregnancy. No complications were observed during pregnancy. The conclusion is that both patients with and those without radiologic evidence of a prolactin-secreting pituitary adenoma can be safely treated with bromocriptine. In addition, the resumption of ovulatory cycles is more important than the absolute normalization of serum prolactin.
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PMID:Management of patients with hyperprolactinemia and normal or abnormal tomograms. 663 94

Prolactin (PRL) and other pituitary hormones (luteinizing hormone, follicle-stimulating hormone, growth hormone [GH], thyrotropin stimulating hormone) were measured before, during, and after transphenoidal pituitary adenomectomy in 16 patients with hyperprolactinemia. The diagnosis of prolactinoma was made in three of the 16 patients by the absence of PRL response to thyrotropin-releasing factor (TRF) and a dopamine receptor antagonist, metoclopramide, without radiologic evidence of an adenoma. Contrary to findings in subjects with normal PRL values, the PRL rise in response to anesthesia and operation was absent. Other pituitary hormones, with the exception of GH, which increased during anesthesia and operation, exhibited no acute changes. In 11 of 16 cases, complete tumor removal was achieved as determined by the rapid decline of PRL levels to normal values within 24 to 48 hours after operation and by subsequent clinical follow-up. This finding documents that the adenoma is the main source of excessive PRL secretion. The circulating half time of immunoreactive PRL determined by frequent sampling in these patients was variable, ranging from 74 to 190 minutes, significantly longer than the previously reported value of 15 minutes determined by bioassay. Although a transient decline was evident, serum PRL levels remained elevated in those patients with incomplete tumor removal. These findings suggest that a single measurement of serum PRL within 24 to 48 following transphenoidal adenomectomy is a reliable indicator of the success or failure of the procedure.
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PMID:Changes in pituitary hormones during and following transsphenoidal removal of prolactinomas. 676 67

Giant invasive pituitary adenomas are rare tumors that have been reported to extensively involve the cranial base, as well as other intra- and extra-cranial structures, making surgical resection by traditional approaches impossible. We report two cases, each of a giant invasive adenoma involving the entire length of the clivus and adjacent structures that was resected via a transfacial approach with excellent results. Both tumors were in middle-aged men; one was nonsecreting, and the other secreted follicle-stimulating hormone alpha-subunit. Most previously reported giant invasive adenomas have been prolactinomas. Both tumors were resected via a transfacial approach that incorporated an osteoplastic maxillotomy with palatal division and a posterior pharyngeal incision that provided exposure from the suprasellar region to C2. Both of the patients received postoperative radiation and have done very well. Their cosmetic results were excellent. The complications included postoperative meningitis in one patient and a nasal voice in the other. The transfacial approach provides excellent access for this type of extensive midline tumor requiring resection from the suprasellar region down to the foramen magnum.
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PMID:Resection of giant invasive pituitary tumors through a transfacial approach: technical case report. 750 Nov 26

The anterior pituitary hormone serum levels of 13 patients of both sexes were examined for basal secretion and response to TRH-GnRH stimulus before and after parathyroidectomy. The patients were suffering from hyperparathyroidism of parathyroid adenoma origin. After the operation, the previously high serum calcium and low serum phosphate levels decreased (P < 0.001). The serum parathyroid hormone (PTH) concentration, too, decreased significantly. After surgery, the basal and stimulated secretion of thyrotropin (TSH) showed a significant increase (P < 0.02 and P < 0.05, respectively). Significantly higher prolactin (PRL) levels were measured after surgery in those patients whose PRL levels were normal both before and after the operation. No significant change was observed in patients with hyperprolactinaemia. After surgery an increased spontaneous growth hormone (GH) secretion was found, while the basal luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretions remained unchanged. In postmenopausal women the stimulated FSH secretion decreased (P < 0.05), while the decrease of the stimulated LH secretion was not significant. The results suggest that extracellular calcium may modify the secretion of certain adenohypophysis hormones and their stimulus-induced response.
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PMID:The reaction of adenohypophysis hormones in primary hyperparathyroidism and after surgical treatment. 763 37

A 40-year-old Black man presenting with increasing nasal discharge of bloody, mucoid pus as well as nasal obstruction over a 2-month period is described. Magnetic resonance imaging of the skull showed a tumor eroding through the skull base into the clivus and extending into the sphenoid sinus. Endoscopy of the sphenoid sinus demonstrated a polypoid mass extending into the posterior choanae. The lesion was partially resected. Histologic evaluation showed a cellular small blue cell tumor punctuated by bland, epithelial-lined microcysts. Electron microscopy revealed epithelial cells with abundant rough endoplasmic reticulum and electron-dense membrane-bound endocrine granules, some undergoing misplaced exocytosis. Immunohistochemical evaluation demonstrated cytoplasmic reactivity for neuron-specific enolase, synaptophysin, and prolactin. Stains for leukocyte common antigen, HMB-45, desmin, cytokeratin, chromogranin, and the remaining spectrum of pituitary hormones including growth hormone, corticotropin, luteinizing hormone, follicle-stimulating hormone, and thyrotrophic hormone were negative. In contrast, the epithelium lining the cysts was cytokeratin positive and synaptophysin negative. This ostensibly small cell tumor therefore represented a remarkably extensive and aggressive prolactin cell adenoma with unusual light microscopic features. Characterization of the lesion required electron microscopy and further confirmation by immunocytology. The distinction of pituitary adenomas and particularly of prolactin cell tumors from other adenoma types and from other small cell lesions markedly affects therapy and patient prognosis.
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PMID:Aggressive small cell tumor of the skull base. 819 26

Interleukin-6 (IL-6) was secreted by cultured cells of 7 out of 11 human pituitary adenomas that were examined. Interleukin-1 (IL-1) stimulated IL-6 release after a 24-h incubation period in five of the seven IL-6-secreting adenoma cultures and in all seven after 72 h. Tumour necrosis factor, interferon-gamma and epidermal growth factor did not significantly affect IL-6 secretion. Interleukin-1 failed to induce measurable IL-6 in the cultures that did not secrete IL-6 under basal conditions. Prostaglandin E2 did not influence basal IL-6 secretion and indomethacin did not inhibit IL-1-stimulated IL-6 release. In addition, pertussis toxin had no effect on IL-1-stimulated IL-6 release. The growth hormone (GH) secretory response to IL-1 varied, with stimulation in one GH-secreting adenoma culture, no significant effect in a second and inhibition in a third. Interleukin-1 did not significantly affect the release of prolactin, thyrotrophin, luteinizing hormone or follicle-stimulating hormone in any of the adenoma cultures. This study provides evidence that IL-1 is a stimulator of IL-6 release from cultured human pituitary adenoma cells that secrete IL-6. Stimulation of IL-6 release by IL-1 in these tumour cells is probably not mediated by prostaglandins or by a pertussis toxin-sensitive mechanism.
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PMID:Interleukin-1 stimulates the release of interleukin-6 from cultured human pituitary adenoma cells. 839 Nov 94

Pancreastatin, a carboxyl-terminal amidated peptide derived from chromogranin (Cg)A, inhibits secretion of insulin and parathyroid hormone. Our recent studies found significant amounts of immunoreactive pancreastatin in all pituitary adenomas except prolactin adenomas. To analyze the effects of pancreastatin on pituitary cell function, 17 cultured pituitary adenomas were examined for immunoreactive pancreastatin and pancreastatin secretion by the tumors. The effects of pancreastatin on pituitary hormone secretion and on pituitary hormone (follicle-stimulating hormone and prolactin), CgA, and CgB mRNA levels were also examined. Immunoreactive pancreastatin and CgA were present diffusely in gonadotroph and null cell adenomas, but only a few prolactin adenoma cells expressed pancreastatin or CgA. When cells were treated with hypothalamic peptides, gonadotroph adenomas were the only group that released increased amounts of pancreastatin in response to gonadotropin-releasing hormone (10(-7) mol/L). Pancreastatin (10(-7) mol/L) treatment did not stimulate pituitary hormone secretion significantly. In situ hybridization analyses showed that gonadotropin-releasing hormone and pancreastatin treatment led to significant increases in CgB and follicle-stimulating hormone mRNAs in gonadotroph adenomas, whereas CgA mRNA levels did not change significantly. These results show that there is a differential distribution of pancreastatin secretion in pituitary adenomas and that the hypothalamic hormone gonadotropin-releasing hormone and the CgA-derived peptide pancreastatin can regulate CgB mRNA in gonadotroph adenomas, suggesting an autocrine effect of pancreastatin on pituitary tumor function.
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PMID:Pancreastatin secretion by pituitary adenomas and regulation of chromogranin B mRNA expression. 866 89


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