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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pituitary glands of 18 patients with untreated Addison's disease were studied by histologic and immunocytochemical methods. Adrenal destruction was caused by tuberculosis (13 cases) or autoimmune adrenalitis (five cases), and the duration of the adrenal insufficiency ranged from one to 16 years. Both diffuse and nodular hyperplasia of corticotropic cells were evident in each case, and the extent of hyperplasia correlated with the duration of disease. In five cases, nodular proliferations with morphologic features between those of hyperplasia and those of adenoma, termed tumorlets, were identified, as were two microadenomas, only one of which was available for study. In all instances, the proliferating corticotrophs stained positively with PAS and were immunoreactive for adrenocorticotropic hormone and beta-endorphin. We conclude that diffuse and nodular corticotroph hyperplasia are common in untreated Addison's disease, although frank adenoma formation seems to be rare. The latter may be related to the short duration of disease or may imply the absence of additional, unknown factors that are required for adenoma growth.
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PMID:The pituitary gland in untreated Addison's disease. A histologic and immunocytologic study of 18 adenohypophyses. 630 13

We studied 107 adenomas, found incidentally at autopsy in 100 pituitaries, by histologic and immunohistochemical techniques to elucidate their cellular composition and hormone content. No adenohypophyseal hormones were found in 54 (50%) of the adenomas, whereas prolactin was shown in 45 (42%). Of the remaining tumors, two contained prolactin and growth hormone, four contained adrenocorticotropic hormone, one contained thyroid-stimulating hormone, and one contained luteinizing hormone. These findings are consistent with the view that all adenohypophyseal cell types can give rise to neoplasms. No correlation was found between clinical history, autopsy findings, or cause of death and the presence or type of adenoma. The adenomas caused neither local symptoms nor endocrine abnormalities. The prevalence of various adenoma types differed between autopsy specimens and surgical material.
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PMID:Subclinical adenomas of the human pituitary. New light on old problems. 630 14

A dopaminergic mechanism has been proposed to suppress aldosterone secretion. To assess the possibility that a defect in the dopaminergic mechanism might enhance aldosterone secretion in hypertensive patients, we determined basal and adrenocorticotropic hormone (ACTH)-stimulated plasma aldosterone (PA), cortisol, renin activity, and potassium concentrations before and during dopamine receptor stimulation with dopamine infusion and bromocriptine administration and dopamine receptor blockade with metoclopramide. The patient study groups included: (a) seven patients with low-renin hypertension and abnormal aldosterone suppression with sodium loading and presumed bilateral zona glomerulosa hyperplasia (ZGHP); (b) two patients with aldosterone-producing adenoma; (c) five patients with low-renin hypertension but normal aldosterone suppression with sodium loading; and (d) six patients with normal-renin hypertension. Dopamine infusion in patients with ZGHP caused PA to fall (P less than 0.01) into the normal range, but did not block the enhanced (P less than 0.05) aldosterone response to ACTH that is characteristic of these patients. Dopamine infusion in patients with low-renin hypertension but normal aldosterone suppression also suppressed PA (P less than 0.01), whereas it had no effect upon PA in patients with normal-renin hypertension or aldosterone-producing adenoma and did not blunt the PA response to ACTH in either group. Bromocriptine administration had no effect upon basal or ACTH-stimulated PA. Dopamine infusion in patients with ZGHP also enhanced (P less than 0.05) diuresis and natriuresis in comparison with normal-renin patients. Metoclopramide administration increased (P less than 0.01) PA in all patients. Thus, a dopaminergic mechanism appears to be important in the regulation of aldosterone secretion in patients with ZGHP and in other low-renin hypertensives with normal aldosterone suppression with sodium loading. In contrast, this latter group does not exhibit an enhanced aldosterone response to ACTH. Both of these groups differ from normal-renin hypertensives, who have no PA suppression with dopamine infusion.
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PMID:Aldosterone suppression with dopamine infusion in low-renin hypertension. 630 9

With the use of electron microscopic morphology and immunochemistry, 5 tumors were studied: a spontaneous prolactin-producing adenoma (LEP rats); an estrogen-induced intrasellar tumor (R-Amsterdam rats); and 3 transplanted tumors, MtT.W10 and MtT.W5 (WF rats) and MtT.F4 (F344 rats). All tumors were derived from rat adenohypophysis and are known to secrete prolactin, growth hormone, or adrenocorticotropic hormone. The spontaneous tumor consisted of a uniform population of cells containing only immunoreactive prolactin. In the estrogen-induced tumor, prolactin and growth hormone were localized in separate cell types with the use of the immunoperoxidase technique. In the MtT.W10 tumor, both immunoreactive prolactin and growth hormone were observed in the same cell and in separate cell types. In the MtT.F4 and MtT.W5 tumors, one cell type was identified that was characterized by lack of morphologic differentiation, reduced secretory granule number, and inconclusive immunopositivity.
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PMID:Five different adenomas derived from the rat adenohypophysis: immunocytochemical and ultrastructural study. 701 14

Previous series of pediatric pituitary adenomas have been small and have not been analyzed by age group. We analyzed the frequency, manifestation, course, and biology of these tumors before, during, and after puberty in 136 children younger than 20 years old at surgery, identified by review of 2230 patients treated from 1969 to 1993. Tumors were classified by clinical phenotype. Adrenocorticotropic hormone-releasing adenomas were most common before puberty, and prolactinomas were most common during and after. The frequencies of adrenocorticotropic hormone-releasing adenomas, prolactinomas, and endocrine-inactive adenomas differed from those in adults. Growth arrest was common with all types except growth hormone (GH)-releasing adenomas; menstrual irregularities were common with all but adenomas causing Nelson syndrome. Among girls with prolactinomas, the preoperative duration of primary amenorrhea was longer than that of other symptoms. Tumor size differed by adenoma type. Serum hormone levels shortly after surgery correlated with the recurrence of prolactinomas and GH-releasing adenomas. The prolactinoma size correlated with the maximum preoperative serum prolactin level; boys had larger tumors and higher preoperative and postoperative prolactin levels. We conclude that pediatric pituitary adenomas vary in size, age at symptom onset, and frequency before, during, and after puberty. Most adenomas can cause menstrual irregularities, and primary amenorrhea should prompt investigation of the sella. Growth arrest is common with all adenomas except GH-releasing adenomas. Serum prolactin and GH levels measured at 1 to 5 days after surgery indicate the risk of recurrence of prolactinomas and GH-releasing adenomas, respectively.
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PMID:Pediatric pituitary adenomas. 773 5

Our followup study of 48 patients with primary aldosteronism concerns the results of 2 different operative methods. After preoperative localization of the unilateral solitary tumor 22 patients underwent unilateral adrenalectomy and 26 underwent enucleation of aldosterone-producing adenoma. Both operative methods improved hypertension, hypokalemia, the low urinary sodium-to-potassium ratio, suppressed plasma renin activity, high plasma aldosterone concentration, high urinary aldosterone excretion and high urinary kallikrein excretion in similar orders of magnitude for 5 years. Levels of plasma cortisol and plasma adrenocorticotropic hormone following respective operations were also identical. Five years postoperatively, ambulation and furosemide administration under low sodium diet stimuli remarkably enhanced plasma renin activity and plasma aldosterone concentration in the aldosterone-producing adenoma enucleation group (p < 0.001), almost similar to that of normal subjects but increment magnitudes were slight (p < 0.05 to < 0.01) in the adrenalectomy group. Preoperatively, angiotensin II infusion failed to increase plasma aldosterone concentration in patients with primary aldosteronism. After respective operations, responses of plasma aldosterone concentration to angiotensin II infusion and of plasma cortisol to adrenocorticotropic hormone administration in the aldosterone-producing adenoma enucleation group were more sensitive than those in the adrenalectomy group. There was no remission of recurrent hyperaldosteronism in either group throughout the study. These results suggest that angiotensin II induces aldosterone release by an activation of tumor uninvolved cortical cells and that the enucleation of aldosterone-producing adenoma is more preferable than unilateral adrenalectomy.
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PMID:Therapeutic outcome of primary aldosteronism: adrenalectomy versus enucleation of aldosterone-producing adenoma. 775 16

A location of copper and zinc- superoxide dismutase (Cu, Zn-SOD) in adenohypophysis and pituitary adenomas was examined with immunohistochemical technique. Pituitary adenomas include thirteen functioning, five nonfunctioning; functioning adenomas consist seven prolactinomas, four growth hormone (GH) secreting, two adrenocorticotropic hormone (ACTH) secreting adenomas. Three specimens of normal adenohypophysis were used for control study. The Cu, Zn-SOD was localized diffusely in the cytoplasm of normal adenohypophyseal cells and the tumor cells. Sometimes immunoreactive products of Cu, Zn-SOD revealed in the cytoplasm of endothelial cell, neutrophil, macrophage and the cell membrane of erythrocyte in the vessels. The content of Cu, Zn-SOD in normal adenohypophyseal cells and pituitary adenomas was markedly higher in normal cells than adenoma cells. No significant difference of the SOD content was observed not only in non-functioning adenoma but also in functioning adenoma cells including PRL, GH and ACTH cells.
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PMID:[Immunohistochemical study on the expression of copper and zinc-superoxide dismutase (Cu, Zn-SOD) in human adenohypophysis and pituitary adenomas]. 782 10

Touch preparations from surgically removed pituitary adenomas were studied by both routine staining and immunocytochemistry for all anterior pituitary hormones. The results were correlated with the histologic, histochemical, immunohistochemical and ultrastructural findings. Several features were recognized, some of them applicable in diagnosing various adenoma types: high cellularity, cell monomorphism, nuclear irregularities and heterogeneity of immunoreactivity, all major diagnostic criteria of pituitary adenoma. The presence of numerous fibrous bodies associated with nuclear pleomorphism, multinucleation and peripheral displacement of nuclei, in association with growth hormone (GH) immunopositivity, represent diagnostic criteria for sparsely granulated GH cell adenoma. The "Golgi" pattern of prolactin (PRL) immunopositivity in conjunction with the small size of cell and nucleus and the presence of microcalcifications represents diagnostic features of PRL-secreting adenoma. Cytoplasmic accumulation of hyaline material in association with peripheral distribution of periodic acid-Schiff stain and adrenocorticotropic hormone immunoreactivity is characteristic of sparsely granulated corticotroph cell adenoma. Knowledge and application of the described features may contribute significantly to the diagnostic approach to pituitary adenomas.
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PMID:Diagnosis of pituitary adenomas on touch preparations assisted by immunocytochemistry. 788 60

Three cases of a composite sellar tumour composed of a gangliocytoma and an adenoma are presented. Two patients who showed acromegaly and hyperprolactinaemia had a gangliocytoma and a growth hormone (GH)-prolactin cell adenoma in close proximity. The gangliocytoma contained growth hormone-releasing hormone (GHRH) by immunohistochemistry. At the electron microscopical level, the gangliocytoma was characterized by numerous synaptic vesicles. The third patient, a child with Cushing's disease, presented a corticotropin-releasing hormone (CRH)-positive gangliocytoma in close contact with an adrenocorticotropic hormone (ACTH) secreting adenoma, the latter a typical densely granulated ACTH cell adenoma. Ultrastructurally, the gangliocytoma revealed synaptic vesicles and sparse secretory granules. The results suggest that gangliocytomas may promote the development of pituitary adenomas by hypersecretion of releasing hormones. Whereas 20 cases of sellar GHRH producing gangliocytomas in acromegaly are reported in the literature, the combination of a CRH-positive gangliocytoma and an ACTH cell adenoma in Cushing's disease is apparently the first case.
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PMID:Combined sellar gangliocytoma and pituitary adenoma in acromegaly or Cushing's disease. A report of 3 cases. 792 20

Fourteen patients with adrenocorticotropic hormone (ACTH)-dependent hypercortisolism underwent pituitary scanning with computed axial tomography (CT) and magnetic resonance imaging (MRI). Computed tomography revealed pituitary macroadenomas in two patients, pituitary hyperplasia in one and a suspicion of pituitary microadenoma in one. Thirteen patients underwent MRI. One with a macroadenoma diagnosed on CT did not undergo MRI. The MRI revealed a pituitary macroadenoma in one, microadenoma in three and hyperplasia in two cases. Magnetic resonance imaging following gadolinium diethylene triamine penta acetic acid (gd-DTPA) enhancement revealed four more pituitary microadenomas. All patients who had pituitary adenomas (micro and macro) and hyperplasia underwent trans-sphenoidal pituitary surgery. One of the two patients, who had an enlarged pituitary on imaging but no demonstrable adenoma, was found to have a microadenoma at surgery. Patients with ACTH-dependent hypercortisolism should undergo MRI of the pituitary gland to identify/localize corticotroph pituitary adenomas. The study should include gd-DTPA enhancement in cases where the scan is normal.
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PMID:Cushing's disease: pituitary imaging. 794 10


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