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Biomedical subjects

E Horvath

Publications and source records attributed to E Horvath.

At least 181 records · Page 10Linked to original sources
PubMed1984

Sellar glomangioma.

A glomangioma (glomus tumor) arising in the pituitary region is described. The histologic and ultrastructural features were characteristic. The tumor was composed of epithelioid cells arranged in an organoid fashion around vascular channels and contained scattered mast cells. Electron microscopy revealed tumor cells that showed features of smooth muscle differentiation. Immunocytology demonstrated the presence of actin, desmin, and myoglobin within tumor cells and basement membrane antigen surrounding them; factor VIII was localized in endothelial cells and not within tumor cells. Pituitary hormones were not detected in the tumor by the immunoperoxidase technique. This is the first report of a glomangioma of the sella turcica. The gomitoli of the hypophyseal portal vessels are structures that resemble glomera found in other sites. Derivation of this tumor from gomitoli is suggested.

Adult↗
PubMed1984

Clinical and pathological effects of bromocriptine on prolactin-secreting and other pituitary tumors.

Bromocriptine inhibits prolactin secretion and causes size reduction of prolactin-secreting adenomas. The effect of the drug upon pituitary tumors other than prolactinomas is uncertain. The authors report a prospective series of 12 patients with pituitary macroadenomas in whom bromocriptine was administered for 6 weeks prior to transsphenoidal surgery. Five of the patients had computerized tomographic documentation of significant reductions in tumor size (Group A) and six had no change (Group B) during 3 and 6 weeks of bromocriptine administration. One patient who demonstrated size reduction in his tumor was not assigned to either group as he was treated with high-dose dexamethasone concurrently with the bromocriptine. Pathological examination (light and electron microscopy and immunocytochemistry) indicated that all Group A patients harbored tumors with prolactin granules whereas all Group B tumors lacked such granules. Adenoma cells in the responsive tumors were involuted with reduced cytoplasmic, nuclear, and nucleolar areas. Neither widespread cell necrosis, infarction, nor vascular injury was observed. Two of the five Group A patients discontinued bromocriptine prior to completion of the 6-week protocol and had a rapid return of their tumors to pre-treatment size. Although bromocriptine has been reported to cause shrinkage of nonfunctional tumors, there was no radiological evidence of size reduction or pathological changes in the nonfunctional tumors of this series. Interestingly, serum levels of prolactin were modestly elevated (84 and 113 ng/ml) in two of the six Group B patients, an elevation due to stalk compression rather than secretion by adenoma cells. This finding underscores the fact that failure of bromocriptine to reduce pituitary tumor size in the presence of hyperprolactinemia may occur because the tumor is other than a prolactinoma. This is the first moderate-sized group of patients in whom pathological changes in responsive prolactinomas during bromocriptine therapy have been demonstrated. As bromocriptine is not tumoricidal, and thus not curative, there is insufficient evidence to recommend this drug as primary therapy for either prolactin-secreting or nonfunctional macroadenomas, but the drug may have potential as a preoperative adjunct to effect shrinkage of prolactinomas and theoretically, at least, make excision easier and possibly more complete.

Adenoma↗
PubMed1984

Cushing's disease associated with an intrasellar gangliocytoma producing corticotrophin-releasing factor.

A 58-year-old woman had Cushing's disease with elevated plasma adrenocorticotrophin and an intrasellar tumor. Light microscopy showed that the tumor was a gangliocytoma containing immunoreactive corticotrophin-releasing factor accompanied by pituitary corticotroph hyperplasia. Ultrastructural examination identified an intimate association and desmosomal attachments between interdigitating cell processes of neurons and corticotrophs. It is suggested that Cushing's disease was due to the effect of corticotrophin-releasing factor on corticotrophs; this case represents a syndrome supporting the concept that, in some patients, Cushing's disease may have a hypothalamic origin.

Corticotropin-Releasing Hormone↗
PubMed1984

Gonadotroph adenomas of the human pituitary: sex-related fine-structural dichotomy. A histologic, immunocytochemical, and electron-microscopic study of 30 tumors.

Thirty pituitary tumors, removed from 14 men and 15 women, were diagnosed as gonadotroph adenomas on the basis of their immunocytochemical and/or ultrastructural features. Serum follicle-stimulating hormone (FSH), but not luteinizing hormone (LH), was elevated in 8 men, whereas none of the women had gonadotropin levels, as measured by radioimmunoassay, inappropriately high for their age. Immunoreactive FSH (sometimes also LH) was present in 13 of 15 tumors in men but only 6 of 13 adenomas in women. By electron microscopy, gonadotroph adenomas in men had uncharacteristic features often similar to those of null-cell adenomas with poorly or moderately developed cytoplasmic organelles. In women, all tumors were well differentiated, with a highly distinctive vesicular dilatation of the Golgi complex ("honeycomb Golgi") as a diagnostic marker present in 14 of 15 adenomas. To the author's knowledge, this is the first example of sex-linked dichotomy within a tumor type expressed as the markedly different ultrastructural appearance of cytoplasmic organelles, especially the Golgi apparatus.

Adenoma↗
PubMed1984

Quantitative autoradiography of [125I] apamin binding sites in the central nervous system.

The binding sites for [125I] apamin in the central nervous system of rat, guinea-pig, chicken and frog were assessed by quantitative autoradiography on X-ray film. In rat and guinea-pig brain apamin labels preferentially the limbic-olfactory system, i.e. nucleus olfactorius, nuclei septi, habenula and hippocampus. In the rat spinal cord the peptide binds preferentially to the substantia gelatinosa. Tectum opticum and nuclei isthmi are labelled in chicken brain. In frog brain no preferentially "apamin-stained" area was found. The role of the cerebral binding sites is still unknown, whereas the spinal sites may be involved in apamin poisoning.

Animals↗
PubMed1983

Mammosomatotroph cell adenoma of the human pituitary: a morphologic entity.

Nine cases of a hitherto undescribed morphologic entity, termed mammosomatotroph cell adenoma of the human pituitary, are reported. These tumors, occurring mostly in men, are invariably associated with acromegaly (or gigantism) and high-normal or slightly elevated blood prolactin levels, and it cannot be distinguished clinically from well-differentiated growth hormone cell or mixed growth hormone cell-prolactin cell adenomas. They show a slow growth rate and usually exhibit a diffuse pattern and intense cytoplasmic acidophilia by histology. The immunoperoxidase technique detects both growth hormone and prolactin within the same cells. Electron microscopy reveals monomorphous tumors with a fine structure markedly similar to that of well-differentiated, densely granulated growth hormone cell adenomas. An added feature and diagnostic marker of mammosomatotroph cell adenoma is the presence of extracellular deposits of secretory material. One tumor shows a marked abnormality of hormone packaging and storage, resulting in the cytoplasmic accumulation of pleomorphic bodies containing semicrystalline secretory material.

Acromegaly↗
PubMed1983

Pathophysiology of acromegaly.

This review discusses the pathophysiology of acromegaly. Acromegaly has been classified in this paper into distinct entities based on etiology, ultrastructural features of the pituitary, and cytogenesis. This classification has been proposed based on clinical signs, immunoperoxidase techniques, transmission electromicroscopy and immunoelectron microscopy. Pituitary causes of acromegaly include densely granulated adenomas, sparsely granulated adenomas, mixed growth hormone and prolactin cell adenomas, acidophil stem cell adenomas, mammosomatotroph cell adenomas, and pleurihormonal adenomas. GH cell hyperplasia and GH cell carcinoma are also discussed. Extrapituitary causes of acromegaly include eutopic GH cell adenoma in the sphenoid sinus or parapharyngeal region and excess GHRF secretion which may be eutopic or ectopic. The pathological, clinical, and biochemical evidence in favor of a pituitary or hypothalamic etiology of acromegaly has been reviewed. Finally, a multistage theory of GH cell tumorigenesis has been proposed as a model in an attempt to unify the genetic, environmental and biochemical factors implicated in the pathogenesis of acromegaly.

Acromegaly↗
PubMed1983

Subclinical adenomas of the human pituitary. New light on old problems.

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.

Adenoma↗
PubMed1983

Hypothalamic neuronal hamartoma and adenohypophyseal neuronal choristoma: their association with growth hormone adenoma of the pituitary gland.

Hypothalamic neuronal hamartomas and neuronal choristomas of the anterior pituitary are rare lesions; either may be associated with endocrinopathy. We describe a case of each with associated growth hormone-producing pituitary adenomas and clinical acromegaly, both well documented and studied by immunocytochemistry and electron microscopy. That a functional relationship exists between the neuronal malformation and the pituitary neoplasm remains speculative. We suggest that a growth hormone-releasing factor-like substance may have been elaborated by hypothalamic-type neurons, which, by a trophic effect, may have resulted in the production of an adenohypophyseal neoplasm. Our study supports the concept that secretory neurons, either outside or within the sella, may induce adenomas.

Acromegaly↗
PubMed1983

Unusual configurations of endoplasmic reticulum in human pituitary adenomas.

Electron microscopic study of 435 surgically-removed human pituitary adenomas and 43 nontumorous adenohypophyses revealed unusual configurations of endoplasmic reticulum in 102 adenohypophysial tumors (23%) and in 12 nontumorous adenohypophyses (28%). These configurations classified as paired reticulum, annulate lamellae and ribosome-lamellar complexes were noted in various adenomatous and nontumorous adenohypophysial cells, indicating that they could not be used as specific markers for pituitary adenomas or for a particular adenohypophysial cell type. Paired reticulum was a common finding, whereas annulate lamellae and ribosome-lamellar complexes were rarely encountered. Whether or not these endoplasmic reticulum configurations could be considered as normal constituents of adenohypophysial cells was difficult to assess, since nontumorous cells studied were from patients who had various diseases and who had been treated with different hormones. The presence of endoplasmic reticulum configurations was neither related to age, sex of the patients nor degree of differentiation or endocrine activity of pituitary adenomas.

Adenoma↗
PubMed1982

Malignant Leydig cell tumor: clinical, histologic and electron microscopic features.

A 51-year-old man had a malignant Leydig cell tumor of the testis with elevation of serum estrone and androstenedione as well as urine chorionic gonadotropin. The fine structural features of the neoplasm resembled those of nontumorous Leydig cells as well as cells of Leydig cell adenomas, except for, nuclear pleomorphism, the absence of Reinke's crystals and the infrequency of microvilli. The abundance of smooth surfaced endoplasmic reticulum, well-developed mitochondria with tubular and vesicular cristae were regarded as representing ultrastructural expressions of enhanced secretory activity and consistent with the biochemical findings of increased hormonal production by tumor cells. Since Leydig cells have distinct ultrastructural features, ultrastructural investigation represents a valuable tool in establishing the Leydig cell origin of a tumor.

Androstenedione↗
PubMed1982

Adenoma of the human pituitary producing growth hormone and thyrotropin. A histologic, immunocytologic and fine-structural study.

A pituitary adenoma removed by surgery from a 22-year-old man was studied by histology, immunocytology, transmission electron microscopy and immunoelectron microscopy. Clinically, the patient had acromegaly and euthyroidism with elevated blood GH concentrations. Blood TSH and T4 levels were within the normal range. Histologically, the adenoma was chromophobic and exhibited no PAS, lead hematoxylin, aldehyde thionin or Grimelius silver positivity. By the immunoperoxidase technique GH, beta-TSH and alpha-subunit but no PRL, ACTH, alpha-endorphin, beta-FSH or beta-LH were demonstrated in the adenoma cells. Electron microscopy revealed adenoma cells which were similar to TSH cells and showed no resemblance to GH cells of nontumorous pituitaries or GH-secreting tumors. Immunoelectron microscopy demonstrated GH and beta-TSH in the secretory granules. It is concluded that pituitary adenomas composed of TSH-like cells may secret GH, resulting in acromegaly. Production of GH by adenomatous TSH cells cannot be explained on the basis of the one cell- one hormone theory. The question is raised whether bihormonal or multihormonal clones, capable of synthesizing more than one hormone, exist in the human pituitary. These cells are apparently dormant under normal conditions, but in the course of neoplastic transformation may undergo functional dedifferentiation and acquire the ability to produce two or more different hormones.

Adenoma, Chromophobe↗
PubMed1982

Somatotroph hyperplasia. Successful treatment of acromegaly by removal of a pancreatic islet tumor secreting a growth hormone-releasing factor.

A 21-yr-old woman with Turner's syndrome presented with signs and symptoms of acromegaly. The serum growth hormone (GH) (95+/-9.4 ng/ml; mean+/-SEM) and somatomedin C (11 U/ml) levels were elevated, and an increase in GH levels after glucose instead of normal suppression, increase after thyrotropin-releasing hormone (TRH) administration instead of no change, and decrease after dopamine administration instead of stimulation were observed. The pituitary fossa volume was greater than normal (1,440 mm(3)) and the presence of a pituitary tumor was assumed. After tissue removal at transsphenoidal surgery, histological study revealed somatotroph hyperplasia rather than a discrete adenoma. Postoperatively, she remained clinically acromegalic and continued to show increased GH and somatomedin levels. A search was made for ectopic source of a growth hormone-releasing factor (GRF). Computer tomographic scan revealed a 5-cm Diam tumor in the tail of the pancreas. Following removal of this tumor, serum GH fell from 70 to 3 ng/ml over 2 h, and remained low for the subsequent 5 mo. Serum somatomedin C levels fell from 7.2 to normal by 6 wk postoperatively. There were no longer paradoxical GH responses to glucose, TRH, and dopamine. Both the medium that held the tumor cells at surgery and extracts of the tumor contained a peptide with GRF activity. The GRF contained in the tumor extract coeluted on Sephadex G-50 chromatography with rat hypothalamic GH-releasing activity. Stimulation of GH from rat somatotrophs in vitro was achieved at the nanomolar range, using the tumor extract. The patient's course demonstrates the importance of careful interpretation of pituitary histology. Elevated serum GH and somatomedin C levels in a patient with an enlarged sella turcica and the characteristic responses seen in acromegaly to TRH, dopamine, and glucose do not occur exclusively in patients with discrete pituitary tumors and acromegaly. This condition can also occur with somatotroph hyperplasia and then revert to normal after removal of the GRF source. Thus, in patients with acromegaly a consideration of ectopic GRF secretion should be made, and therefore, careful pituitary histology is mandatory. Consideration for chest and abdominal computer tomographic scans before pituitary surgery, in spite of their low yield, may be justified.

Acromegaly↗
PubMed1981

Acidophil stem cell adenoma of the human pituitary: clinicopathologic analysis of 15 cases.

In material of 347 surgically removed pituitary adenomas, 15 tumors (4.3%) were diagnosed as acidophil stem cell adenomas. These are immature neoplasms, assumed to derive from the common progenitor of growth hormone and prolactin cells, and usually containing both hormones by the immunoperoxidase technique. Clinically, they are regularly associated with hyperprolactinemia. Some patients may exhibit physical stigmata of acromegaly without biochemical evidence of the disease ("fugitive acromegaly"). The entity is also characterized by (1) relatively short clinical history; (2) large (grade III--IV), locally invasive adenoma, and (3) relatively low hormonal activity. By electron microscopy, these tumors are unicellular with immature cytoplasm, exhibiting some features of adenomatous growth hormone and prolactin with immature cytoplasm, exhibiting some features of adenomatous growth hormone and prolactin cells and frequently mitochondrial abnormalities as well. They are more aggressive than the well-differentiated adenomas of the "acidophil" cell line--a fact to be considered in postoperative management.

Adenoma, Acidophil↗