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Biomedical subjects

S L Asa

Publications and source records attributed to S L Asa.

At least 181 records · Page 10Linked to original sources
PubMed1986

Human fetal adenohypophysis. Histologic and immunocytochemical analysis.

One hundred and forty human fetal pituitary glands were removed from fetuses at 7-40 weeks of gestation and studied by light microscopy and immunocytochemistry to localize adenohypophysial hormones. For immunocytology, the avidin-biotin-peroxidase complex technique was more sensitive and identified hormones in younger fetuses than did the immunoperoxidase method. Adrenocorticotrophin, beta-endorphin, and growth hormone were the first hormones detected; they were identified by intense cytoplasmic immunopositivity at 8 weeks of gestation. Between 10 and 20 weeks, many growth hormone containing cells were large and showed scattered, faint positivity; after 20 weeks, smaller cells with intense positivity predominated. alpha-Subunit of the glycoprotein hormones was identified at 9 weeks of development; beta-subunits of thyroid-stimulating hormone, follicle-stimulating hormone, and luteinizing hormone appeared by 12 weeks. Gonadotrophs differed in numbers related to fetal age and sex. From 15 to 25 weeks, glands of female fetuses contained more gonadotrophs than did those of males; after 25 weeks, there was no significant difference in total gonadotroph numbers. Throughout gestation, adenohypophyses of male fetuses had more luteinizing hormone containing cells than follicle-stimulating hormone containing cells; pituitaries of females had approximately the same numbers of follicle-stimulating hormone containing and luteinizing hormone containing cells. Prolactin was identified in few small cells at 12 weeks; at term, prolactin-containing cells were numerous, comparable to those seen in the hyperplasia of maternal glands in late gestation and during lactation. This comprehensive study indicates morphologic correlations with pituitary hormone extraction data and with the appearance of the various hormones in the fetal circulation.

Adrenocorticotropic Hormone↗
PubMed1986

Gonadotropin secretion in vitro by human pituitary null cell adenomas and oncocytomas.

Pituitary null cell adenomas and oncocytomas are tumors not associated with clinical or biochemical evidence of hormone excess; morphological studies have not hitherto revealed their origin or the nature of their hormone production, if any. We examined the in vitro secretory activity of seven null cell adenomas and five oncocytomas which caused symptoms of a mass lesion and variable degrees of hypopituitarism. All tumors were classified at the time of surgical resection using immunohistochemistry and electron microscopy. RIA revealed the presence of FSH, LH, and alpha-subunit of pituitary glycoprotein hormones in the culture medium of eight tumors, FSH and alpha-subunit in the medium of one tumor, and TSH, FSH, LH, and alpha-subunit in the medium of three adenomas. Morphological examination of cultured tissues confirmed the presence of tumor resembling those in the initial surgical specimen. Thus, we conclude that null cell adenomas and oncocytomas contain cells that can produce pituitary glycoprotein hormones, and that the majority produce gonadotropins.

Adenoma↗
PubMed1986

Microscopic peliosis of pancreatic islets in a woman with MEN-1 syndrome.

We report herein a case of histologically identified peliosis of pancreatic islets in the surgically removed portion of the pancreas of a 30-year-old woman with multiple endocrine neoplasm, type 1 (MEN-1) syndrome. In addition to microscopic peliosis, the pancreas contained multiple endocrine tumors producing insulin, glucagon, somatostatin, and growth hormone-releasing factor and showed evidence of widespread nesidioblastosis. It is uncertain whether peliosis of pancreatic islets and MEN-1 syndrome were coincidental or whether the two diseases were causally related. Since hormonal factors can result in hepatic peliosis, it is tempting to speculate that the endocrine imbalance secondary to MEN-1 syndrome might have played a role in the genesis of peliosis in this case. Although no direct proof of vascular damage was encountered, it is conceivable that escape of red blood cells from the circulation and their accumulation in tissue spaces was due to abnormal islet blood flow and increased capillary permeability.

Adult↗
PubMed1985

Immunohistological localization of growth hormone-releasing hormone in human tumors.

Two forms of GH-releasing factor (GHRH), which play a role in the regulation of GH secretion, have been isolated from pancreatic endocrine tumors in two patients with acromegaly. We examined formalin-fixed, paraffin-embedded human tissues from autopsies and surgical specimens for the presence of human pancreatic GHRH-40 using the avidin-biotin-peroxidase complex technique to assess the prevalence of tumors containing GHRH, to define their primary sites and cellular derivations, and to correlate clinical and pathological features. Immunopositivity was demonstrated in 4 of 24 pancreatic endocrine tumors, 1 of 5 bronchial and 2 of 15 gut carcinoids, 1 of 2 thymic carcinoids, 2 of 20 medullary carcinomas of the thyroid, 1 of 12 pheochromocytomas, and 5 of 20 small cell carcinomas of the lung. Of the GHRH-containing tumors, only 2 of the pancreatic endocrine tumors and the bronchial carcinoid were associated with acromegaly. No GHRH was found in 35 tumors derived from cells that are not known to produce peptide hormones. Immunoreactivity was not detected in the nontumorous tissues from which GHRH-containing tumors were derived. It can be concluded that GHRH may be found in a variety of tumors arising from and composed of peptide hormone-producing endocrine cells. The significance of immunoreactive GHRH detected in tumors unassociated with clinical evidence of acromegaly remains to be established.

Acromegaly↗
PubMed1984

The influence of pituitary hormones on adjuvant arthritis.

Adjuvant arthritis was induced in female Fisher rats by injecting their right hind paw with 0.1 ml Freund's complete adjuvant. The development of adjuvant arthritis was inhibited by hypophysectomy and by daily treatment of intact animals with the dopaminergic agent bromocriptine. Adjuvant arthritis developed normally if hypophysectomized or bromocriptine-suppressed animals were treated with either prolactin or growth hormone. Additional treatment with adrenocorticotropic hormone inhibited this restoration. Treatment of hypophysectomized rats with follicle-stimulating hormone, luteinizing hormone, and thyroid-stimulating hormone had no effect. These results indicate that prolactin and/or growth hormone are necessary for the development of adjuvant arthritis, whereas adrenocorticotropic hormone has an inhibitory effect.

Adrenocorticotropic Hormone↗
PubMed1984

Report of a case of pheochromocytoma producing immunoreactive ACTH and beta-endorphin.

A 47-year old woman is presented who had a left adrenal pheochromocytoma with manifestations also indicative of ectopic ACTH syndrome. The excised adrenal gland showed both an adrenal medullary tumor and adrenal cortical hyperplasia. Immunostaining also showed the presence in the tumor of ACTH and beta endorphins. The immediate post-adrenalectomy decline of catecholamines, ACTH, cortisol and beta endorphins indicate that the adrenal itself was the source of these hormones. This patient, the thirteenth now reported in the literature, represents one form of ectopic ACTH syndrome in which the lesion is benign, and in which a successful outcome can be anticipated.

Adrenal Cortex↗
PubMed1984

A case for hypothalamic acromegaly: a clinicopathological study of six patients with hypothalamic gangliocytomas producing growth hormone-releasing factor.

We report the histological, ultrastructural, and immunocytochemical features of six hypothalamic gangliocytomas associated with pituitary GH cell adenomas and/or acromegaly. In four patients, the gangliocytoma was intrasellar, and no hypothalamic investigation was performed; in two patients, autopsy confirmed hypothalamic involvement. Four patients had a gangliocytoma associated with pituitary GH cell adenoma and acromegaly; electron microscopy demonstrated an intimate association between neurons and adenomatous GH cells. One patient had a gangliocytoma and a GH cell adenoma but no clinical evidence of acromegaly. In the sixth patient, clinical and biochemical acromegaly was manifest, but no pituitary adenoma was demonstrated. Using immunocytochemistry, human pancreatic tumor GRF (hptGRF-40) was localized in the majority of neurons of all six gangliocytomas. The pituitary adenomas and nontumorous adenohypophyses were negative for hptGRF-40. In addition, somatostatin, glucagon, and GnRH were demonstrated within some neurons of several tumors; insulin and gastrin stains were equivocal. These findings confirm previous proposals of production of a GRF by such gangliocytomas. While the significance of other peptides found in some of the tumors is uncertain, the presence of hptGRF-40 in neurons of these gangliocytomas supports the theory that GRF excess is the mechanism responsible for over-production of GH and provides evidence for a syndrome of hypothalamic acromegaly.

Acromegaly↗
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

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

Immunohistochemical localization of neuron-specific enolase in the human hypophysis and pituitary adenomas.

Neuron-specific enolase (NSE) was localized, using the immunoperoxidase technique, in the cytoplasm of the five adenohypophyseal hormone-secreting cell types, and in nerve fibers of the pars nervosa of the human pituitary. Crooke's hyaline material was negative. Neuron-specific enolase was found in all pituitary adenoma types; there was no correlation between degree of granularity or differentiation of tumor cells and intensity of NSE immunopositivity. One hypothalamic hamartoma was positive for NSE; a craniopharyngioma and a neurohypophyseal granular cell tumor were not. Neuron-specific enolase was present in peptide hormone-producing endocrine cells outside the pituitary and in their tumors; the majority of other tumors were negative for NSE, although one breast carcinoma, one ovarian cystadenocarcinoma, and one lymphoma were positive for NSE. In control studies, absorption of NSE antisera with growth hormone abolished immunoreactivity; there was no immunologic cross-reaction demonstrable by radioimmunoassay.

Adenoma↗
PubMed1983

The pars tuberalis of the human pituitary. A histologic, immunohistochemical, ultrastructural and immunoelectron microscopic analysis.

Forty autopsy pituitaries were studied to elucidate the histology, immunocytology and ultrastructure of pars tuberalis in subjects with normal and abnormal endocrine homeostasis. Pars tuberalis consisted mainly of gonadotrophs interspersed with few corticotrophs and thyrotrophs, histologically resembling those of pars distalis. Somatotrophs and lactotrophs were not identified. There were no histologic differences attributable to age or sex. In cases of glucocorticoid excess, pars tuberalis corticotrophs showed Crooke's hyalinization. Following castration or hypophysectomy, pars tuberalis gonadotrophs exhibited more intense immunostaining for FSH and LH than did normals. Ultrastructural analysis revealed gonadotrophs and corticotrophs showing no evidence of active secretion; immunoelectron microscopy demonstrated FSH, LH and ACTH in secretory granules. By light microscopy, squamous nests, often identified in pars tuberalis, were positive for immunoreactive keratin; cells at their periphery contained FSH, LH or ACTH, indicating derivation of nests by squamous metaplasia from gonadotrophs and corticotrophs. By electron microscopy, clusters of epithelial cells containing desmosomes and tonofilaments were surrounded by granulated gonadotrophs. Human pars tuberalis cells represent mainly a subpopulation of gonadotrophs possessing all organelles required for synthesis and storage of hormones but showing ultrastructural features of functional inactivity; the reasons for this inactivity and for the formation of squamous nests remain unexplained.

Adrenocorticotropic Hormone↗
PubMed1983

Immunomodulation by bromocriptine.

Treatment of rats with the dopaminergic ergot alkaloid bromocriptine (BRC) inhibited the following immune reactions: contact sensitivity skin reaction to dinitrochlorobenzene (DNCB); antibody formation to sheep red blood cells and to bacterial lipopolysaccharide; adjuvant arthritis; and experimental allergic encephalitis. Immunosuppressive doses of BRC (5 mg/kg) decreased the serum prolactin (PRL) levels from 84.8 +/- 15.9 ng/ml to 4.9 +/- 1.6 ng/ml. Further studies on DNCB contact sensitivity and on antibody formation revealed that the immunocompetence of BRC-suppressed animals could be restored by additional treatment with either prolactin (PRL) or growth hormone (GH). Treatment with adrenocorticotropic hormone antagonized the restoring effect of PRL and GH. These results suggest that BRC suppressed immunity by its inhibition of PRL, and possibly also by inhibition of GH secretion.

Animals↗
PubMed1983

Histological classification of pituitary disease.

Morphological features of pituitary disease are classified according to increased and decreased hormone production to allow clinical correlation with pathological processes. Increased hormone synthesis and secretion may be due to pituitary adenomas or carcinomas derived from the five hormone-secreting cell types, or to extrapituitary stimuli causing hypertrophy and hyperplasia of those cells. Various tumour-like conditions can mimic functioning adenomas. Rarely, no lesion is detected and intrinsic abnormalities of adenohypophyseal cells are implicated. Hypopituitarism can be selective or generalized. Diffuse hormone deficiency is usually attributable to tissue destruction by tumours, inflammatory or infiltrative conditions or vascular lesions. Congenital abnormalities of pituitary development may result in hypophyseal dysfunction. Hypothalamic abnormalities may cause generalized hypopituitarism or may involve only selective releasing factors and hormones. Feedback inhibition and receptor abnormalities may be implicated in pituitary hypofunction, and selective deficiencies may be the result of genetic abnormalities, immune reactions or toxic damage to one cell type.

Adenoma↗
PubMed1983

Pituitary hormones and contact sensitivity in rats.

Hypophysectomized (Hypo-X) rats do not develop contact sensitivity to dinitrochlorobenzene (DNCB). Daily treatment with prolactin or growth hormone completely restores the DNCB-reactivity of Hypo-X animals. Treatment of such animals with ACTH, FSH, LH, TSH or HCG has no restoring potential. Treatment with ACTH in addition to prolactin or growth hormone antagonizes restoration of Hypo-X rats. These experiments indicate that the pituitary gland has the potential of regulating contact sensitivity.

Adrenocorticotropic Hormone↗
PubMed1982

Prolactin cells in the human pituitary. A quantitative immunocytochemical analysis.

Sixty adult human pituitary glands taken at autopsy were stained for prolactin using the immunoperoxidase technique, and percentages of prolactin-bearing cells were assessed. There was no difference between the percentages of prolactin cells seen in the adenohypophyses of adult men and nulliparous women; they averaged 16.9%, with an average of from 8.6% to 31.3%. Percentages did not vary with age, and were higher in women in the perinatal period. In multiparous women percentages were increased, which indicates that prolactin cell hyperplasia of pregnancy does not completely reverse. No regression of prolactin cells was evident in the nontumorous portion of glands that harbored prolactinomas; however, percentages were elevated in glands with non-prolactin-producing adenomas. Quantitative adenohypophysial cell classification provides a basis for defining hyperplasia and abnormal distribution of cells that result from various pathologic conditions, drug therapies, and changes in the hormonal environment.

Age Factors↗
PubMed1981

Immunohistochemical localization of keratin in craniopharyngiomas and squamous cell nests of the human pituitary.

To identify keratin, the immunoperoxidase technique was performed on 41 nontumourous pituitaries, 14 pituitary adenomas composed of different cell types and 15 craniopharyngiomas. No keratin was demonstrated in adenohypophysial cells, neurohypophysis or hypophysial vessels, however, it was occasionally identified in the pairs intermedia within cells lining cystic structures. Crooke's hyaline material and all pituitary adenomas were negative for keratin. The epithelial portions of craniopharyngiomas exhibited positive keratin immunostaining, as did squamous cell nests, which are frequently found in hypophysial stalk. Immunostaining for keratin can effectively be used in the differential diagnosis of pituitary tumours and may prove valuable in the investigation of histogenesis and embryology.

Adenoma↗