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C Ezrin

Publications and source records attributed to C Ezrin.

At least 19 recordsLinked to original sources
PubMed1993

Recurrent acromegaly resulting from ectopic growth hormone gene expression by a metastatic pancreatic tumor.

BACKGROUND: Acromegaly is usually the result of a pituitary growth hormone (GH)-cell adenoma or is more rarely due to ectopic secretion of GH-releasing hormone (GHRH). The authors previously described a more unusual form of acromegaly secondary to ectopic GH synthesis by a pancreatic islet cell tumor. METHODS: One year after tumor resection and transient disease remission, multiple abdominal metastases were identified with accompanying elevated levels of circulating GH and insulin-like growth factor-1 (IGF-1). Serial 24-hour GH sampling was performed before and after intravenous GHRH or thyrotropin releasing hormone (TRH) administration during treatment with bromocriptine; treatment with the somatostatin (SRIF) analogue octreotide; or no treatment. RNA from abdominal tumor tissue was extracted and subjected to Northern gel electrophoresis and GH hybridization analysis. RESULTS: Neither GHRH nor TRH resulted in stimulation of the elevated GH levels. Bromocriptine and octreotide did not suppress GH secretion but attenuated the thyroid stimulating hormone (TSH) response to TRH administration. Octreotide (as much as 1500 micrograms/d) was clinically, biochemically, and radiographically ineffective. GH-secreting abdominal tumor tissue expressed a 0.9-kb mRNA transcript consistent with the size of authentic human GH mRNA. CONCLUSION: The natural history and ectopic nature of a GH-producing pancreatic carcinoma has been documented, with biochemical remission occurring after initial tumor resection, with autonomous GH hypersecretion after tumor recurrence, and with RNA analysis demonstrating ectopic activation of GH gene transcription.

Acromegaly↗
PubMed1991

Hereditary diabetes insipidus: an immunohistochemical study of the hypothalamus and pituitary gland.

We report the histological findings in a case of hereditary diabetes insipidus (HDI) using vasopressin (VP) immunohistochemistry. The hypothalamus displayed a marked loss of magnocellular VP neurons, with preservation of the smaller cells. The neurohypophysis was severely atrophic with scanty immunoreactivity. Our results support the hypothesis that HDI results from a selective degeneration of VP neurons affecting chiefly the magnocellular elements projecting to the neurohypophysis. The sparing of the parvocellular component may reflect the projection of these neurons to non-pituitary targets.

Aged↗
PubMed1991

Sustained pulsatile insulin secretion from adenomatous human beta-cells. Synchronous cycling of insulin, C-peptide, and proinsulin.

The endocrine pancreas secretes insulin in a pulsatile fashion. This rhythm is generated at a site within the pancreas, although its precise location has not been determined. With an in vitro system, we tested the possibility that beta-cells might generate spontaneous pulsatile insulin secretion in the absence of any external influence. Human insulinoma tissue from five patients was perifused for 7-10 h with RPMI-1640 medium and constant concentrations of glucose (5.5 mM). Insulin, C-peptide, and proinsulin were measured in the effluent collected at 3.3-min intervals. All three peptides demonstrated pulsatility of secretion in a similar, synchronous fashion that was sustained throughout each study. The Clifton cycle detection program demonstrated cycling in all five tumors, with an average period for all tumors of 28, 29, and 26 min for insulin, C-peptide, and proinsulin, respectively. Spectral analysis confirmed the regularity and consistency of the hormonal secretory patterns. Mean hormone concentrations secreted by different tumors varied, but insulin and C-peptide were secreted in a nearly 1:1 ratio. This study demonstrates 1) that beta-cells are able to generate spontaneous pulsatile insulin secretory activity, which is independent of innervation or the presence of other islet cells, and 2) proinsulin secretion from the beta-cell also has an inherent pulsatility. The synchrony observed in the cycles of proinsulin and its peptide products confirms their common secretory pathway in the beta-cell. We conclude that the beta-cell may be the originator of insulin cycling.

Adenoma↗
PubMed1988

Metastatic carcinoma to pituitary adenomas: a report of two cases.

Two cases of carcinoma metastatic to pituitary adenomas are reported. One patient had a prostatic adenocarcinoma, giving rise to metastases in an adenoma found incidentally at autopsy; clinically and immunohistochemically, the adenoma showed lack of endocrine activity. The second patient had symptoms of cortisol excess. A corticotroph adenoma associated with a malignant neoplasm was diagnosed ante mortem; at autopsy a pancreatic endocrine neoplasm was found. Immunohistochemistry and electron microscopy were important in elucidating the primary tumor. The formation of extraportal vascular channels and altered blood flow may have importance in the pathogenesis of cancer metastases to pituitary adenomas.

Adenocarcinoma↗
PubMed1987

Rhabdomyosarcoma in the region of the sella turcica.

Intracranial extension of rhabdomyosarcoma from the face, nasopharynx or middle ear is rare. A 16-year-old boy presented with deterioration of vision and headache. CT scan revealed a soft tissue mass occupying the sphenoid and ethmoid sinuses, extending to the suprasellar fossa and impinging on the optic chiasm. The tumour, mimicking pituitary carcinoma, was removed by transsphenoidal craniotomy. Morphologic studies, including immunohistochemistry and electron microscopy, revealed that the tumour was a rhabdomyosarcoma. This case stresses the value of immunohistochemical and ultrastructural studies in the diagnosis of tumours occurring in the region of the sella turcica. The origin of this tumour was thought to be the sphenoid or ethmoid sinus. The pituitary gland appeared intact.

Adolescent↗
PubMed1986

Effects of caloric restriction and exercise on insulin receptors in obesity: association with changes in membrane lipids.

We have studied the effects of supervised caloric restriction and exercise on mononuclear leukocyte lipid composition, membrane fluidity, and insulin receptors in ten nondiabetic obese adults, (175 +/- 9.3% of ideal body weight) and ten normal adult subjects. In a second study, we examined the effects of caloric restriction alone using a very low calorie liquid diet in the treatment of another ten obese adults. In both groups of obese adults, fasting insulin levels were elevated and fell to normal levels following treatment. Insulin binding to monocytes, which was reduced in obese subjects, increased toward normal after short-term treatment; this was due to the restoration of total insulin binding capacity to levels one half of that seen in the normal adult group. Obese subjects undergoing either treatment had elevated membrane cholesterol/phospholipid ratios prior to treatment (0.499 +/- 0.050 and 0.446 +/- 0.011 v 0.400 +/- 0.025 mol/mol in normal adults P less than 0.005 by ANOVA). Prior to treatment, for all subjects there was a significant inverse correlation between insulin tracer binding and membrane cholesterol/phospholipid ratios (r = .484, n = 34, P less than 0.005). This relationship did not change significantly in obese subjects in either treatment group. Cell membrane microviscosity was determined by fluorescence polarization (FP) using DPH (2 X 10(-6) mol/L). Prior to weight loss, obese subjects had significantly higher FP values than controls (0.304 +/- 0.006 and 0.319 v 0.259 +/- 0.009, P less than 0.005, by ANOVA) indicating greater microviscosity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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↗
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↗
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↗
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

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↗
PubMed1980

Predicted ovulatory response to 2-brom-alpha-ergocryptine (CB-154) in amenorrhea-galactorrhea syndromes.

Adenohypophyseal function was evaluated in 20 consecutive patients with hyperprolactinemic amenorrhea-galactorrhea in an attempt to predict ovulatory response with 2-brom-alpha-ergocryptine (CB-154) therapy. Pituitary fossa tomography and response to insulin, thyrotropin-releasing hormone, and luteinizing hormone--releasing hormone were correlated with the return of ovulatory cycles. Fourteen of 15 patients demonstrating normal pretreatment sellar volume ovulated, compared with 0 of 5 showing increased volume. Thirteen of 14 with adequate adenophypophyseal reserve of growth hormone and luteinizing hormone ovulated, compared with 0 of 6 and 1 of 6, respectively, with inadequate reserve. Serum prolactin suppression to normal occurred in 19 of 20 patients but could not predict response. Only 2 of 10 patients receiving clomiphene citrate ovulated and neither conceived, while 8 of the 10 ovulated with CB-154 and 6 of 7 desiring pregnancy conceived. CB-154 is an effective "fertility drug" and response to therapy can usually be predicted.

Adult↗
PubMed1980

The effect of pregnancy on suspected pituitary adenomas after conservative management of ovulation defects associated with galactorrhea.

Thirty infertile patients with ovulation defects and galactorrhea conceived after medical therapy: four after clomiphene stimulation (with or without hCG) and 26 after receiving CB-154 (2-Br-alpha-ergocryptine or bromergocryptine). Pregnancies were followed closely; sellar tomography and perimetry were repeated at 36 weeks' and 8 weeks' post partum. One patient required transsphenoidal adenectomy because of acute pituitary enlargement. Two developed minimal asymptomatic fossa enlargement. Lactation was suppressed with Lactostat in the first eight patients delivered; hyperprolactinemia, amenorrhea, and galactorrhea recurred. Five of eight showed asymptomatic enlargement of the sella. Bromergocryptine was used to suppress lactation in the rest. Long-term bromergocryptine therapy resulted in the restoration of euprolactinemic ovulatory cycles in all patients. These data suggest that patients with ovulation defects associated with galactorrhea can conceive with medical therapy now available. However, there is a risk of significant pituitary enlargement during pregnancy and the puerperium. Lactation should be suppressed with bromergocryptine.

Adenoma↗
PubMed1980

Null cell adenoma of the human pituitary.

Among 343 surgically-removed pituitary adenomas, 56 tumors were unassociated clinically or biochemically with increased hormone secretion and contained no adenohypophysial hormones by the immunoperoxidase technique, except for 10 cases in which a few scattered cells showed positive immunostaining for beta-TSH or beta-FSH, beta-LH, prolactin and/or alpha-subunit. These tumors were chromophobic adenomas with no PAS, lead hematoxylin or carmoisine positivity and electron microscopy failed to reveal their morphogenesis. The term null cell adenoma of the pituitary is proposed to designate this tumor type. This term recognizes the most obvious features of these tumors: the absence of markers which would permit the disclosure of their cellular origin. Null cells are also found in the nontumorous adenohypophysis, suggesting that null cell adenomas derive from preexisting nonneoplastic null cells. The question of whether pituitary null cells are hormonally inactive committed precursors, uncommitted stem cells or dedifferentiated cells remains to be elucidated.

Adenoma↗
PubMed1980

Correlative ultrastructural morphometry of human prolactin-producing adenomas.

Ultrastructural morphometry was applied to 24 surgically removed human sparsely granulated prolactin cell adenomas in an attempt to correlate the measurements with blood prolactin levels, size of tumour, and age and sex of patient. No correlation was apparent. However, further evaluation revealed that correlation existed between size of tumour and blood prolactin levels, indicating that tumour mass, and not subcellular morphology, was related to the amount of prolactin released.

Adenoma↗
PubMed1980

Gonadotroph cell adenoma of the pituitary in a women with long-standing hypogonadism.

A 57-year-old woman, with long-standing hypogonadism secondary to irradiation of the ovaries, was found to have a pituitary tumor which was removed and investigated by histology, immunocytology and electron microscopy. Histologically, the tumor corresponded to a chromophobe, slightly PAS positive adenoma and the immunoperoxidase stain revealed the presence of both FSH and LH in the cytoplasm of the adenoma cells. The structural features of the adenoma cells resembled those of FSH cells in the nontumorous adenohypophysis. We thus believe that pituitary adenomas consisting of gonadotrophin-producing cells occur and that these may produce both FSH and LH. The relation between the gonadotrophin-producing adenoma and the preceding hypogonadism is uncertain.

Adenoma↗