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S Ezzat

Publications and source records attributed to S Ezzat.

At least 55 records · Page 3Linked to original sources

The c-erbB-2/neu proto-oncogene in human pituitary tumours.

OBJECTIVE: The aetiology of most pituitary tumours remains unknown. We have examined the potential role of neu receptor proto-oncogene in human pituitary tumorigenesis. MATERIALS AND METHODS: Ten non-tumorous pituitary glands and 16 morphologically characterized functional and clinically non-functioning pituitary adenomas were studied. Protein expression was examined by immunohistochemistry, mRNA expression by RT-PCR and competitive PCR, gene amplification by differential PCR, and point mutations by DNA sequencing. RESULTS: Cytoplasmic positivity for neu was identified in a few scattered cells of the non-tumorous adenohypophysis using an antibody to the intracytoplasmic domain of neu, but no membrane staining was found with an antibody to the extracellular domain; the latter is said to reflect gene amplification. mRNA transcript signals of the expected size were identified in the normal adenohypophysis and in all 16 adenomas examined. No increase in the degree of mRNA expression, however, was noted in the different tumour types compared to normal human pituitary tissue as determined by competitive PCR. As neu can be activated to an oncogene by a point mutation in the transmembrane region, nucleotide substitutions in this domain were investigated. Direct sequencing of codon 659 revealed no point mutations in any of the tumours. Furthermore, since amplification of neu has been noted in various human malignancies, DNA from these tumours was examined by differential PCR. No detectable differences were noted between the neu gene and the single-copy reference gene IFN-gamma. CONCLUSION: The neu gene is expressed in adenohypophysial cells and their tumours. In pituitary adenomas, this expression is not associated with gene amplification or activating mutations to suggest a direct role in pituitary tumorigenesis.

Adenoma↗

Altered expression of fibroblast growth factor receptors in human pituitary adenomas.

We have shown that basic fibroblast growth factor (FGF) is heterogeneously expressed by human pituitary adenomas and may be implicated as a growth stimulus for these tumors. There are four mammalian FGF receptor (FGFR) genes encoding a complex family of transmembrane tyrosine kinases. The prototypic receptor is composed of three Ig-like extracellular ligand-binding domains, a transmembrane domain, and a cytoplasmic split tyrosine kinase. Multiple forms of cell-bound or secretable isoforms of FGFR-1, -2, and -3 can be generated by cell- and tissue-specific alternative splicing, resulting in tissue-specific FGF function. Shifts in isoform expression accompany tumor progression in some systems. We examined the normal human adenohypophysis and 40 pituitary adenomas to determine the pattern of FGFR expression by reverse transcription-PCR; all tumors were characterized clinically and morphologically. Ribonucleic acid (RNA) was extracted from frozen tumor tissue and primers were used to distinguish messenger RNA of the secretable first Ig-like domain (I) and those of the transmembrane and kinase domains (K) of each FGFR subtype. The normal pituitary-expressed mRNAs for FGFR-1 I and K, FGFR-2 I and K, FGFR-3 I and K, and FGFR-4 I but not FGFR-4 K; this represents the first report of a truncated isoform of FGFR-4, indicating possible alternative polyadenylation sites in this receptor. Only 3 tumors had the same pattern of expression of the 4 FGFRs as the normal gland. Although all tumors expressed FGFR-1 I, 1 tumor did not express FGFR-1 K, suggesting the production of only a secretable form of FGFR-1 by this tumor. Four tumors were negative for FGFR-2 I and K; 6 expressed the secretable form only, and 17 expressed FGFR-2 K but not I. All tumors expressed FGFR-3 I; 14 had secretable forms only, and no tumors expressed FGFR-3 K alone. As in the normal gland, 13 tumors expressed only the secretable I form of FGFR-4. Unlike the normal pituitary, however, 22 expressed FGFR-4 I and K, indicating a possible tumor-specific transmembrane receptor. Five tumors were negative for FGFR-4 I and K. Expression of FGFR proteins was confirmed by immunohistochemical localization of the C-terminal portion of FGFR-1, -2, -3, and -4; the results correlated with the RNA data in each case. There was no correlation between tumor type, size, or aggressiveness and the expression pattern of FGFRs. Our study suggests that pituitary adenomas have altered FGFR subtype and isoform expression, which may determine their hormonal and proliferative responses to FGFs.

Adenoma↗

Prevalence of activating ras mutations in morphologically characterized thyroid nodules.

Ras proteins are signal-transducing proteins that share common properties with membrane-anchored G proteins. Mutations at codon 12/13 or codon 61 alter GTP-binding or GTPase activity, respectively. Such activating mutations are present in nearly 30-50% of various malignancies including colon, breast, and lung carcinomas. There are conflicting data regarding the prevalence of ras mutations in the thyroid and their possible pathogenetic role in the different tumor types. To address this question, we examined 45 morphologically characterized thyroid carcinomas, adenomas, and hyperplastic nodules using a highly sensitive single-stranded conformation polymorphism (SSCP) approach combined with DNA-sequencing. DNA from cell lines with known mutations served as controls. A G to A H13 codon substitution replacing an Asp for a Gly residue was detected in 1 papillary carcinoma. Although no H12 or H61 codon substitutions were identified, 2 discrete alterations were identified in codons H17 and 22. No N12/13 codon substitutions were identified. N61 codon substitutions of A to G resulting in a Gly to Arg substitution were detected in 2 papillary carcinomas; the same mutation was also found in one follicular adenoma. Interestingly, K12/13 and K61 ras mutations were not present in any of the tumors examined. These data establish a low prevalence of mutations in all ras gene family members in human thyroid neoplasms. This difference from neoplasms of other organs may explain the relatively indolent biologic behavior of many thyroid tumors and supports an alternate early genetic mutation that is more characteristic of these neoplasms.

Adult↗

Expression of steroidogenic factor-1 (SF-1) mRNA and protein in the human placenta.

Steroidogenic factor-1 (SF-1), also known as adrenal-4-binding protein (Ad4BP), is a recently-described transcription factor, which has been shown to be important for the differentiation of steroidogenic tissues. In addition, SF-1 has been implicated in regulating the glycoprotein hormone alpha-subunit gene in a pituitary gonadotroph cell line. Considering that the human placenta produces both steroids and human chorionic gonadotrophin (HCG), we studied the expression of SF-1 in this tissue. Human first trimester and term placentas were collected at the time of therapeutic abortion and birth respectively. Messenger RNA was extracted, reverse transcribed, and used for polymerase chain reaction (PCR) amplification with primers specific for the human SF-1 cDNA sequence. A band of the expected size was obtained from both first and third trimester samples, indicating that SF-1 expression in the human placenta starts early in pregnancy and is maintained until birth. In addition to normal placental samples, JEG3 and JAR choriocarcinoma cells were also analysed and found to express SF-1 mRNA. The identity of the amplified products was confirmed by diagnostic restriction digest and Southern hybridization. SF-1 protein was localized mainly to the nuclei of the cyto- and syncytiotrophoblast and to some mesenchymal villous nuclei by immunocytochemistry using a specific antibody. We conclude that SF-1 is expressed in human first trimester and term placenta, where it could be implicated in the regulation of HCG production, in steroidogenesis, or both.

Base Sequence↗

Epidermal growth factor and its receptor (EGF-R) in human pituitary adenomas: EGF-R correlates with tumor aggressiveness.

Epidermal growth factor (EGF) has been localized in several human neoplasms and has been shown to have a significant correlation to prognosis. We investigated the potential role of the EGF receptor (EGF-R) system in pituitary tumorigenesis by examining the expression of EGF and EGF-R in the different types of human pituitary adenomas. EGF was identified by immunohistochemistry in all cell types of the nontumorous adenohypophysis and in all types of morphologically characterized functional (n = 9) and nonfunctional (n = 17) adenomas. To confirm local EGF synthesis, ribonucleic acid (RNA) from human pituitary adenomas was reverse transcribed and PCR amplified. Transcript signals of the expected size were identified, with marked variation in 41 of 48 adenomas. To assess possible secretion in vitro, EGF was measured in pituitary tumor culture medium. No measurable quantities of EGF were present in conditioned culture medium from all 35 adenomas examined, consistent with the rapid uptake of EGF by unoccupied functional EGF-R sites. Using a specific monoclonal antibody that recognizes the extracellular ligand-binding domain of the human EGF-R, we found EGF-R in cells in the normal pituitary and in some functional and nonfunctional adenomas with extremely variable intensity. By RT-PCR, EGF-R messenger RNA (mRNA) expression was also identified, with marked variation in all 48 adenomas examined and in the nontumorous pituitary. The highest degrees of EGF-R mRNA expression were present in somatotroph adenomas and the aggressive silent subtype 3 adenomas. Tumors from patients with recurrent acromegaly demonstrated significantly higher levels of EGF-R mRNA than those from patients with nonrecurrent disease. In conclusion, EGF and EGF-R are expressed in a variable manner in all types of human pituitary adenomas. The overexpression of EGF-R in recurrent somatotroph adenomas and aggressive silent subtype 3 adenomas suggests a selective mechanism for the EGF/EGF-R family in the growth of aggressive pituitary tumors.

Adenoma↗

The transcription activator steroidogenic factor-1 is preferentially expressed in the human pituitary gonadotroph.

Steroidogenic factor-1 (SF-1), also known as adrenal-4-binding protein, is a transcription factor that is important for the differentiation of steroidogenic tissues. We investigated whether SF-1 is expressed in specific hormone-producing cell types in the human pituitary and its adenomas. Pituitary adenomas (n = 35) were collected at the time of surgery, and normal adenohypophyses were obtained from autopsies; 3 corticotroph adenomas were excluded because pit-1 messenger ribonucleic acid (mRNA) expression indicated contamination by nontumorous elements. Expression of SF-1 mRNA was determined by reverse transcription-PCR. SF-1 protein was localized with immunocytochemistry. By reverse transcription-PCR, SF-1 mRNA was found in the nontumorous pituitary and in pituitary adenomas expressing gonadotropins. All 8 gonadotroph adenomas had a strong signal for SF-1. SF-1 mRNA was also detected in 2 of 3 corticotroph adenomas, 2 of 13 somatotroph/mammosomatotroph adenomas, 1 of 6 lactotroph adenomas, and 2 silent subtype 3 adenomas; however, in most of the positive tumors there was also positivity for FSH beta and/or LH beta mRNA, suggesting that contaminating nontumorous gonadotrophs may be the source of SF-1 mRNA signal. SF-1 protein was localized by immunocytochemistry in the nuclei of scattered cells of the nontumorous adenohypophysis that were shown to be gonadotrophs with double immunostaining and in gonadotroph adenomas; nuclear staining was not found in other adenoma types, except in areas shown to contain trapped nontumorous tissue. We conclude that SF-1 expression correlates with the expression of gonadotropins. These findings implicate SF-1 as a cell-specific transcription factor that may regulate gonadotroph differentiation in the pituitary.

Adenoma↗

ret/PTC-1, -2, and -3 oncogene rearrangements in human thyroid carcinomas: implications for metastatic potential?

The ret/PTC oncogene is unique to papillary thyroid cancer. Three forms of this oncogene, formed by translocation of three different genes to the tyrosine kinase domain of the ret protooncogene, result in constitutive kinase activation. Correlation with clinical outcome is controversial; ret/PTC-1 has been suggested to predict aggressive behavior. There is no morphological description of ret/PTC-positive tumors. We analyzed 60 thyroid carcinomas for ret/PTC expression to determine correlation with clinical history, disease stage, or tumor morphology. Ribonucleic acid extracted from frozen tissue was reverse transcribed; PCR was performed to amplify ret/PTC-1, 2, and -3. The TPC-1 cell line was the positive control for ret/PTC-1. All tumors were characterized morphologically. Clinical data were collected. The 57 papillary and 3 follicular carcinomas were resected from 44 female patients and 15 males. The average age at diagnosis was 46.2 yr (range. 24-83 yr). Three patients had a history of neck irradiation. At diagnosis, 11 patients had extrathyroidal tumor extension, 20 had lymph node metastases, and 1 had lung metastasis. Thirteen patients had tall cell papillary carcinomas; 3 tumors had focal insular or anaplastic dedifferentiation. The average follow-up was 13.4 months, during which 4 patients had recurrent disease. No deaths occurred. One papillary carcinoma (1.7%) was positive for ret/PTC-1, none was positive for ret/PTC-2, and 2(3.4%) were positive for ret/PTC-3. Although all 3 patients who had tumors containing ret/PTC rearrangements were under the age of 45 yr (range, 26-44 yr) and had small tumors (< 1.2 cm), 2 of these 3 patients presented with lymph node metastases, and the third had lymphatic invasion. ret/PTC oncogene expression did not correlate with radiation history. In summary, ret/PTC oncogene rearrangements were found in 3 of 60 (5%) thyroid carcinomas and were not present in tumors with aggressive morphological features. However, we found ret/PTC rearrangements in young patients (< 45 yr of age) with small thyroid carcinomas showing a predisposition for lymphatic involvement, suggesting a possible role in the development of this subgroup of tumors.

Adult↗

The diagnosis and management of acromegaly: a Canadian consensus report.

OBJECTIVE: To reach a Canadian consensus on the diagnosis and management of acromegaly. OPTIONS DIAGNOSIS: documenting autonomous growth-hormone hypersecretion and imaging of the pituitary. TREATMENT: surgical resection, adjunctive therapy with bromocriptine or octreotide and radiation therapy. OUTCOMES: Reduction of the morbidity and mortality associated with acromegaly. EVIDENCE: Review of international literature. VALUES: Achievement of consensus among a panel of Canadian endocrinologists. BENEFITS, HARMS AND COSTS: Acromegaly is a chronic debilitating condition that is associated with morbidity and mortality. This consensus statement is designed to improve the diagnosis and management of this rare condition in order to minimize the negative outcomes. Costs were not considered. RECOMMENDATIONS: The diagnosis of acromegaly is established by documenting autonomous growth-hormone hypersecretion and by imaging the pituitary. Surgical resection is the cornerstone of treatment; however, adjunctive therapy is often needed. Although growth-hormone reduction is often associated with alleviation of symptoms, an attempt should also be made to normalize levels of growth hormone and its target growth factor, insulin-like growth factor-I (IGF-I). Persistent secretion of excess growth hormone and IGF-I may pose significant long-term health risks. A suggested therapeutic algorithm is provided. The ease of administration of bromocriptine should prompt a trial of therapy with this agent. The subcutaneous use of octreotide is of particular benefit to those patients with persistently high levels of growth hormone and IGF-I that cannot be suppressed by other means. Because acromegaly is relatively rare and complex, its diagnosis and treatment require the concerted efforts of an endocrinologist, an neurosurgeon and a radiation oncologist.

Acromegaly↗

Continuous versus intermittent subcutaneous infusion of octreotide in the treatment of acromegaly.

This review evaluates the efficacy, tolerability, and safety of continuous subcutaneous infusion (CSI) relative to intermittent subcutaneous injection (ISI) of the somatostatin analog, octreotide in the treatment of acromegaly. Data was extracted from five clinical series using CSI octreotide in acromegaly, six reports comparing CSI to ISI, and three studies comparing pulsatile subcutaneous infusion (PSI) to ISI. Effects of each drug regimen on the control of growth hormone (GH), insulin-like growth factor (IGF-1), clinical symptomatology, pituitary tumor size, and adverse effects were evaluated. Normalization of serum GH or IGF-1 levels, as well as improvement in clinical symptoms was reported in the majority of the patients studied. Cases in which pituitary adenomas decreased in size were also documented during the study period. When the effects of CSI were compared with ISI, a more pronounced control of GH and IGF-1 was observed. In addition, diurnal GH fluctuation during CSI was significantly reduced relative to ISI in two reports. Moreover, in two patients, CSI achieved similar clinical and biochemical effects at lower doses than when the drug was given by ISI. Finally, adverse effects with CSI may be less severe than with ISI. Continuous subcutaneous infusion of octreotide produced biochemical improvement in 67 of the 88 patients reviewed. When compared with ISI, CSI induced more pronounced biochemical control, often with less fluctuation in GH and IGF-1 levels. Because of a lack of data, definite conclusions regarding the differences between regimens on clinical symptomatology and tolerability could not be discerned. A large prospective, long-term randomized crossover study is recommended to make these determinations.

Acromegaly↗

A prospective multicenter octreotide dose response study in the treatment of acromegaly.

The somatostatin analog octreotide has proven to be an effective form of treatment for various hypersecretory states including acromegaly. This report describes the effects of escalating doses of octreotide on the growth hormone (GH) profiles, insulin-like growth factor-1 (IGF-1), prolactin (PRL), and adverse effects in 99 patients with acromegaly. Treatment with octreotide was initiated at 50 micrograms sc every 8 h and the dose gradually titrated to a maximum of 1500 micrograms/d if more than 75% of GH determinations in a 12-h day profile were above detection limits. This dose was maintained for the duration of 6 months. Seventy-three percent of patients did not reach the GH reduction criterion at the 300 micrograms dose. Mean GH levels decreased from 33 +/- 4 micrograms/l to 10 +/- 1 microgram/l (p < 0.001) while receiving the 300 micrograms/d dose. The percentage decrease in mean GH levels, however, was dose-independent reaching 50 +/- 5% of baseline with 300 micrograms/d, 55 +/- 5% with 600 micrograms/d, 57 +/- 6% with 900 micrograms/d, and 56 +/- 5% with 1500 micrograms/d. Maximal GH suppression, however, was achieved in 40%, 17%, 7%, and 16% of subjects by the 300 micrograms, 600 mg, 900 micrograms, and 1500 micrograms doses respectively. GH suppression was independent of duration of treatment. While there was a tendency for a greater degree of IGF-1 reduction with the higher doses, the rate of normalization (30-37%) was not influenced by the dose of octreotide administered. Elevated PRL levels also declined with the use of higher doses of octreotide.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗

Clonality of thyroid nodules in sporadic goiter.

Clonality studies have suggested that neoplasms are monoclonal and hyperplasias are polyclonal. To investigate this question in thyroid, we analyzed the clonality of 26 morphologically characterized hyperplastic nodules from 19 patients with sporadic goiters. For comparison we studied six thyroid carcinomas. We used the highly informative M27 beta probe that maps to the X-chromosome DXS255 locus (X cen-p11.22). Material was obtained from 52 nodules; tissue from nine nodules was rejected because of contamination with normal elements, five patients (eight nodules) were homozygous at Pst I sites in nonnodular thyroid tissue, and three nodules were excluded for technical reasons. Methylation patterns after Hpa II digestion confirmed polyclonality in all nontumorous thyroids of informative patients. Seven hyperplastic nodules were polyclonal, and 18 were monoclonal; one showed loss of heterozygosity. One nodule exhibited aberrant methylation. Multiple nodules were obtained from four patients; in three, all were monoclonal with activation of the same allele. Three papillary carcinomas were monoclonal; two exhibited aberrant methylation. One follicular carcinoma showed loss of heterozygosity. Our data indicate that morphologically indistinguishable hyperplastic thyroid nodules may be monoclonal or polyclonal. These findings suggest that variable molecular mechanisms are involved in the pathogenesis of nodules in sporadic goiter. Future studies will need to explore the biological significance of nodules of variable clonal origin.

Adult↗

Effects of acromegaly treatment and growth hormone on adipose tissue lipoprotein lipase.

Lipoprotein lipase (LPL) hydrolyzes lipoprotein triglyceride into nonesterified fatty acids, which are then reesterified and stored in adipose tissue. Previous studies have demonstrated increases in LPL in response to insulin-like growth factor I and GH when added in vitro. This study examined the effects of acromegaly treatment on adipose tissue LPL. Ten patients with clinically active acromegaly were recruited. A fasting adipose tissue biopsy was performed both before and 3 months after treatment with octreotide (8 patients) or surgery plus octreotide (2 patients). With treatment, mean baseline insulin-like growth factor I levels fell from 6.41 to 3.98 U/mL (normal, < 2.2 U/mL; P < 0.05), and serum glycohemoglobin fell from 8.6 to 7.2 (normal, < 6.8). Adipose LPL was measured in the heparin-released fraction as well as the cellular fraction extracted with nonionic detergent (EXT). After treatment of acromegaly, there was no change in heparin-released fraction LPL activity or immunoreactive mass. However, there was an increase in EXT activity from 0.73 +/- 0.33 to 1.83 +/- 0.58 nEq/min.10(6) cells (mean +/- SEM; P < 0.05) and an increase in EXT mass from 4.1 +/- 0.89 to 11.4 +/- 2.0 ng/10(6) cells (P < 0.05). There was no change in LPL messenger ribonucleic acid levels with treatment, determined using both quantitative polymerase chain reaction and Northern blotting. Thus, treatment of acromegaly resulted in an increase in the intracellular level of the LPL protein, with no change in messenger ribonucleic acid levels, suggesting posttranscriptional regulation of LPL. These changes in LPL may be due to improved insulin sensitivity, or to other changes associated with acromegaly treatment.

Acromegaly↗

Cell-specific expression of estrogen receptor in the human pituitary and its adenomas.

Estrogen affects the synthesis and release of several pituitary hormones. The estrogen receptor (ER), a member of the steroid hormone receptor family, is thought to mediate transcriptional effects in a cell-specific fashion. We investigated whether ER is expressed in specific hormone-producing cell types in the human pituitary and its adenomas. Pituitary adenomas (n = 34) were collected at the time of surgery, and normal glands were obtained from autopsy. Expression of ER messenger ribonucleic acid (mRNA) was determined by reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization. ER was also localized with immunohistochemistry and protein extraction. By RT-PCR, ER mRNA was found in the nontumorous pituitary and in pituitary adenomas expressing only PRL, in those producing GH and PRL, and in adenomas expressing the gonadotropic hormones. No ER mRNA was detected in adenomas expressing only GH without PRL or gonadotropins, nor in tumors producing ACTH without PRL or gonadotropins. In situ hybridization was not as sensitive or specific as RT-PCR. Biochemical analysis performed on seven tumors that were positive for ER mRNA by RT-PCR detected ER protein in only one PRL adenoma and one oncocytoma and yielded negative or equivocal results in one PRL adenoma, three GH-PRL adenomas, and one null cell adenoma. ER protein was localized by immunohistochemistry in scattered cells of the nontumorous adenohypophysis and in a few PRL and gonadotroph adenomas. We conclude that ER expression, as determined by RT-PCR, correlates with the expression of PRL or gonadotropins; in contrast, ER mRNA was not detected in adenomas that express only GH or ACTH. These findings implicate ER as a cell-specific transcription factor that may regulate cytodifferentiation in the pituitary.

Adenoma↗

Membrane-anchored expression of transforming growth factor-alpha in human pituitary adenoma cells.

Growth factors induce cell proliferation and are implicated in the multistep process of tumorigenesis. Transforming growth factor-alpha (TGF alpha), a peptide that binds to the epidermal growth factor receptor, is expressed by carcinomas and normal tissues. To investigate the possible role of TGF alpha in adenohypophysial tumorigenesis, we studied its expression in nontumorous human pituitary and different clinically and morphologically characterized human pituitary adenomas. Ribonucleic acid was reverse transcribed and amplified by polymerase chain reaction; transcript signals were identified with marked variation in 14 of 15 adenomas, and a weak signal was detected in nontumorous pituitary. Immunohistochemical positivity was found with variable intensity in all adenoma types, but not all tumors. Ultrastructural immunogold localized TGF alpha in endoplasmic reticulum, in Golgi apparatus, and on cell membranes; surface localization was confirmed by immunofluorescence. To assess possible secretion, the reverse hemolytic plaque assay was performed; small plaques were identified using an antibody that recognizes the extracellular domain of pro-TGF alpha; however, the plaques did not increase in size with time, suggesting that they detected membrane-anchored TGF alpha. Moreover, TGF alpha was undetectable by enzyme-linked immunosorbent assay in pituitary tumor-conditioned culture media. The marked variable expression of TGF alpha, the absence of secretion in measurable quantities, and the preferential membrane localization suggest a specific juxtacrine mechanism for TGF alpha in pituitary tumorigenesis.

Adenoma↗

Heterogenous in vivo and in vitro expression of basic fibroblast growth factor by human pituitary adenomas.

Basic fibroblast growth factor (bFGF) is a potent mitogenic and angiogenic factor that is known to regulate GH, PRL, and TSH secretion. Sequences within a bFGF gene family member have been detected in transforming DNA samples derived from human PRL-secreting tumors. Furthermore, elevated serum concentrations of bFGF have been noted in patients with multiple endocrine neoplasia-1. To further examine the significance of bFGF in sporadic human pituitary adenomas, we investigated the expression of bFGF by these tumors. Using an enzyme-linked immunoassay that recognizes all 16-24 kilodalton molecular mass forms of bFGF, we measured circulating serum concentrations in 21 patients with sporadic pituitary adenomas; they ranged from less than 0.5-84 pg/mL and declined following surgical adenomectomy. To confirm the pituitary source of this growth factor, we determined in vitro bFGF release from 43 adenomas (10 GH, 7 PRL, 10 ACTH, 14 gonadotrope adenomas/oncocytomas, and 2 silent subtype 3 adenomas). bFGF was present with wide variability (0.75-2100 pg/24 h.10(5) cells) in conditioned culture media of all adenomas examined. The adenohypophysial source of this growth factor was further demonstrated by the reverse hemolytic plaque assay. Variable bFGF messenger RNA expression was identified by the reverse-transcription polymerase chain reaction technique in 9 functional (2 PRL, 5 GH, 2 ACTH) and 7 nonfunctional (1 oncocytoma, 2 null cell, 2 gonadotrope, 2 Silent Subtype 3) adenomas examined. bFGF levels were unaltered in vitro following hypothalamic hormone stimulation/inhibition. The lack of a bFGF signal peptide sequence and hypothalamic hormone-independence suggest that secretion of this factor may be independent of pituitary hormone regulation. Immunocytochemistry failed to localize bFGF in tumors that released this factor in vitro, suggesting that storage of this peptide does not correlate with its synthesis and release. In conclusion, the heterogenous expression of bFGF suggests that it may play a specific and selective role in the tumorigenic process of some pituitary adenomas.

Adenoma↗

Clinical case seminar: lymphocytic hypophysitis: clinicopathological findings.

This report describes the clinicopathological features of 16 patients with lymphocytic hypophysitis and compares the results with the published literature. There were 2 males and 14 females in this series. In 10 of the 14 females (71%), the presentation was associated with pregnancy. Nine patients (56%) presented with symptoms of an expanding pituitary sellar mass, 10 (63%) had anterior pituitary hypofunction, 3 had diabetes insipidus (19%). Progressive undiagnosed hypopituitarism led to the demise of 3 patients (19%). Hyperprolactinemia was encountered in 6 patients (38%), and elevated growth hormone levels (GH) resulted in IGF-1 excess in one patient. Computed tomography (CT) and magnetic resonance (MR) imaging revealed features of a pituitary mass mimicking an adenoma in 10 cases (83%). Four patients (25%) had associated autoimmune thyroiditis. Morphologic examination of the pituitary and immunohistochemistry showed a polyclonal lymphoplasmacytic infiltrate as well as occasional neutrophils, eosinophils, and macrophages; the chronic inflammatory process resulted in focal or diffuse adenohypophysial destruction of variable severity with associated fibrosis. The inflammatory infiltrate involved the neurohypophysis in 2 cases and one of these patients had diabetes insipidus; the posterior lobe of two other patients with diabetes insipidus was not examined morphologically. We conclude that lymphocytic hypophysitis should be considered in the differential diagnosis of females with pituitary enlargement presenting in the peripartum period as well as those patients in whom pituitary hormone deficiency and/or excess is noted in association with a co-existing autoimmune disorder. This clinical suspicion should probably also be extended to include patients presenting with rapidly growing pituitary masses associated with compressive symptoms with or without pituitary hormone dysfunction. Because of the transient endocrine and compressive features of this condition in many instances, conservative treatment on the basis of clinical suspicion alone may obviate the need for aggressive pituitary surgery.

Adult↗

In vivo responsiveness of morphological variants of growth hormone-producing pituitary adenomas to octreotide.

The somatostatin analog, octreotide, is an inhibitor of growth hormone (GH) secretion that has been used to treat patients with GH-producing pituitary tumors. In this study we investigated the in vivo responsiveness to treatment with this analog in patients harboring different morphological types of GH-producing pituitary adenomas. Both GH and insulin-like growth factor I (IGF-I) plasma levels in 30 patients treated with octreotide (300 micrograms/day) for 4 months preoperatively were compared with those from 30 patients who did not receive treatment preoperatively. Tissue samples were studied using ultrastructural and immunohistochemical techniques. Amongst patients harboring densely granulated (DG) adenomas, mean GH levels were reduced to 32 +/- 9% by octreotide, to 30 +/- 7% by surgery and to 26 +/- 9% of baseline by both interventions. Surgery was equally as effective in lowering GH levels in patients with sparsely granulated (SG) adenomas as it was in those with DG adenomas; in patients with SG adenomas, GH levels were reduced by surgery alone to 37 +/- 16% and to 24 +/- 15% when performed following octreotide pretreatment. In contrast, treatment with octreotide alone in patients harbouring SG adenomas reduced GH levels to only 70 +/- 13% of baseline (p < 0.02 compared to surgery alone, or surgery and octreotide). We conclude that the GH inhibitory effects of octreotide are significantly better in patients harboring DG somatotroph adenomas compared with those harboring SG adenomas.

Acromegaly↗

Asynchronous pituitary adenomas with differing morphology.

Recurrent pituitary tumors can sometimes pose a diagnostic and therapeutic challenge. We report a case of a 43-year-old man who presented twice, 13 years apart, with pituitary adenoma marked by headaches, visual impairment, and no signs of endocrinologic abnormality. At initial presentation computed tomographic scan documented a pituitary mass eroding the sellar floor, with suprasellar and parasellar extension. The patient underwent transsphenoidal surgery and the tumor was classified as a silent corticotroph adenoma, subtype 2. Thirteen years later, clinical symptoms of a destructive pituitary mass reappeared. This time, the adenoma revealed typical ultrastructural features of an oncocytoma; it had a different immunocytochemical profile from the first tumor. Given these striking morphologic differences, we consider the two adenomas to represent asynchronous, de novo formations. We conclude that the recurrence of a resected pituitary tumor may also represent a metachronous development of two distinct pituitary adenomas.

Adenoma↗