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Biomedical subjects

C Bordi

Publications and source records attributed to C Bordi.

At least 91 records · Page 5Linked to original sources
PubMed1995

Lack of allelic loss at the multiple endocrine neoplasia type 1 (MEN-1) gene locus in a pancreatic ductal (non-endocrine) adenocarcinoma of a patient with the MEN-1 syndrome.

The gene responsible for multiple endocrine neoplasia type I (MEN-1) syndrome has been mapped to chromosome 11q13. It appears to function as a tumour-suppressor gene analogous to that for retinoblastoma and allelic losses involving the wild-type of the MEN-1 allele have been found in parathyroid and pancreatic endocrine tumours of MEN-1 patients. No genetic information has been provided so far on non-endocrine malignancies that may occur in MEN-1 patients. A case of exocrine pancreatic adenocarcinoma presenting as the terminal event in a woman with a long standing history of MEN-1 syndrome and multiple endocrine tumours of the pancreas was investigated for possible allelic losses at the MEN-1 gene locus using restriction fragment length polymorphisms (RFLPs) closely linked to the MEN-1 gene and polymerase chain reaction (PCR) for D11S533 locus. No allelic losses were found in tumour tissue with two informative RFLPs (D11S97, D11S146) or with PCR analysis. These findings suggest that the MEN-1 gene does not confer a predisposition to develop tumours other than those that typify the syndrome.

Adenocarcinoma↗
PubMed1995

Endocrine tumours of the stomach.

This review illustrates the current classification of gastric endocrine tumors: a) carcinoid tumors (associated with chromic atrophic gastritis; with Zollinger-Ellison syndrome and multiple endocrine neoplasia type I; sporadic) and b) neuroendocrine carcinomas. The pathogenetic characteristics and clinical implications that justify this classification are discussed.

Carcinoid Tumor↗
PubMed1995

[Thoracic actinomycosis with lung, mediastinal and pericardial involvement. A case report].

A case of actinomycosis is reported in a 17-years-old woman with pleural and pericardial effusions and anterior mediastinal mass. Histopathological diagnosis of actinomycosis was performed by mediastinal mass biopsy. There was no evidence of immunodeficit or neoplasia. Probably a dental manipulation favoured the Actinomyces infection. Treatment with antibiotics resulted in a reduction of mediastinal mass and in a complete resolution of pleural and pericardial effusions.

Actinomycosis↗
PubMed1995

Hypergastrinemia and gastric enterochromaffin-like cells.

The enterochromaffin-like (ECL) cell of the oxyntic, acid-secreting mucosa is at present the most extensively studied endocrine cell type in the gastrointestinal tract. It is functionally related to acid secretion through paracrine release of histamine. Its ability to undergo proliferation in response to the trophic stimulus of hypergastrinemia has important implications in pathology, being involved in the development of ECL-cell carcinoid tumors of rodents treated with powerful inhibitors of acid secretion as well as in that of most human gastric carcinoids which, with rare exceptions, are composed of ECL cells. The various aspects of the ECL-cell response to hypergastrinemia in humans are discussed in this review. The trophic effect of gastrin is specific for ECL cells and its sensitivity is enhanced by the female sex and by the genetic background of the multiple endocrine neoplasia type 1 (MEN-1) syndrome. Exposure of ECL cells to hypergastrinemia induces peculiar changes in the structure of cytoplasmic granules and triggers the phenotypic expression of a novel protein, the alpha subunit of glycoprotein hormones, absent in normal cells. The ECL-cell hyperplasia driven by hypergastrinemia may influence the hypersecretory gastric state of patients with Zollinger-Ellison syndrome (ZES) by inappropriate intramucosal secretion of histamine and may contribute to the high circulating levels of basic fibroblast growth factor (bFGF), an ECL-cell product responsible for parathyroid mitogenic effects in MEN-1 patients. However, hypergastrinemia per se cannot promote evolution of hyperplasia into carcinoid tumors, for which additional unknown factors, particularly associated with atrophic gastritis or MEN-1 syndrome, are required. ECL-cell carcinoids developing within these backgrounds have a strikingly more favorable course than their gastrin-independent counterpart. Suppression of hypergastrinemia, either by antrectomy or treatment with somatostatin analogues, may induce regression of both ECL-cell hyperplasia and gastrin-sensitive ECL-cell carcinoids.

Carcinoid Tumor↗
PubMed1994

Production of basic fibroblast growth factor by gastric carcinoid tumors and their putative cells of origin.

Using immunohistochemical techniques a subpopulation of endocrine cells in the human oxyntic mucosa was found to react with antibodies against basic fibroblast growth factor (bFGF). These cells were identified as histamine-producing enterochromaffin-like (ECL) cells and, to a minor extent, serotonin-producing enterochromaffin cells. Basic fibroblast growth factor immunoreactive cells were most frequently found in hyperplastic lesions of ECL cells occurring in hypergastrinemic patients (20 of 27 cases) and in ECL cell carcinoid tumors (10 of 17 cases). In addition, bFGF mRNA was demonstrated by Northern blot analysis of homogenates from two gastric carcinoids cytologically characterized as pure ECL cell tumors. Although the function of bFGF in normal cells remains unknown, its production in neoplastic conditions may be responsible for the associated desmoplastic and angioblastic proliferations. Moreover, secretion of bFGF by hyperplastic or neoplastic ECL cells may contribute to the circulating levels of the bFGF-like mitogenic factor identified in patients affected by multiple endocrine neoplasia type 1 syndrome.

Carcinoid Tumor↗
PubMed1994

Three months of octreotide treatment decreases gastric acid secretion and argyrophil cell density in patients with Zollinger-Ellison syndrome and antral G-cell hyperfunction.

METHODS: The effects of three months of treatment with octreotide on gastric acid hypersecretion induced by hypergastrinaemia were investigated in patients with Zollinger-Ellison syndrome (n = 5) or antral G-cell hyperfunction (n = 4). Gastric acid secretion, fasting plasma gastrin concentrations and clinical findings were examined, and a morphometrical analysis of oxyntic endocrine cells was performed. RESULTS: Administration of octreotide 100 mcg b.d. subcutaneously significantly decreased the volume density of argyrophil cells (P < 0.05) as well as basal and pentagastrin-stimulated acid secretion (P < 0.05). Although partial or complete loss of inhibition was found in most patients after 3 months, gastrin levels were decreased during the first 2 months of treatment (P < 0.05). Fundic D-cells were not affected by treatment. Positive correlations were observed between volume density of argyrophil cells and basal acid output (r = 0.65); plasma gastrin and basal acid output (r = 0.74); plasma gastrin concentrations and volume density of argyrophil cells (r = 0.80). CONCLUSION: These results support the important role of the enterochromaffin-like cell in maintaining acid secretion, and indicate a specific role for octreotide in the therapy of gastric acid hypersecretion associated with hypergastrinaemic diseases.

Administration, Oral↗
PubMed1994

Gastric carcinoid tumor and its precursor lesions. Ultrastructural study of a case before and after antrectomy.

Antrectomy has been proposed as the preferential treatment of hypergastrinemic patients with nonantral gastric carcinoids since it removes the main growth factor for the tumors and their precursor lesions, ie, hypergastrinemia. To investigate the cellular basis of the mechanism for postantrectomy regression in nonantral endocrine cells, a light and electron microscopic morphometric study was performed in a case of enterochromaffinlike-cell gastric carcinoid associated with hypergastrinemia before and 4 and 10 months after antrectomy. The withdrawal of sustained hypergastrinemia obtained by antrectomy was associated with a progressive reduction of the volume density, cross-sectional area, and number of profiles of endocrine cells in the remaining nonantral mucosa, in which gastrin-dependent proliferations were regarded as the carcinoid precursor lesions. Ultrastructural morphometry demonstrated that the changes selectively involved the enterochromaffinlike cells, ie, the specific cell target for the trophic action of gastrin and the usual component of gastric carcinoids. The volume fractions of enterochromaffin and X cells (producing serotonin and endothelin, respectively) were increased 10 months after antrectomy. Persistence of a modest elevation of gastrin levels, likely due to the occurrence of gastrin cells in areas of pyloric metaplasia of the nonantral mucosa, did not prevent the hypotrophic effects of antrectomy.

Aged↗
PubMed1993

Morphometry of gastric endocrine cells in hypergastrinemic patients treated with the somatostatin analogue octreotide.

The aim of the study was to evaluate whether treatment with 200 micrograms/d of the somatostatin analogue octreotide (SMS 201-995) for three months can influence the trophic action exerted by hypergastrinemia on endocrine cells of the oxyntic mucosa, a condition potentially leading to hyperplasia and carcinoid tumors. Endocrine cells were morphometrically investigated in Grimelius silver stained sections of endoscopic biopsies of oxyntic mucosa collected from 13 hypergastrinemic patients with Zollinger-Ellison syndrome (ZES) (n = 5), antral G cell hyperfunction (AGCH) (n = 4) and atrophic gastritis type A (AG-A) (n = 4) before and after 3 months treatment and 3 months after drug discontinuance. The treatment induced a reduction of the volume density (P < 0.015), profile cross sectional area (P < 0.05) and number of cell profiles per unit area (P < 0.015) of argyrophil cells. A rebound of all these parameters was observed 3 months after drug withdrawal with values usually exceeding those at the entry, except in cases of AG-A. The patients' plasma gastrin concentrations presented similar variations showing a significant relation with all morphometric parameters of argyrophil cells. Also, the cell content in alpha subunit of human chorionic gonadotropin was related to the plasma gastrin levels, a finding confirming the close gastrin dependence of the expression of this protein by oxyntic endocrine cells. No significant changes were observed in mucosal somatostatin D cells. These results indicate that variations in circulating gastrin levels are the most likely factor responsible for the hypotrophic effect of octreotide on oxyntic argyrophil cells (mostly corresponding to the ECL cells) of hypergastrinemic patients.

Adult↗
PubMed1993

Amyloid stroma in meningiomas.

Twenty-three cases of meningiomas with psammoma bodies (PBs) and 15 without PBs have been studied using histochemical, ultrastructural and immunohistochemical methods for amyloid. Amyloid was found in all cases showing PBs and in only 5 cases in the group devoid of PBs. Meningiomas may contain amyloid in their stroma.

Adult↗
PubMed1993

Progression of uremic hyperparathyroidism involves allelic loss on chromosome 11.

In occasional cases of secondary hyperparathyroidism, long term stimulation of the parathyroid glands leads from compensatory to autonomous hyperfunction, and thus, hypercalcemia develops. This clinical entity, named tertiary hyperparathyroidism, is possibly due to the formation of an adenoma in one of the hyperplastic glands. Previous studies have shown that parathyroid adenomas may arise with allelic loss on chromosome 11. We tested for allelic loss at several loci on chromosome 11 in 12 enlarged parathyroid glands from 6 uremic patients and found loss of heterozygosity in 2 of the glands from 2 different patients with higher serum calcium levels (11.3 +/- 0.29 vs. 9.8 +/- 0.28 mg/dL; P < 0.004) and, therefore, ascribable to the so-called tertiary hyperparathyroidism. The 2 glands with allelic loss were significantly greater in mass than those without loss (3.42 +/- 0.37 vs. 1.60 +/- 0.54 g; P < 0.001). These data offer new evidence that autonomous parathyroid proliferation in uremic patients can develop through overgrowth by a monoclonal tumor, presumably with inactivation of a tumor suppressor gene(s) on chromosome 11.

Adenoma↗
PubMed1993

Endocrine tumors of the pancreas: the pathologist's approach.

The introduction of modern cytological techniques has provided the pathologist of tools that considerably improved his analysis of pancreatic endocrine tumors and that are discussed in this review. Hormonal characterization of the tumors by immunohistochemistry significantly contributed to the definition of the current functional classification of the tumors and proved that ectopic tumors (producing extrapancreatic hormones) are as common as entopic tumors synthesizing pancreatic hormones. The identification of neuroendocrine markers and of other active non-hormonal substances extended our knowledge on the functional properties of tumor cells often with significant fall out on the biology of the corresponding normal cells. Current studies are mostly oriented toward the analysis of cell proliferation and appear to open promising perspectives for the prognostic evaluation of the tumor course.

Adenoma, Islet Cell↗
PubMed1993

Proliferation of endothelial component of parathyroid gland in multiple endocrine neoplasia type 1. Potential relationship with a mitogenic factor.

The basic fibroblast growth factor-like mitogen detected in the plasma of patients with the multiple endocrine neoplasia type 1 (MEN-1) syndrome was found to have a specific mitogenic effect on parathyroid endothelial cells in vitro. To investigate its pathogenic role in humans, the endothelial component of parathyroid glands was evaluated by ultrastructural morphometry in six MEN-1 patients. The results were compared with those found in six patients with uremic hyperparathyroidism (UHPT) and in three subjects with histologically normal glands. Plasma mitogenic activity was found in all MEN-1 patients but not in those with UHPT or in normal subjects. All morphometric parameters investigated (fractional volume and nuclear density of capillary endothelial cells, volume fraction and number per unit area of capillaries) showed 1.5- to 2-fold higher values in patients with MEN-1 than in those with UHPT (P < 0.05). In contrast, no difference was found between MEN-1 cases and normal subjects. Quantitative evaluation of parathyroid pericytes yielded results similar to those of endothelial cells. These data indicate that the proliferation of parathyroid cells in MEN-1 patients is accompanied by parallel increase in the associated endothelial component that does not occur in patients with UHPT and may support the hypothesis of an in vivo role of the MEN-1 mitogen factor on the endothelial component of parathyroid glands in MEN-1 patients.

Adult↗
PubMed1992

Progesterone receptor immunoreactivity in pancreatic endocrine tumors. An immunocytochemical study of 156 neuroendocrine tumors of the pancreas, gastrointestinal and respiratory tracts, and skin.

BACKGROUND: The immunoreactivity for progesterone receptors (PR) of the majority of endocrine cells of the human pancreas has prompted the authors to investigate if PR expression is maintained in pancreatic endocrine tumors and is correlated with the main clinicopathologic features of these neoplasms. Furthermore, the study has been extended to other neuroendocrine cells and tumors to determine whether PR immunoreactivity is a common feature of neuroendocrine cells and tumors other than those of the pancreas. METHODS: One hundred fifty six neuroendocrine tumors of the pancreas, gastrointestinal and respiratory tracts, and skin were immunostained for PR with three different monoclonal antibodies and for estrogen receptors (ER). Additional immunostainings for general neuroendocrine markers and for pancreatic hormones were performed in selected cases. RESULTS: Nuclear immunoreactivity for PR has been documented in the neoplastic cells of 56 (58.33%) of 96 pancreatic endocrine tumors. PR immunoreactivity was not influenced by the sex and age of the patients or the occurrence of a clinical syndrome related to inappropriate hormone secretion. Tumors synthesizing pancreatic polypeptide, glucagon, and insulin expressed PR in higher percentages (80%, 75%, and 66%, respectively) than those producing other pancreatic hormones or those that were not functioning. Irrespective of the functionally different tumor types, PR immunoreactivity showed a significant correlation (P = 0.0003) with the absence of metastases and the lack of tumor invasion of neighboring organs or of large vessels. As opposed to normal and neoplastic islet cells, the neuroendocrine cells and tumors of the gastrointestinal tract, respiratory tract, and skin did not show any PR immunoreactivity, with the single exception of a typical carcinoid tumor of the lung. ER were not identified in any pancreatic or extrapancreatic neuroendocrine cells or tumors. CONCLUSIONS: Nuclear PR are immunocytochemically detectable in most pancreatic endocrine tumors and are correlated significantly to the absence of pathologic evidence for malignancy. Conversely, PR expression has not been found in normal and neoplastic endocrine cells and tumors investigated.

Adenoma, Islet Cell↗
PubMed1992

Studies on co-localization of 7B2 and pancreatic hormones in normal and tumoural islet cells.

The distribution of protein 7B2, a protein with structural characteristics of GTP-binding proteins, has been studied in normal pancreatic islets and in a series of 70 pancreatic endocrine tumours with emphasis on the co-localization of 7B2 and the different pancreatic hormones. Although all cell types of normal islets were found to store 7B2, variations from intense expression to absence of reaction were seen within each cell type. In particular, B cells showed intense immunostaining for 7B2 in small compact islets and weak or no staining in larger islets with lobular arrangement. Pancreatic polypeptide (PP) cells expressed 7B2 intensely in the PP-rich area of ventral embryological origin, but were mostly non-reactive in the PP-poor area. The A cells, located along intralobular blood vessels, were more frequently immunoreactive for 7B2 than those at the periphery of the islets. Immuno-electron microscopy revealed a preferential localization of 7B2 in secretory granules of islet cells, with more intense localization in the peripheral halo of alpha granules. Benign islet cell tumours more frequently expressed 7B2 than their malignant counterparts. Although often expressed in a lower number of tumour cells than the tumour-specific hormone, 7B2 was usually co-localized with the latter. In contrast, no relationship was found with the localization of proinsulin. It is concluded that 7B2 is a non-permanent component of the cell granule compartment, probably involved in events related to exocytosis and without relationship to intracellular prohormone processing.

Cytoplasmic Granules↗
PubMed1992

Focal oxyntic gland atrophy with endocrine cell hyperplasia in Zollinger-Ellison syndrome during omeprazole treatment.

Development of focal gland atrophy of the oxyntic mucosa was found in two patients with the Zollinger-Ellison syndrome undergoing long-term treatment with omeprazole. The atrophic areas revealed florid proliferation of endocrine cells in the form of both intraglandular crescents and micronodular hyperplasia. This proliferation was significantly more pronounced than in the remaining non-atrophic mucosa. The possible relationship of these changes to long-standing pharmacological therapy for gastric acid suppression is discussed.

Adult↗
PubMed1991

Gastric carcinoids and their precursor lesions. A histologic and immunohistochemical study of 23 cases.

A histologic and immunohistochemical study was carried out in 23 unselected nonantral gastric carcinoids and their precursor lesions classified according to Solcia et al. None of the patients showed Zollinger-Ellison syndrome. Two variants of carcinoids showing distinctive pathologic and pathogenetic characteristics were identified on the basis of presence or absence of associated chronic atrophic gastritis type A (A-CAG). Chronic atrophic gastritis type A was found in 19 cases showing either single or multiple neoplasms, tumor extension limited to the mucosa or submucosa, consistent endocrine cell precursor changes in extratumoral mucosa, and consistent hypergastrinemia and/or G cell hyperplasia. Associated precursor lesions were only hyperplastic in all but two cases with single carcinoids whereas they were also dysplastic in all but one case with multiple carcinoids. The four tumors arising in nonatrophic mucosa were all single, more aggressive, and not associated with extratumoral endocrine cell proliferations or with signs of gastrin hypersecretion. Tumor cells were diffusely immunoreactive for chromogranin A and synaptophysin but usually negative for chromogranin B or HISL-19. Scattered serotonin cells were found in ten carcinoids. They were more frequent in infiltrating than in intramucosal tumors as were the less represented pancreatic polypeptide cells whereas the reverse was found for alpha-subunit-containing cells. These results are of relevance for tumor pathogenesis and may provide the rationale for a less aggressive therapeutic approach in the patients.

Adolescent↗