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C Bordi

Publications and source records attributed to C Bordi.

At least 55 records · Page 3Linked to original sources
PubMed1999

Heterotopic mesenteric ossification ('intraabdominal myositis ossificans'): report of five cases.

Intraabdominal heterotopic ossification is a very uncommon disorder. We report five new cases, review the previous literature, and discuss the clinical and pathologic features of these lesions. The clinical features of the current cases and of those previously reported are remarkably similar. All patients were middle-aged to elderly men (range, 43-80 years; mean, 61 years) who had small bowel obstruction associated with heterotopic bone formation in the small bowel mesentery, often after one or more abdominal operations. In one case, an initial diagnosis of extraosseous osteosarcoma was considered. This unusual reactive process shares many of the clinical and pathologic features of myositis ossificans, as classically described in somatic soft tissues. We propose to designate this condition heterotopic mesenteric ossification.

Adult↗
PubMed1999

High prevalence of atrophic body gastritis in patients with unexplained microcytic and macrocytic anemia: a prospective screening study.

OBJECTIVE: Atrophic body gastritis (ABG) is characterized by atrophy of the gastric body mucosa, hypergastrinemia, and hypo/achlorhydria. Its association with pernicious anemia is well recognized. Gastric hypo/achlorhydria is known to affect iron absorption but ABG is rarely considered as a possible cause of iron deficiency (microcytic) anemia. The aims of this study were to validate a screening methodology for the detection of ABG in a consecutive series of patients with microcytic and macrocytic anemia and to investigate the clinical and gastric morphofunctional characteristics of the two hematological presentations of ABG. METHODS: A two-part prospective study was carried out. Part A aimed to validate the screening methodology to detect the presence of ABG in patients with macrocytic and microcytic anemia who have no specific GI symptoms, by measuring their gastrin levels and verified by performing gastroscopy with biopsy. Part B aimed to detect the presence of ABG in a larger sample of anemic patients by our validated method and, by pooling the data of ABG patients, to determine the clinical, gastric histological, and functional characteristics pertaining to the macrocytic and microcytic presentations of ABG. RESULTS: In part A, ABG was detected in 37.5% of patients with macrocytic and in 19.5% of those with microcytic anemia. Pooling the data of the ABG patients from part A and part B, microcytic ABG patients were on average 20 yr younger than those with macrocytic anemia. The majority of microcytic ABG patients were female, most of whom were premenopausal. H. pylori infection was widely represented in the microcytic ABG group (61.1%). They also had a lesser grade of body mucosal atrophy and lower hypergastrinemia levels, suggesting a less severe oxyntic damage of shorter duration. CONCLUSIONS: Macrocytic anemia is not the only hematological presentation of ABG. Physicians evaluating patients with unexplained iron deficiency anemia should consider ABG as a possible cause by determining fasting gastrin levels and performing gastroscopy with biopsies of the body mucosa.

Adult↗
PubMed1999

Prevalence and causes of hypergastrinemia in primary hyperparathyroidism: a prospective study.

Gastrin levels have been reported to be often increased in patients with primary hyperparathyroidism (PHPT) considered to be caused by hypercalcemia. To determine the prevalence of increased basal gastrin and to investigate its causes, 52 consecutive patients with PHPT were studied prospectively, undergoing a clinical, biochemical, and gastric morphofunctional assessment before any parathyroid surgical procedure. This included evaluation of basal and secretin-stimulated gastrin, basal and pentagastrin-stimulated gastric acid secretion, upper gastrointestinal endoscopy, with histological evaluation for gastritis and Helicobacter pylori infection. Twenty of the 52 PHPT patients (38.5%) had increased fasting gastrin. Further investigation allowed us to clearly demonstrate the causes of hypergastrinemia in 16 of these 20 patients. In 7 of 20 (35%), hypergastrinemia was caused by gastric fundus atrophy; in 3 patients (15%), Zollinger-Ellison syndrome with Multiple Endocrine Neoplasia type I was diagnosed; whereas in another 20% of patients, mild hypergastrinemia was ascribed to Helicobacter pylori gastritis. Finally, in 2 patients, additional clinical history revealed an occasional use of the gastric antisecretory drug omeprazole a few days before the serum gastrin determination. This study shows that the hypercalcemic status per se is not sufficient to produce an increase in fasting gastrin levels. Furthermore, gastric fundus atrophy, and not gastrinoma, is the major cause of relevant (>160 pg/mL) hypergastrinemia.

Adult↗
PubMed1999

Loss of heterozygosity in 11q13-14 regions in gastric neuroendocrine tumors not associated with multiple endocrine neoplasia type 1 syndrome.

Loss of heterozygosity (LOH) at the MEN1 gene locus at 11q13 is commonly found in type II gastric carcinoid tumors, which are associated with multiple endocrine neoplasia type 1 (MEN-1). In contrast, information is scanty or absent for other types of gastric neuroendocrine tumors, represented by type I carcinoids (associated with chronic atrophic gastritis), type III (sporadic) carcinoids, and neuroendocrine carcinomas. Moreover, LOH analysis of the allelic region distal to the MEN1 gene, which is postulated to contain an additional tumor suppressor gene effective in MEN-1-associated and sporadic endocrine tumors, has never been performed. To clarify these issues, DNA extracted from archival tissue from 25 type I carcinoids, 4 type III carcinoids, and 2 neuroendocrine carcinomas was amplified by PCR, using primers for six polymorphic markers located on chromosome 11q13 (PYGM, D11S4946, and D11S913) and 11q14 (D11S916, D11S901, and D11S1365), for analysis of LOH. Allelic losses in the 11q13-14 region with at least two polymorphic markers were found in 12 of 25 (48%) type I carcinoids. When LOH was found in the 11q13 region, it was large and continuous and extended to the most telomeric marker investigated. In one tumor, retention of heterozygosity for markers in the MEN1 region and LOH for distal markers were observed. No LOH was found in three of four type III carcinoids. Large deletions in both the 11q13 and 11q14 regions were observed in both neuroendocrine carcinomas investigated. In conclusion, LOH in the 11q13-14 regions is frequently found in type I carcinoids and neuroendocrine carcinomas of the stomach, suggesting the involvement of the MEN1 gene and/or a more telomeric tumor suppressor gene in the pathogenesis of these non-MEN-1-associated neuroendocrine tumors. The low rate of LOH at 11q13-14 suggests the predominance of different genetic mechanisms in type III carcinoids, which also differ from other types of gastric carcinoids in the lack of a promoter role for gastrin.

Carcinoid Tumor↗
PubMed1999

Gastric carcinoids.

Gastric carcinoids are classified into three types mostly on the basis of their pathological associations: 1) type I, associated with atrophic corporal gastritis; 2) types II, associated with Multiple Endocrine Neoplasia type 1; 3) type III, sporadic. Type I and II carcinoids develop through a histologically recognizable sequence: hyperplasia-dysplasia-neoplasia. Their pathogenesis depends on the combined action of promoting agents, mostly hypergastrinaemia, and of transforming agents, the role of which is currently under investigation. Their prognosis is generally favourable. In contrast, type III tumours are often malignant and their pathogenesis has not been clarified yet.

Carcinoid Tumor↗
PubMed1998

Expression of the alpha- and beta-subunits of human chorionic gonadotropin by subsets of parathyroid cells in states of hyperparathyroidism.

The alpha-subunit of human chorionic gonadotropin (hCG-alpha) has previously been found to be expressed in hyperplasias and tumours of numerous endocrine tissues including all those involved in MEN-I syndrome except the parathyroid glands. In the present immunohistochemical investigation of 86 patients with various states of hyperparathyroidism, expression of hCG-alpha by subsets of parathyroid cells was shown in 46 cases (54 per cent) including all states of hyperparathyroidism investigated: primary adenoma (n = 34, 44 per cent); uraemic secondary hyperplasia (n = 34, 53 per cent); MEN-I (n = 13, 77 per cent); MEN-II (n = 2, 100 per cent); and parathyroid carcinoma (n = 3, 100 per cent). Although the number of parathyroid cells expressing hCG-alpha was in general low, the occurrence of numerous immunoreactive cells appeared to be concentrated in primary adenoma and MEN-I (20 and 33 per cent of positive cases, respectively). No expression was found in ten normal control glands, except for very rare cells in one case. Expression of hCG-alpha was in part associated with that of hCG-beta, which appeared to be more commonly expressed than hCG-alpha in cases of secondary hyperparathyroidism. In separate experiments, Bouin fixation was found to preserve the immunoreactivity of hCG-alpha and hCG-beta better than the formalin fixation used in this study, suggesting that the figures may be underestimates. These immunohistochemical results are in agreement with a previous biochemical study showing hCG-alpha and hCG-beta in extracts of parathyroid tumours and extend to the parathyroid glands the otherwise ubiquitous finding of hCG-alpha expression in MEN-I-related neoplasms.

Adenoma↗
PubMed1998

Pancreatic endocrine tumours: evidence for a tumour suppressor pathogenesis and for a tumour suppressor gene on chromosome 17p.

Two molecular pathways leading to cancer are known. Common-type cancers arise from the 'tumour suppressor' pathway, characterized by gross chromosomal changes and allelic losses (LOH) in an average of 25 per cent or more of randomly chosen chromosomal loci. The 'mutator pathway' has been recognized in a subset of cancers, characterized by widespread microsatellite DNA instability and rarity of chromosomal losses. The present study has investigated 20 pancreatic endocrine tumours (PETs) for loss of heterozygosity (LOH) at seven chromosomal loci (3p14, 7q31-32, 11q13, 13q14, 18q21, 17p13, and 17q21); microsatellite instability; and Ki-ras, N-ras, and p53 gene mutations. LOH was found in an average of 24 per cent of the chromosomal loci analysed. No tumour showed microsatellite instability. Ki-ras and p53 mutations were each found in one case. The frequency of losses was higher in malignant (40 per cent) than in benign (17 per cent) tumours (p = 0.009), and the specific chromosome 17p13 LOH was associated with extrapancreatic extension of disease (p = 0.007), high proliferative activity (p = 0.001), and absence of progesterone receptors (p = 0.01). A common deleted region on chromosome 17p13 and the rarity of p53 gene mutations suggest the existence of a novel tumour suppressor gene involved in the pathogenesis of PETs in this chromosomal area.

Adolescent↗
PubMed1998

Functioning human insulinomas. An immunohistochemical analysis of intracellular insulin processing.

Sixty-seven insulinomas were investigated by immunohistochemistry using site-directed antibodies against insulin, proinsulin, chromogranin A, HISL-19, and four proteins directly or indirectly involved in the proteolytic processing of proinsulin: the prohormone convertases PC2 and PC3, carboxypeptidase H (CPH) and 7B2. Results were expressed in a six-grade score according to the frequency of immunoreactive tumour cells. Insulin was expressed by all tumours, appearing in either a diffuse or a polarized pattern and being detected in more than 30% of tumour cells in all cases but three. Proinsulin was also expressed in all tumours, with more than 50% of tumour cells immunoreactive in all cases but 5. It was consistently localized in the Golgi apparatus. In about half the cases, moreover, it also showed diffuse cytoplasmic staining, usually with a very sparse distribution. Trabecular and solid insulinomas did not present specific, homogeneous patterns of insulin immunostaining. However, insulin immunoreactivity was much more abundant in trabecular than in solid neoplasms, being present in virtually all tumour cells (score 6) in 50% and 8% of cases, respectively. Virtually all insulinomas expressed PC2, PC3, CPH and 7B2, usually in 30-100% of tumour cells, with a frequency significantly related to that of insulin. However, detection of PC2 and 7B2 was slightly less frequent than that of PC3 and CPH. In consecutive sections these proteins were found to be mostly co-localized with insulin and chromogranin A but not with proinsulin. They were heavily expressed in all 10 tumours with more than 10% of cells showing cytoplasmic proinsulin immunoreactivity, indicating that the leakage of proinsulin from the Golgi compartment is not associated with faulty expression of converting enzymes and possibly reflects a saturated processing capacity. HISL-19 immunoreactivity was found in both Golgi apparatus and insulin stores, indicating that the relevant antigen is different from all other proteins investigated. These results do not support a defect in expression or localization of proinsulin-processing enzymes in most insulinomas.

Adolescent↗
PubMed1998

Relationship between fundic endocrine cells and gastric acid secretion in hypersecretory duodenal ulcer diseases.

BACKGROUND: Acid hypersecretion is associated with duodenal ulcer disease in the following conditions: Zollinger-Ellison syndrome (ZES) and antral gastrin cell hyperfunction (AGCH) due to hypergastrinaemia, or hypersecretory duodenal ulcer (HDU) without hypergastrinaemia. AIM: To evaluate whether quantitative changes in fundic ECL and D cells may be involved in acid hypersecretion. PATIENTS AND METHODS: Seven ZES, six AGCH and six HDU Helicobacter pylori-positive patients were compared. Basal (BAO) and pentagastrin-stimulated gastric acid secretions (PAO), and morphometry of fundic ECL and D cells were performed. The six AGCH and six HDU patients were investigated again using the same tests 1 year after H. pylori eradication. RESULTS: Median PAO values were no different in all the hypersecretory conditions studied. The median volume density of ECL cells in ZES was significantly higher than in controls (2.75, range 1.74-5.8 vs. 0.73, 0.52-1.11: P < 0.05), whereas it was in the control range in AGCH and HDU patients (0.77, range 0.20-1.39 and 0.99, range 0.42-1.51; respectively). The count of fundic D cells was significantly lower in AGCH patients than in all other investigated groups (median 0.16, range 0.1-0.52; P < 0.05). Cure of infection in AGCH and HDU patients did not modify the ECL cell volume density, whereas a significant increase in the count of fundic D cells was observed in AGCH patients. Thus, the ECL/D cell index was significantly affected in AGCH patients (P < 0.05), being higher during H. pylori infection (median 6, range 0.7-9.25) than after the cure (median 2.12, range 1.10-3.5). BAO and PAO were not affected by H. pylori eradication in either group. CONCLUSIONS: The study provides evidence, for the first time, that quantitative alterations in the fundic endocrine cells are not involved in acid hypersecretion of patients with hypersecretory states, and that eradication of H. pylori does not restore normal acid secretion values.

Adult↗
PubMed1998

Use of the somatostatin analogue octreotide to localise and manage somatostatin-producing tumours.

BACKGROUND: Somatostatin receptor scintigraphy (SRS) and octreotide therapy have both changed the management of gastroenteropancreatic endocrine tumours, but very few data are available on the use of SRS and octreotide to visualise and treat somatostatinomas. METHOD: The results of SRS and octreotide treatment in three somatostatinoma patients were examined. RESULTS: SRS was able to detect extensive hepatic involvement in patient 1, one hepatic and one pancreatic lesion in patient 2, and one hepatic lesion in patient 3. Octreotide therapy (0.5 mg/day subcutaneously) was effective in decreasing plasma levels of somatostatin in all three patients. Symptoms (diabetes and diarrhoea) were greatly improved in the two patients with "somatostatinoma syndrome". CONCLUSION: The study shows that somatostatinoma, like most other gastroenteropancreatic endocrine tumours, possesses functioning somatostatin receptors.

Aged↗
PubMed1998

Classification of gastric neuroendocrine tumors and its clinicopathologic significance.

AIMS:To study the pathologic classification of gastric neuroendocrine tumors and its clinicopathologic significance.METHODS:Paraffin-embedded sections of 52 gastric neuroendocrine tumors including 42 carcinoid tumors, and 10 cases of neuroendocrine carcinoma from 326 patients who underwent resection of stomach carcinomas were studied by immunohistochemical methods including 10 endocrine markers or hormones antibodies and endocrine cells in gastric neuroendocrine tumors and extratumoral mucosa were observed under electromicroscope.RESULTS:The 52 gastric neuroendocrine tumors were divided into three types:(1) Gastrin dependent type of carcinoid (26 cases) accompanied by chronic atrophic gastritis (CAG) and tumor extension limited to the mucosa or submucosa complicated with hypergastrinemia and G cell hyperplasia.This type was consistently preceded by and associated with generalized proliferation of endocrine cells in the extratomoral fundic mucosa.(2)Non-gastrin dependent type of carcinoids (16 cases)associated with neither CAG nor hypergastrinemia. This type was more aggressive; and (3)Neuroendocrie carcinomas (10 cases), which are highly aggressive tumors.CONCLUSIONS:A correct identification of different types of gastric endocrine tumors has major implications for the treatment and prognosis of the patients.

Journal Article↗
PubMed1997

Endocrine cell growths in atrophic body gastritis. Critical evaluation of a histological classification.

The aim of the present study was to evaluate the correspondence of the classification of non-antral endocrine cell growths proposed by Solcia and co-workers with clinical features and non-endocrine mucosal changes. For this purpose, 94 cases of newly diagnosed atrophic body gastritis were investigated using endoscopic biopsies and compared with 18 control subjects. The patients were subdivided into the following four groups according to the most severe pattern of endocrine cell proliferation found in the body mucosa, as shown by chromogranin A immunostaining: group 1, normal pattern (7 cases, 7.5 per cent); group 2, simple hyperplasia (6 cases, 6.5 per cent); group 3, linear hyperplasia (24 cases, 25.8 per cent); group 4; micronodular hyperplasia (56 cases, 60.2 per cent). Adenomatoid hyperplasia was found in only one case, thus precluding further analysis. Patients in groups 1 and 2 had lower acid secretion, higher gastrin level, and higher mean scores in all histopathological variables of chronic gastritis considered by the Sydney system when compared with controls, but did not differ among them in any parameter investigated. When compared with groups 1 and 2, patients of groups 3 and 4 showed higher values of circulating gastrin, higher scores of glandular atrophy, and lower values of acid secretion and of mononuclear and neutrophil inflammatory cell infiltration. Moreover, group 4 patients differed significantly from those of group 3 in their higher gastrin levels and atrophy scores, and lower scores of neutrophil cell infiltration. On the basis of these results, it is proposed that for practical purposes the normal and the simple hyperplasia patterns may be incorporated into a single group. It is concluded that this classification in its simplified form, based on a qualitative histological approach, shows clinical relevance without the need to perform expensive, time-consuming morphometric evaluations.

Adult↗
PubMed1997

[Neuroendocrine tumors of the stomach. Pathogenesis, classification and clinical aspects].

Neuroendocrine tumors of the stomach are classified into four types mostly on the basis of their pathological associations: 1) carcinoid type I, associated with atrophic corporal gastritis, 2) carcinoid type II, associated with multiple endocrine neoplasia type 1, 3) carcinoid type III, sporadic, and 4) neuroendocrine carcinoma. The first two types develop through a histologically recognizable sequence hyperplasia--dysplasia--neoplasia. Their pathogenesis depends on the combined action of promoting agents, mostly hypergastrinemia, and of transforming agents, the role of which is currently under investigation. Their prognosis is generally favourable in sharp contrast with that of the other two types of tumors, which is usually poor. The pathogenesis and the precursor lesions of the latter neoplasms have not been clarified yet.

Carcinoid Tumor↗
PubMed1997

Pancreatic-polypeptide cell hyperplasia associated with pancreatic or duodenal gastrinomas.

An immunohistochemical investigation of pancreatic-polypeptide (PP) cells in the PP-rich region of the pancreas, of ventral embryological origin, was performed in three female patients affected by or previously operated on for functioning duodenal or pancreatic gastrinomas not associated with multiple endocrine neoplasia syndrome. A pronounced PP-cell hyperplasia showing histological patterns of endocrine cell dysplasia and focal adenomatosis as defined by Jaffe et al was found in all cases. Morphometric analysis showed that in these patients the fraction of ventral-type pancreatic lobules occupied by PP-immunoreactive cells was 14.77 +/- 5.73%, 8.94 +/- 2.92%, and 10.83 +/- 5.64%, respectively. These values were three to five times higher than the upper values found in controls (mean, 2.20%; range, 1.54 to 2.93%; P < .0001). PP-cell hyperplasia may contribute for the increased circulating levels of PP found in gastrinoma patients. In this regard, elevation of fasting blood PP was found in one of four determinations done in one patient, indicating that PP-cell hyperplasia may be responsible for, at least, transient PP hypersecretion. In one of our patients, PP-cell hyperplasia was found 15 years after normalization of gastrin levels by removal of a single pancreatic gastrinoma. This finding is against a trophic role for hypergastrinemia in the development of PP-cell hyperplasia. In one of two patients in whom the pancreatic regions of dorsal embryological origin (ie, body and tail of the gland) were examined, ventral-type, PP-rich islets were frequently encountered, a finding at variance with their exceptional detection in control cases. This finding suggests that PP cell hyperplasia of the PP-rich pancreatic region may be a feature of a more diffuse disorder of PP cell development in the pancreas of gastrinoma patients.

Aged↗
PubMed1997

Aggressive forms of gastric neuroendocrine tumors in multiple endocrine neoplasia type I.

In recent classifications of gastric endocrine tumors, tumors arising in patients with multiple endocrine neoplasia type 1 (MEN-1) are regarded to be regulated by the concomitant hypergastrinemia resulting from to pancreatic or, most commonly, duodenal gastrinomas and to have a benign behavior. In this article, we report on two cases of MEN-1 gastric neuroendocrine tumors having a fatal course. Case 1 was a young male with hyperparathyroidism and Zollinger-Ellison syndrome and with florid development of multiple gastric carcinoids and multiple duodenal gastrinomas. Metastases occurred in the liver, of exclusive gastric origin, in periduodenal lymph nodes, of exclusive duodenal origin, and in perigastric lymph nodes, of mixed origin. The patient died 48 months after diagnosis. Case 2 was an adult female patient with hyperparathyroidism, adrenocortical disorders, and gastric tumors but no hypergastrinemia. The patient died 3 months after tumor diagnosis. At autopsy, the stomach showed multiple benign carcinoids and two independent neuroendocrine carcinomas not reported before in MEN-1 and massively metastatizing to lymph nodes, liver, and peritoneum. Multiple islet cell tumors mostly producing pancreatic polypeptide were found, whereas gastrinomas were seen in neither the pancreas nor the duodenum. Allelic losses at the MEN-1 gene locus in chromosome 11q13, the mechanism responsible for tumor development in MEN-1 syndrome, were demonstrated in the carcinoid tumors of case 1 and in the neuroendocrine carcinoma of case 2. We conclude that gastric neuroendocrine tumors in patients with MEN-1 may have a poor outcome, they have the same genetic mechanism as MEN-1 tumors in other organs, and they may be independent of the trophic effect of hypergastrinemia.

Adult↗
PubMed1997

Atrophic body gastritis: distinct features associated with Helicobacter pylori infection.

BACKGROUND: Usually, atrophic body gastritis has been considered an autoimmune disease characterized by the presence of parietal cell antibodies. Previous investigations into the role of Helicobacter pylori infection have obtained conflicting results. The aim of this study was to investigate the prevalence and role of H. pylori in a prospectively investigated population of patients with corpus-predominant atrophic gastritis. PATIENTS AND METHODS: A consecutive series of 67 newly diagnosed cases of atrophic body gastritis was derived from a screening of 326 patients with unexplained anemia or dyspepsia. Criteria for diagnosis were fasting hypergastrinemia, pentagastrin-resistant achlorhydria, and histological confirmation of body atrophy. In all 67 patients, H. pylori infection was evaluated independently by histological assay and urease test. The gastritis status of both the fundic and antral mucosa were graded according to the Sydney system. Parietal cell and intrinsic factor antibodies also were determined. RESULTS: Active H. pylori infection was present in 26.8% of our patients and allowed us to identify a patient's subpopulation with a significantly smaller degree of body mucosa damage as shown by functional parameters (gastrin, gastric acid secretion, pepsinogen I) and histological assessment. In this subpopulation, a higher prevalence of gastric cancer familial history was found. Presence of parietal cell antibodies showed a similar prevalence in H. pylori-positive and H. pylori-negative patients (61.1% vs. 69.4%) and was not associated with significant functional and histological differences. Cure of infection determined an evident improvement of corporal atrophy as well as a reduction of hypergastrinemia. CONCLUSION: Active H. pylori infection, a potential cause of oxyntic gland atrophy, is found in one-fourth of patients with newly diagnosed atrophic body gastritis.

Adult↗