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M Marignani

Publications and source records attributed to M Marignani.

32 records · Page 2Linked to original sources
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

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↗
PubMed1997

Reversal of long-standing iron deficiency anaemia after eradication of Helicobacter pylori infection.

Helicobacter pylori has been proposed as a major determinant in multiple gastric disorders. We describe the case of a young adult with a long-standing medical history of sideropenic anaemia and of oral iron consumption dependence with a chronic superficial H. pylori-positive gastritis. All other causes of sideropenic anaemia were carefully excluded. Histology showed a peculiar pattern of non-active H. pylori-positive gastritis. The bacterium was a non-VacA-producing strain. The first attempt at eradication caused a reduction in bacterial load and led to a partial normalization of haematologic variables without improving the ferritin level. A successful second course of eradication therapy completely reversed the anaemia and restored the iron deposit, which persisted at the 29-month follow-up. H. pylori infection can be involved in unexplained cases of iron deficiency anaemia in adults, and its cure can normalize the haematologic picture.

Adult↗
PubMed1997

Does pretreatment with omeprazole decrease the chance of eradication of Helicobacter pylori in peptic ulcer patients?

OBJECTIVE: It has been reported that pretreatment with omeprazole could decrease the efficacy of Helicobacter pylori eradication. Our aim was to compare the efficacy, safety, and tolerability of the eradicating regimen, omeprazole/amoxicillin/metronidazole. The two antibiotics were scheduled either during the first or during the last 2 wk of omeprazole administration. METHODS: In this prospective controlled study conducted in a single center, 78 symptomatic peptic ulcer patients were treated for 4 wk with omeprazole 40 mg o.m.; the patients were randomly assigned to receive amoxicillin 1 g t.i.d. postprandially and metronidazole 250 mg t.i.d. postprandially, either during the first 2 wk (group A, n = 40) or the last 2 wk of therapy with omeprazole (group B, n = 38). H. pylori status was assessed by culture, histology, urease test, and IgG antibodies. Each patient's course was followed for 1 yr. RESULTS: H. pylori infection was cured in 97.4% of group A (95% CI: 0.84-0.99) and in 89% of group B (95% CI: 0.73-0.96, p = 0.28). Healing was achieved in 80% of the patients in group A (95% CI: 0.63-0.90) and in 75.7% of patients in group B (95% CI: 0.60-0.90, p = 0.60) At 12-month follow-up, 72 patients were evaluated: 37/38 (97%) of patients in group A and 33/33 (100%) in group B were confirmed as cured of the infection (NS). Peptic ulcer healing rate reached 100% in the two groups. Furthermore, between the two groups, there were no significant differences in symptom relief or improvement. Both regimens were well tolerated, and no patient had to be withdrawn from therapy because of an adverse event. Minor side-effects appeared to be similar in the two groups (40% vs. 38%). CONCLUSIONS: This randomized study clearly indicates that omeprazole pretreatment does not significantly reduce the efficacy of eradicating therapy for H. pylori in peptic ulcer patients.

Adult↗
PubMed1996

Somatostatin receptor localization of pancreatic endocrine tumors.

Gastroenteropancreatic endocrine tumors are difficult to localize. At the same time the tumor is localized, though, there is an opportunity for cure or to remove tumor tissue. In this study we have prospectively examined the ability of 111In-octreotide scintigraphy, magnetic resonance imaging (MRI), and computed tomography (CT) to localize tumor lesions in 24 patients with a biochemical or histologic diagnosis of neuroendocrine tumor. In eight patients a surgical assessment of the imaging results was prospectively performed. Planar and abdominal single-photon emission tomography (SPET) images acquired 4 and 24 hours after 180 to 220 MBq of 111In-octreotide injection were evaluated and compared with conventional imaging techniques. SPET scintigraphy visualized more presumed tumor lesions (n = 39) than conventional imaging studies (MRI,n = 25; CT,n = 13); 23 of 24 patients had positive octreotide scintigraphy, 17 of 24 had positive MRI-scans, and 12 of 24 patients had positive CT scans. It was concluded that 111In-octreotide scintigraphy combined with conventional imaging improves the preoperative localization of presumably tumorous lesions in patients with gastroenterohepatic endocrine tumors.

Adenoma, Islet Cell↗
PubMed1996

Antral gastrin cell hyperfunction and Helicobacter pylori infection.

BACKGROUND: Antral gastrin cell hyperfunction (AGCH), is a rare cause of duodenal ulcer associated with non-tumour hypergastrinaemia and acid hypersecretion. AIM: To investigate the role of Helicobacter pylori in AGCH. PATIENTS: Twelve AGCH patients and eight H. pyloripositive non-hypergastrinaemic duodenal ulcer patients were compared. METHODS: Basal and peak acid outputs, gastrin-stimulation (meal and bombesin) tests, and immunohistochemistry for antral G and D cells were performed. One year after H. pylori eradication, six AGCH patients were again investigated with the same tests. RESULTS: Significantly more basal, and stimulated gastrin and acid secretion, were found in AGCH compared to the H. pylori-positive duodenal ulcer patients (P < 0.01). G cell counts were significantly higher in AGCH than in duodenal ulcer patients (118.8, range 58-192.4, vs. 86.1, range 49-184; P < 0.05), and the resulting G/D cell ratio was also higher in AGCH patients (4.2, range 2.6-5.6, vs. 3.3, range 1.9-4.3; P < 0.05). H. pylori was present in the gastric mucosa of all 12 AGCH patients. Cure of infection in six AGCH individuals resulted in marked a decrease of gastrin levels associated with a significant (23.7%: P < 0.05) decrease of G cell count and an increase (12%; P < 0.05) of D cell count. CONCLUSIONS: The results indicate that AGCH may result from H. pylori overstimulation of gastrin cell function in patients with some presently undefined, familial predisposition and that an imbalance of the G/D cell ratio may have a role in the genesis of hypergastrinaemia.

Adolescent↗
PubMed1996

Effectiveness of octreotide in controlling fasting hypergastrinemia and related enterochromaffin-like cell growth.

The effects of long term (6-month), high (500-micrograms), once a day administration of octreotide on enterochromaffin-like (ECL) cell proliferation were evaluated in eight patients with hypergastrinemic atrophic gastritis at risk for the development of gastric carcinoids. Fasting gastrin levels were determined during treatment and up to 6 months after the end of treatment. Chromogranin A, hCG alpha, and somatostatin-immunostained cells were morphometrically evaluated in biopsy specimens of corpus mucosa taken before and after treatment. The results showed that gastrin levels significantly decreased from 950 to 238 ng/L (-74.9%; P < 0.01) at the end of treatment, a decrease that persisted 6 months after the end of treatment (450 ng/L; P < 0.05). The volume density of CgA cells (mostly ECL cells) decreased from 3.7% to 2.1% of the epithelial component (-43%; P < 0.014), that of hCG alpha-storing ECL cells decreased by 85% (P < 0.0007), and that of somatostatin-stained cells decreased by 74% (P < 0.04). No clinically significant side-effects were found. It is concluded that octreotide treatment as used in the present study is safe and effective in reducing hypergastrinemia and associated ECL cell changes in patients with atrophic gastritis. The decrease in D cells is consistent with the occurrence of somatostatin receptors and related autocrine regulation in these cells.

Adult↗
PubMed1994

Zollinger-Ellison syndrome and antral G-cell hyperfunction in patients with resistant duodenal ulcer disease.

We measured basal and pentagastrin-stimulated acid secretion, as well as basal and meal-stimulated plasma gastrin concentration to determine, in 67 patients affected by resistant duodenal ulcer, whether their condition could be related to gastric acid secretion and/or gastrin-related syndromes. We then compared them to 46 duodenal ulcer control patients. The outpatients were investigated consecutively. The resistant duodenal ulcer patients differed from the controls only in their higher complication rates (bleeding or perforation, P < 0.05). We identified five patients in the resistant duodenal ulcer group with Zollinger-Ellison syndrome and 12 with antral G cell hyperfunction, whereas in the control group only one patient was affected by antral G cell hyperfunction. IgG anti-Helicobacter pylori antibodies were positive for the presence of infection in 7 of the hypergastrinaemic patients. When Zollinger-Ellison syndrome or antral G cell hyperfunction were excluded, no differences could be found in gastric acid secretion, or basal and meal-stimulated plasma gastrin levels, between the resistant and control duodenal ulcer patients, except for basal acid hypersecretion (resistant duodenal ulcer 16% vs duodenal ulcer 2% P = 0.0144). In the presence of duodenal ulcer disease resistant to H2-blockers, it is mandatory to measure basal plasma gastrin concentration since it was possible to diagnose the gastrin-related syndromes, Zollinger-Ellison syndrome and antral G cell hyperfunction, in 26% of this group of patients.

Adult↗
PubMedDate not supplied

Atrophic body gastritis in patients with autoimmune thyroid disease: an underdiagnosed association.

BACKGROUND: Atrophic body gastritis (ABG) has never been histologically characterized in patients with autoimmune thyroid disease (AITD), and its prevalence may be substantially different from that previously assessed based on only indirect evidence. OBJECTIVE: To detect and characterize the presence of ABG in patients with AITD. METHODS: Sixty-two patients with AITD (5 men and 57 women), aged between 21 and 74 years, have been screened for the presence of ABG by assaying serum gastrin levels. Patients with hypergastrinemia underwent gastroscopy followed by the histological examination of multiple biopsy specimens. The diagnosis of ABG was based on hypergastrinemia and pentagastrin-resistent achlorhydria, confirmed by histological examination. RESULTS: Twenty-two (35%) of 62 patients had hypergastrinemia (mean +/- SEM gastrin level, 1070+/-288 pmol/L). The diagnosis of ABG has been histologically confirmed in all 22 patients, and the score of atrophy was moderate to severe. In group A (patients aged 20-40 years; n = 21), 6 patients (29%) had ABG, compared with 11 patients (37%) in group B (patients aged 41-60 years; n = 30) and 5 patients (45%) in group C (patients aged 61-80 years; n = 11). Antiparietal cell antibodies were detected in only 68% (15/22) of patients with ABG. Anemia was observed in 82% (18/ 22) of patients with AITD and ABG but only in 22% (9/40) of patients without ABG (P<.0001). CONCLUSIONS: In the patients with AITD studied, about one third had ABG, which was diagnosed also in young patients; the measurement of gastrin levels represented the most reliable tool in the diagnosis of ABG; and the presence of anemia, even microcytic, was suggestive of undiagnosed ABG.

Achlorhydria↗
PubMedDate not supplied

Hypergastrinemia and enterochromaffin-like cell hyperplasia.

UNLABELLED: The enterochromaffin-like (ECL) cells, the most frequent endocrine cells of the oxyntic mucosa of the stomach, are under the trophic stimulus of gastrin. These cells undergo a hyperplastic increase in variety of hypergastrinemic diseases. The most widely accepted nomenclature for the description of hyperplastic proliferation has been retrospectively arranged in a sequence presumed to reflect a temporal evolution of the proliferative process. A comparative, prospective study aimed to verify, in human hypergastrinemic diseases such as atrophic body gastritis (ABG), Zollinger-Ellison syndrome (ZES) and antral gastrin cell hyperfunction (AGCH), the effect of exposure of ECL cells to different pattern of gastrin hypersecretion, is lacking. To this purpose, we studied a series of consecutive patients with ABG, ZES and AGCH at the time of first diagnosis. MATERIAL AND METHODS: The patients included in this study (124 ABG, 18 ZES and 10 AGCH) were selected on the basis of two previously performed screening studies aimed to diagnose these diseases. All patients at the time of diagnosis underwent gastroscopy, with multiple biopsies of the gastric body mucosa for the evaluation of qualitative pattern of ECL cells hyperplasia, and basal fasting gastrin determination. A sample of hypergastrinemic patients from each group was further investigated by meal-stimulation of gastrin secretion and quantitative morphometry for CgA positive gastric body endocrine cells. RESULTS: AGCH patients showed only the normal or simple hyperplasia pattern. In the ZES group, simple and linear grades accounted for 38.4 percent and 46.1 percent, respectively. MEN-I patients showed only these two patterns. The majority of ABG patients showed the presence of micronodular pattern (59.7 percent). A correlation analysis between fasting gastrin levels and grade of hyperplasia (r = 0.5580, p < 0.0001), indicates that the greater the gastrin levels, the higher is the degree of severity of ECL hyperplasia pattern. In conclusion, our data support the role of gastrin as the selective contributor to the progression of ECL cell hyperplasia in humans.

Adolescent↗
PubMedDate not supplied

Peptic ulcer and duodenal stenosis: role of Helicobacter pylori infection.

A 17-year-old boy who developed a symptomatic duodenal ulcer at 10 years of age with melena, and was then treated continuously for 6 years with ranitidine therapy that only partially controlled symptoms and peptic lesions, came to us with vomiting due to duodenal bulb stenosis and active ulcer. Four months of omeprazole (40 mg/die o.m.) did not modify the endoscopic picture. The diagnosis of H. pylori infection and its treatment with triple therapy led to the cure of both duodenal ulcer and bulbar stenosis. Afterwards he remained asymptomatic without any lesions or complications for 18 months. This case illustrates that H. pylori eradication: a) is able to cure refractory duodenal ulcer; b) resolves severe complications such as duodenal stenosis.

Amoxicillin↗
PubMedDate not supplied

Single photon emission computerized tomography increases the sensitivity of indium-111-pentetreotide scintigraphy in detecting abdominal carcinoids.

Somatostatin (sms) receptors have been identified in carcinoids (c), so enabling their visualization with 111In-pentetreotide scintigraphy. The aim of this study was to evaluate if single photon emission computerized tomography (SPECT) can increase the sensitivity of sms receptor scintigraphy in the detection of abdominal c. 26 patients (pts) with a present, or previously operated, abdominal carcinoid were submitted to SPECT over the abdomen and multiple planar views after the injection of 111In-pentetreotide. Magnetic resonance imaging and computed tomography were also performed. In 19 pts abnormal sites of uptake were found by SPECT which localized 13 abdominal extrahepatic (in 11 pts) and 45 hepatic lesions (in 15 pts). No pathologic accumulation was seen in 7 pts in complete remission after surgery. Planar images visualized 7 abdominal extrahepatic (in 6 pts) and 26 liver tumor sites (in 10 pts), conventional procedures detected 5 abdominal extrahepatic (in 4 pts) and 36 hepatic lesions (in 10 pts). 111In-pentetreotide SPECT is more sensitive than planar scanning and conventional methods to detect abdominal c, and so may play a major role in the early and accurate mapping of tumour spread.

Abdominal Neoplasms↗
PubMedDate not supplied

111In-pentetreotide detection of gastrinoma before and after surgery.

Eighteen patients with Zollinger-Ellison syndrome were studied with 111In-pentetreotide SPECT in order to localize gastrinoma, the tumour responsible for this pathology. NMR imaging was also carried out. Eight patients were operated. 111In-pentetreotide was reinjected 4 hours before operation and the radioactivity of the excised tumours counted. The nature of the withdrawn tissues was assessed by immunohistochemistry (chromogranina A). The scintigraphy was repeated 3-6 months after surgery. 111In pentetreotide SPECT was more sensitive than NMR. It was also absolutely specific because all the radioactive tumours excised showed positive chromogranin A staining. The radioactivity/gram counted in gastrinomas exceeded 10 fold the hepatic and biliary radioactivity and 20-100 folds the radioactivity of blood and omentum. In all the operated patients but three, the scintigraphy performed after surgery did not detect tumours. However complete eradication did not occur, because though 3-6 months after surgery the gastrinemia was significantly lower with respect to pre-surgery results it did not return to normal values in all patients but two.

Chromogranin A↗