Biomedical subjects

G D'Ambra

Publications and source records attributed to G D'Ambra.

At least 19 recordsLinked to original sources

PubMed2005

Effects of an appropriate oral diet on the nutritional status of patients with HCV-related liver cirrhosis: a prospective study.

BACKGROUND AND AIMS: In patients with liver cirrhosis, protein-energy malnutrition is a frequent finding and a risk factor influencing survival. The aim was to estimate the effects of an adequate diet on malnutrition and clinical outcome in patients with Child A or B HCV-related liver cirrhosis. METHODS: We enrolled 90 consecutive outpatients (M/F=52/38) with liver cirrhosis, 30 in Child class A and 60 in class B. Patients were evaluated by anamnesis, clinical examination, estimation of daily caloric intake and measurement of anthropometrical and biochemical indexes. Patients were randomized into two groups: group 1 with a 3-month oral controlled diet started one week after the first examination and this was followed by a 3-month of spontaneous dietary intake, and group 2 which started a 3-month spontaneous dietary intake followed by a 3-month of controlled diet. The follow-up was performed every month. RESULTS: During the period of controlled diet in patients of both groups, protein malnutrition assessed by midarm muscle circumference, creatinine-height index and serum albumin significantly improved independently of the Child class. Lipid malnutrition, assessed by triceps skin fold thickness values, did not improve during the course of the study. The compliance to the prescribed diet was very high in both groups, and no carry over effect of the previous dietary intake was observed during the follow-up period. CONCLUSIONS: The results emphasize the importance of both nutritional status evaluation and improvement in the Child A and B cirrhotic patients with HCV-related disease. The proposed nutritional approach was able to influence their protein malnutrition positively.

Anthropometry↗

PubMed2005

Occurrence and risk factors for benign epithelial gastric polyps in atrophic body gastritis on diagnosis and follow-up.

BACKGROUND: Benign epithelial gastric polyps have been reported to be more common in atrophic body gastritis. The role of Helicobacter pylori infection in the induction of gastric atrophy is well-known. The development of hyperplastic polyps may be in relation to H. pylori infection. AIM: To investigate occurrence of benign epithelial gastric polyps in atrophic body gastritis patients at diagnosis and follow-up, and the role of H. pylori and other risk factors for the development of benign epithelial gastric polyps. METHODS: A total of 259 consecutive atrophic body gastritis patients included in a follow-up programme, of whom 202 were followed up for median period of 4 years (range: 2-11). At baseline and follow-up gastroscopies, the presence of benign epithelial gastric polyps was evaluated. Biopsies for histology were obtained from all detected benign epithelial gastric polyps. RESULTS: Frequency of benign epithelial gastric polyps in atrophic body gastritis patients were 4.6% at baseline and 5.9% at follow-up. About 91.7% were hyperplastic polyps. H. pylori infection was detected in 79.2% atrophic body gastritis patients with benign epithelial gastric polyps, and in 70.8% without benign epithelial gastric polyps. Smoking was more frequent among patients with benign epithelial gastric polyps [42% vs. 20%, OR 2.8 (95% CI: 1.2-6.9)]. CONCLUSIONS: Benign epithelial gastric polyps occur in about 5% of atrophic body gastritis patients, and the vast majority are hyperplastic polyps. Smoking habit, but not H. pylori infection, increases the risk for benign epithelial gastric polyps in atrophic body gastritis patients.

Adolescent↗

PubMed2004

Large hiatal hernia in patients with iron deficiency anaemia: a prospective study on prevalence and treatment.

BACKGROUND: Although large hiatal hernia may cause bleeding from Cameron erosions, its role in iron deficiency anaemia has been debated, and no data are available on the treatment of these patients with proton pump inhibitors. Aims : To determine the prevalence of large hiatal hernia in out-patients with iron deficiency anaemia and the role of proton pump inhibitors in the prevention of recurrence of anaemia. METHODS: Two hundred and twenty-eight out-patients underwent upper/lower endoscopy. Those with large hiatal hernia were given an oesophagogram, discontinued iron supplementation and received proton pump inhibitor treatment with (group 1) or without (group 2) surgery. Anaemia was re-assessed during 1 year of follow-up. RESULTS: Large hiatal hernia was the likely cause of anaemia in 21 patients (9.2%). The median haemoglobin and ferritin values at the diagnosis of anaemia were 7.9 g/dL and 6 micro g/L, respectively. Cameron erosions were found in 33% of patients. Ten and eleven patients were included in groups 1 and 2, respectively. Haemoglobin values were 13.8 g/dL and 13.4 g/dL at 3 months of follow-up, and 13.4 g/dL and 13.8 g/dL at 1 year of follow-up, in groups 1 and 2, respectively. CONCLUSIONS: Large hiatal hernia may cause iron deficiency anaemia, even without Cameron erosions. Surgery in combination with proton pump inhibitor therapy is no better than proton pump inhibitor therapy alone in preventing the recurrence of anaemia.

Adult↗

PubMed2003

Abdominal tuberculosis with pancreatic involvement: a case report.

A case of abdominal tuberculosis with pancreatic involvement is described. A 27-year-old Italian male, with no known cause of immunodeficiency and with no evidence of pulmonary tuberculosis, was admitted to our division because of acute pancreatitis. Abdominal imaging revealed a large 'tumour-like' mass in the pancreas head compressing the distal choledochous, and multiple adenopathy. Histological examination of multiple specimens removed during explorative laparotomy revealed granulomas with giant cells, caseous necrosis, and positive Ziehl-Neelsen staining. Tissue culture was positive for Mycobacterium tuberculosis. Once specific medical treatment was started, the pancreatic damage completely resolved.

Adult↗

PubMed2003

Role of small bowel investigation in iron deficiency anaemia after negative endoscopic/histologic evaluation of the upper and lower gastrointestinal tract.

BACKGROUND: The usefulness of small bowel investigation in iron deficiency anaemia (IDA) patients is controversial. AIM: To evaluate the presence of small bowel lesions likely to cause IDA in patients with unexplained IDA after negative gastroscopy with biopsies and colonoscopy (CS). METHODS: A total of 117 outpatients, referred for unexplained IDA, underwent gastroscopy with biopsies and colonscopy. In 17 (14.5%) patients, endoscopic/histological investigations were negative. Of these patients, 13 underwent small bowel follow-through (SBFT) and if necessary to confirm the diagnosis, further gastrointestinal (GI) investigations. RESULTS: Small bowel lesions likely to cause IDA were found in five (38%) patients. Four of these lesions were detected by SBFT, two of them were malignant. These findings, confirmed at surgery and ileoscopy (IS), led to the final diagnoses ofjejunal and ileal adenocarcinoma, idiopathic ileal ulcers and ileal Crohn's disease. In one case, after negative SBFT, jejunal angiodysplasia was detected by video capsule endoscopy (VCE). Faecal occult blood test (FOBT) was positive in four (31%) patients, all of whom presented lesions likely to cause IDA, detected in three cases by SBFT and in one case by VCE. CONCLUSIONS: This study shows the importance of investigating the small bowel in IDA patients after negative upper and lower GI endoscopy, particularly if FOBT is positive.

Adenocarcinoma↗

PubMed2002

Progression of gastric enterochromaffin-like cells growth in Zollinger-Ellison syndrome and atrophic body gastritis patients.

BACKGROUND: Enterochromaffin-like cell hyperplasia of the gastric body mucosa occurs in hypergastrinaemic conditions such as atrophic body gastritis and Zollinger-Ellison syndrome. However, the time course of change or factors involved are not known. AIMS: To compare the rate of change of enterochromaffin-like cell proliferation in patients with atrophic body gastritis and Zollinger-Ellison syndrome. PATIENTS: From a consecutive series of atrophic body gastritis and Zollinger-Ellison syndrome patients, studied at the time of first diagnosis, 10 atrophic body gastritis (4 with pernicious anaemia) and 14 Zollinger-Ellison syndrome (4 with multiple endocrine neoplasia type 1) patients were followed-up for a median time of 48 months. METHODS: At entry and during follow-up patients underwent: plasma gastrin determination, endoscopic sampling of body mucosa for qualitative assessment of enterochromaffin-like cell hyperplasia pattern and degree of glandular atrophy, qualitative and morphometric analyses of body mucosa endocrine cells. RESULTS: At time of diagnosis, enterochromaffin-like cell lesions were more severe in atrophic body gastritis than in Zollinger-Ellison syndrome. During follow-up, no significant variations were observed in gastrin values, enterochromaffin-like cell patterns and grade of body mucosa atrophy in atrophic body gastritis. In contrast, gastrin levels were significantly increased [median 1200 (235-2625) vs 1947 (225-5200) pg/ml; p<0.001)] as was total volume density of enterochromaffin-like cells [median 1.60 (0.53-4.06) vs 3.18 (1.35-21.13)% of mucosal epithelial component; (p<0.005)] in Zollinger-Ellison syndrome. Micronodular hyperplasia of enterochromaffin-like cells, present in only one patient at diagnosis, was observed in 8 Zollinger-Ellison syndrome patients at follow-up. CONCLUSIONS: These data suggest that the progression of enterochromaffin-like cell growth in human gastric mucosa requires an increase of and/or a prolonged exposure to severe hypergastrinaemia.

Adult↗

PubMed2002

Role of Helicobacter pylori serology in atrophic body gastritis after eradication treatment.

BACKGROUND: It has been reported that 50% of patients with atrophic body gastritis have positive Helicobacter pylori antibody titres only. In atrophic body gastritis, a decrease in H. pylori antibodies after eradication treatment has been reported, suggesting that serology may indicate an active H. pylori infection. AIM: To investigate the time course of H. pylori antibodies and gastric inflammation after eradication treatment in patients with atrophic body gastritis, and to determine whether serology alone can be considered as a valid tool to assess the efficacy of eradication treatment in patients with atrophic body gastritis. METHODS: Twenty-seven patients with atrophic body gastritis (12 serologically H. pylori-positive only, ABG-S+; 15 H. pylori-positive at histology and serology, ABG-H+) were included in the treatment group, and 17 patients (all ABG-S+) in the no treatment group. All patients had gastroscopy plus biopsies evaluated according to the updated Sydney system and H. pylori immunoglobulin G determination: in the treatment group, at baseline and 6 and 24 months after eradication (bismuth-based triple regimens); in the no treatment group, at baseline and after 3 years. RESULTS: In the treatment group, in ABG-S+ patients, H. pylori antibodies decreased significantly 6 months after treatment [37.5 U/mL (16-100 U/mL) vs. 15 U/mL (0--100 U/mL), P < 0.01], but 2 years after treatment no further decrease occurred. In addition, in ABG-H+ patients, a significant decrease in H. pylori antibodies occurred 6 months after treatment [45 U/mL (12.5-100 U/mL) vs. 31 U/mL (0-65 U/mL), P < 0.01], but a further decrease was also observed 2 years after treatment [20 U/mL (0-56 U/mL), P < 0.01]. In ABG-S+ patients, no correlation was observed between the H. pylori antibodies and gastric inflammation score, whereas, in the ABG-H+ group, this correlation was extremely significant (r=0.5991, P < 0.0001). In the no treatment group, at follow-up, a significant decrease in H. pylori antibodies was observed [26 U/mL (15-100 U/mL) vs. 22 U/mL (0-53 U/mL), P < 0.05], but the gastric body inflammation remained unchanged. CONCLUSIONS: This study shows that, in ABG-S+ patients after eradication treatment, serology does not keep in step with gastric inflammation. This suggests that, in patients with atrophic body gastritis, serology alone may not be valid for the assessment of the efficacy of eradication treatment.

Acute Disease↗

PubMed2001

Gastrointestinal causes of refractory iron deficiency anemia in patients without gastrointestinal symptoms.

BACKGROUND: The standard evaluation of a patient with iron deficiency anemia includes a complete evaluation of the gastrointestinal tract to identify a source of bleeding. However, even after a careful examination, many patients remain without a diagnosis. Because iron deficiency anemia results from iron loss or defective absorption, we sought to determine the prevalence of potential gastrointestinal sources for iron deficiency anemia in patients without gastrointestinal symptoms. METHODS: Over a 10-month period, 668 outpatients were referred to the University Hematology Department with iron deficiency anemia, defined by a hemoglobin concentration less than 14 g/dL (less than 12 g/dL in women), mean corpuscular volume less than 80 fL, and ferritin level less than 30 microg/L. After excluding patients with obvious causes of blood loss, inadequate diet, chronic diseases, or malignancies, there were 81 eligible patients, 10 of whom refused investigation. The remaining 71 patients (51 women, median age 59 years) underwent colonoscopy, as well as gastroscopy with gastric (antrum and body) and duodenal biopsies. RESULTS: A likely cause of iron deficiency anemia was detected in 60 patients (85%). Diseases associated with bleeding were found in 26 patients (37%), including colon cancer (10 patients), gastric cancer (2), peptic ulcer (7), hiatal hernia with linear erosions (5), colonic vascular ectasia (3), colonic polyps (2), and Crohn's disease (1). Causes not associated with bleeding were found in 36 patients (51%), including 19 with atrophic gastritis, 4 with celiac disease, and 13 with Helicobacter pylori gastritis. Six (8%) patients had coincident gastrointestinal findings, and 11 (15%) had no cause identified. Patients with an identified nonbleeding-associated cause were younger than those with a bleeding-associated cause (median, 56 vs 70 years; P = 0.001) and included 59% of women (n = 30) versus 30% of men (n = 6) (P = 0.04). Hemoglobin level was not related to the site and severity of disease. CONCLUSION: Gastrointestinal diseases that do not usually cause bleeding are frequently associated with iron deficiency anemia in patients without gastrointestinal symptom or other potential causes of gastrointestinal bleeding.

Adult↗

PubMed2001

Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infection.

BACKGROUND: Helicobacter pylori infection, gastric acid hypersecretion and NSAID consumption may cause peptic ulcer. AIM: To investigate the respective roles of H. pylori and acid secretion in bleeding duodenal ulcer. PATIENTS AND METHODS: A total of 99 duodenal ulcer patients were referred for evaluation of acid secretion: seven with Zollinger-Ellison Syndrome; 14 with hypersecretory duodenal ulcer, defined by the coexistence of elevated basal acid output and pentagastrin acid output; and 78 duodenal ulcer patients with normal acid output. All non-Zollinger-Ellison Syndrome patients were H. pylori-positive and cured of infection. All patients were followed-up for a 36-month period, to assess the occurrence of bleeding episodes. RESULTS: Twenty-nine patients had at least one bleeding episode in the 4 years before the study. Bleeding was more frequent in males and in patients on NSAIDs. The mean basal acid output was not higher among bleeders. In the 21 patients (14 hypersecretory duodenal ulcer, seven Zollinger-Ellison Syndrome) with basal acid output > 10 meg/h and pentagastrin acid output > 44.5 meg/h, the risk of bleeding was higher (OR 6.5; 95% CI: 2-21). In the follow-up period, three out of 83 (3.3%) non-Zollinger-Ellison Syndrome patients had a H. pylori-negative duodenal ulcer with bleeding. The risk of bleeding after H. pylori cure was not higher in hypersecretory duodenal ulcer patients (P > 0.3), nor among patients with previous bleeding episodes (P > 0.2). CONCLUSIONS: In H. pylori-positive duodenal ulcer patients, the coexistence of elevated basal acid output and pentagastrin acid output leads to a sixfold increase in the risk of bleeding. After H. pylori cure, gastric acid hypersecretion is not a risk factor for bleeding. However, duodenal ulcer recurrence with bleeding may occasionally occur in patients cured of H. pylori, even if acid output is normal.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2001

First endoscopic-histologic follow-up in patients with body-predominant atrophic gastritis: when should it be done?

BACKGROUND: Body-predominant atrophic gastritis is considered a risk factor for gastric cancer and carcinoid. Timing of follow-up for patients with this disorder has not been defined. This study was undertaken to determine the optimal time for the first endoscopic/histologic follow-up in patients with body-predominant atrophic gastritis. METHODS: Forty-two patients with body-predominant atrophic gastritis were randomly assigned to 1 of 2 follow-up intervals: group A (n = 22) at 24 months and group B (n = 20) at 48 months. At baseline and follow-up patients underwent gastroscopy at which biopsies were obtained from the antrum and body for histopathology and evaluation for enterochromaffin-like cells. RESULTS: In group A patients, 2 antral hyperplastic polyps (9.1%) were present at baseline and 4 antral hyperplastic polyps (18.2%) were found at follow-up. In group B patients, baseline gastroscopy revealed 2 antral hyperplastic polyps (10%) and follow-up 2 antral hyperplastic polyps (10%) and 1 carcinoid tumor (5%) in the body. Atrophy and intestinal metaplasia scores in gastric body and antral mucosa in both groups did not change significantly between baseline and follow-up, except an increase in antral mucosa atrophy in group B patients (p = 0.02) was revealed. CONCLUSIONS: The results of this study indicate that performing the first follow-up in patients with body-predominant atrophic gastritis need not be earlier than at 4 years after diagnosis. This interval is satisfactory for detection of potential neoplastic lesions.

Adult↗

PubMed2001

Atrophic body gastritis patients with enterochromaffin-like cell dysplasia are at increased risk for the development of type I gastric carcinoid.

BACKGROUND/AIMS: In the presence of atrophic body gastritis, gastric carcinoid develops from gastric-body mucosa enterochromaffin-like cells. Few data exist on the prevalence of enterochromaffin-like dysplastic lesions in atrophic body gastritis patients and their presumed risk of evolution to carcinoid has never been assessed prospectively in humans. The aim of the present study was to investigate the prevalence and incidence of dysplastic and neoplastic enterochromaffin-like cell lesions in a consecutive series of patients with atrophic body gastritis. METHODS: A total of 130 atrophic body gastritis patients at diagnosis and 96 atrophic body gastritis patients at follow-up (median 30 months) underwent gastroscopy with multiple biopsies and fasting gastrinaemia evaluation. In patients with enterochromaffin-like cell dysplasia, a more detailed bioptic sampling at follow-up was performed. RESULTS: Of the 130 atrophic body gastritis patients, only one (0.7%) had a gastric carcinoid polyp, whereas enterochromaffin-like cell dysplasia was found in five patients (3.8%). At follow-up only one out of the 96 atrophic body gastritis patients (1%) was diagnosed as having a carcinoid polyp at 41 months. Enterochromaffin-like cell dysplasia was present in four additional patients (4.2%). Two atrophic body gastritis pernicious anaemia patients with enterochromaffin-like cell dysplasia developed a gastric carcinoid in the follow-up. Among nine atrophic body gastritis patients with enterochromaffin-like cell dysplasia, the incidence of carcinoid tumour was 22% compared to 1.1% of atrophic body gastritis patients without dysplasia (odds ratio: 26.00; 95% confidence interval: 2.089-323.52). During the follow-up, fasting gastrin levels increased significantly only in atrophic body gastritis patients with enterochromaffin-like cell dysplasia (mean 677.4 +/- 66.1 vs 1112.2 +/- 185.6; P = 0.0287). CONCLUSION: This study provides the first clinical evidence that, in hypergastrinaemic atrophic body gastritis patients, enterochromaffin-like cell dysplasia carries a markedly increased risk for development of type I gastric carcinoid. This suggests that a more detailed endoscopic/bioptic procedure in this subgroup of atrophic body gastritis patients is able to detect gastric carcinoid at an early stage.

Adult↗

PubMed2001

[Association between breast and colorectal cancer and polyps. Screening and epidemiological study].

BACKGROUND: Studies regarding the associations between different types of cancer in the same patient are very few and not always come to the same conclusions. Several hypothesis are suggested and particularly genetic and socioeconomical ones seem to offer an interpretation of this issue. Early detection of a second neoplasm allows to improve prognosis and survival. The knowledge of correlations between tumors help to select a population, with a high risk to develop a second cancer, to be included in a screening program. Nowadays thanks to early detection of breast cancer, ten years survival is more than 75%. Women who had breast cancer now live longer and so could have a higher risk to develop a second cancer. METHODS: From September 1998 to September 1999 in our Department 71 patients operated for breast cancer, underwent screening colonscopy. No patients refused to be included in the study. Mean age was 61 years (range 36-87). Each patient had a clinician interview in order to explain the goals of the study. RESULTS: Results show that among all patients 3 (4.2%) presented a history of colon cancer, 18.3% (13 cases) presented large bowel polyps. In 84.60% patients (11 cases) polyps were found not over 40 cm. This study shows that 93% of patients (66 cases) had a relative with cancer history. CONCLUSIONS: Our results compared with those of other authors seem to show an increased risk for breast cancer patients in developing polyps or colon cancer, so we suggest to insert sigmoidoscopy in standard follow-up of breast cancer patients.

Adult↗

PubMed1999

Duodenal ulcer relapse is not always associated with recurrence of H. pylori infection: a prospective three-year follow-up study.

BACKGROUND: Long-term data concerning the reappearance of Helicobacter pylori infection and duodenal ulcer (DU) recurrence after successful eradication are still few and conflicting. Inadequate histological assessment or use of indirect tests for the determination of H. pylori and bias in the selection of patients to be controlled can influence reported results. The aim of this study was to determine the rate of recurrence of H. pylori infection and ulcer relapse in a population of cured DU patients followed up for 3 years irrespective of their symptomatology. METHODS: Between 1992 and 1994, 126 patients with DU disease were treated with double or triple therapy. Patients using nonsteroidal antiinflammatory drugs or aspirin or receiving maintenance antisecretory therapy were excluded. H. pylori infection was assessed by three bioptic tests from both the antrum and the body (culture, urease, histopathological examination). After 2 months from cessation of treatment, DU had healed and H. pylori infection was cured in 102 of 126 patients (81%). These patients were endoscopically followed up after 1 and 3 years, respectively, and were advised to contact us at symptom recurrence. At 1 and 3 years, we studied 95 (93.2%) and 79 (77.4%) patients, respectively, of the 102 who were cured. The other patients were untraceable or refused endoscopy because they were asymptomatic. RESULTS: After 1 year, no patient had H. pylori recurrence, whereas three patients had a relapse of DU without evidence of infection. After 3 years, recurrence of H. pylori occurred in six patients (annual rate, 2.5%), DU relapsed in five H. pylori-positive patients (6.3%) and in two H. pylori-negative patients (annual rate, 1.9%). Fasting gastrin and acid secretion values studied in all relapsed patients were within the normal range except for one H. pylori-positive patient. CONCLUSIONS: Recurrence of H. pylori infection is very low where treatment is effective, but a DU relapse, not related to acid hypersecretion, can occur in a small percentage of cured patients.

Adolescent↗

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↗

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↗

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

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↗