Anti-gastric parietal cell antibodies for autoimmune gastritis screening in juvenile autoimmune thyroid disease.

OBJECTIVE: Patients with autoimmune thyroid disease (ATD) have a higher prevalence of autoimmune gastritis (AIG) compared with the general population. The association between ATD and AIG is poorly characterized in the pediatric age. We reviewed the prevalence of anti-gastric parietal cell antibodies (PCA) in young patients with ATD to evaluate its usefulness as a marker for AIG screening. METHODS: We evaluated 220 children and adolescents (11.28 ± 6.37 years) with ATD (186 with autoimmune thyroiditis (AT) and 34 with Graves' disease (GD). At ATD diagnosis and annually thereafter, blood counts and PCA levels were measured. In patients positive for PCA, plasma gastrin, chromogranin A, vitamin B12, iron and ferritin levels and H. pylori antigen were measured. PCA-positive patients > 18 years were invited to undergo a gastroscopic exam. RESULTS: PCA positivity was detected in ten (4.5%) subjects (5F/5M; 12.6 ± 3.4 years). The prevalence of PCA positivity was not significantly different in the comparison of GD and AT patients (p = 0.9). PCA positivity was detected after 2.7 ± 2.7 years of follow-up in AT and 4.4 ± 4.0 years in GD (p = 0.4). Autoantibody positivity was more prevalent in female patients, in both AT and GD (p = 0.02 and p = 0.03, respectively). At detection of PCA positivity, five out of ten PCA-positive patients had iron deficiency, four vitamin B12 deficiency, two anemia, three hypergastrinemia and two elevated chromogranin values. Two patients had H. pylori infection. Gastroscopy was performed in the five ATD patients and in all patients, AIG was confirmed. CONCLUSION: In the juvenile population, ATD and AIG may also be associated. PCA screening is useful to detect subjects at risk for this condition. Due to the longer life expectancy of the pediatric population and considering the relatively high risk of malignant transformation, early surveillance monitoring is mandatory for children and adolescents with ATD.

The prevalence and the causes of minimal intestinal lesions in patients complaining of symptoms suggestive of enteropathy: a follow-up study.

AIMS: Although they are non-specific, minimal intestinal lesions are at the end of the coeliac histological damage spectrum. To investigate whether minimal intestinal lesions in patients without endomysial antibodies are due to coeliac disease, their prevalence, causes and risk of evolving into frank coeliac disease were studied. METHODS: From January 2000 to December 2005, 645 duodenal biopsies were performed. In 209 patients, duodenal biopsies were performed independently of endomysial antibody results. Clinical data and HLA-typing of all the patients negative to endomysial antibodies but with minimal mucosal lesions were re-evaluated. Three years later, they were offered to be seen again, and further investigations were proposed. RESULTS: 14 out of 209 patients had minimal mucosal lesions and negative endomysial antibodies. Two patients were lost to follow-up; in 7/12 patients, symptoms and histological lesions were due to a different condition, not related to coeliac disease. In 11/12 patients, HLA-typing made diagnosis of coeliac disease very unlikely. Only one patient was on a gluten-free diet because of gluten-sensitive symptoms and was DQ2(+)/DQ8(+). CONCLUSIONS: Minimal duodenal lesions in patients negative to endomysial antibodies are rare and are likely to be due to conditions unrelated to coeliac disease.

New insights into the role of age and carcinoembryonic antigen in the prognosis of colorectal cancer.

The aim of this study was to verify through relative survival (an estimate of cancer-specific survival) the true prognostic factors of colorectal cancer. The study involved 506 patients who underwent locally radical resection. All the clinical, histological and laboratory parameters were prognostically analysed for both overall and relative survival. This latter was calculated from the expected survival of the general population with identical age, sex and calendar years of observation. Univariate and multivariate analyses were applied to the proportional hazards model. Liver metastases, age, lymph node involvement and depth of bowel wall involvement were independent prognosticators of both overall and relative survival, whereas carcinoembryonic antigen (CEA) was predictive only of relative survival. Increasing age was unfavourably related to overall survival, but mildly protective with regard to relative survival. Three out of the five prognostic factors identified are the cornerstones of the current staging systems, and were confirmed as adequate by the analysis of relative survival. The results regarding age explain the conflicting findings so far obtained from studies considering overall survival only and advise against the adoption of absolute age limits in therapeutic protocols. Moreover, the prechemotherapy CEA level showed a high clinical value.

[Molecular biology, basic research and diagnosis of Hirschsprung's disease]. / Molekularbiologie, Grundlagenforschung und Diagnose des Morbus Hirschsprung.

The proto-oncogene RET is the major gene responsible for Hirschsprung's disease (HSCR), with RET mutations also implied in different pathologies. A variety of mutations of the RET proto-oncogene have been detected in HSCR patients. Special attention should be paid to rare patients who carry mutations of one of the critical cysteine residues of these exons, known to predispose to MEN2A. In these cases, HSCR can be associated with the development of neuroendocrine tumors such as medullary thyroid carcinoma (MTC) or MEN2A, for which a prophylactic thyroidectomy is advisable in the presence of a tumor causing RET mutation. In combined MEN2A/HSCR families, RET gene testing, tumor screening and prophylactic thyroidectomy are indicated as in MEN2A. The multigenic origin of HSCR and the absence of a "standard" RET mutation associated with HSCR currently make a routine molecular diagnosis impossible.

Intraepithelial lymphocytes in the villous tip: do they indicate potential coeliac disease?

BACKGROUND: The counting of intraepithelial lymphocytes (IELs) in the villous tips of architecturally normal small bowel biopsy specimens was proposed as a method to measure mucosal infiltration in gluten sensitive patients. AIMS: To apply this straightforward method in duodenal biopsy specimens from patients affected by potential coeliac disease (PCD) to verify whether it can discriminate these patients from controls. METHODS: Paraffin wax embedded duodenal sections from 11 patients affected by PCD were stained with an antihuman CD3 antibody. Sections from 19 patients affected by treated coeliac disease (TCD) and 17 patients in whom coeliac disease was excluded were stained with the same antibody to serve as controls. The slides were examined blindly. IELs/20 enterocytes in five randomly chosen villous tips were counted. Patients affected by PCD were all on a gluten containing diet. They had an architecturally normal duodenal mucosa and were positive for endomysial antibody. Both TCD and non-coeliac controls were negative for endomysial antibody. RESULTS: The mean villous tip IEL scores were 4.6 (SD, 1.5; range, 1.4-7.8) in non-coeliac controls, 7.9 (SD, 4.0; range, 2.0-18.6) in TCD, and 9.2 (SD, 4.7; range, 5.8-21.8) in patients with PCD. The difference between PCD and non-coeliac controls was significant. CONCLUSIONS: This is a very simple and sufficiently reliable method to count IELs. In patients with an architecturally normal duodenal mucosa, the IEL count in villous tips helps to distinguish between patients with PCD and non-coeliac controls.

Loss of heterozygosity at 18q21 region in gastric cancer involves a number of cancer-related genes and correlates with stage and histology, but lacks independent prognostic value.

Several studies support a role of 18q21 LOH, involving the DCC locus, in colorectal cancer progression; however, its contribution to the natural history of gastric cancer is less clear. Recently, a number of cancer-related genes have been mapped in the 18q21 region, either centromeric or telomeric to DCC. This study searched for 18q21 LOH in 161 gastric cancers representative of all tumour stages and main histological types. To this purpose, seven highly polymorphic markers were used flanking the 18q21 band and spanning the entire region. Thirty-four out of 147 (23.1%) informative cases showed LOH. In 27 of 34 cases (79%), LOH involved all the informative loci. The remaining seven cases showed LOH at more telomeric sites and retained heterozygosity at more centromeric markers, mostly those proximal to the DCC gene. A strong correlation between 18q21 LOH and level of gastric wall invasion, lymph node metastases, or stage was found in cohesive (glandular+solid) and mixed tumours, but not in diffuse cancers. Cox univariate and multivariate analysis showed that invasion level, lymph node metastases, distant metastases, TNM stage, and histology were effective predictors of survival, whereas 18q21 LOH did not show predictive power. The simultaneous deletion of a variety of cancer-related genes with different and even opposite roles might explain why, apparently, 18q21 LOH does not per se contribute significantly to the natural history of gastric cancer, despite strong correlation with stage.

Small bowel enterocyte apoptosis and proliferation are increased in the elderly.

BACKGROUND: It is known that in the elderly the small bowel does not reveal structural and functional deteriorations in normal conditions, whereas the absorptive function is impaired in stress conditions. OBJECTIVE: The balance between enterocyte apoptosis and proliferation being responsible for the maintenance of tissue size, mucosal morphology and function in the gastrointestinal tract, the aim of our study was to evaluate the rates of enterocyte apoptosis and proliferation in the duodenal mucosa of aged human beings in comparison to adults. METHODS: For this purpose, the terminal deoxynucleotidyl transferase-mediated digoxigenin-deoxyuridine triphosphate nick end labelling (TUNEL) technique and immunohistochemistry for MIB-1 detection were applied on histological sections of endoscopic duodenal biopsy specimens obtained from 12 healthy elderly subjects (mean age 77.6 years; M/F 7/5) and 12 healthy adult subjects (mean age 37.7 years; M/F 8/4). Counts were performed, at a constant magnification (x200), by computer-aided analysis and the results expressed as median percentages of positive enterocytes. RESULTS: The results showed a significant increase in enterocyte apoptosis in the elderly (15.3 vs. 2.1% in the adults, p < 0.001) which was positively correlated (r(s) = 0.65, p < 0.05) with a significant increase in enterocyte proliferation (37.7 vs. 15.8% in the adults, p < 0.0001). CONCLUSIONS: These data suggest that the maintenance of mucosal architecture throughout the process of aging is due to either a hyperproliferative state or an exaggerated apoptosis with a consequent cellular immaturity, which may impair the absorptive function observed in stress conditions.

Nasal paraganglioma. A case report.

Nasal paraganglioma. A case report. Nonchromaffin paragangliomas or chemodectomas arise in paraganglia distributed in various parts of the body. The jugular bulb, the vagal body and the bifurcation of the carotid artery are the most common sites of origin of paraganglioma in the head and neck region. Paragangliomas in the nose and paranasal sinuses are extremely rare and very few cases of definite paraganglioma arising primarily in the nose or paranasal sinuses have been reported. The paraganglioma is a slow-growing tumour that produces nasal obstruction, profuse epistaxis and facial swelling. Complete excision of the glomus tumour is normally curative. We report a case of nasal paraganglioma and discuss the diagnosis and therapy.

Molecular mechanisms involved in the pathogenesis of gastric carcinoma: interactions between genetic alterations, cellular phenotype and cancer histotype.

Gastric cancer develops through the accumulation of multiple genetic lesions that involve oncogenes, tumor suppressor genes and DNA mismatch repair genes. Lauren's classification of gastric carcinoma does not correlate with cellular phenotypes expressed by neoplastic cells and gastric and intestinal cell differentiation markers are widely expressed in both types (intestinal and diffuse) of gastric carcinoma. In contrast, the study of the correlation between morphologic events and genetic alterations, which come about in the cancerogenetic process, seems to indicate the existence of distinct cancerogenetic pathways for the intestinal (or glandular) and diffuse type carcinoma, both originating from a HP-positive gastritis. In particular there seem to be three different profiles of cancerogenesis: 1) p53 mutations which accompany the onset of dysplasia and intestinal-type carcinoma; 2) DNA repair mechanism alterations conditioning microsatellite instability, seem mutually exclusive with regards to p53 mutations. Microsatellite instability correlates with antrally located intestinal-type carcinoma, with little metastatic tendency and a better prognosis; microsatellite instability frequently involves the TGF beta RII, IGF II R genes or the BAX proapoptotic gene, in as much as these contain microsatellite sequences; 3) alterations of E-cadherin, both with regards to mutations and abnormal expression. These lead to junctional and cell polarity loss and are primarily associated with diffuse type carcinoma, which is characterized by poorly cohesive neoplastic cells. Some tumors, initially arising as intestinal-type (glandular structure), acquire a mixed histotype during neoplastic progression, in which both the typical alterations of the intestinal cancerogenesis (p53, microsatellite instability) and those of the diffuse carcinoma (E-cadherin) coexist. The identification of a mixed histotype could have importance both in epidemiologic, pathogenetic and prognostic terms.

Eosinophilic pleural effusion due to mesalamine. Report of a rare occurrence.

Mesalamine-induced lung toxicity has often been described. We report on a case of a patient who underwent mesalamine treatment, though in the absence of established criteria required for diagnosing Crohn's disease (CD) or ulcerative colitis (UC). He developed an adverse respiratory reaction to the drug, thus definitely proving its lung damaging capacity. The clinical presentation included eosinophilic pleural effusion, a feature never previously described in association with mesalamine intake.

Altered intercellular glycoconjugates and dilated intercellular spaces of esophageal epithelium in reflux disease.

BACKGROUND AND AIMS: The usefulness of histological diagnosis of gastroesophageal reflux disease (GERD) is limited by poor specificity or sensitivity of available diagnostic tools. Recently, ultrastructural morphometry showed interstitial space dilation (ISD) to be a reliable sign of reflux disease. Aims of this study were to (a) search for a light microscopy equivalent of ISD, (b) test its diagnostic value, and (c) look for a possible role of intercellular glycoconjugates in its genesis. METHODS: Esophageal grasp biopsies were taken during endoscopy, 2-3 cm and 6-7 cm above the squamocolumnar junction, from patients under investigation for GERD symptoms. The biopsies were fixed in aldehyde solutions and embedded in resin for electron microscopy or in paraffin for routine histology, and the glycoconjugates underwent immunohistochemistry using 3-fucosyl-N-acetylactosamine antibodies. RESULTS: Irregular intercellular space dilation was detected in the basal and prickle layers using both light and electron microscopy. Hematoxylin-eosin preparations showed ISD in 20 of 22 (90%) erosive esophagitis cases, 30 of 44 (68%) endoscopy negative GERD cases, and 1 of 12 (8%) controls, with good interobserver (K = 0.75) and bioptic site reproducibility. ISD correlated with loss or rearrangement of intercellular glycoconjugates of the overlying layers and with granulocyte (eosinophil and/or neutrophil) infiltration. CONCLUSIONS: Light microscopy ISD is a suitable index of GERD. Alterations of intercellular glycoconjugates are likely to have a role in the genesis of ISD and GERD.

[Inflammatory pseudotumor of the lung. Diagnostic-therapeutic effectiveness of its radical resection]. / Pseudotumore infiammatorio del polmone. Utilità diagnostico-terapeutica della resezione radicale.

Clinical, therapeutical observations and experience in 3 cases of pulmonary inflammatory pseudotumors (PIP) are presented. A retrospective analysis is made of cases with pulmonary "mass" suspected as malignant tumor, resected in a general surgery department between 1988 and 1995, and finally diagnosed as inflammatory pseudotumor. Three of the 10 cases originally diagnosed as malignant lung tumor were inflammatory pseudotumor (30%). Pulmonary inflammatory pseudotumors, may be a pitfall diagnosing a lung mass and implicate legal problems. Surgical resection leads to the final diagnosis in doubtful cases. A wide resection has a diagnostic aim and may preserve healthy parenchyma. Clinicians, pathologists and surgeons should accurately inform patients with doubtful diagnosis of pulmonary malignancy. Any decision should be kept altogether either choosing the simple observation or the timely surgical diagnostic and therapeutical approach.

Early onset of gastric carcinoma and constitutional deletion of 18p.

We report on the association of a gastric carcinoma and a constitutional deletion of the short arm of chromosome 18 in a 14-year-old patient. The phenotype of the patient, including microcephaly, ptosis, micrognathia, tetralogy of Fallot, and mental retardation, fits well with previously reported cases of del(18p); she also showed a positive serology against Helicobacter pylori. The comparison of the alleles of polymorphic loci located on the short arm of chromosome 18 between the patient and her parents showed a maternal origin of the abnormal chromosome. Loss of heterozygosity (LOH) for loci located in the long arm of chromosome 18 is a frequent event in gastric carcinomas; it was observed in the tumoral mass of our patient and again, the alleles lost were of maternal origin. We postulate that the constitutional chromosomal abnormality may have favored the loss of the abnormal chromosome in some cells and that the loss of the deleted chromosome 18 (demonstrated by LOH for this chromosome in the tumoral mass) has been an early step in the pathogenesis of the gastric carcinoma of our patient with Helicobacter pylori infection acting as a cofactor.

Genetic pattern, histological structure, and cellular phenotype in early and advanced gastric cancers: evidence for structure-related genetic subsets and for loss of glandular structure during progression of some tumors.

Gastric cancer shows remarkable heterogeneity in histological pattern, cellular phenotype, and genotype. Tumor subsets identified by varying procedures have shown limited reciprocal correlation and have failed to provide a sound rationale for the characterization and classification of all tumors. Based on a case series of 130 gastric cancers that covered both early (70 cases) and advanced (60 cases) stages and that represented most histological types and structural patterns, this study investigated (1) microsatellite instability and p53 gene mutation by means of PCR-based molecular techniques and (2) p53 protein accumulation or tumor cell immunophenotype by means of immunoperoxidase procedures. It was found that microsatellite instability and p53 gene mutation involve two distinct subsets of both early and advanced-stage glandular (intestinal) cancer, and that, contrastingly, they leave purely diffuse cancers unaffected. Mixed cancers, namely, those in which glandular admixed with diffuse growths, showed scarce microsatellite instability at all stages, whereas prominent p53 gene mutation and p53 protein accumulation was limited to the advanced stage alone. No significant correlation was found between tumor cell immunophenotype and either genotype or histotype, although some correlation with particular structural patterns was detected. Comparison of intramucosal with invasive growths within any given tumor suggested that invasive cancers with diffuse-type growth arise in part from mucosal cancers of glandular or mixed structure through progressive loss of intercellular junctional systems. It is concluded that at least two genetically distinct subsets of glandular cancer, one with microsatellite instability and the other with p53 lesions, should be separated both from purely diffuse cancer and, at least in the advanced stage, from mixed cancer. Available evidence suggests distinct clinicopathologic profiles for such tumor entities.

Analysis of gastroduodenitis and oesophagitis in relation to dyspeptic/reflux symptoms.

BACKGROUND/AIMS: The pathogenesis of dyspeptic/reflux symptoms and the clinico-pathologic profile of affected patients are still poorly understood. To improve our knowledge in this field we carried out a systematic, comparative analysis of symptom profiles and histopathologic patterns of oesophagogastroduodenal mucosa in a series of 221 subjects, 140 with and 81 without endoscopic evidence of hiatal hernia. Of these, 190 showed reflux and/or dyspeptic symptoms. METHODS: Before endoscopy, all the subjects were questioned about the presence and severity of 12 individual symptoms. Biopsies were taken from the distal oesophagus, cardia, corpus, angulus, antrum and duodenal bulb, and were scored in accordance with the Sydney system. RESULTS: Patient groups with a distinct clinico-pathologic profile were better identified when symptoms of adequate severity were compared with histopathologic parameters. A correlation between gastroesophageal reflux disease (GORD) symptoms and histologic signs of oesophagitis was mostly restricted to patients endoscopically positive for oesophagitis. Retroxiphoid pyrosis correlated with cardial gastritis but not with oesophagitis, either endoscopic or histologic, while ulcer-like epigastric pain correlated with active duodenitis and distal gastritis. No definite histopathologic background was detected in patients with putative dysmotility-like symptoms, endoscopy-negative GORD and low score or mixed symptoms. CONCLUSION: A contribution of Helicobacter pylori gastroduodenitis to the pathogenesis of some dyspeptic symptoms seems likely. However, the identification of specific histologic changes causing individual symptoms remains rather elusive, with the exception of active antroduodenitis in patients with ulcer-like pain and of active proximal gastritis in patients with severe retroxiphoid pyrosis.

Natural history, clinicopathologic classification and prognosis of gastric ECL cell tumors.

A series of 50 gastric endocrine tumors classified according to Rindi et al. [1] comprised 12 small cell neuroendocrine carcinomas (NEC) and 38 ECL cell carcinoids, of which 22 associated with type A chronic atrophic gastritis (A-CAG), eight with hypertrophic gastropathy due to combined Multiple Endocrine Neoplasia and Zollinger/Ellison syndrome (MEN/ZES), and eight sporadic. Variables found to predict tumor malignancy were: size > 2 cm, > 2 mitoses and > 130 Ki67 positive cells/10 high power fields (HPF), grade 2 or 3 histology, angioinvasion, p53 protein nuclear accumulation, and the presence of a single tumor. None of these factors increased significantly the predicting ability of tumor classification itself, although grade 2 + 3 shows 100 percent negative predictive value and Ki67 and angioinvasion 100 percent positive predictive value. When the mostly non-malignant A-CAG and MEN-ZES tumors were analysed against the mostly malignant sporadic and NEC tumors, a positive predictive value of 90 percent and a negative predictive value of 93 percent was obtained. Investigation of a larger tumor series is under way with the aim to develop an optimal model for prognostic evaluation of gastric endocrine tumors.

Microsatellite instability in intestinal- and diffuse-type gastric carcinoma.

To investigate the role of genetic instability in the development of intestinal- and diffuse-type gastric cancers, six microsatellite loci were analysed in 98 carcinomas of the two main histotypes, at both early and advanced stages of progression, and in five preneoplastic lesions. RER+ phenotype frequency proved to be significantly higher (P = 0.013) in intestinal (23 per cent) than in diffuse cancers (5 per cent) and slightly higher in advanced (19 per cent) than in early (12 per cent) tumours. When comparing early and advanced tumours of the same histotype, a similar frequency was found for diffuse tumours (4 per cent vs. 6 per cent), and an increase from 19 to 30 per cent for intestinal cancers. Instability at more than one locus was limited to intestinal tumours and replication errors were also detected in an intestinal dysplasia. On the whole, these data suggest that genetic instability has an important and early role in gastric carcinogenesis of the intestinal type and a less important role in gastric carcinogenesis of the diffuse type. Most tumours of this panel had previously been characterized for p53 gene mutations. p53 screening was extended to all samples, to investigate the possible association between gene mutations and microsatellite instability. Analysis showed a trend (P = 0.07, Fisher's exact test) towards a negative association between these two genetic lesions in tumours of the intestinal type.

Omeprazole for severe reflux esophagitis in children.

BACKGROUND: Severe esophagitis is a rare complication of gastroesophageal reflux in children. In adults, omeprazole therapy of severe erosive esophagitis has become the gold standard short-term treatment of the disease. In children, data on its use are limited, and problems about the dosage are unresolved. The aim of this study was to evaluate the efficacy of a simplified, body-weight-based daily dosage of omeprazole in children with severe esophagitis. METHODS: Ten children (median age 75.6 months; range 25-109 months) with severe esophagitis were prospectively investigated. All patients were evaluated by endoscopy, histology, and 24-h pH-metry study before and after 3 months of omeprazole. The starting dose of omeprazole was 20 mg as a single daily dose in children weighing less than 30 kg, and 40 mg daily for those weighing over 30 kg. RESULTS: A significant improvement in all the children was demonstrated after 3 months of treatment by clinical, endoscopic, and pH-metry assessment. However, histologic study failed to show significant improvement of both inflammatory and hyperplastic findings. Relapse occurred in six of 10 patients after discontinuation of therapy. CONCLUSIONS: Omeprazole is effective in the short-term treatment of severe oesophagitis in children. The daily dose of the drug could be easily based on the body weight. The persistence of histologic features of esophagitis in spite of clinical and endoscopic healing could be an indicator of poor outcome.

Omeprazole coupled with two antibiotics for Helicobacter pylori eradication and prevention of ulcer recurrence.

BACKGROUND: Numerous therapeutic trials aimed at eradicating Helicobacter pylori (HP) from the gastric mucosa and preventing ulcer recurrence have been carried out; however, an optimal treatment has not yet been established with carefully controlled randomized studies. OBJECTIVE: The aim of our study was to evaluate the efficacy of an association of omeprazole (OM) coupled with two antibiotics in the eradication of HP and prevention of duodenal ulcer (DU) recurrence. METHODS: One hundred and eighty three patients with active DU were randomized under double-blind conditions to receive either OM 20 mg for 4 wk plus amoxycillin 3 g daily and metronidazole 1 g daily during the 2nd and 3rd wk (91 patients, group A) or OM 20 mg for 4 wk plus matching placebo (92 patients, group B). Endoscopy was performed before and at the end of the 4-wk treatment as well as 2, 6, and 12 months later. Biopsies were taken from the duodenum, antrum, and gastric body at each endoscopic examination for HP histological detection and for evaluation of inflammatory changes according to the Sydney system. RESULTS: After 4 wk, 84/86 patients (98%) of group A and 80/86 (93%) of group B were healed of their ulcers. The percentage of eradication was 90% in group A and 1% in group B. During a 12-month follow-up, DU relapsed in 4/63 (6%, including two of three reinfected cases) HP-eradicated group A patients, 4/8 (50%) HP-noneradicated group A patients, and 52/65 (80%) persistently HP-positive group B patients. Rapid, complete, and persistent suppression of gastroduodenitis activity and gastric surface epithelium lesions was observed in most HP-eradicated group A patients, whereas a transient decrease of bacterial colonization and inflammatory scores in the antrum and a transient worsening of corpus gastritis were found in group B patients. CONCLUSIONS: The combined therapy with amoxycillin, metronidazole, and omeprazole is highly effective in both HP eradication and prevention of duodenal ulcer recurrence.