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.

Intestinal bacterial overgrowth during chronic pancreatitis.

INTRODUCTION: The presence of an intestinal bacterial overgrowth (IBO) in patients with pancreatic insufficiency has been recently suggested to justify the worsening of their clinical conditions despite pancreatic enzyme supplementation. AIM: The purposes of this study were (a) to verify IBO frequency in patients with pancreatic insufficiency owing to chronic pancreatitis and (b) to evaluate the effect of chronic administration of a non-absorbable antibiotic, Rifaximin, in reducing IBO frequency and influencing the clinical picture of the disease. MATERIAL AND METHODS: Thirty-five patients with pancreatic insufficiency owing to chronic pancreatitis and 61 gastro-resected patients without pancreatic disease were studied. The presence of IBO was tested in both groups of patients using the hydrogen breath test with glucose. Chronic pancreatitis patients were subsequently treated with Rifaximin, 400 mg t.i.d for seven consecutive days each month for three months. RESULTS: A positive hydrogen breath test was present in 12 out of 35 (34%) chronic pancreatitis patients and in 13 out 61 (21%) controls (p < 0.002). In chronic pancreatitis patients an IBO was most likely to be present in the presence of a high ethanol intake, pancreatic microcalcifications, concomitant gallstones, diarrhoea and a history of gastric resection. In all patients with IBO, Rifaximin administration normalised the hydrogen breath test and reduced symptoms. CONCLUSIONS: IBO is frequent in patients with pancreatic insufficiency, particularly in those with a history of gastroduodenal surgery. Treatment with Rifaximin reduces IBO frequency and improves symptoms.

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.

[Efficacy of low dose mesalazine (5-ASA) in the treatment of acute inflammation and prevention of complications in patients with symptomatic diverticular disease. Preliminary results]. / Efficacia della mesalazina (5-ASA) a basse dosi nel trattamento della flogosi acuta e nella prevenzione delle complicanze in pazienti con malattia diverticolare sintomatica. Risultati preliminari.

MATERIALS AND METHODS: To assess the efficacy of mesalazine in treating acute diverticulitis and preventing diverticular disease (DD) complication. 166 patients with symptomatic DD were randomly assigned to receive mesalazine Pentacol (400 mg b.i.d., orally; M group) or no additional treatment (controls; C group). RESULTS: After a 12 months follow-up, 26 patients experienced a symptomatic relapse (8%M vs 27% C, p=0.003), with a higher rate in C group for the patients with a history of previous diverticulitis (p=0.006) and independently of the diverticular site (sigmoid p=0.041; colon and sigmoid p=0.044). Minor diverticular haemorrhages were less frequent in M group (p=0.016), with a significant difference only for the patients with sigmoid diverticula (p=0.023); abdominal pain persisted for a shorter time in the treated group (p=0.0015). CONCLUSIONS: No significant difference was found between the two groups for the incidence of DD major complications.

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.

Distinct profiles of gastritis in dyspepsia subgroups. Their different clinical responses to gastritis healing after Helicobacter pylori eradication.

BACKGROUND: A contribution of Helicobacter pylori gastritis to the pathogenesis of non-ulcer dyspepsia (NUD) remains uncertain. METHODS: Administration of an appropriate clinical questionnaire followed by endoscopy allowed us to select, among 139 outpatients with dyspepsia, 87 non-ulcer dyspepsia patients with more severe and group-distinctive symptoms, 35 of whom were classified as having ulcer-like (ULD). 38 as dysmotility-like (DLD), and 14 as reflux-like dyspepsia (RLD). Biopsy specimens were evaluated for H. pylori gastritis in accordance with the Sydney system. The 70 H. pylori-positive cases were treated with omeprazole, 20 mg twice daily, and amoxycillin, 1 g three times daily for 2 weeks. RESULTS: Higher rates of H. pylori colonization were found histologically in the gastric mucosa of ULD (91%) and RLD (86%) than in that of DLD (68%) or asymptomatic (42%) patients. ULD differed from RLD patients in their higher score of antritis activity. Three and 6 months after H. pylori eradication ULD (but not DLD) showed significant regression of dypspetic symptoms scores. CONCLUSIONS: It seems likely that H. pylori gastritis, with special reference to active antritis, is among causative factors of ULD. Its role in the pathogenesis of RLD and DLD needs further investigation.

Effects of eradication of Helicobacter pylori on gastritis in duodenal ulcer patients.

The incidence and mean score of Helicobacter pylori-related, active antroduodenitis, lesions of superficial antral epithelium and duodenal gastric-type metaplasia were higher in endoscopic biopsies from a large series of patients with duodenal ulcer, when compared with asymptomatic patients or patients with non-ulcer dyspepsia. In 65 out of 73 patients with duodenal ulcer who could be followed up, H. pylori was eradicated using a combination of amoxycillin, 3 g daily, metronidazole, 1 g daily, and omeprazole, 20 mg daily. Rapid and permanent (6-month follow-up) abolition of both gastroduodenitis activity and lesions of the gastric surface epithelium was observed in these 65 patients. There was also a progressive decrease in total immune-inflammatory cells but without a substantial change in duodenal gastric-type metaplasia. Similar, but transient and quantitatively less prominent, improvements were observed in the antroduodenal mucosa, which had been temporarily cleared of H. pylori by treatment with omeprazole alone. Conversely, increased gastritis activity, epithelial lesions and immune-inflammatory cell scores were found in the short term in the corpus mucosa, which was not cleared of H. pylori after omeprazole treatment. It is concluded that, of the various H. pylori-related mucosal changes, antroduodenitis activity and antral epithelial lesions most closely reflect the severity of mucosal damage and are probably the most important factors in duodenal ulcerogenesis. Their complete and rapid suppression after bacterial eradication may be a key factor in preventing ulcer relapse.

Radioimmuno-guided endoscopy (RIGE) in the detection of primary and recurrent rectal tumor.

The usefulness of radioimmunoguided endoscopy in the detection of primary and recurrent rectal cancer was investigated. Of the 15 patients included in our study, 4 with suspected primary rectal cancer were examined preoperatively, while the remaining 11 were studied after radical resection of rectal carcinoma with the aim of detecting local recurrence. Radioimmunoguided endoscopy was performed employing a hand-held gamma-detecting probe (mod. 2 Oris, France), after the administration of a 111In labeled monoclonal antibody to CEA. Radioimmuno-guided endoscopy results detected the presence of primary or recurrent periluminal cancer in seven cases. In four it modified the preoperative stage based on the findings of conventional investigation and it influenced the surgical decision in five cases. No toxicity was noted and none of the patients developed HAMAs.

[Helicobacter pylori and gastro-duodenal pathology]. / Helicobacter pylori e patologia gastro-duodenale.

Helicobacter Pylori (HP) were found in 878 (73%) of 1205 patients undergoing upper G-I endoscopy with multiple biopsies for gastroduodenal diseases. HP were present in similar percentages among patients with active (89%) or healed (81%) peptic ulcer as well as in non ulcerous dyspeptics affected with gastritis (85%). 96% of active chronic gastritis were infected by HP as compared with 55% of quiescent gastritis. Antral gastritis was more frequently active in patients with ulcer diseases (76%) than in dyspeptic and asyntomatic patients (50%). Healed gastric and duodenal ulcers showed decreased incidence of active antral gastritis (69) as compared with active ulcers. Conversely body gastritis was more frequently active in healed (37%) than in overt (18%) duodenal ulcers. 95 histologically normal stomachs as well as 9 cases exhibiting type A gastritis were devoid of HP. High rates of infection were found in 610 cases of chronic gastritis without atrophy as well as in 151 atrophic antral (type B) gastritis. Cytoplasmic vacuolization and swelling of foveolar-superficial cells with adhering bacteria, micropapillae and microerosions were commonly found in HP-infected mucosa. In 16 of 19 children with type B chronic gastritis antibacterial therapy eradicated HP. This was followed by resolution or striking improvement of gastritis and disappearance of epithelial lesions.

Morphological evidence of Campylobacter pylori pathogenicity in chronic gastritis and peptic ulcer.

Campylobacter pylori (CP) were found in 84% of 384 patients with chronic gastritis and in none of 49 subjects without inflammation. CP were present in similar percentages among patients with active (90%) or healed peptic ulcer (84%), as well as in non-ulcerous dyspepsia complicated by gastritis (91%). Cytoplasmic vacuolization and swelling of foveolar-superficial cells with adhering bacteria, micropapillae and microerosions were commonly found in CP-infected mucosa. In 100 cases with gastritis both intraepithelial granulocytes and epithelial lesions were prominent features of heavily CP-infected antral mucosa. The occurrence of some cases with abundant, adhering CP but lacking epithelial lesions is in keeping with the different ability of various CP-strains to produce cytotoxins. In 16 of 19 children with type B chronic gastritis antibacterial therapy eradicated CP. This was followed by resolution or striking improvement of gastritis and disappearance of epithelial lesions. These data provide further morphological evidence of direct cytotoxic activity of CP toward gastric mucosal cells.