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AIM: Some endoscopic features of duodenal mucosa are marker of mucosal injury, the most common cause being celiac disease (CD). The aim of this study was to prospectively assess the diagnostic value of the endoscopic markers for the diagnosis of CD in the adult population undergoing routine upper endoscopy. METHODS: This was a prospective multicenter study conducted at 37 Italian endoscopic centers. A total of 509 consecutive patients submitted to routine upper endoscopy who presented one or more of following endoscopic markers were included: 1) mucosal mosaic pattern in the bulb and/or descending duodenum (DD); 2) nodularity in the bulb and/or DD; 3) scalloping of Kerkring's folds; 4) reduction in the number or absence of folds in the DD. 4 biopsies samples were taken from descending duodenum. In patients with histological findings consistent with CD, according to Oberhuber classification, sierologic test (EMA, tTGA) were performed for confirm the diagnosis. RESULTS: At endoscopy, 249 patients showed an isolated marker; 260 subjects showed a coexistence of more than one marker; 369 patients (72.5%) presented mucosal lesions at histological examination and in 347 of these patients the diagnosis of CD was confirmed by serologic markers (94.0%). For 10 patients the diagnosis remained uncertain because of negative sierology and exclusion of other other cause of mucosal lesions. The diagnosis of CD was made in 61.3% patients who showed the mosaic pattern, in 65.7% of patients with nodular mucosa, in 64.4% of patients with scalloping of folds, in 40.2% of patients with reduction of folds, and in 61.5% of patients with loss of folds and in 83.6% of patients who showed the coexistence of more than one marker. The endoscopic markers overall had a PPV of 68% for the diagnosis of CD; the markers that singularly have demonstrated a higher correlation with CD are: mosaic mucosa of DD (PPV 65.0%), nodular mucosa of the bulb and DD (PPV 75.5%), and scalloping of folds (PPV 64.4%). CONCLUSION: The study confirms the important role of endoscopy in the diagnostic process of CD not only for the bioptic sampling in patients with clinical suspicion of CD, but especially for the opportunity to evaluate alterations of the duodenal mucosa suggestive of CD in the general population and, consequently, to identify those patients who should undergo a duodenal biopsy.

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BACKGROUND: Incidence of adenocarcinoma of distal oesophagus and gastric cardia, probably arising from areas of intestinal metaplasia, has been increasing rapidly. AIMS: To define prevalence of intestinal metaplasia of distal oesophagus, oesophagogastric junction and gastric cardia and to evaluate potential associated factors, by means of a prospective multicentre study including University and teaching hospitals, and primary and tertiary care centres. PATIENTS: Each of 24 institutions involved in study enrolled 10 consecutive patients undergoing first-time routine endoscopy for dyspeptic symptoms. METHODS: Patients answered symptom questionnaires and underwent gastroscopy Three biopsies were taken from distal oesophagus, oesophago-gastric junction and gastric cardia, and were stained with haematoxylin and eosin. Specimens were also evaluated for Helicobacter pylori infection. RESULTS: A total of 240 patients (124 male, 116 female; median age 56 years, range 20-90) were enrolled in study. Intestinal metaplasia affected distal oesophagus in 5, oesophago-gastric junction in 19 and gastric cardia in 10 patients. Low-grade dysplasia was found at distal oesophagus and/or oesophago-gastric junction of 3/24 patients with intestinal metaplasia vs 2/216 without intestinal metaplasia (p<0.05). A significant association was found between symptoms and presence of intestinal metaplasia, regardless of location, and between Helicobacter pylori infection and intestinal metaplasia at oesophago-gastric junction. CONCLUSIONS: Intestinal metaplasia of distal oesophagus, oesophagogastric-junction and gastric cardia is found in a significant proportion of symptomatic patients undergoing gastroscopy and is associated with dysplasia in many cases. Although prevalence of dysplasia seems to decrease when specialized columnar epithelium is found in short segment, or even focally in oesophago-gastric junction, these small foci of intestinal metaplastic cells may represent source of most adenocarcinomas of cardia.

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OBJECTIVES: Azithromycin, a new antibiotic chemically related to erythromycin, has been proposed for the cure of Helicobacter pylori, achieving high gastric tissue levels (above the MIC for H. pylori) after oral administration. The aim of the study was to establish whether azithromycin plus metronidazole in association with either omeprazole or bismuth subcitrate is useful in curing H. pylori infection of the stomach. PATIENTS AND METHODS: The study involved 132 dispeptic patients who proved to be H. pylori infected by antral and corpus histology (Giemsa, modified) and rapid urease test (CLOtest); the Sydney system was used to classify the gastritis. Sixty-three patients received bismuth subcitrate 120 mg q.i.d. for 14 days plus azithromycin 500 mg o.d. for the first 3 days plus metronidazole 250 mg q.i.d. for the first 7 days; 69 patients received omeprazole 40 mg for 14 days plus azithromycin 500 mg o.d. for the first 3 days plus metronidazole 250 mg q.i.d. for the first 7 days. Patients were well matched for common clinical variables. Cure of H. pylori infection was assessed by the same methods 2 months after completion of treatment. RESULTS: Eleven patients dropped out of the study, only one reporting side effects (nausea, vomiting, and epigastric pain). Cumulative "per protocol" cure rate was 66.1% (CI 95%, 58.5-75.3%). There was no statistically significant difference between the two treatment groups: 58.9% (CI 95% 48.4-74.6%) versus 72.3% (CI 95%, 60.7-82.5%). Intention to treat does not substantially modify results. Few side effects were recorded. Cured patients showed a significant reduction in the activity of gastritis. CONCLUSION: Azithromycin, combined with omeprazole and metronidazole, the cure rate of H. pylori was about 70%. The cure of H. pylori infection improves the activity of gastritis.

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BACKGROUND: Common etiopathogenic factors may explain the association of systemic sarcoidosis with inflammatory bowel disease. METHODS: We report two cases of such an association: one of sarcoidosis that developed 2 years after proctocolectomy for ulcerative colitis and one of sarcoidosis and Crohn's colitis. Factors like increased cellular immunity or circulating immunocomplexes or autoantibodies may have a role. Exogenous agents or familiarity may also be involved. CONCLUSIONS: It is postulated that the association between sarcoidosis and inflammatory bowel disease (both ulcerative colitis and Crohn's disease) does not occur by chance alone and that the two conditions may share some genetic or immunologic alterations. The two diseases, however, follow an independent clinical course.

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Several studies have shown that cigarette smoking affects duodenal ulcer (DU) recurrence. To verify any correlation between smoking and complications of ulcer disease, we studied 33 DU smokers, 16 DU ex-smokers and 87 DU non-smokers for up to 48 months, recording age, sex, family history of ulcer, ulcer symptoms, non-steroidal anti-inflammatory drug use, length of DU history, alcohol consumption, smoking habit, relapses and bleeding episodes. Nicotine contents were also obtained for the type of cigarettes smoked. Statistics used were: Analysis of variance with Bonferroni's test. Pearson's chi-squared test and stepwise logistic regression analysis. Smokers were found to have significantly more relapses but fewer bleeding episodes than ex-smokers and non-smokers (63.3%, 31.2% and 34.5%, p = 0.029; 12.1%, 43.7% and 34.5%, p = 0.017). Bleeders were significantly more often males than non-bleeders (82.9% vs. 61.0%, p = 0.01) and had ulcer symptoms less frequently (9.7% vs. 26.3%, p = 0.02). Multivariate analysis confirmed sex as a risk factor (OR = 3.0) and smoking as a "protective" factor (OR = 0.4) for bleeding, while nicotine intake was found to be unrelated to this complication. We concluded that smoking (but not nicotine intake) and male sex are factors to take into account in evaluating the risk of DU bleeding.

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A modification of Berstad's spectrophotometric method was tested and proved capable of detecting pepsin concentrations in mucosal perendoscopic biopsy homogenates. The relationship between this parameter and pepsin in gastric juice and pepsinogen group I in serum and in biopsy homogenates was analyzed. From the biochemical point of view, the assay was found sufficiently accurate. Mucosal pepsinogen group I, but not mucosal pepsin, concentration was found higher in gastric and duodenal ulcer patients than in controls. Patients with corpus-fundic gastric ulcer showed significantly lower mucosal pepsin and mucosal pepsinogen group (PG) I. Aging and smoking did not influence either parameter but male duodenal ulcer subjects presented higher mucosal pepsinogen group I concentration. The lack of any relationship between serum and mucosal PG I and between pepsin in gastric juice and in mucosa raises a question, at least in methodological terms, about the validity of using serum pepsinogen group I and pepsin as indicators of peptic output.

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Gastric bicarbonate secretion has been evaluated by Feldman's method in 48 duodenal-ulcer patients. The relationship between smoking, clinical ulcer outcome (healing and recurrence) and bicarbonate secretion has been analysed. Heavy smokers secreted higher bicarbonate ions than did non-smokers. High-relapsing patients produced lower bicarbonate output. These preliminary data suggest that an impaired gastric bicarbonate secretion is associated with smoking, a well-known ulcer-associated factor; further-more, it may single out high-relapsing duodenal ulcer patients.

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UNLABELLED: Aim of the present study has been to investigate the possible modifications of peptic secretion after a period with H2 blockers and omeprazole, evaluating in the same patient pepsinogen group A levels in gastric mucosa and pepsin in gastric juice. 54 active duodenal ulcer were studied: during an upper gastrointestinal endoscopy a sample of gastric juice and one fundus biopsy were taken before and after four weeks 300 mg/daily ranitidine (23 patients), 40 mg/daily famotidine (7 patients), 300 mg/daily nizatidine (12 patients) therapy and 40 mg/daily omeprazole (12 patients) therapy. RESULTS: H2-blockers and omeprazole treatment determines a non statistically significant decrease of pepsin in gastric juice and in pepsinogen group A in gastric mucosa.

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UNLABELLED: A substantial number of duodenal ulcer (DU) patients relapse despite maintenance treatment with antisecretory drugs. The influence of certain risk factors and the heterogeneity of the disease could explain such behavior. The present prospective, open study compares the one-year clinical outcome (with upper GI endoscopy at the beginning of the study, at 6 and 12 months, and at every symptomatic relapse) of four groups of DU subjects, consecutively recruited from December 1987 to December 1988, separated in accordance with whether or not a bleeding DU episode had previously occurred, and whether or not an evaluation of gastric acid secretion had been made. Thus, Group I (17 patients; 12 males, 5 females) included heavy smokers and/or gastric acid hypersecretors; Group II (13 patients; 12 males, 1 female) non- or light smokers non-hypersecretors; Group III (34 patients; 22 males, 12 females) subjects with unknown gastric acid secretion; Group IV (33 patients; 30 males, 3 females) previously bleeding DU patients. All patients, except those in Group II (who were left untreated), were given ranitidine 150 mg at bedtime. The outcome of Groups I+II was compared with that of Group III (considered as "standard therapy") and Group IV patients, the latter presumably with a low risk of relapse because of the low prevalence of smokers. STATISTICS: Chi-square test, Fisher's exact test, analysis of variance and the logrank test. During the year of follow-up, 27/97 patients withdrew from the study, while 18 had a DU relapse (remission rates 82.1% +/- 7.4% in Groups I+II, 70.5% +/- 8.4% in Group III, 87.5% +/- 5.9% in Group IV).(ABSTRACT TRUNCATED AT 250 WORDS)

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The clinical course of gastric and duodenal ulcer and the efficacy of H2 blockers in ulcer healing and the prevention of relapse in cirrhotic liver patients were studied. Seventy-four cirrhotic patients with endoscopically proven acute gastric ulcer (30), duodenal ulcer (34) or a combination of both gastric and duodenal ulcers (10) were treated for six weeks with either Cimetidine 800 mg/daily (27) or Ranitidine 300 mg/daily (47). Of the 77 patients 49 (66.2%) were healed after therapy, 11 cases (14.8%) remained unhealed even after two additional cycles of the same treatment and four were lost to follow-up. After an endoscopically proven healing of the active ulcer, 51 patients took part in the long-term study over a mean period of 24 months: 21.5% of the 27 patients were treated with a maintenance dosage of H2 blockers and 29.1% of the 24 patients left without therapy relapsed during the first year. We conclude that the ulcer healing rate with H2 blockers is lower and the relapse rate higher in cirrhotic patients than in the general ulcer population.

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Mucosal blood flow performs an extremely important role in microcirculation wherein alterations necessarily lead to severe gastric and duodenal mucosal lesions. The removal of back-diffused H+ ions through the adaptation of microcirculatory flow represents a valid defence mechanism. The blood flow's inability to contain H+ back-diffusion lies at the bottom of rapid-onset acute mucosal lesions; moreover, it probably contributes to the onset of chronic ulcer in certain areas already precariously supplied, because of the breakdown of the mucosal barrier or a further reduction in blood supply. Portal hypertension leads to altered blood flow in the gastric microcirculation. This haemo-dynamic condition brings about a series of endoscopically evident changes which are probably a consequence of the conspicuous increase in mucosal and submucosal vascular area. This haemodynamic situation may be an aetiopatho-genetic factor in the cirrhotic subject's marked sensitivity to gastric mucosal damage.

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The effects of Nizatidine, an H2-receptor antagonist, and Misoprostol, a PGE1 analogue, on gastric pH, pepsin, pepsinogen group I and N-acetylneuraminic acid concentration were evaluated in a group of 20 patients with duodenal ulcer. Nizatidine decreased pepsin concentration while it increased gastric pH, although not to a significant degree and left pepsinogen group I and N-acetylneuraminic acid concentration unchanged. Misoprostol did not modify gastric pH, pepsin and N-acetylneuraminic acid values but it increased pepsinogen group I levels. These data support the view that H2-receptor antagonists, especially Nizatidine, and Misoprostol do not directly affect pepsin and/or N-acetylneuraminic acid concentration.

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The histamine H2-receptor antagonists, cimetidine, ranitidine, famotidine and nizatidine are effective in promoting the healing of both gastric and duodenal ulcer. Unfortunately the recurrence rate after withdrawal of the therapy does not appear modified and many studies indicate an increased rate of relapse after antisecretory treatment. The difference between various H2-blockers in terms of duration of acid inhibition and then increasing in gastrin levels may play a role in explaining the phenomenon, the exception represented by the last H2-blocker, nizatidine. It is reasonable, therefore, to analyze the different therapeutical approaches proposed for ulcer relapse prevention, such as continuous maintenance therapy, seasonal on demand, intermittent, week-end therapy, association of drugs with different mechanisms of action, etc. Four categories of patients can be characterized both for gastric and duodenal localization: 1. Subjects with low rate of relapses, i.e. less than one each fifteen months; 2. Subjects with episodic relapses, i.e.; one or two per year; 3. Subjects with frequent relapses, i.e. more than three per year; 4. Subjects with complications (bleeding, perforation).

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UNLABELLED: The aim of this study was to evaluate the clinical efficacy of short and long-term treatment with famotidine 40 mg/daily at bed time in duodenal ulcer disease. 45 patients with endoscopically proven active duodenal ulcer undertaken the study. Endoscopic evaluations were performed at 6 weeks, 3 and 6 months from the start of the study. The following parameters were evaluated: pepsinogen group I and gastrin levels in serum, pH, acid and neutral glycoprotein, N-acetylneuraminic acid, pepsin in gastric juice collected during the upper gastrointestinal endoscopy. 6 weeks healing rate was 91.1%. After the third month of follow-up 14.2% of the patients presented an endoscopical proven episode of relapse. No relapses were observed at the end of the study (after 6 months of treatment). Acid glycoprotein, N- acetylneuraminic acid and pepsin concentrations significantly decreased after 6 weeks of treatment (p less than 0.0125, p less than 0.025, p less than 0.005 respectively), while serum levels of pepsinogen group I, gastrin and gastric pH increased (p less than 0.0005, p less than 0.005, p less than 0.025). After 6 months period of therapy, a significant increase of neutral glycoproteins (p less than 0.01) and a decrease of pepsin (p less than 0.005) and acid glycoproteins (p less than 0.01) was observed. On the contrary, gastric N- acetylneuraminic acid, pH, serum gastrin and pepsinogen group I presented the pre-trial values. IN CONCLUSION: 1) famotidine appears to be an effective and safe therapy for duodenal ulcer treatment; 2) it seems to act not only by inhibiting gastric acid secretion but also influencing some parameters related to the gastric mucosal barrier.

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