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Background The management of bloating is unclear and its relationship with patients' well-being and treatment satisfaction independent of other abdominal symptoms is uncharacterized. We evaluated the association of bloating with patient-reported outcomes. Methods Thirty-nine centers for functional gastrointestinal disorders joined the laxative inadequate relief survey. We enrolled 2203 consecutive outpatients with functional constipation (FC) or constipation-predominant irritable bowel syndrome (IBS-C) in two cross-sectional waves. Both wave 1 and 2 included the SF-12, the patient assessment of constipation-symptoms (PAC-SYM), and the treatment satisfaction questionnaire for medication (TSQM-2). Wave 2 only included a global rating of change (GRC) scale to assess patients' assessment of efficacy concerning treatment switches occurred in the 3 months prior to the interview. Bloating in the abdomen was defined on the basis of PAC-SYM item 3. Key Results The average age was 50.1 years (SD, 16.7) and 82.1% of patients were women. The prevalence of bloating was 91.6% (n = 1970). Bloating was associated with SF-12 Physical Composite Score (p < 0.01), SF-12 Mental Composite Score (p < 0.01), GRC (p < 0.01), Satisfaction with treatment effectiveness (p < 0.01), convenience of administration (p < 0.01), and side effects (p < 0.01) after adjustment for possible confounders. Conclusions & Inferences Our data suggest that patients regard bloating as a key element in assessing clinical changes and treatments' efficacy as this symptom exerts a strong influence on patient-reported outcomes independent of possible confounders and other symptoms of constipation. Our data provide the rationale to investigate the efficacy and tolerability of new treatments specifically addressing this important, yet disregarded, patients' complain.

Background and aim: PAC-SYM is widely adopted to asses constipation severity. However, it has been validated in a small sample, few items have been included based on expert opinion and not on empirical grounds, and its factor structure has never been replicated. We aimed at evaluating the psychometric properties of PAC-SYM in patients with chronic constipation. Methods: We enrolled 2,203 outpatients with chronic constipation in two waves. We used wave I sample to test the psychometric properties of the PAC-SYM and wave II sample to cross-validate its factor structure, to assess criterion validity, responsiveness to clinical change, and its minimal clinically important difference. Results: Only a minority of patients reported any rectal tearing (38 %). Deletion of such item leads to a 11-item version (M:PAC-SYM). The remaining items in the rectal domain were moderately correlated with the stool domain. Exploratory factor analysis and confirmatory factor analysis revealed a bifactor structure with two subscales (stool and abdominal symptoms) and a general severity factor. The M:PAC-SYM demonstrated excellent reliability, moderate correlation with SF-12 and treatment satisfaction (r = 0.28–0.45), discrimination across Rome III criteria for functional constipation and abdominal pain, and responsiveness to clinical change (β = −0.49; ω 2 = 0.25). M:PAC-SYM minimal clinically important difference was 0.24. Conclusion: Our analysis shows that the rectal domain may not represent a relevant cluster of symptoms for patients with chronic constipation. We developed a modified version of the PAC-SYM which might better represent symptom severity of most patients seeking care in gastroenterology referral centers

Prevalence of gastroduodenal lesions is changing in the last decades. Prevalence of Helicobacter pylori infection, non-steroidal anti-inflammatory drugs (NSAIDs), and proton pump inhibitor (PPI) therapy may be involved in such a phenomenon. We assessed gastroduodenal lesions prevalence in a nationwide study.Consecutive patients who underwent upper endoscopy for the first time in 24 Italian centres between January 2012 and 31 March 2012 were enrolled. Prevalence of gastric ulcer (GU), duodenal ulcer (DU), gastric erosions (GE), duodenal erosions (DE), gastric polyp (GP), Barrett's oesophagus (BE), and neoplasia was assessed.Overall, 1054 (M/F: 388/666; Mean age: 57.5 ± 5 years) patients were enrolled. H. pylori infection was detected in 356 (33.9%) patients, 358 (34%) were taking NSAIDs, and 532 (50.5%) PPIs. PPI therapy was associated with a significantly lower H. pylori detection rate (27.8% vs 39.8%; OR: 0.6, 95% CI 0.45-0.77; P0.001). GU, DU, GE, DE, GP and BE were detected in 17 (1.6%), 13 (1.2%), 150 (14.2%), 50 (4.7%), 51 (4.8%) and 17 (1.6%), respectively. Moreover, 3 (0.3%) distal gastric cancers were observed. H. pylori infection remained the most prevalent factor for all gastroduodenal lesions, but gastric polyp. One third of patients with GU and GE were taking only NSAIDs therapy.The prevalence of peptic ulcer was very low (3%), with a similar rate between DU and GU. As many as half patients were on ongoing PPI therapy. Such a therapy could affect both the detection rate of H. pylori infection and the real prevalence of gastroduodenal lesions.

Summary Background Cure rates for eradication of Helicobacter pylori appear to be decreasing, thus more effective therapies must be identified. Aim To evaluate the efficacy of bovine lactoferrin in the treatment of H. pylori infection. Methods In a multicentred prospective study, 402 (mean age 52.4, range 19–84 years) H. pylori-positive patients were assigned to one of three regimens: group A – esomeprazole 20 mg b.d., clarithromycin 500 mg b.d. and tinidazole 500 mg b.d. for 7 days; group B – lactoferrin 200 mg b.d. for 7 days followed by the same schedule of group A; group C – esomeprazole 20 mg b.d., clarithromycin 500 mg b.d. and tinidazole 500 mg b.d. plus lactoferrin 200 mg b.d. for 7 days. Results Of the 402 patients, 389 completed the study. Six patients were discontinued due to side effects, one patient in group B died and six patients were lost to follow up. The eradication rate (intention-to-treat analysis) was 77% in group A (105/136), 73% in group B (97/132) and 90% in group C (120/134) (χ2-test P

Numerous studies have shown that alcohol causes both acute and chronic damage to gastroduodenal mucosa. The methods of damage differ however, and experimental studies in animals have shown that the degranulation of mast cells in gastric mucosa causes acute hemorrhagic lesions after the consumption of alcohol. It is not known whether this mechanism also operates in man. The aim of the present study was therefore to evaluate whether there is a correlation between mast-cell activation, determined by assaying tryptase levels in gastric mucosa, and the consumption of alcohol in patients with ulcerative diseases. Thirty-one patients with cicatrized ulcerative lesions (13 gastric ulcers, 18 duodenal ulcers) were included in the study. Biopsies at the level of the gastric fundus and antrum and the duodenal bulb were performed in all patients to determine tryptase levels. Biopsy material was frozen and subsequently homogenized; the enzyme was assayed in the supernatant using a radioimmunometric method. The mean daily alcohol consumption was calculated in clinical terms for each patient over the past 5 years and patients were subdivided into non-drinkers and moderate (60 g alcohol/day) and excessive (60 g alcohol/day) drinkers. It was found that tryptase concentrations were higher in the fundus compared to the gastric antrum and duodenal bulb, irrespective of alcohol consumption both in patients with gastric ulcer and duodenal ulcer. The importance of mast cells in provoking alcohol-dependent damage was studied at a gastric level. Alcohol leads to their degranulation and therefore contributes to the formation of gastric lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Fifty-nine cases of gastric dysplasia (46 of which were mild, 11 moderate and 2 severe) were studied in relation to their association with atrophic gastritis and intestinal metaplasia. Atrophic gastritis was found in 39 cases (28 of which were mild, 10 moderate and 1 severe). Dysplasia was considered "persistent" when found of the same degree in at least two consecutive check-ups after initial diagnosis (13 cases); it was considered "progressive" if found more severe or evolving as cancer (5 cases) or "regressive" if detected in a lesser degree or no longer detected (13 cases). Sixteen of the 18 persistent or progressive cases of dysplasia were associated with atrophic gastritis, whereas 10 of the 13 cases with regressive dysplasia revealed no concomitant pattern of gastric mucosa atrophy (p less than 0.005). These findings suggest that dysplasia represents a truly pre-neoplastic change particularly when associated with atrophic gastritis and which must therefore be more carefully monitored.

Several studies have shown an influence of cigarette smoking on serum pepsinogen group I (PGI) levels in duodenal ulcer patients and in control subjects. The elevation of PGI in smokers has just been interpreted as reflecting some degree of smoking-induced inflammation of the gastric mucosa. We have determined fasting serum PGI by radioimmunoassay in 163 healthy subjects investigated by a survey conducted on a sample population of an urban area in the North-East of Italy by means of a random selection based on the public registers of home addresses. The data reported confirmed that PGI levels are increased by smoking in a healthy population. The main contribution of this study consists in demonstrating in a non-selected population an increase of the only parameter up to date claimed to be a possible serological predictive index for ulcer disease.

Several studies are present in the literature about the efficacy of medical treatment with biliary acid, orally administered, on the symptomatic gallstone patients. Both this drugs act, with different mechanisms, on the same pathophysiological pathway, represented by the supersaturated bile in cholesterol. Aim of the present investigation was to study the possible modifications of serum bile acids pattern and of lipoproteins in a large sample of gallstone patients under long-term treatment with biliary acids. One hundred and twelve patients with radiolucent gallstones entered the study; 54 received chenodeoxycholic acid (CDCA) and 58 ursodeoxycholic (UDCA) at dosage of 15 mg/kg/daily. Blood samples for determination of serum cholesterol, triglycerides, phospholipids, lipoproteins, total and fractionated biliary acids were collected from each subjects every three months for a mean "follow-up" of 24 months. The levels of serum cholesterol, triglycerides and phospholipids showed a mild decrease only in the patients under therapy with CDCA, while no modifications were detected using UDCA. The same was found for two other parameters, HDL-cholesterol and lipoproteins, with both treatments during the overall period of follow-up. The biliary acids levels showed a significant increase only in the patients treated with CDCA, but no differences were found between "responders" and "non responders" to the therapy.

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.

A study of potentially benign or malignant ulcer in the stomach was made to assess its role in the differential diagnosis between these two conditions. In the 201 patients observed, no statistically significant differences in frequency in the various sites were noted as regard either benign or malignant lesions. The site of the ulcer cannot be taken as indicative of its nature.

Discriminant analysis was used in evaluating the importance of clinical aspects and the value of routine and experimental biochemical markers in the differential diagnosis of primary liver cancer (PLC) and chronic, non-neoplastic, liver diseases. Our results show that: 1) Clinical signs, such as the presence of pain, weight loss or mass, correctly indicate the diagnosis in 76% of the cases; 2) The determination of alkaline phosphatase isoenzymes is shown by the computer to be the most useful marker and provides an overall diagnostic accuracy which is higher than that of alpha-fetoprotein. We also found that, by using these two markers together, "by intersection," the best overall accuracy (85%) is obtained. We, therefore, suggest determination of alkaline phosphatase isoenzymes and alpha-fetoprotein in screening the populations at risk for liver cancer.

Objectives The aim of this study was to investigate the contribution of smoking and alcohol intake and pancreas divisum on the risk of developing chronic pancreatitis (CP). Methods Consecutive patients with CP who underwent secretin-enhanced magnetic resonance cholangiopancreatography were compared with consecutive patients without pancreatic disease who underwent secretin-enhanced magnetic resonance cholangiopancreatography for irritable bowel syndrome. Results We enrolled 145 consecutive CP patients and 103 irritable bowel syndrome patients from 2010 to 2014. In a univariate analysis, statistically significant differences in sex, mean age, and the duration and amount of cigarette and alcohol use were found. Per a receiver operating characteristic curve analysis, thresholds for cigarette and alcohol consumption were, respectively, 5.5 cigarettes and 13.5 g daily. In a multivariate analysis, independent risk factors for CP were male sex (odds ratio [OR], 2.05), smoking more than 5.5 cigarettes per day (OR, 2.72), and drinking more than 13.5 g/d (OR, 6.35). Conclusions In an Italian population, we confirmed smoking and alcohol as cofactors in the development of CP. This study shows that alcohol intake and smoking habits are 2 of the most important risk factors for the development of CP.