A Primary-Care Interventional Model on the Diverticular Disease: Searching for the Optimal Therapeutic Schedule.

INTRODUCTION: In routine colonoscopy, diverticulosis is the most commonly found feature, but only a minority of these cases show symptoms of diverticular disease.From June 2014 to December 2014, we enrolled prospectively 178 patients affected by symptomatic uncomplicated diverticular disease (Male/Female=0.47, mean age 71.7±11.5 y, range 41 to 95 y) from 15 General Pratictioners patient files. All patients were symptomatic; in all cases, diagnosis was been confirmed by a colonoscopy performed at least 1 year before. Patients with acute diverticulitis were excluded.On the basis of the predominant symptoms (abdominal complaints or constipation), patients were addressed to 4 different therapeutic approaches using mesalamine, rifaximine, probiotics (in a consortium of different species of Lactobacillus and Bifidobacterium), and fibers (Plantago Ovata Husk). All treatments lasted 3 months. RESULTS: Sixty-three patients were enrolled in group A (rifaximine), 43 in group A1 (rifaximine+fibers+probiotics), 23 in group B (mesalamine), and 31 in group B1 (mesalamine+fibers).Analysis of variance suggested a statistically significant difference (P<0.003) among groups at the end of the observation period, with Groups A1 and B1 showing a higher number of bowel movement per week. Global linear measurement confirmed the role of treatment as a significant factor (F=2.858; P=0.039) associated with body mass index (F=6.972; P<0.009). CONCLUSIONS: In accordance with the baseline clinical presentation, the supplementation of fiber and/or probiotics is associated with a statistically significant improvement in the clinical pattern of symptoms in patients with diverticular disease in a primary-care/family physician setting.

Barrett's esophagus and adenocarcinoma risk: the experience of the North-Eastern Italian Registry (EBRA).

OBJECTIVE: To establish the incidence and risk factors for progression to high-grade intraepithelial neoplasia (HG-IEN) or Barrett's esophageal adenocarcinoma (BAc) in a prospective cohort of patients with esophageal intestinal metaplasia [(BE)]. BACKGROUND: BE is associated with an increased risk of BAc unless cases are detected early by surveillance. No consistent data are available on the prevalence of BE-related cancer, the ideal surveillance schedule, or the risk factors for cancer. METHODS: In 2003, a regional registry of BE patients was created in north-east Italy, establishing the related diagnostic criteria (endoscopic landmarks, biopsy protocol, histological classification) and timing of follow-up (tailored to histology) and recording patient outcomes. Thirteen centers were involved and audited yearly. The probability of progression to HG-IEN/BAc was calculated using the Kaplan-Meier method; the Cox regression model was used to calculate the risk of progression. RESULTS: HG-IEN (10 cases) and EAc (7 cases) detected at the index endoscopy or in the first year of follow-up were considered to be cases of preexisting disease and excluded; 841 patients with at least 2 endoscopies {median, 3 [interquartile range (IQR): 2-4); median follow-up = 44.6 [IQR: 24.7-60.5] months; total 3083 patient-years} formed the study group [male/female = 646/195; median age, 60 (IQR: 51-68) years]. Twenty-two patients progressed to HG-IEN or BAc (incidence: 0.72 per 100 patient-years) after a median of 40.2 (26.9-50.4) months. At multivariate analysis, endoscopic abnormalities, that is, ulceration or nodularity (P = 0.0002; relative risk [RR] = 7.6; 95% confidence interval, 2.63-21.9), LG-IEN (P = 0.02, RR = 3.7; 95% confidence interval, 1.22-11.43), and BE length (P = 0.01; RR = 1.16; 95% confidence interval, 1.03-1.30) were associated with BE progression. Among the LG-IEN patients, the incidence of HG-IEN/EAc was 3.17 patient-years, that is, 6 times higher than in BE patients without LG-IEN. CONCLUSIONS: These results suggest that in the absence of intraepithelial neoplastic changes, BE carries a low risk of progression to HG-IEN/BAc, and strict surveillance (or ablative therapy) is advisable in cases with endoscopic abnormalities, LG-IEN or long BE segments.

Changing trends in acute upper-GI bleeding: a population-based study.

BACKGROUND: Advances in medical practice in recent decades have influenced the etiology and management of acute upper-GI bleeding (UGIB), but their impact on the incidence and mortality is unclear. OBJECTIVE: To analyze the time trends of UGIB in 2 different management eras. DESIGN: Prospective observational study. SETTING: General university-affiliated hospital. PATIENTS AND INTERVENTIONS: A total of 587 patients who presented with UGIB during the 1983-to-1985 period were compared with 539 patient in the 2002-to-2004 period. RESULTS: The overall incidence of UGIB decreased from 112.5 to 89.8 per 100,000/y, which corresponds to a 35.5% decrease after adjustment for age (95% CI, 24.2%-46.8%). The age standardized incidence of ulcer bleeding decreased by 41.6% (95% CI, 27.2%-56%); the decrease occurred only in people younger than 70 years of age. The rate of history of peptic ulcer disease decreased from 32.7% in the 1983-to-1985 period versus 19.5% in the 2002-to-2004 period (P < .001). The mean age increased from 61.0 to 68.7 years (P < .001), and the male:female ratio decreased from 2.7 to 1.8 (P = .002). The comorbidities increased from 69% to 75% (P = .01), the use of nonsteroidal anti-inflammatory drugs from 40.0% to 46.4% (P = .03), and the cases of bleeding occurring during hospitalization from 10.4% to 17.1% (P < .001). In the 1983-to-1985 cohort, the endoscopy was solely diagnostic, and antisecretory therapy consisted of H2-antagonists drugs. In the second period, 39.3% of patients underwent endoscopic therapy, whereas proton pump inhibitors were administered in 47%. Rebleeding rates decreased from 32.5% to 7.4% (P < .001) and surgery from 10.2% to 2.0% (P < .001). Overall mortality decreased from 17.1 to 8.2 per 100,000/y, which corresponded to a 60.8% decrease after adjustment for age (95% CI, 46.5%-75.1%). The age standardized mortality rate for ulcer bleeding decreased by 56.5% (95% CI, 41.9%-71.1%). LIMITATIONS: A single-center study and a potential lack of generalizability. CONCLUSIONS: From the 1983-to-1985 period to the 2002-to-2004 period, major changes occurred in the incidence of UGIB, features of patients, management, and outcomes. The incidence and mortality of UGIB overall and ulcer bleeding decreased significantly, and the decline of incidence occurred only in patients younger than 70 years old.

Does Helicobacter pylori infection eradication modify peptic ulcer prevalence? A 10 years' endoscopical survey.

AIM: To compare peptic ulcer prevalence in patients referred for upper gastrointestinal endoscopy in two Italian hospitals in pre-Helicobacter era and ten years after the progressive diffusion of eradication therapy. METHODS: We checked all the endoscopic examinations consecutively performed in the Gastroenterology Unit of Padova during 1986-1987 and 1995-1996, and in the Gastroenterology Unit of Parma during 1992 and 2002. Chi Square test was used for statistic analysis. RESULTS: Data from both the endoscopic centers showed a statistically significant decrease in the prevalence of ulcers: from 12.7% to 6.3% (P<0.001) in Padova and from 15.6% to 12% (P<0.001) in Parma. The decrease was significant both for duodenal (from 8.8% to 4.8%, P<0.001) and gastric ulcer (3.9% to 1.5%, P<0.001) in Padova, and only for duodenal ulcer in Parma (9.2% to 6.1%, P<0.001; gastric ulcer: 6.3% to 5.8%, NS). CONCLUSION: Ten years of extensive Helicobacter pylori (H pylori) eradication in symptomatic patients led to a significant reduction in peptic ulcer prevalence. This reduction was particularly evident in Padova, where a project for the sensibilization of H pylori eradication among general practioners was carried out between 1990 and 1992. Should our hypothesis be true, H pylori eradication might in the future lead to peptic ulcer as a rare endoscopic finding.

Usefulness of serum pepsinogens in Helicobacter pylori chronic gastritis: relationship with inflammation, activity, and density of the bacterium.

We sought to study the relationship between serum pepsinogens and different histopathologic features of Helicobacter pylori-related chronic gastritis. One hundred forty-nine consecutive dyspeptic patients underwent endoscopy with biopsies; serum pepsinogens I and II were measured by immunoassay. Serum levels of pepsinogens (sPG) were significantly correlated with H. pylori density both of the corpus (sPGI: r = 0.32, P < .001; sPGII: r = 0.56, P < .001) and antrum (sPGI: r = 0.41, P < .001; sPGII: r = 0.43, P < .001) as well as with chronic inflammation (sPGI: r = 0.26, P < .001; sPGII: r = 0.49, P < .001) and activity (sPGI: r = 0.38, P < .001; sPGII: r = 0.50, P < .001) in the antrum. Only sPGII was correlated with chronic inflammation (r = 0.44, P < .001) and activity (r = 0.40, P < .001) in the corpus. SPGI was inversely correlated with atrophy (r = -0.33, P < .001) and intestinal metaplasia (r = -0.37, P < .001) in the corpus. sPGII levels could be considered as markers of gastric inflammation all over in the stomach. sPGI levels are inversely related to atrophic body gastritis.

Recovery of gastric function after Helicobacter pylori eradication in subjects with body atrophic gastritis: prospective 4-year study.

BACKGROUND: The relationship between Helicobacter pylori (H. pylori) eradication and atrophic changes in the gastric mucosa has not yet been fully defined. Although studies report a partial restoration of serum pepsinogen I (sPGI) levels after eradication, it is not clear if this finding reflects gastric mucosal healing on a morphological level. AIM: To assess alterations in gastric function after H. pylori eradication on moderate/severe body atrophic gastritis by determination of sPGI levels. METHODS: Twenty-three dyspeptic patients, selected from 284 consecutive H. pylori positive patients, with histological features of moderate/severe body atrophic gastritis and sPGI < 25 microg/L (11 men, mean age: 51.8 years, range: 29-79 years), underwent an upper gastrointestinal endoscopy with gastric biopsies and sPGI determination at baseline. All patients underwent eradication therapy. Serum pepsinogen I was measured again after 6 months, and at 1, 2, 3 and 4 years after eradication therapy. RESULTS: Mean sPGI levels prior to eradication were 11.9 microg/L (range: 4-23 microg/L). Six months after eradication therapy, mean sPGI levels significantly increased to 17.4 microg/L (P = 0.04). At the completion of the study, 4 years after eradication, sPGI levels increased from 17.4 to 32.7 microg/L (P = 0.01). A significant progressive increase in sPGI levels was observed from 6 months to 1 year (17.4 to 23.9 microg/L) and from 1 to 2 years (23.9 to 26.0 microg/L, P = 0.01). Serum pepsinogen I levels higher than the cut-off value of 25 microg/L were observed at various time-points: 6.3% of patients at 6 months (1/16), 33.3% (5/15) at 1 year, 50% (7/14) at 24 months, 66.7% (6/9) at 36 months and 87.5% (7/8) at 4 years. CONCLUSION: After H. pylori eradication, subjects with body atrophic gastritis showed long-term improvement of physiological gastric function, reflected by significantly and continually increasing sPGI levels over a 4-year period.

Clinical usefulness of serum pepsinogen II in the management of Helicobacter pylori infection.

BACKGROUND: Serum pepsinogen II (sPGII) levels are known to increase during Helicobacter pylori infection. AIM: To assess H. pylori infection and success of H. pylori therapy by means of sPGII levels. METHODS: sPGII levels were determined in 156 H. pylori-positive and 157 H. pylori-negative consecutive patients with dyspeptic symptoms. Additionally, sPGII determination was performed in 70 H. pylori-positive patients 2 months after H. pylori eradication therapy. In 29 of these 70 patients, gastroscopy was performed to evaluate the effect of H. pylori therapy on gastric activity. RESULTS: H. pylori-positive subjects demonstrated a significantly higher mean of sPGII levels than H. pylori-negative subjects (16.8 +/- 7.4 vs. 8.6 +/- 3.7 microg/l; p < 0.001). The best sPGII cut-off for predicting H. pylori infection was 9.93 microg/l (sensitivity 83%, specificity 73%). The best cut-off values to evaluate success of therapy were: sPGII of 9.47 microg/l, a sPGII variation level (difference between baseline and after therapy) of 4.54 microg/l, and a sPGII Deltavalue (sPGII variation divided by sPGII before therapy) of 25% (sensitivity 93%, specificity 91%). CONCLUSIONS: sPGII levels may be used as a reliable marker of H. pylori infection in the initial diagnosis as well as to evaluate H. pylori eradication and subsequent changes in gastric inflammation.

Rabeprazole in a one-week eradication therapy of Helicobacter pylori: comparison of different dosages.

AIM: Many data regarding omeprazole-, lanzoprazole- and pantoprazole-based triple therapy for Helicobacter pylori (H. pylori) eradication have been reported, but there is few data present regarding rabeprazole (R). We report the efficacy and tolerability of rabeprazole in different dosages in association with clarithromycin (C)and tinidazole (T) in H. pylori eradication. DESIGN AND METHODS: Ninety-four H. pylori-positive patients with dyspeptic symptoms were enrolled and randomly allocated to eradication therapy in two different one-week regimens. In regimen A, 47 patients received R 20 mg b.i.d, C 500 mg b.i.d and T 500 mg b.i.d, while in regimen B, 47 patients received R 10 mg b.i.d, C 500 mg b.i.d and T 500 mg b.i.d. Eradication of H. pylori was evaluated by a 13C urea breath test (UBT) two months after the end of the therapy. RESULTS: Four patients (two in each regimen) did not complete treatment. The H. pylori eradication rate was 91.4% in group A compared to 89.3% in group B (P-value not significant). Minor side-effects were reported in 4.2% of group A and 6.4% of group B patients. CONCLUSION: Rabeprazole showed good efficacy and tolerability in one-week H. pylori therapy at 20 mg b.i.d and 10 mg b.i.d, suggesting the use of the lower dosage.

Lactoferrin: mechanism of action, clinical significance and therapeutic relevance.

Lactoferrin is an iron binding protein involved in a large spectrum of biological actions including antimicrobial actions. Lactoferrin plays a central role in ferrokinetics: it binds free iron with great affinity limiting the amount of ions available for microorganism's metabolism. Its role in the host defence mechanisms consists in bacteriostatic and bactericidal effects; moreover it inhibits the proliferation of other microbes such as fungi and viruses. Lactoferrin is also involved in the modulation of immune system and recent studies indicate that lactoferrin directly modulates both production and function of neutrophils and monocytes.