Ali M. Moussa

Efficacy of mesalazine in the treatment of symptomatic diverticular disease.

We aimed to improve symptoms by means of mesalazine in symptomatic colonic diverticular disease patients. One hundred seventy outpatients (98 M, 72 F; age, 67.1 years; range, 39–84 years) were assigned to four different schedules: rifaximin, 200 mg bid (Group R1: 39 pts), rifaximin, 400 mg bid (Group R2: 43 pts), mesalazine, 400 mg bid (Group M1: 40 pts), and mesalazine, 800 mg bid (Group M2: 48 pts), for 10 days per month. At baseline and after 3 months we recorded 11 clinical variables (upper/lower abdominal pain/discomfort, bloating, tenesmus, diarrhea, abdominal tenderness, fever, general illness, nausea, emesis, dysuria), scored from 0 = no symptoms to 3 = severe. The global symptomatic score was the sum of all symptom scores. After 3 months in all schedules but Group R1, 3 of the 11 symptoms improved (P < 0.03); the global score decreased in all groups but Group R1 (P < 0.0001). Mesalazine-treated patients had the lowest global score at 3 months (P < 0.001). Mesalazine is as effective as rifaximin (higher dosage schedule) for diminishing some symptoms, but it appears to be better than rifaximin for improving the global score in those patients.

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.

Use of lactoferrin for Helicobacter pylori eradication: Preliminary results

BACKGROUND One-week triple therapy is the most frequently recommended treatment of Helicobacter pylori infection. The associated eradication rate is satisfactory; nevertheless, it is advisable to look for more effective therapies. Our aim was to test the efficacy of a standard triple therapy plus bovine lactoferrin for the eradication of H. pylori infection. STUDY This open, randomized, single-center study was designed to include 150 consecutive H. pylori-positive patients with dyspeptic symptoms and gastritis who received triple therapy with rabeprazole, clarithromycin, and tinidazole plus lactoferrin for 7 days (group A), rabeprazole, clarithromycin, and tinidazole for 7 days (group B), or rabeprazole, clarithromycin, and tinidazole for 10 days (group C). H. pylori status was assessed 8 weeks after the end of treatment by means of the 13C-urea breath test or H. pylori stool antigen test. RESULTS The 7-day treatment including lactoferrin (group A) was successful in 100% (24/24) of the patients. The eradication rates in groups B and C were 76.9% (20/26 patients; 95% CI, 61%-93%) and 70.8% (17/24 patients; 95% CI, 53%-89%), respectively. A significant difference was found between group A and group B (P = 0.023) and group A and group C (P = 0.022). No differences were found between group B and group C (P = 1.00). CONCLUSION These results suggest that lactoferrin could be a new, effective agent when added to antimicrobial therapy for the eradication of H. pylori. This treatment schedule could be proposed for larger trials of H. pylori eradication therapy, focusing on the excellent preliminary cure rate, good compliance to the treatment schedule, and relatively low price of lactoferrin for full treatment.

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 µg/l; p < 0.001). The best sPGII cut-off for predicting H. pylori infection was 9.93 µg/l (sensitivity 83%, specificity 73%). The best cut-off values to evaluate success of therapy were: sPGII of 9.47 µg/l, a sPGII variation level (difference between baseline and after therapy) of 4.54 µg/l, and a sPGII Δvalue (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.

Usefulness of a serological panel test in the assessment of gastritis in symptomatic children.

Background: Non-invasive methods are advisable for the detection of Helicobacter pylori-related chronic gastritis in pediatric patients. Serum pepsinogens I and II (sPGII and sPGII), gastrin-17 (G-17) and anti-H. pylori antibodies (IgG-Hp) have been proposed as a ‘serological gastric biopsy’. Aim: To assess H. pylori infection and to evaluate gastric mucosa status in a pediatric population by means of serological parameters such as sPGI, sPGII, G-17 and IgG-Hp. Methods: 45 consecutively children evaluated for upper gastrointestinal symptoms were analyzed. All children were submitted to upper gastrointestinal endoscopy with biopsies. Serum samples were analyzed for IgG-Hp, sPGII, sPGI and G-17 (Biohit, Helsinki, Finland). Results: 18 children had H. pylori-related mild or moderate non-atrophic chronic gastritis. They presented significantly higher mean levels of sPGII and of IgG-Hp than negative ones, eitherunder or up to 10 years. sPGI showed significantly increased levels in H. pylori-positive patients only over 10 years. G-17 levels were not different between H. pylori-positive and -negative ones. The best cut-offs of IgG-Hp, sPGII and of product IgG-Hp·sPGII, to identify H. pylori infection, were 30 IU/l, 9 µg/l, and 241 IU/l·µg/l, respectively. The product IgG-Hp·sPGII identified H. pylori infection with a 100% sensitivity, 92% specificity, 90% positive predictive value and 100% negative predictive value. IgG-Hp and IgG-Hp showed a correlation (r = 0.94; p < 0.001). Conclusions: Combined analysis of sPGII and IgG-Hp antibody levels could be recommended as a non-invasive panel for the assessment of H. pylori-related histological alterations of gastric mucosa in childhood.

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.

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.