Is a one-week course of triple anti-Helicobacter pylori therapy sufficient to control active duodenal ulcer?

BACKGROUND: Triple therapy currently forms the cornerstone of the treatment of patients with Helicobacter pylori-positive duodenal ulcer. AIM: To establish whether prolonged antisecretory therapy is necessary in patients with active duodenal ulcer. METHODS: A total of 77 patients with H. pylori-positive duodenal ulcer were included in a prospective, controlled, double-blind study. All patients received a 7-day treatment with omeprazole 20 mg b.d., clarithromycin 500 mg b.d. and amoxicillin 1000 mg b.d. Patients in the omeprazole group underwent an additional 14-day therapy with omeprazole 20 mg; patients in placebo group received placebo. Endoscopy was performed upon inclusion in the study and after 3 and 8 weeks. RESULTS: Seventy-four patients were eligible for a per protocol analysis after 3 weeks, and 65 after 8 weeks. After 3 weeks, the healing rate was 89% in the omeprazole group and 81% in the placebo group (P=0.51). After 8 weeks, the ulcer healed in 97% of the patients in the total group (95% CI: 92.7-100%). H. pylori was eradicated in 88% of patients in the omeprazole group and in 91% in the placebo group (P=1.0). No statistically significant differences between the groups were found in ulcer-related symptoms or in ulcer healing. CONCLUSION: In patients with H. pylori-positive duodenal ulcer, a 7-day triple therapy alone is sufficient to control the disease.

Effects of ondansetron on portal hemodynamics in liver cirrhosis.

OBJECTIVE: The double-blind randomized pilot study was undertaken to compare the effects of a 10-day course of ondansetron 8 mg/day and propranolol 80 mg/day perorally in treating portal hypertension. SUBIECTS AND METHODS: 16 patients with liver disease were enrolled in the study. Measurements of portal vein diameter, portal blood flow velocity and portal blood flow volume were done at days 1, 5 and 10 of treatment using duplex Doppler sonography. RESULTS: The propranolol group demonstrated a decrease in portal venous diameter, while patients treated with ondansetron exhibited reduced portal blood flow velocity values. A decreased portal blood flow volume was found in both groups after 10 days of therapy. CONCLUSION: No statistically significant differences were found between the groups with the exception of portal venous diameter which is significantly lower at the end of the treatment in the case of propranolol.

Evidence that hereditary pancreatitis is genetically heterogeneous disorder.

Hereditary pancreatitis (HP) is an autosomal dominant disorder characterized by recurrent acute attacks of severe abdominal pain with an onset in early childhood. Many HP patients progress to complicated chronic pancreatitis and/or pancreatic cancer. Initially, a single mutation R117H in the cationic trypsinogen gene was detected in all affected members of five unrelated HP families. Further studies identified a second mutation (N21L) in two HP families without the R117H mutation. Before the association between cationic trypsinogen and HP was found, we detected a cystic fibrosis transmembrane conductance regulator (CFTR) gene mutation (L327R) in all affected individuals of a family with HP. We therefore performed a mutational analysis for R117H and N21L in cationic trypsinogen in this and three additional unrelated families with HP. The R117H mutation was detected in all 9 affected members of three HP families and in 3 asymptomatic but at-risk relatives. However, neither the R117H nor the N21L mutation in the cationic trypsinogen were found in the HP family with the L327R alteration in CFTR. The L327R allele segregates with the disease within this HP family and was not detected on 360 unrelated Caucasian non-CF chromosomes. Although close to 800 different mutations have been detected in the CF gene of cystic fibrosis patients, L327R is a new alteration, not yet reported in connection with CF. The results of this study indicate that the CFTR gene may play a role in the etiology of minority of cases with HP and suggest that hereditary pancreatitis is genetically heterogeneous disease.

A four-year follow-up of duodenal ulcer patients after Helicobacter pylori eradication.

BACKGROUND/AIMS: The aim of our study was to evaluate the clinical course of disease in 63 duodenal ulcer (DU) patients during a 4-year follow-up after Helicobacter pylori (H. pylori) eradication. METHODOLOGY: Upper gastrointestinal endoscopy and a clinical interview were performed before antimicrobial therapy, 2 months after, yearly and when symptoms recurred. Two antral and two corporal specimens were taken for histology, and one additional specimen from antrum was taken for rapid urease test at the first endoscopy and for culture at the following endoscopies. All patients received triple antimicrobial regimens based on colloidal bismuth subcitrate, amoxycillin and metronidazole for at least 2 weeks. Patients with a negative histology and culture 2 months after antimicrobial therapy were included in the study. RESULTS: After H. pylori eradication, ulcer recurrence dropped from 84.1% per year in the year before H. pylori eradication to a mean value of 5.2% per year during 2076 patient months (p<0.01). The increased incidence of gastroesophageal reflux disease (GERD) was found only in the first year of the follow-up period. The average percentage of anti-ulcer drug users per year was 30.8% because of GERD, reflux symptoms, ulcer recurrence or non-ulcer dyspepsia. Ulcers or acute erosions recurred in 9 H. pylori-negative patients; recurrences were attributable to non-steroidal anti-inflammatory drugs (NSAID) in 4 out of 9 cases (44.4%). CONCLUSIONS: H. pylori eradication changed the long-term course of DU disease.

Two- to four-year histological follow-up of gastric mucosa after Helicobacter pylori eradication.

In a 2- to 4-year prospective study, the reversibility of gastritis after Helicobacter pylori eradication was analysed. Sixty-three H. pylori-positive, chronic duodenal ulcer patients were studied after the successful eradication of bacteria in the period from 1990 to 1993. H. pylori eradication was obtained by triple antimicrobial regimens (colloidal bismuth subcitrate, amoxycillin, and metronidazole) applied for at least 14 days. The criteria for eradication were the absence of bacteria from two antral and two body of stomach biopsies stained with haematoxylin, eosin, and Warthin Starry, and a negative antral biopsy culture. The same diagnostic procedures were repeated, at regular follow-up endoscopies, each year for up to 4 years. Neutrophil-granulocyte infiltration of gastric mucosa disappeared in 2 months after bacterial eradication. Mononuclear cellular infiltration was disappearing with statistical significance up to the second year and normal mucosa was observed in the majority of patients in the fourth year of follow-up. Degeneratively changed lymphoid aggregates were also present in the fourth year in the antrum (12.5 per cent of patients) and in the body of stomach (14 per cent of patients). There was no significant change in antral intestinal metaplasia during the 4 years of follow-up. Antral atrophy declined significantly in the period from 1 to 3 years of follow-up. In conclusion, 3-4 years are needed for gastric mucosa to become normal after H. pylori eradication, although some residual lymphoid aggregates persist even after that period.

HLA-DR expression on CD8 lymphocytes from gastric mucosa in urease-positive and urease-negative gastritis.

We isolated lymphocytes from chronically inflamed gastric mucosa. We analysed the expression of IL-2 receptors (CD25), transferin receptors (CD71) and HLA-DR molecules on T lymphocytes by flow cytometric analysis in 16 patients with urease-positive and in 7 patients with urease-negative chronic gastritis. In G0, G1 and G2 histological type (Sydney classification) of gastritis the number of lymphocytes obtained from the gastric mucosa biopsies was too low for the flow cytometric analysis. However, in G3 histological type of chronic gastritis we obtained enough cells for the flow cytometric analysis in 75%. We demonstrated a significant increase in HLA-DR expression on CD8 cells from patients with urease-positive gastritis compared to urease-negative gastritis. We also observed a statistically non-significant increase in HLA-DR expression on CD3 cells, and in CD71 expression on both CD3 and CD8 cells in urease-positive gastritis. However, no difference in CD25 expression was found between the two types of gastritis.