M Schraier

Helicobacter pylori is one of the main causes of type B gastritis and is frequently found in the gastric antrum or in areas of gastric metaplasia in duodenal ulcer patients. The aim of this study was to evaluate Helicobacter pylori and gastric metaplasia prevalence in duodenal ulcer patients within their first diagnosed episode compared to those with chronic ulcer disease. Eighty three patients were prospectively studied in a 2-year period, they were divided into 3 groups: Group I, control, included 29 patients; Group II, 17 patients, included patients with first diagnosed duodenal ulcer episode; and Group III, 37 patients, with chronic ulcer disease. Helicobacter pylori prevalence in duodenum was significatively lower in Group II versus Group III and controls (67.5%, 0% and 3.2% respectively) (p < 0.001). In the antrum Hp prevalence was also lower in Group II compared to Group III and I (41%, 78.3% and 24.1%) with a significative difference (p < 0.001). Gastric metaplasia was significantly higher in Group III versus Group II and controls. These results suggest that Helicobacter pylori plays an important but not exclusive role in the pathogenesis of these disease together with other factors.

Helicobacter pylori (Hp) infection affects almost half of the world population, it is almost a pandemia, and has been associated to poverty in underdeveloped countries. The Club Argentino del Estómago y Duodeno decided to fulfill the lack of information upon this subject in Argentina designing a seroprevalence, multicentric, prospective study performed in voluntary adults donors in blood banks and in children seen during normal growth controls. Seven hundred and nineteen individuals were evaluated, 645 of them were included: 178 children (age 0-18 years) and 467 adults. In all cases a serological IgG Hp test (Flex-Pack Abbott) was performed and an epidemiological questionnaire was completed by a physician. General prevalence of Hp infection was 44.8% of individuals. In the paediatric population prevalence was 15.7% and in adults 55.9%. The highest prevalence was observed in the fifth decade: 64%. In concordance with other similar studies carried out in different countries, we may conclude that the risk of acquisition of Hp infection is directly related to age, area of residence, social-economical status, sanitary facilities, and educational level reached. Even though the prevalence of Hp infection in Argentina is intermediate between highly developed and underdeveloped countries, the number of people infected is very high and the incidence of Hp-associated pathologies in the future represents a formidable task for gastroenterologists and sanitary authorities.

INTRODUCTION: The action of non-steroidal anti-inflammatory drugs (NSAIDs) on the Helicobacter Pylori (Hp) infected mucosa is a matter of debate. Some authors consider them to cause additive iatrogeny whilst others attribute a purportedly protective action to them. The development of on experimental animal model could help clarify this phenomenon. OBJECTIVES: 1--To develop an animal model of Hp gastric infection. 2--To evaluate the aggressiveness of NSAIDs in this model. MATERIALS AND METHODS: Male 6 month old BALC/C mice weighing 38 g were studied. Pylori Hp infection was ruled out. On three occasions, in the same week, 18 mice were inoculated intra-gastrically with 0.6 ml of Hp culture broth (brain-heart infusion) containing 1 x 10 8-1 x 10 9 CFU/ml. Another group of mice were inoculated with sterile saline. After two months the mice were killed and their stomachs studied. They were divided into groups: a) 6 Hp negative control mice. b) 8 Hp negative mice with prior intra-peritoneal injection of 25 mg/Kg indomethacin (24 hs.) c) 8 mice inoculated with Hp with indomethacin. d) 8 mice inoculated with Hp, without indomethacin. The stomachs were opened along the greater curvature and photographed macroscopically in order to map the necrotic area. The antrums were biopsied to test for urease and separate antrum and body specimens were send for staining with Warthin-Starry H & B and histopathology. RESULTS: All the mice inoculated with Hp acquired the infection. The necrotic area was larger in Group B: 55.5 +/- 7.87 mm than in Group C: 15 +/- 1.82 mm P < 0.00019. HISTOLOGY: Group A: normal mucosa. Group B: extensive coagulation necrosis and focal erosions. Group C: ulcers with inflammatory infiltrate and smaller necrotic area, presence of Hp on the surface epithelium. Group D: no ulcers, Hp present. CONCLUSION: An animal model of Hp infection was successfully developed Hp infection could play a potentially protective role against indomethacin aggression in the mouse.