Modelo experimental de infeccion por Helicobacter pylori en el raton. Estudio del dano gastrico producido por indometacina / Experimental model of infection of Helicobacter pylori in the mouse. A study of gastric damage caused by indomethacin

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.

Helicobacter pylori in recently-diagnosed versus Chronic duodenal ulcer

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 percent; 0 percent and 3.2 percent respectively) p<0.001). In the antrum Hp prevalnce was also lower in Group II compared to Group III and I (41 percent, 78,3 percent and 24.1 percent) 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.

Gastroenteritis eosinofilica con compromiso esofagico / Eosinophilic gastroenteritis with esophageal involuement

Se describe el caso de un varón de 29 años portador desde 1979 de gastroenteritis eosinofílica con compromiso mucos a nivel de intestino delgado, manifestado por infiltración de eosinófilos y malabsorción; alteraciones de la capa muscular con obstrucción de intestino delgado y suboclusión pilórica; y compromiso seroso con ascitis. En 1985 es reinternado con un cuadro de suboclusión intestinal y ascitis que mejoran espontáneamente. A pesar de no presentar síntomas esofágicos se realizó una esofagogastroscopía que mostró una hernia hiatal e imposibilidad para franquear el pilóro. Las biopsias de esófago mostraron una marcada infiltración eosinófila intraepitelial y en corion. Así establecido el diagnóstico de sofagitis eosinofílica a nivel mucosa se trató de comprobar si el compromiso llegaba a la capa muscular. Se recurrió a dos métodos indirectos que evaluaron la función motora del esófago. El tránsito con 99Tc mostró una incoordinación motora en los dos tercios inferiores con retardo del vaciamiento. La electromanometría mostró un esfínter esofágico inferior con presiones ligeralmente elevadas y relajación normal; en el cuerpo esofágico había un gran porcentaje de ondas aperistálicas, algunas de tipo vigoroso y duración prolongada. La prueba de urecoline fue negativa. Basados en estos datos, inferimos que existía infiltración eosinófila de la capa muscular sin un compromiso a nivel neuronal. La revisión posterior de la literatura desde el primer caso documentado en 1977, demostró que existen siete comunicaciones previas de esofagitis eosinofílica, y en una de ellas con trastornos motores similares a los hallados en nuestro paciente