Helicobacter pylori is a well-known cause of chronic antral gastritis and plays an important role in the pathogenesis of peptic ulcer disease in adults.
However, because of the relatively low incidence of duodenal ulcer in childhood, few studies have been directed specifically at the relation between the treatment of H. pylori infection and duodenal ulcer in children.
An evaluation in a larger patient population is necessary to draw a conclusion.
Twenty-six children with duodenal ulcer and H. pylori antral gastritis received triple therapy (amoxicillin, bismuth, and metronidazole) to investigate whether eradication of the organisms can promote healing and prevent relapse of the ulcers in children.
Endoscopic examinations were performed before. 2 months, and 12 months after the beginning of treatment.
H. pylori infection was eradicated in 25 (96%) of the 26 patients who underwent upper endoscopic follow-up.
Clinical improvement and ulcer healing were achieved in 24 (92%) of 26 children.
During a mean follow-up of nearly 2 years, the annual ulcer relapse rate was estimated to be 9%. Conclusions : Triple therapy is the treatment of choice for endoscopically proven duodenal ulcer and histologically proven H. pylori antral gastritis in children.
It strongly supports a causal relation between H. pylori and duodenal ulcer disease in children.
Mots-clés Pascal : Ulcère, Duodénum, Complication, Helicobacter pylori, Spirillaceae, Spirillales, Bactérie, Etude longitudinale, Prétraitement chimique, Eradication, Efficacité traitement, Evaluation, Enfant, Homme, Appareil digestif pathologie, Intestin pathologie, Bactériose, Infection
Mots-clés Pascal anglais : Ulcer, Duodenum, Complication, Helicobacter pylori, Spirillaceae, Spirillales, Bacteria, Follow up study, Chemical pretreatment, Eradication, Treatment efficiency, Evaluation, Child, Human, Digestive diseases, Intestinal disease, Bacteriosis, Infection
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 99-0073960
Code Inist : 002B05B02F. Création : 31/05/1999.