Helicobacter pylori infection and childhood idiopathic thrombocytopenic purpura. 2007

Kuan-Sheng Wu, and Chih-Cheng Hsiao, and Hong-Ren Yu, and Eng-Yen Huang, and Wan-Li Mai, and Jiunn-Ming Sheen
Department of Pediatrics, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung Hsien, Taiwan, ROC.

BACKGROUND Several studies showed some chronic idiopathic thrombocytopenic purpura (ITP) patients with complete platelet recovery after Helicobacter pylori (H. pylori) eradication and cited the cause of persistent thrombocytopenia as inability to eradicate H. pylori. So we studied H. pylori infection status in pediatric ITP patients at diagnosis and address whether such infection played a role in the development of childhood ITP. METHODS We compared H. pylori infection status by stool H. pylori antigen test of an ITP group including 32 childhood ITP patients at diagnosis from September 2004 to June 2006 and a control group including 30 unselected patients with no history of thrombocytopenia seen consecutively with clinical manifestations of pharyngotonsillitis, bronchitis, or bronchopneumonia in our ward during a one-month span. We further analyzed parameters between H. pylori infection-positive (H. pylori(+)) and H. pylori infection-negative (H. pylori(-)) childhood ITP patients. RESULTS The H. pylori-positive (H. pylori(+)) rate was 19% in the study group and 17% in the control group, with not statistically significant difference. As for the characteristics and treatment response about H. pylori status, they were also not statistically different. Although the ratio of chronic ITP cases showed higher tendency in H. pylori(+) patients (2/6) than the H. pylori(-) ones (3/26), it was not statistically significant. CONCLUSIONS It seems that H. pylori infection played a minor role in the development of childhood ITP in this small-scale study. A large-scale study is necessary to further confirm the relationship between H. pylori infection and the development of childhood ITP.

UI MeSH Term Description Entries
D007223 Infant A child between 1 and 23 months of age. Infants
D008297 Male Males
D002648 Child A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL. Children
D002675 Child, Preschool A child between the ages of 2 and 5. Children, Preschool,Preschool Child,Preschool Children
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000293 Adolescent A person 13 to 18 years of age. Adolescence,Youth,Adolescents,Adolescents, Female,Adolescents, Male,Teenagers,Teens,Adolescent, Female,Adolescent, Male,Female Adolescent,Female Adolescents,Male Adolescent,Male Adolescents,Teen,Teenager,Youths
D016480 Helicobacter pylori A spiral bacterium active as a human gastric pathogen. It is a gram-negative, urease-positive, curved or slightly spiral organism initially isolated in 1982 from patients with lesions of gastritis or peptic ulcers in Western Australia. Helicobacter pylori was originally classified in the genus CAMPYLOBACTER, but RNA sequencing, cellular fatty acid profiles, growth patterns, and other taxonomic characteristics indicate that the micro-organism should be included in the genus HELICOBACTER. It has been officially transferred to Helicobacter gen. nov. (see Int J Syst Bacteriol 1989 Oct;39(4):297-405). Campylobacter pylori,Campylobacter pylori subsp. pylori,Campylobacter pyloridis,Helicobacter nemestrinae
D016481 Helicobacter Infections Infections with organisms of the genus HELICOBACTER, particularly, in humans, HELICOBACTER PYLORI. The clinical manifestations are focused in the stomach, usually the gastric mucosa and antrum, and the upper duodenum. This infection plays a major role in the pathogenesis of type B gastritis and peptic ulcer disease. Infections, Helicobacter,Helicobacter Infection,Infection, Helicobacter
D016553 Purpura, Thrombocytopenic, Idiopathic Thrombocytopenia occurring in the absence of toxic exposure or a disease associated with decreased platelets. It is mediated by immune mechanisms, in most cases IMMUNOGLOBULIN G autoantibodies which attach to platelets and subsequently undergo destruction by macrophages. The disease is seen in acute (affecting children) and chronic (adult) forms. Autoimmune Thrombocytopenic Purpura,Idiopathic Thrombocytopenic Purpura,Purpura, Thrombocytopenic, Autoimmune,Werlhof's Disease,Autoimmune Thrombocytopenia,Immune Thrombocytopenia,Immune Thrombocytopenic Purpura,Thrombocytopenic Purpura, Autoimmune,Werlhof Disease,Autoimmune Thrombocytopenias,Autoimmune Thrombocytopenic Purpuras,Disease, Werlhof,Disease, Werlhof's,Idiopathic Thrombocytopenic Purpuras,Immune Thrombocytopenias,Immune Thrombocytopenic Purpuras,Purpura, Autoimmune Thrombocytopenic,Purpura, Idiopathic Thrombocytopenic,Purpura, Immune Thrombocytopenic,Purpuras, Autoimmune Thrombocytopenic,Purpuras, Idiopathic Thrombocytopenic,Purpuras, Immune Thrombocytopenic,Thrombocytopenia, Autoimmune,Thrombocytopenia, Immune,Thrombocytopenias, Autoimmune,Thrombocytopenias, Immune,Thrombocytopenic Purpura, Idiopathic,Thrombocytopenic Purpura, Immune,Thrombocytopenic Purpuras, Idiopathic,Thrombocytopenic Purpuras, Immune,Werlhofs Disease

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