EVALUATION STUDY
JOURNAL ARTICLE
MULTICENTER STUDY
Eradication of Helicobacter pylori increases platelet count in patients with idiopathic thrombocytopenic purpura in Japan.
European Journal of Clinical Investigation 2005 March
BACKGROUND: The effect of Helicobacter pylori eradication on the platelet count in patients with thrombocytopenic purpura is controversial. In this multicentre study, we prospectively assessed the effect of H. pylori eradication therapy in idiopathic thrombocytopenic purpura patients.
MATERIALS AND METHODS: Thirty-five consecutive patients with chronic idiopathic thrombocytopenic purpura (11 males and 24 females, a median age of 57) were assessed for H. pylori infection by use of a urea breath test. All patients received 1-week triple therapy (amoxicillin, clarithromycin, and lansoprazole) to eradicate H. pylori. At 6 months, idiopathic thrombocytopenic purpura patients with a platelet count recovery of greater than 100 x 10(9) L(-1) were defined as idiopathic thrombocytopenic purpura responders.
RESULTS: Helicobacter pylori infection was observed in 25 (71%) of the 35 patients. All infected patients were cured. Eleven patients were identified as idiopathic thrombocytopenic purpura responders; 24 were considered nonresponders. Platelet counts improved by more than 100 x 10(9) L(-1) in 11 (44%) of the 25 patients cured of H. pylori infection, while none of the 10 patients H. pylori-negative patients experienced the same improvement (P = 0.015). Univariate analysis showed that H. pylori infection and its eradication were significant factors associated with platelet recovery (P = 0.015).
CONCLUSIONS: Helicobacter pylori infection played a role in the pathogenesis of idiopathic thrombocytopenic purpura in approximately 30% of all patients assessed and 45% of the patients with H. pylori infection. Eradication of H. pylori in idiopathic thrombocytopenic purpura patients led to improved disease activity.
MATERIALS AND METHODS: Thirty-five consecutive patients with chronic idiopathic thrombocytopenic purpura (11 males and 24 females, a median age of 57) were assessed for H. pylori infection by use of a urea breath test. All patients received 1-week triple therapy (amoxicillin, clarithromycin, and lansoprazole) to eradicate H. pylori. At 6 months, idiopathic thrombocytopenic purpura patients with a platelet count recovery of greater than 100 x 10(9) L(-1) were defined as idiopathic thrombocytopenic purpura responders.
RESULTS: Helicobacter pylori infection was observed in 25 (71%) of the 35 patients. All infected patients were cured. Eleven patients were identified as idiopathic thrombocytopenic purpura responders; 24 were considered nonresponders. Platelet counts improved by more than 100 x 10(9) L(-1) in 11 (44%) of the 25 patients cured of H. pylori infection, while none of the 10 patients H. pylori-negative patients experienced the same improvement (P = 0.015). Univariate analysis showed that H. pylori infection and its eradication were significant factors associated with platelet recovery (P = 0.015).
CONCLUSIONS: Helicobacter pylori infection played a role in the pathogenesis of idiopathic thrombocytopenic purpura in approximately 30% of all patients assessed and 45% of the patients with H. pylori infection. Eradication of H. pylori in idiopathic thrombocytopenic purpura patients led to improved disease activity.
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