• Eur Rev Med Pharmacol Sci · Aug 2015

    Helicobacter pylori and mean platelet volume: a relation way before ımmune thrombocytopenia?

    • H Umit and E G Umit.
    • Department of Gastroenterology, Trakya University Medical Faculty, Edirne, Turkey. hasanumit@hotmail.com.
    • Eur Rev Med Pharmacol Sci. 2015 Aug 1; 19 (15): 2818-23.

    ObjectiveHelicobacter pylori is associated with chronic immune thrombocytopenia. Eradication of H. pylori has been related with a platelet response and this treatment has been included within management strategies for a certain group of patients. However, in patients with normal platelet counts, the effects of H. pylori infection on platelet count and mean platelet volume as an important platelet index have not been investigated. In this study, we aimed to assess the relation between platelet indices and H. pylori infection in patients with dyspepsia who have otherwise normal platelet counts.Patients And MethodsIn a retrospective manner, 4823 patients with dyspeptic complaints who have underwent an upper gastrointestinal endoscopy and a rapid urease test were included. Data of whole blood counts before the procedure were recorded from their files. Patients with normal endoscopic findings or simple gastritis were included. Patients with malignancy, GI bleeding, portal hypertension, liver or kidney disease and taking nonsteroidal anti-inflammatory drugs, proton pump inhibitors, cytotoxic medications were excluded.ResultsMean platelet count in H. pylori positive and negative patients were 246381± 92225/mm3 and 258135 ± 89912/mm3, respectively (p<0.001). Mean MPV was higher in H. pylori positive group (8.9± 1.3 vs. 8.23 ± 0.94, p<0.001). This difference was observed in both genders. MPV was observed to be higher than 10 fL in 20.5% of HP positive patients while in only 2.8% of H. pylori negative patients (p<0.0001).ConclusionsIn patients with H. pylori infection and normal platelet counts, it may be speculated that an ongoing and compensated platelet destruction-production process may be responsible for the increase in MPV. Likewise, in conditions exclusive for the host or the H. pylori strain, platelet destruction may be enhanced leading to immune thrombocytopenia. As our study is the first study to investigate the effect of H. pylori in patients with normal platelet counts, our findings may give way to further prospective researches.

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