DISCUSSION
The pathogenesis of ITP is not completely clear, and its exact cause has not yet been elucidated. However, the main underlying mechanisms are considered to be an antibody–induced increase in platelet destruction, shortened platelet lifespan and diminished platelet production (9). Although there is no proven mechanism concerning the pathogenesis, certain theories based on the molecular similarity between platelets andH. pylori antigens, platelet aggregation, and down–regulation of the reticuloendothelial system have been propounded in an attempt to explain the role of H. pylori in the development of ITP (10).
The prevalence of H. pylori infection varies between 22% and 85% in patients with chronic ITP (7). There is not enough evidence to support the routine screening of ITP patients for H. pylori or the administration of eradication therapy to patients who are H. pylori –negative or patients whose H. pylori states are unknown (11). The predominant view is that appropriate patients with typical ITP can be administered eradication therapy, both due to its low cost and toxicity, and because it can achieve an increase in the platelet count in H. pylori –positive patients (7). Prospective controlled studies conducted on this matter by Rostami et al. (12) and Suzuki et al. (13) showed that platelet count increased in response to H. pylori eradication and that this was an appropriate therapeutic option for the patients. Following from this, the present study included patients who had never received eradication therapy in order to eliminate potential influence on the targeted treatment outcomes, and compared treatment outcomes between H. pylori –positive andH. pylori –negative patients by assigning them to two different groups.
The primary objective of ITP treatment is to prevent bleeding by raising the platelet count to a constant level. In the absence of bleeding or predisposing comorbid conditions, treatment is rarely required if a platelet count >50×109/L is present; and it is reported that treatment must only be considered in symptomatic patients with a platelet count lower than 30×109/L (14). All patients in this study had symptoms of active bleeding and/or required treatment according to their platelet count.
The treatment involves medications that increase the platelet count by decreasing the scale of platelet destruction through different mechanisms, and immunosuppressive corticosteroid medications constitute the first–line option among these. In patients who have active bleeding or in whom corticosteroid use is contraindicated, intravenous immunoglobulin or anti–D globulin can be used, either in combination with corticosteroids or as a standalone treatment (15). First–line treatment options for ITP are similar for all patients, regardless of whether or not a H. pylori infection are present (14). Accordingly, the treatment options received by the two groups in our study were similar and the great majority of the patients had received corticosteroid as the first–line treatment. Where symptoms of bleeding were present and/or a fast increase in platelet count was required, patients received IVIG in combination with standard or high–dose corticosteroids.
The main mechanism underlying the low platelet count seen in H. pylori– positive ITP patients is thought to be the destruction of existing platelets by an immune–mediated mechanism rather than a diminution of platelet production. This mechanism was first introduced to the literature by Byrne et al. (16) and later confirmed by another study conducted by Teawtrakul et al. (17). In our study, the response rates achieved by the first–line use of immunosuppressive or immunomodulatory medications were comparable betweenH.pylori –positive and H.pylori –negative patients. Accordingly, the results we obtained in this study corroborate the mechanism described above.
A review of the literature reveals that previous clinical and review studies and have mainly focused on the effects of eradication therapy on the platelet count response in H.pylori –positive andH.pylori –negative ITP patients (18, 19). The methods and the results of the present retrospective investigation are distinct from other studies. To the best of our knowledge, the present study is unique as its main component is the direct evaluation of response rates to the first–line treatment in H.pylori –positive andH.pylori –negative ITP patients who did not undergo eradication therapy; and it is valuable in this aspect.
Although the findings of this study may suggest that it is not necessary to routinely screen ITP patients for H.pylori before initiating the first–line treatment, the difference between the groups with respect to recurrence rates and response rates to post–recurrence treatment during long–term follow–up have not yet been elucidated.
In conclusion, although the literature suggests that the platelet count could be increased by standalone eradication therapy without administering conventional ITP treatment, it can be stated based on the present study that response rates to the first–line treatment without eradication therapy are comparable between H.pylori –positive andH.pylori –negative ITP patients in whom treatment is indicated.