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.