Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by production of auto
antibodies against platelet surface antigens. ITP affects women more often than men and is more common
in children than adults. ITP is a diagnosis of exclusion after other identifiable etiologies have been
ruled out. After the first report by Gasbarrini et al. (1998) showing rising platelet counts in ITP patients
following Helicobacter pylori (HP) eradication therapy, there is growing evidence that highlights the role
of HP in triggering ITP. The H-pylori infection induced ITP is validated by many proposed mechanisms
such as molecular mimicry due to production of auto antibodies against H-pylori surface virulent factors
(CagA) and cross reactivity of these antibodies with platelet surface antigens (GP IIb/IIIa, GP Ib/IX,
and GP Ia/IIa), phagocytic perturbation due to enhanced phagocytic activity of monocytes, enhanced
dendritic cell numbers and response, platelets aggregation due to presence of anti- H-pylori IgG and von
Willebrand factor (vWf) and finally host immune response against H-pylori virulent factors CagA and
VacA leading to ITP.
Eradication of Helicobacter pylori infection has been variably associated with a platelet response in
patients with immune thrombocytopenic purpura (ITP). Eradication therapy is simple and inexpensive,
with limited toxicity and the advantage of avoiding long-term immunosuppressive treatment for those
who respond. Although the evidence and follow-up are limited, it appears reasonable to routinely screen
patients with ITP for H pylori, particularly in those populations with a high background prevalence of
H pylori infection.
