Helicobacter pylori Eradication in Patients with Immune Thrombocytopenic Purpura: A Review and the Role of Biogeography

Abstract

Idiopathic thrombocytopenic purpura (ITP) is typically a diagnosis of exclusion, assigned by clinicians after ruling out other identifiable etiologies. Since a report by Gasbarrini et al. in 1998, an accumulating body of evidence has proposed a pathophysiological link between ITP and chronic Helicobacter pylori (H. pylori) infection. Clinical reports have described a spontaneous resolution of ITP symptoms in about 50% of chronic ITP patients following empirical treatment of H. pylori infection, but response appears to be geography dependent. Studies have also documented that ITP patients in East Asian countries are more likely to express positive antibody titers against H. pylori-specific cytotoxic-associated gene A (CagA), a virulence factor that is associated with an increased risk for gastric diseases including carcinoma. While a definitive mechanism by which H. pylori may induce thrombocytopenia remains elusive, proposed pathways include molecular mimicry of CagA by host autoantibodies against platelet surface glycoproteins, as well as perturbations in the phagocytic activity of monocytes. Traditional treatments of ITP have been largely empirical, involving the use of immunosuppressive agents and immunoglobulin therapy. However, based on the findings of clinical reports emerging over the past 20 years, health organizations around the world increasingly suggest the detection and eradication of H. pylori as a treatment for ITP. Elucidating the exact molecular mechanisms of platelet activation in H. pylori-positive ITP patients, while considering biogeographical differences in response rates, could offer insight into how best to use clinical H. pylori eradication to treat ITP, but will require well-designed studies to confirm the suggested causative relationship between bacterial infection and an autoimmune disease state.

Epidemiology, clinical impacts and current clinical management of Helicobacter pylori infection

“…In most cases, the association has not been shown to be causal, and common conditions will inevitably coexist in some patients. There are modest data linking H. pylori to immune thrombocytopenic purpura, and eradication therapy is often tried, with variable results 35 …”

Adult‐onset, chronic, cyclic thrombocytopenia in a Rhesus macaque (Macaca mulatta) after dengue virus vaccination and viral challenge

“…5 Because H. pylori , the human gastric pathogen, has been linked to thrombocytopenia in select patients, the monkey was treated with a H. pylori eradication antibiotic therapy consisting of clarithromycin 15 mg/kg PO BID and amoxicillin 20 mg/kg PO BID for 10 days, and omeprazole 0.6 mg/kg PO SID for 21 days. 6 Antibiotic treatment for the H. suis infection did not resolve the coagulopathy and the episodes of petechiae +/− ecchymoses recurred. Although there was negative silver staining on gastric tissue collected during necropsy, 16S rRNA revealed that this antibiotic treatment did not completely eradicate the Helicobacter infection.…”

Prevalence of Helicobacter pylori Antibodies in Egyptians with Idiopathic Thrombocytopenic purpura and in the General Egyptian Population: A Comparative Study

“…While a definitive mechanism by which H. pylori may induce thrombocytopenia remains elusive, proposed pathways include molecular mimicry of CagA by host auto antibodies against platelet surface glycoproteins, as well as alterations in the phagocytic activity of monocytes (Frydman et al, 2015).…”