Helicobacter pylori Eradication in Patients with Immune Thrombocytopenic Purpura: A Review and the Role of Biogeography.
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.
Department of Biological Engineering, Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA, USA.
Galit H
GH
Frydman
Department of Biological Engineering, Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA, USA.
Nick
N
Davis
The Gastrointestinal Research Group, Division of Gastroenterology, University of Calgary, Calgary, AB, Canada.
Paul L
PL
Beck
Department of Biological Engineering, Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA, USA.
James G
JG
Fox
D000328:Adult; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D000942:Antigens, Bacterial / Q000235:genetics / Q000276:immunology; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D015551:Autoimmunity / Q000235:genetics / Q000276:immunology; D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology; D001792:Blood Platelets / Q000276:immunology; D019295:Computational Biology; D016481:Helicobacter Infections / Q000276:immunology* / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics / Q000276:immunology*; D006801:Humans; D007116:Immunization, Passive; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008875:Middle Aged; D018716:Molecular Mimicry / Q000235:genetics / Q000276:immunology; D058974:Phylogeography; D015539:Platelet Activation / Q000276:immunology; D010980:Platelet Membrane Glycoproteins / Q000276:immunology; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology
D000900:Anti-Bacterial Agents; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D007166:Immunosuppressive Agents; D010980:Platelet Membrane Glycoproteins; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori
CagA; Helicobacter; biogeography; immune-mediated; infectious; thrombocytopenia