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Immune Thrombocytopenic Purpura and Helicobacter pylori Infection

Immune Thrombocytopenic Purpura and Helicobacter pylori Infection We read with great interest the article by Michel et al1 on a possible association between Helicobacter pylori infection and autoimmune thrombocytopenic purpura (AITP) in adults. The authors found no cross-reactivity between platelet and H pylori antibodies and, on this basis, they excluded the evidence of an association between bacterial infection and AITP. In their series of adults of white French origin, Michel et al detected a similar seroprevalence of H pylori in patients with AITP and in control subjects (29%). These data, although related to a small series, may be of interest, even if it is well known that seroprevalence of H pylori is greatly variable from country to country also in healthy individuals. A recent review2 of the literature found that of 193 patients with AITP investigated so far in various countries, 112 (58%) were positive for H pylori infection. Michel et al chose the serologic antibody detection method for H pylori isolation. This choice might be misleading because antibody titers may remain positive for years after successful treatment, and, unlike the urea breath test and stool antigen testing, this method does not denote active H pylori infection.3 In our opinion, a temporal correlation between bacterial infection and AITP should be considered to establish an association between such 2 conditions. The investigation of a molecular mimicry mechanism was performed in only 3 patients with AITP.1 This series seems too small to draw consistent conclusions. Furthermore, no information was provided about the responsiveness of such patients to bacterial eradication treatment. Considering that, to our knowledge, only 49% of infected patients with AITP respond well to antibiotics with platelet count increase,2 the pathogenetic mechanisms might be different between responders and nonresponders. Molecular mimicry is only one of the possible pathogenetic mechanisms. Early studies indicated the possible occurrence of B-cell clonal population in patients with AITP.4 Moreover, gastric extranodal marginal zone B-cell lymphomas were found associated with H pylori infection in virtually all cases, suggesting a possible H pylori direct antigenic stimulation.5 The etiopathogenetic link between such gastric lymphoma and bacterial infection has also been shown by the regression of some cases by antibiotic treatment.6 Nevertheless, in a subset of gastric extranodal marginal zone B-cell lymphomas, tumor immunoglobulins seem to be autoantigen related rather than specific to H pylori, and the neoplastic growth seems to be sustained by stimulation through a H pylori–specific T-cell reaction.7 In this context, we cannot exclude that H pylori may be one of the possible antigens involved in the benign, clonal B-cell selection in gastric germinal centers, with an indirect association with AITP. Finally, the short time span between bacterial eradication and platelet increase in infected patients with AITP investigated so far may rule out the occurrence of spontaneous remission of thrombocytopenia. This eventuality is greatly variable in adult patients with chronic AITP, spanning from 0%8 to 9%,9 and seems to not contradict the evidence, even if indirect, of an association between H pylori infection and AITP. References 1. Michel MKhellaf MDesforges L et al. Autoimmune thrombocytopenic purpura and Helicobacter pylori infection. Arch Intern Med. 2002;1621033- 1036Google ScholarCrossref 2. Emilia GLuppi MMorselli MPotenza LD'Apollo NTorelli G Helicobacter pylori infection and idiopathic thrombocytopenic purpura. Br J Haematol. 2002;1181198- 1199Google ScholarCrossref 3. Peterson WLFendrick MCave DR et al. Helicobacter pylori–related disease. Arch Intern Med. 2000;1601285- 1291Google ScholarCrossref 4. van der Harst Dde Jong DLimpens J et al. Clonal B-cell populations in patients with idiopathic thrombocytopenic purpura. Blood. 1990;762321- 2326Google Scholar 5. Wotherspoon ACOrtiz-Hidalgo CFalzon MFIsaacson PG Helicobacter pylori–associated gastritis and primary B-cell gastric lymphoma. Lancet. 1991;3381175- 1176Google ScholarCrossref 6. Wotherspoon ACDoglioni CDiss TC et al. Regression of primary low-grade B-cell gastric lymphoma of mucosa associated lymphoid tissue type after eradication of Helicobacter pylori. Lancet. 1993;342575- 577Google ScholarCrossref 7. Hussel TIsaacson PGCrabtree JESpencer J The response of cells from low-grade B-cell gastric lymphoma of mucosa associated lymphoid tissue to Helicobacter pylori. Lancet. 1993;342571- 574Google ScholarCrossref 8. Vianelli NValdre LFiacchini M et al. Long-term follow-up of idiopathic thrombocytopenic purpura in 310 patients. Haematologica. 2001;86504- 509Google Scholar 9. Stasi RStipa EMasi M et al. Long-term observation of 208 adults with chronic idiopathic thrombocytpenic purpura. Am J Med. 1995;98436- 442Google ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Internal Medicine American Medical Association

Immune Thrombocytopenic Purpura and Helicobacter pylori Infection

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Immune Thrombocytopenic Purpura and Helicobacter pylori Infection

Abstract

We read with great interest the article by Michel et al1 on a possible association between Helicobacter pylori infection and autoimmune thrombocytopenic purpura (AITP) in adults. The authors found no cross-reactivity between platelet and H pylori antibodies and, on this basis, they excluded the evidence of an association between bacterial infection and AITP. In their series of adults of white French origin, Michel et al detected a similar seroprevalence of H pylori in patients with AITP and...
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Publisher
American Medical Association
Copyright
Copyright © 2003 American Medical Association. All Rights Reserved.
ISSN
0003-9926
eISSN
1538-3679
DOI
10.1001/archinte.163.1.120-a
Publisher site
See Article on Publisher Site

Abstract

We read with great interest the article by Michel et al1 on a possible association between Helicobacter pylori infection and autoimmune thrombocytopenic purpura (AITP) in adults. The authors found no cross-reactivity between platelet and H pylori antibodies and, on this basis, they excluded the evidence of an association between bacterial infection and AITP. In their series of adults of white French origin, Michel et al detected a similar seroprevalence of H pylori in patients with AITP and in control subjects (29%). These data, although related to a small series, may be of interest, even if it is well known that seroprevalence of H pylori is greatly variable from country to country also in healthy individuals. A recent review2 of the literature found that of 193 patients with AITP investigated so far in various countries, 112 (58%) were positive for H pylori infection. Michel et al chose the serologic antibody detection method for H pylori isolation. This choice might be misleading because antibody titers may remain positive for years after successful treatment, and, unlike the urea breath test and stool antigen testing, this method does not denote active H pylori infection.3 In our opinion, a temporal correlation between bacterial infection and AITP should be considered to establish an association between such 2 conditions. The investigation of a molecular mimicry mechanism was performed in only 3 patients with AITP.1 This series seems too small to draw consistent conclusions. Furthermore, no information was provided about the responsiveness of such patients to bacterial eradication treatment. Considering that, to our knowledge, only 49% of infected patients with AITP respond well to antibiotics with platelet count increase,2 the pathogenetic mechanisms might be different between responders and nonresponders. Molecular mimicry is only one of the possible pathogenetic mechanisms. Early studies indicated the possible occurrence of B-cell clonal population in patients with AITP.4 Moreover, gastric extranodal marginal zone B-cell lymphomas were found associated with H pylori infection in virtually all cases, suggesting a possible H pylori direct antigenic stimulation.5 The etiopathogenetic link between such gastric lymphoma and bacterial infection has also been shown by the regression of some cases by antibiotic treatment.6 Nevertheless, in a subset of gastric extranodal marginal zone B-cell lymphomas, tumor immunoglobulins seem to be autoantigen related rather than specific to H pylori, and the neoplastic growth seems to be sustained by stimulation through a H pylori–specific T-cell reaction.7 In this context, we cannot exclude that H pylori may be one of the possible antigens involved in the benign, clonal B-cell selection in gastric germinal centers, with an indirect association with AITP. Finally, the short time span between bacterial eradication and platelet increase in infected patients with AITP investigated so far may rule out the occurrence of spontaneous remission of thrombocytopenia. This eventuality is greatly variable in adult patients with chronic AITP, spanning from 0%8 to 9%,9 and seems to not contradict the evidence, even if indirect, of an association between H pylori infection and AITP. References 1. Michel MKhellaf MDesforges L et al. Autoimmune thrombocytopenic purpura and Helicobacter pylori infection. Arch Intern Med. 2002;1621033- 1036Google ScholarCrossref 2. Emilia GLuppi MMorselli MPotenza LD'Apollo NTorelli G Helicobacter pylori infection and idiopathic thrombocytopenic purpura. Br J Haematol. 2002;1181198- 1199Google ScholarCrossref 3. Peterson WLFendrick MCave DR et al. Helicobacter pylori–related disease. Arch Intern Med. 2000;1601285- 1291Google ScholarCrossref 4. van der Harst Dde Jong DLimpens J et al. Clonal B-cell populations in patients with idiopathic thrombocytopenic purpura. Blood. 1990;762321- 2326Google Scholar 5. Wotherspoon ACOrtiz-Hidalgo CFalzon MFIsaacson PG Helicobacter pylori–associated gastritis and primary B-cell gastric lymphoma. Lancet. 1991;3381175- 1176Google ScholarCrossref 6. Wotherspoon ACDoglioni CDiss TC et al. Regression of primary low-grade B-cell gastric lymphoma of mucosa associated lymphoid tissue type after eradication of Helicobacter pylori. Lancet. 1993;342575- 577Google ScholarCrossref 7. Hussel TIsaacson PGCrabtree JESpencer J The response of cells from low-grade B-cell gastric lymphoma of mucosa associated lymphoid tissue to Helicobacter pylori. Lancet. 1993;342571- 574Google ScholarCrossref 8. Vianelli NValdre LFiacchini M et al. Long-term follow-up of idiopathic thrombocytopenic purpura in 310 patients. Haematologica. 2001;86504- 509Google Scholar 9. Stasi RStipa EMasi M et al. Long-term observation of 208 adults with chronic idiopathic thrombocytpenic purpura. Am J Med. 1995;98436- 442Google ScholarCrossref

Journal

Archives of Internal Medicine – American Medical Association

Published: Jan 13, 2003

Keywords: helicobacter infections,purpura, thrombocytopenic, idiopathic

References

  • Autoimmune thrombocytopenic purpura and Helicobacter pylori infection.
    Desforges L; Arch Intern Med.
  • Helicobacter pylori infection and idiopathic thrombocytopenic purpura.
    Torelli G; Br J Haematol.
  • Helicobacter pylori–related disease.
    Cave DR; Arch Intern Med.
  • Clonal B-cell populations in patients with idiopathic thrombocytopenic purpura.
    Limpens J; Blood.
  • Helicobacter pylori–associated gastritis and primary B-cell gastric lymphoma.
    Isaacson PG; Lancet.
  • Regression of primary low-grade B-cell gastric lymphoma of mucosa associated lymphoid tissue type after eradication of Helicobacter pylori.
    Diss TC; Lancet.
  • The response of cells from low-grade B-cell gastric lymphoma of mucosa associated lymphoid tissue to Helicobacter pylori.
    Spencer J; Lancet.
  • Long-term follow-up of idiopathic thrombocytopenic purpura in 310 patients.
    Fiacchini M; Haematologica.
  • Long-term observation of 208 adults with chronic idiopathic thrombocytpenic purpura.
    Masi M; Am J Med.

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