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Helicobacter pylori and Idiopathic Thrombocytopenic Purpura

Francesco Franceschi, MD; Nicholas Christodoulides, PhD; Michael H. Kroll, MD; and Robert M. Genta, MD
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From Catholic University of Rome, 00168 Rome, Italy; and Baylor College of Medicine and Veterans Affairs Medical Center, Houston, TX 77030.


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Ann Intern Med. 2004;140(9):766-767. doi:10.7326/0003-4819-140-9-200405040-00028
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Grahic Jump Location
Figure.
Cross-reactivity between anti–cytotoxin-associated gene A (anti-CagA) antibodies and human platelet antigens.

Monoclonal anti-CagA antibodies recognized 2 platelet antigens (50 and 55 kDa) in patients with previous idiopathic thrombocytopenic purpura (ITP ) (patients A, B, G, and H) or active ITP (patients C, D, I, and L [patients C and D were Helicobacter pylori–positive]), but only 1 antigen (50 kDa) in 3 of 4 normal controls (patients E, F, and M) (P< 0.01 by chi-square analysis). Among the normal cofntrols, only patient N showed the additional 55-kDa band.

Grahic Jump Location

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Idiopathic thrombocytopenic purpura and Helicobacter pylori
Posted on May 20, 2004
Giovanni Emilia
Department of Oncology and Hematology. University of Modena and Reggio Emilia. Modena, Italy
Conflict of Interest: None Declared

The interesting report by Franceschi and colleagues (1) arouses some perplexities, we would like to address. The authors investigated the cross-reactivity between H.pylori and platelet antigens in patients previously studied in 1998 (Ref.:10), whose platelet counts increased "after eradication of CagA-positive H.pylori infection". Unfortunately, in the cited paper there is no mention about anti-CagA antibodies. Has the detection of antibodies been performed on archival specimens?. Moreover, it is stated that "no patient received treatment for ITP". Since in their previous paper the authors stated "patients were given steroids"¦" it is important to know when and how long steroids were administered. Similarly, it is not clear when and from which material the platelet lysates of the 6 patients eradicated and responsive were isolated. Again, are the 6 patients "with active and untreated ITP" new patients? It is stated that "before therapy, 5 of these 11 patients had anti-glycoprotein (GP) IIb/IIIa antibodies" and "no changes in antibody levels were observed"¦". In the previous paper, related to the same patients, it is stated that "six out of these eight patients had disappearance of autoantibodies against platelets". Is it concerning different antibodies or different observations? The presence, in the Figure (Figure 2 ?), of a gel artifact (lane F), makes the evaluation of the data in controls problematic. Have the controls been investigated for H. pylori infection? Finally, a not negligible question is whether the suggestive presence of an additional antigen of 55 kDa is actually specific for ITP platelets or may be related to other cell types in ITP patients. Recently, Takahashi et al. (2) found that platelet eluates recognized H.pylori CagA protein of 140kDa in 12 ITP patients (nine H.pylori-positive and three H.pylori-negative). Whether these platelet antigens are "native" in the general population or specifically expressed in ITP platelets, should be deeply addressed.

References 1. Franceschi F, Christodoulides N, Kroll MH, Genta RM. Helicobacter pylori and idiopathic thrombocytopenic purpura. Ann Intern Med. 2004;140:766-67. 2. Takahashi T, Yujiri T, Shinohara K, Inoue Y, Sato Y, Fujii Y, et al. Molecular mimicry by Helicobacter pylori CagA protein may be involved in the pathogenesis of H. pylori-associated chronic idiopathic thrombocytopenic purpura. Br J Haematol. 2004;124:91-6.

Conflict of Interest:

None declared

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