Volume 18, Issue 5 pp. 547-551

Association of Helicobacter pylori with thrombotic thrombocytopenic purpura and hemolytic uremic syndrome after bone marrow transplantation

Hiroyuki Takatsuka

Hiroyuki Takatsuka

 Division of Hematology and Oncology, Department of Internal Medicine

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Takeshi Wakae

Takeshi Wakae

 Division of Hematology and Oncology, Department of Internal Medicine

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Akinari Toda

Akinari Toda

 Division of Hematology and Oncology, Department of Internal Medicine

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Hisayuki Itoi

Hisayuki Itoi

 Division of Hematology and Oncology, Department of Internal Medicine

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Masaya Okada

Masaya Okada

 Division of Hematology and Oncology, Department of Internal Medicine

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Mahito Misawa

Mahito Misawa

 Division of Hematology and Oncology, Department of Internal Medicine

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Hiroshi Hara

Hiroshi Hara

 Division of Hematology and Oncology, Department of Internal Medicine

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Eizo Kakishita

Eizo Kakishita

 Division of Thrombosis, Haemostasis and Geriatri Medicine, Department of Medicine, Hyogo College of Medicine, Hyogo, Japan

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First published: 01 September 2004
Citations: 12
H Takatsuka, Division of Hematology and Oncology, Department of Internal Medicine, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan.
Tel.: +81 798 45 6886; fax: +81 798 45 6887
e-mail: [email protected]

Abstract

Abstract: Thrombotic microangiopathy (TMA) has attracted attention as a complication of bone marrow transplantation (BMT). The association of Helicobacter pylori (H. pylori) with thrombotic thrombocytopenic purpura and hemolytic uremic syndrome (TTP/HUS) after BMT was studied. Among 74 consecutive patients undergoing transplantation, six developed TTP/HUS (the TTP/HUS group) and 68 did not (controls). These six patients were compared with the other 68 patients to investigate differences of the IL-12 and 8 levels, H. pylori and various clinical characteristics. The patients who developed TTP/HUS seemed not apparently different from those who did not in background characteristics, except that they had a significantly higher H. pylori-positive rate (p < 0.05). In the TTP/HUS group, however, the levels of interleukin-12 and interleukin-8 increased significantly during the leukocyte recovery after BMT and at the onset of TTP/HUS, respectively, to 45.8 ± 57.6 pg/mL and 274.8 ± 65.9 pg/mL (p < 0.05 for both), when compared with their levels of 5.0 pg/mL in the control group. Thus, H. pylori may play a role in the pathogenesis of TTP/HUS after BMT, with cytokines (interleukin-8 and interleukin-12) also being involved.

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