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Association of Helicobacter pylori with thrombotic thrombocytopenic purpura and hemolytic uremic syndrome after bone marrow transplantation
Author(s) -
Takatsuka Hiroyuki,
Wakae Takeshi,
Toda Akinari,
Itoi Hisayuki,
Okada Masaya,
Misawa Mahito,
Hara Hiroshi,
Kakishita Eizo
Publication year - 2004
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/j.1399-0012.2004.00224.x
Subject(s) - medicine , thrombotic microangiopathy , thrombotic thrombocytopenic purpura , helicobacter pylori , gastroenterology , transplantation , pathogenesis , complication , immunology , platelet , disease
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.