Japanese Journal of Transfusion and Cell Therapy
Online ISSN : 1883-0625
Print ISSN : 1881-3011
ISSN-L : 1881-3011
Volume 52, Issue 5
Displaying 1-4 of 4 articles from this issue
  • Kenji Matsumoto, [in Japanese]
    2006 Volume 52 Issue 5 Pages 583-588
    Published: October 27, 2006
    Released on J-STAGE: March 12, 2010
    JOURNAL FREE ACCESS
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  • Shinobu Wakamoto, Mitsuhiro Fujihara, Toru Miyazaki, Daisuke Takahashi ...
    2006 Volume 52 Issue 5 Pages 589-598
    Published: October 27, 2006
    Released on J-STAGE: March 12, 2010
    JOURNAL FREE ACCESS
    It has been proposed that anti-platelet antibodies having the ability to induce platelet activation are involved in not only thrombocytopenic states, but also in the pathology of nonhemolytic transfusion reactions (NHTRs). Recently, we reported that anti-CD36 Abs-containing plasma, derived from the donor SS, was implicated in NHTRs, and induced platelet activation, suggesting the involvement of anti-CD36 Abs in the occurrence of NHTRs. In addition to the serum derived from donor SS (SS serum), one of 13 anti-CD36 Abs-containing sera (anti-CD36 sera) also caused platelet aggregation. The factors that determine the platelet-activating abilities of anti-CD36 sera might also influence the occurrence of anti-CD36 Abs-related NHTRs. In this study, we focused on the relationship between the anti-CD36 Ab titer in sera and the platelet-activating ability of sera to elucidate the determinants of the platelet-activating action of anti-CD36 sera.
    Sixteen anti-CD36 sera (serum #1∼#15), including the SS serum, were incubated with CD36-positive or-negative platelets. Platelet aggregation, the RANTES release and the titer of anti-CD36 Abs in sera were then determined. The two sera (SS serum and serum #1) that induced CD36-specific platelet activation had higher titers (x512) of anti-CD36 Abs than the other sera (less than x128). When SS serum and serum #1 were diluted to a titer of x128, the platelet-activating ability was lost. Furthermore, a subthreshold dose of epinephrine potentiated the platelet aggregation induced by SS serum and serum #1 at a titer of x256 and x341, respectively. When diluted to a titer of x128, however, both sera, failed to induce aggregation even in presence of epinephrine. Similarly, there was no synergistic platelet activation by epinephrine and any of the other anti-CD36 sera showing a titer of x128 or less.
    These findings demonstrated that the platelet-activating ability of anti-CD36 serum depends on the anti-CD36Ab titer, suggesting that the titer of anti-CD36 Abs in blood components may determine the occurrence of anti-CD36 Abs-related NHTRs.
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  • Shoko Kajimoto, Motohiro Fujii, Yoshiyuki Matsumoto, Hiroyuki Ishii, Y ...
    2006 Volume 52 Issue 5 Pages 599-606
    Published: October 27, 2006
    Released on J-STAGE: March 12, 2010
    JOURNAL FREE ACCESS
    In October 2004, a case of Hepatitis B infection was reported to the Kanagawa Red Cross Blood Center. Individual nucleic amplification testing (ID-NAT) was perfomed to study 33 preserved blood samples of donors whose blood had been transfused to the patient. One donor, a 54-year-old male who had donated 78 times during the past 11 years, was found to be positive by ID-NAT. We had previously received reports from different hospitals of three patients with hepatitis. At that time, although a retrospective study was performed using ID-NAT, all the preserved blood samples were negative. Surprisingly, all three patients had received apheresis platelet concentrates derived from the propositus donor. DNA sequence analysis of the HBV of this donor and of three of the four patients revealed 99.8-9% homology and all were genotype C conclusively confirming that the hepatitis B was transmitted from this donor. We have succeeded in following-up the 12 patients for at least six months after transfusion. All had hematological malignancies and had been transfused during chemotherapy. Four patients did not show any change in serological markers where as four were positive, with transmission confirmed by changes in serological markers.
    To our knowledge, this case is the first to demonstrate that it is not possible to detect all occult HBV carriers, even by the use of ID-NAT. Furthermore, this case demonstrates that even when a sample is ID-NAT-negative, blood from an occult HBV carrier is a possible source of HBV infection for immunocompromised patients.
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  • 2006 Volume 52 Issue 5 Pages 618-619
    Published: October 27, 2006
    Released on J-STAGE: March 12, 2010
    JOURNAL FREE ACCESS
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