Isoantibody against CD36 (anti-Nak^a) can cause platelet transfusion refractoriness and serious adverse reactions, including transfusion-related acute lung injury (TRALI). CD36-deficient individuals may produce anti-Nak^a after immunizing events. Indeed, we previously identified three anti-Nak^a-positive donors when we examined 2,497 TRALI-inducing blood products. Although the 268C>T mutation in exon 4 of the CD36 gene is frequently found in Japanese individuals with CD36 deficiency, the correlation between mutations of the CD36 gene and anti-Nak^a production remains unclear. In this study, to clarify whether specific mutations of the CD36 gene are involved in the production of anti-Nak^a, we performed a sequence analysis of the gene in six anti-Nak^a-positive donors, including the three donors described above. We also analyzed 108 anti-Nak^a-negative donors with CD36 deficiency as controls. All anti-Nak^a-positive donors were homozygous for 329_330delAC and 949insA, whereas 268C>T was not found. In contrast, 268C>T was frequently found in the anti-Nak^a-negative control donors. Some of the healthy male donors in this study were also positive for anti-Nak^a, indicating that anti-Nak^a production is not limited to cases involving transfusion or pregnancy. As such, it may be important to focus on mutations other than 268C>T to identify donors who may potentially produce anti-Nak^a.

To prevent adverse events following platelet transfusion, it is usually recommended that platelet concentrate products (PCs) be washed with a cooling centrifuge. However, the majority of hospitals do not have access to suitable equipment. On the other hand, almost all hospitals have hollow fiber membrane equipment on hand for hemodialysis and plasma exchange. Given this situation, we decided to develop a new method for preparing washed platelet concentrate (WPC) using a membrane plasma separator. We compared the quality with WPC prepared by the centrifuge method (CM) and our newly developed membrane method (MM). The new MM consists of 4 processes; 1) a separator (EC-4A10, Kawasumi Laboratories, INC.) is first rinsed. 2) Platelets are primed outside of the hollow fibers. 3) The platelets are then washed with 1,200 ml of BRS-A (Bicarbonate Ringer's solution with ACD-A) and 4) recovered with 240 ml of BRS-A. The platelet recovery rates were 95.8% in MM and 90.4% in CM (p<0.05). The removal rates of plasma proteins were significantly superior in CM compared to those in MM. Specifically, albumin, IgG, IgA, IgM and total protein removal rates in CM were 97.2%, 96.2%, 96.2%, 97.2%, 95.7%, while those in MM were 93.2%, 92.1%, 78.0%, 7.3%, 85.8% (p<0.05). On the other hand, the CD62P-selectin levels were significantly lower in MM than in CM when measured at 1, 12, 24 hours after the respective procedures. In conclusion, MM was superior in having a higher platelet recovery rate and less platelet activation than CM. However, plasma proteins were more poorly removed in MM. We assume that this result was due to the relation between protein molecular weight and membrane pore size. However, currently it is not clearly known how important of a role these proteins take in adverse transfusion reactions, and further examination is needed.

The B_m and AB_m phenotypes are the most prevalent ABO subgroups in Japanese and are produced via the partial deletion of intron 1 of the B gene. The deleted section is 5.8-kb long and includes a transcription enhancer element, which contains 2 GATA motifs. A case in which an individual who exhibited the B_m phenotype displayed a GATA>GAGA mutation, but not the abovementioned deletion in the transcription enhancer element, has been reported. The individual's serological properties were similar to those of the typical B_m phenotype, but B antigen could not be detected in their saliva because they were a non-secretor.

Here, we report a novel case in which a secretor who exhibited the B_m phenotype was found to be carrying a GATA>GAGA mutation in the B gene. This mutation reduced the expression of B antigen on red blood cells, but did not affect the amount of B antigen in the subject's saliva.

There are two standards of hypertonic albumin products in Japan, a 20% w/v human albumin solution formulation and a 25% formulation, but there have been no guidelines for their proper usage. To reduce waste and use albumin properly in our hospital, the Hospital Transfusion Committee committed to enforcing the switching of 25% albumin formulation to 20% formulation. After this change, although 25% formulation accounted for a dominant 72.8% (20,375 g) of hypertonic albumin products in year 2008, 20% formulation accounted for 77.8% (16,190 g) of hypertonic albumin in 2014, which led to a reduction of 10,507.5 g of total albumin.

We report a case of aplastic anemia in a child complicated by severe infection, for which granulocytes with incompatible red cells (total 160 ml) were transfused. A pediatric patient known to have anti-Jk^a antibodies (titer 1) developed sepsis and multi-organ failure during immunosuppressive therapy. An ABO-compatible related donor was found to be Jk (a+b-). In this instance, no hemolytic transfusion reaction was observed. Among Japanese, only 30% of ABO-compatible donors are Jk (a-). After granulocyte transfusion, the direct antiglobulin test remained negative and anti-Jk^a titers did not rise. No hemolysis of Jk (a+) red cells was evident from biochemical and serological tests.