This study compared test methods for detailed examination of blood type after ABO-incompatible cord blood transplantation. Of the 72 subjects who underwent transplantation between May 2016 and October 2018, 34 had a major mismatch, 25 had a minor mismatch, and 13 had a major/minor mismatch. After transplantation, the first follow up was performed in those with no history of transfusion in the previous 3 months. Conversion to the donor blood type was confirmed by forward cell grouping, changes in antibodies by reverse grouping, and loss of recipient antigens by adsorption elution tests using column tests (C-tests) and test-tube tests (T-tests). Furthermore, ABO genotyping and an intergroup comparison were performed. T-tests are superior for detecting the sensitivity of partial agglutination, while a problem with C-tests is that the nozzle of the automatic machine does not accurately sample new donor blood cells with low specific gravity. The adsorption-elution test revealed remnant recipient antigens in 19 cases (50.0%), indicating missed timing for conversion to the donor blood type. While genotyping showed conversion to the donor blood type in all cases, the results obtained using other methods differed, which was concerning. We conclude that blood type examination after transplantation can be performed using T-tests alone.

To establish preventive measures against transfusion-transmitted Hepatitis E Virus infection (TT-HEV), we analyzed TT-HEV cases (n = 34) identified from 2005 to 2018, including 19 cases previously reported in Transfusion (2017; 57: 280-288).

The causative blood had been donated from across Japan, with more than half donated in the Kanto-Koshinetsu area. Thirty (88.2%) blood components tested positive for HEV-RNA and negative for HEV antibodies, suggesting that most of the causative products were donated in the early stage of HEV infection. On molecular phylogenetic analysis of the 32 HEV strains of TT-HEV, 29 (90.6%) and 3 (9.4%) cases were classified as HEV-3 and HEV-4, respectively. Each was found in a different cluster, showing high genetic diversity.

At least 16 (47.1%) patients were transfused under immunosuppression and developed acute hepatitis. HEV viremia persisted for more than 6 months in 8 immunosuppressed patients. The median maximum ALT level during the clinical course of 34 cases was 631 IU/l. The minimum infectious HEV dose through transfusion was 2.51 log IU. There was no correlation between infused dose or HEV genotype and maximum ALT value.

The risk of TT-HEV has emerged in Japan. HEV RNA screening will be useful to reduce it.

Low-ionic-strength solution (LISS) is commonly used in column agglutination technology as potentiator in the detection of irregular antibody in pretransfusion testing.

In this study we evaluated the usefulness of 0.8% Ortho^® Red Cell Diluent (RCD) with the ORTHO VISION^® analyzer (Ortho Clinical Diagnostics Japan, Tokyo). Use of this test with an 0.8% RBC suspension (0.8% LISS-IAT) resulted in an increase in sensitivity for clinically significant antibodies and a decrease in the detection of clinically insignificant antibodies/nonspecific reactions compared to the test using LISS additive method with 4% RBC suspension (4% LISS-IAT). The 0.8% LISS-IAT detected newly produced antibodies, as early as PEG-IAT and earlier than LISS additive method. We speculate that the improvement in sensitivity with 0.8% LISS-IAT was due to a more appropriate ionic strength for antigen-antibody reaction, and efficient mixing in the reaction chamber.

We conclude that 0.8% LISS-IAT contributes to the safety of transfusion.

Our previous in vitro study suggested that platelet concentrates (PCs) suspended in 35% plasma with 65% platelet additive solution (PAS) can be refrigerated (2-6°C) with good quality for 14 days. In clinical practice, however, refrigerated PAS-PCs may be exposed to room temperature, e. g., when issued to wards. The possibility of a change in platelet function during warming is therefore of concern.

We evaluated the impact of exposure to 25°C (room temperature) for 30 minutes or 4 hours during storage, or to 25°C for 30 minutes followed by 24-hour storage at 22°C (PC-storage temperature) with agitation on the in vitro quality of PAS-PCs after refrigeration for 18 hours.

Temporal warming to 25°C or 24-hour exposure to 22°C did not alter the pH or platelet concentration of refrigerated PAS-PCs. However, hypotonic shock response and maximal platelet aggregation response to collagen and ADP increased as a function of exposure time. The mean fluorescence intensity of CD62P became significantly higher 4 hours after exposure to 25°C than that in continuously refrigerated PAS-PCs, suggesting that temporal warming (except within 30 minutes) to room temperature gradually activates platelets in refrigerated PAS-PCs. Temporal warming may influence the efficacy of refrigerated PAS-PC transfusion. Exposure to room temperature should therefore be minimized to achieve the expected transfusion efficacy.

An 85-year-old man with non-Hodgkin's lymphoma received a platelet transfusion for thrombocytopenia following chemotherapy. He developed wheezing and dyspnea 20min after the start of the transfusion. A transthoracic echocardiogram revealed severe left ventricular dysfunction (EF 27.3%) and severe apical hypokinesis with disproportionately preserved contraction of the basal segment, suggestive of Takotsubo cardiomyopathy. The patient responded well to a diuretic and the echocardiography findings returned to normal. Takotsubo cardiomyopathy is often associated with a physical or psychological stress that induces sympathetic nerve activity. In our case, allergic reaction to platelet transfusion is likely to be such a stress. Our case also fulfilled the diagnostic criteria of transfusion-associated circulatory overload (TACO), which is a representative adverse reaction to blood transfusion. This suggests that patients diagnosed with TACO may have Takotsubo cardiomyopathy, which may be involved in pathogenesis of TACO. A large study is required to elucidate the pathogenesis of heart failure following blood transfusion.

A 65-year-old man was diagnosed with myelodysplastic syndrome 3 years ago. He had blood type O RhD (+), Fy (a+b−) and was negative for irregular antibodies before platelet transfusion. The patient had a history of hemolytic anemia and received a red blood cell (RBC) transfusion about 40 years ago. He subsequently received a platelet transfusion due to progressive disease 3 months ago. Two months thereafter, he underwent irregular antibody screening due to anemia. The indirect antibody test was positive for irregular antibodies, and anti-Fy^b subclass IgG1 levels had increased four-fold. Two out of 14 packs of platelet concentrate administered before RBC transfusion were Fy^b antigen positive. The emergence of anti-Fy^b in our patient was probably due to a secondary immune response associated with his transfusion history, considering the relatively weak immunogenicity of the Fy^b antigen and the extremely low frequency of natural anti-Fy^b IgG antibodies, although contribution by natural IgG antibodies cannot be completely ruled out. It is important to understand that any type of irregular antibody can emerge after transfusion with blood products, including platelets.