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Background and Objectives: Red blood cell (RBC) antibody levels diminish over time and negative antibody screen are commonly seen in patients with a history of antibodies. Most hospitals do not have access to a shared registry of antibodies previously detected at other hospitals., Materials and Methods: We describe a case where the patient was found to be at high risk of bleeding during liver transplantation. Antibody screen on admission was negative but a history of anti-Jk a was identified on reviewing patient's history in local registry of RBC antibodies. The surgery was pushed back to arrange for antigen-negative units. The patient received a total of 16 Jk(a-) RBC units during the admission., Results: No acute or delayed transfusion adverse reactions were seen. However, if the history of anti-Jk a identified at another local hospital was not known, approximately three-quarters of the units transfused would have been Jk(a+). Transfusing Jk(a+) units could have potentially exposed the patient to risk of developing an acute and/or delayed haemolytic transfusion reaction which could have led to significant morbidity and perhaps mortality., Conclusion: With this case report, we build a case for developing a national registry of RBC antibodies to help improve patient safety and outcomes., (© 2022 International Society of Blood Transfusion.)

Early gestation fetal mouse skin heals without scars. Plasminogen activator inhibitor-1 (PAI-1) has been associated with postnatal organ fibrosis. We hypothesized that the relative balance between urokinase-type plasminogen activator (uPA) and PAI-1 expression in favor of uPA prevents scarring in early fetal skin wounds, whereas a change in favor of PAI-1 in late gestation results in wound scarring. To evaluate uPA and PAI-1 expression, 1-mm skin wounds were made in E14.5 and E18 mice and harvested 24, 48, or 96 hours postwounding. Aprotinin (2 mg/ml)-coated beads were injected into selected E14.5 wounds. Normal skin and skin wounds were evaluated for uPA, PAI-1, and collagen expression. We showed that in normal skin uPA level is higher in E14.5 than in E18 mice, while PAI-1 is lower in E14.5 than in E18 mice. After wounding, E14.5 wounds show a moderate increase in uPA and a minimal increase in PAI-1. E18 wounds show a transient increase in uPA but a significant, sustained increase in PAI-1. Addition of aprotinin to E14.5 wounds causes an increase in collagen deposition. We conclude that the differential expression of uPA and PAI-1 in the skin of early vs. late gestation mice may contribute to the degree of scar formation seen after cutaneous injury.