rBGPs enable the identification of antibodies to high-prevalence antigens without the need for rare RBC reagents, which are often unavailable. Underlying antibodies can be reliably detected and cross-matching results validated, resulting in a more efficient blood supply for immunized patients.

BACKGROUND Antenatal cases of Bombay‐phenotype (Oh) individuals and hemolytic disease of the fetus and newborn (HDFN) are not well described in the literature. We present two case reports of high‐titer anti‐H in pregnant Oh individuals and their serologic investigation, clinical management, and subsequent outcomes. We describe current published cases detailing pregnancy in Oh individuals, to add to the evidence base for clinical decision making and management of pregnancy. STUDY DESIGN AND METHODS We describe two case reports of high‐titer anti‐H in pregnancy in Oh individuals. We summarize published cases to date, to inform clinical decision making and antenatal management in individuals with the Bombay phenotype. RESULTS Of the case reports described, neither were affected by HDFN due to anti‐H. Antibody titers were high in both cases (immunoglobulin G titer scores, 512 and 4000, respectively) and would be expected to cause some degree of HDFN, a surprising finding. Regular mean cerebral artery Doppler ultrasound was normal. Patient blood management (PBM) techniques ensured that the patient's hemoglobin (Hb) levels were monitored and maintained. Transfusion intervention was not required, with minimal blood loss recorded at birth in both cases. CONCLUSION High‐titer anti‐H in Oh pregnancies may, in rare cases, cause HDFN, but evidence suggests that this may not be the case in all pregnancies. We recommend a multidisciplinary approach, with prompt referral to a fetomaternal medicine unit, combined with PBM strategies, and a planned delivery with the provision of rare‐phenotype units (if available and if indicated) on standby.

A 50-year-old man presented with worsening, virtually lifelong, chorea and progressive behavioural disturbance, involving disinhibition and hoarding, over 10 years. Clinical assessment revealed chorea, dysarthria, areflexia, an inappropriately jovial, impulsive manner and neuropsychological evidence of frontosubcortical dysfunction. Investigation results included an elevated creatine kinase, caudate atrophy and hypoperfusion, acanthocytes in the peripheral blood and the McLeod phenotype. DNA studies demonstrated a single-base deletion at position 172 in exon 1 of the XK gene, giving rise to a premature stop codon at position 129 in exon 2.

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Objective: Whilst small-scale studies on rates of alloimmunisation of patients on Daratumumab have been undertaken, no large-scale study has been performed to date on this cohort of patients.Background: Patients with multiple myeloma (MM) who are relapsed or refractory to standard treatment are treated with the anti-CD38 therapeutic monoclonal antibody, Daratumumab. Due to the complexity of pre-transfusion compatibility testing, many MM patients in England are referred to Red Cell Immunohaematology (RCI) laboratories for investigation and provision of Red Blood Cell (RBC) components.Methods: Over a 4-month period, patients due to commence, or currently on anti-CD38 therapy were identified and flagged on the RCI Laboratory Information Management System (LIMS). Data was identified and extracted for further analysis.Interrogation of data was performed independently by two subject matter experts, with discrepancies resolved through further enquiry.Results: Of 734 English MM patients, we report an alloimmunisation rate of 0.4% whilst on an anti-CD38 TMAb. This is in line with other smaller cohort studies. Conclusion:Given the low rate of RBC alloimmunisation, consideration should be given to revising the pre-transfusion testing regimen in this cohort. This may improve testing costs, turn-around times and evidence-based patient care.

BACKGROUND The U– phenotype is extremely rare and is found predominantly in black African populations at a frequency of between 0.2 and 1.7%. In European populations, U– units are therefore rare, with limited availability in the United Kingdom. Anti‐U is clinically significant and is known to cause hemolytic transfusion reactions (HTRs) and hemolytic disease of the fetus and newborn. It has been suggested that intravenous immunoglobulin (IVIG) may be considered as an option among supportive therapy for urgent transfusion when clinically significant antigen‐matched units are not available. We report three cases with anti‐U transfused with least‐incompatible RBC units, their outcomes, and their clinical management. STUDY DESIGN AND METHODS Intravenous immunoglobulin was prescribed when least‐incompatible units must be issued in patients with anti‐U to ameliorate acute HTR and prevent the development of delayed HTR. We report the outcome of these cases. RESULTS Of the case reports described, one patient with weak anti‐U developed a delayed HTR after transfusion with incompatible units due to an anamnestic response. Two additional patients are described, with the use of IVIG as a precautionary measure to prevent the development of HTRs when transfused with antigen‐positive incompatible units. No acute HTRs or delayed HTRs were noted upon follow‐up. CONCLUSION U– units are not always readily available and transfusion support requires close collaborative working among a multidisciplinary team. Transfusion with antigen‐positive incompatible units with IVIG cover both ameliorates acute HTRs and prevents the development of delayed HTRs.

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