Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis · 2026
Catastrophic acute haemolytic reaction: The discovery of first Bombay phenotype in Iraq /case report.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Aljebouri Dhargam Muhamed, Al-Musawi Yakoob, Al-Bayati Noor
Аннотация
BACKGROUND: The Bombay (Oh) phenotype results from homozygous FUT1 loss-of-function (hh), causing complete absence of H antigen on red blood cells and preventing expression of A and B antigens. Because routine forward and reverse grouping can mimic group O, affected individuals may be transfused with standard group O units, risking severe hemolysis due to naturally occurring anti-H.
CASE: A 31-year-old man in Baghdad presented with massive traumatic hemorrhage and received an uncrossmatched leukoreduced group O RhD-negative packed red cell unit. Within 10 min he developed fever, rigors, hypotension, and dark urine; transfusion was stopped and managed with fluids, vasopressors, oxygen, and diuresis. Post-reaction testing showed hemoglobin fall to 6.5 g/dL, intravascular hemolysis and rising creatinine. ABO/RhD typing was O, RhD-positive and DAT was negative.
INVESTIGATIONS: Antibody screening with group O cells showed strong pan-reactivity (3 +-4 +) at immediate spin, 37°C and IAT with negative autocontrol. Anti-H was suspected; Ulex europaeus and two commercial anti-H lectins demonstrated no agglutination, confirming absent H antigen and supporting Bombay (Oh) phenotype.
CONCLUSION: This first documented Iraqi Bombay phenotype highlights the need to consider anti-H when "group O" samples show pan-incompatible serology and underscores the importance of rare-donor preparedness and referral testing to prevent catastrophic reactions.
CASE: A 31-year-old man in Baghdad presented with massive traumatic hemorrhage and received an uncrossmatched leukoreduced group O RhD-negative packed red cell unit. Within 10 min he developed fever, rigors, hypotension, and dark urine; transfusion was stopped and managed with fluids, vasopressors, oxygen, and diuresis. Post-reaction testing showed hemoglobin fall to 6.5 g/dL, intravascular hemolysis and rising creatinine. ABO/RhD typing was O, RhD-positive and DAT was negative.
INVESTIGATIONS: Antibody screening with group O cells showed strong pan-reactivity (3 +-4 +) at immediate spin, 37°C and IAT with negative autocontrol. Anti-H was suspected; Ulex europaeus and two commercial anti-H lectins demonstrated no agglutination, confirming absent H antigen and supporting Bombay (Oh) phenotype.
CONCLUSION: This first documented Iraqi Bombay phenotype highlights the need to consider anti-H when "group O" samples show pan-incompatible serology and underscores the importance of rare-donor preparedness and referral testing to prevent catastrophic reactions.