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Posttransfusional Hemolysis in Recipients of Glucose‐6‐Phoiphate Dehydrogenase‐Deficient Erythrocytes

O Shalev, Noga Manny, Raphael Sharon

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Abstract

To test the hypothesis that transfusion of blood donated by individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency may result in a hemolytic reaction, we conducted a prospective longitudinal study in which 10 patients transfused with 1 unit of G6PD-deficient and 1 unit of normal red blood cells (RBC) were compared with 10 patients transfused with 2 units of age-matched normal RBC. We found that 24 h after transfusion serum bilirubin (mumol/l) in the recipients of G6PD-deficient RBC was significantly higher than in the recipients of normal RBC (36 +/- 14 vs. 18 +/- 5, respectively, p > 0.004). A parallel increase was found in the serum lactate dehydrogenase (LDH; IU/l) between the two groups (378 +/- 151 vs. 264 +/- 56, p < 0.001). The difference in serum bilirubin (26 +/- 10 vs. 15 +/- 5, p < 0.03) was still noted 48 h after transfusion, with only a marginal difference (p < 0.08) in LDH. We conclude that an immediate posttransfusional hemolytic reaction can occur in recipients of G6PD-deficient RBC and therefore suggest that the differential diagnosis of posttransfusional hemolysis, particularly in populations where G6PD deficiency is prevalent, includes transfusion of erythrocytes from G6PD-deficient donors.

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What this paper is about

To test the hypothesis that transfusion of blood donated by individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency may result in a hemolytic reaction, we conducted a prospective longitudinal study in which 10 patients transfused with 1 unit of G6PD-deficient and 1 unit of normal red blood cells (RBC) were compared with 10 patients transfused with 2 units of age-matched normal RBC. We found that 24 h after transfusion serum bilirubin (mumol/l) in the recipients of G6PD-deficient RBC was significantly higher than in the recipients of normal RBC (36 +/- 14 vs. 18 +/- 5, respectively, p > 0.004). A parallel increase was found in the serum lactate dehydrogenase (LDH; IU/l) between the two groups (378 +/- 151 vs. 264 +/- 56, p < 0.001). The difference in serum bilirubin (26 +/- 10 vs. 15 +/- 5, p < 0.03) was still noted 48 h after transfusion, with only a marginal difference (p < 0.08) in LDH. We conclude that an immediate posttransfusional hemolytic reaction can occur in recipients of G6PD-deficient RBC and therefore suggest that the differential diagnosis of posttransfusional hemolysis, particularly in populations where G6PD deficiency is prevalent, includes transfusion of erythrocytes from G6PD-deficient donors.

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Available abstract

To test the hypothesis that transfusion of blood donated by individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency may result in a hemolytic reaction, we conducted a prospective longitudinal study in which 10 patients transfused with 1 unit of G6PD-deficient and 1 unit of normal red blood cells (RBC) were compared with 10 patients transfused with 2 units of age-matched normal RBC. We found that 24 h after transfusion serum bilirubin (mumol/l) in the recipients of G6PD-deficient RBC was significantly higher than in the recipients of normal RBC (36 +/- 14 vs. 18 +/- 5, respectively, p > 0.004). A parallel increase was found in the serum lactate dehydrogenase (LDH; IU/l) between the two groups (378 +/- 151 vs. 264 +/- 56, p < 0.001). The difference in serum bilirubin (26 +/- 10 vs. 15 +/- 5, p < 0.03) was still noted 48 h after transfusion, with only a marginal difference (p < 0.08) in LDH. We conclude that an immediate posttransfusional hemolytic reaction can occur in recipients of G6PD-deficient RBC and therefore suggest that the differential diagnosis of posttransfusional hemolysis, particularly in populations where G6PD deficiency is prevalent, includes transfusion of erythrocytes from G6PD-deficient donors.

Key concepts: Hemolysis, Lactate dehydrogenase, Glucose-6-phosphate dehydrogenase deficiency, Medicine, Glucose-6-phosphate dehydrogenase, Bilirubin, Glucosephosphate Dehydrogenase Deficiency, Internal medicine

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