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Normalization of serum lactic dehydrogenase in β‐thalassemia patients following bone marrow transplantation
Author(s) -
Toren Amos,
Or Reuven,
Kapelushnik Joseph,
Chividalli Gabriel,
Aku Memet,
Slavin Shimon,
Nagler Ar
Publication year - 1996
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/(sici)1096-8652(199602)51:2<166::aid-ajh13>3.0.co;2-g
Subject(s) - medicine , thalassemia , ineffective erythropoiesis , transplantation , gastroenterology , hemolysis , erythropoiesis , hemoglobinopathy , bone marrow , hemolytic anemia , surgery , anemia
Serum lactic dehydrogenase (LDH) levels are mildly elevated in β‐thalassemia major due to ineffective erythropoiesis. We reviewed the charts of 15 consecutive thalassemic children who underwent allogeneic, T‐cell‐depleted bone marrow transplantation (BMT) in our department during the last 3 years. Eleven patients had successful engraftment and are alive and well without evidence of disease, according to physical examinations, blood counts, and polymerase chain reaction (PCR) tests, with a median follow‐up of 2 years. Two patients died due to transplantation‐related complications, and two rejected the graft and received their backup autologous marrow. The LDH levels in the transplanted patients gradually decreased from an average of 952 ± 155 IU/L 10 days pre‐transplant (N = 300–620) to 426 ± 56 IU/L at the day of transplantation, and stayed at approximately the same level post‐transplant (489 ± 55 IU/L). By contrast, the LDH levels reverted to the pre‐transplant value in those patients who rejected their marrow. The significance of this clinical observation for the pathophysiologic mechanism of intramedullary hemolysis and ineffective erythropoiesis in β‐thalassemia major is discussed. © 1996 Wiley‐Liss, Inc.