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Deoxyuridine suppression studies in bone marrow in primary refractory sideroblastic anemia
Author(s) -
Goodman Anita,
Bacon Bruce,
Hines John D.
Publication year - 1978
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/ajh.2830050106
Subject(s) - megaloblastic anemia , pyridoxine , bone marrow , sideroblastic anemia , deoxyuridine , ineffective erythropoiesis , medicine , anemia , pyridoxal phosphate , endocrinology , erythropoiesis , biology , biochemistry , cofactor , dna , enzyme
Abstract Because unexplained megaloblastic erythroid maturation occurs in patients with primary refractory sideroblastic anemia (PRSA), deoxyuridine (dU) suppression tests using 125 I‐UdR were performed on bone marrow from five patients with PRSA. All patients had megaloblastic alterations in the marrow erythroid precursors (with normal serum folate and B 12 levels) and numerous ringed sideroblasts, and most had marrow iron overload. Results of the dU suppression tests were normal in all five, both with and without incubation with pharmacologic amounts of folate, B 12 , and pyridoxal phosphate with or without 1‐serine. Despite occasional hematologic improvement subsequent to folate, pyridoxine, or pyridoxal phosphate (PLP) administration in some patients with PRSA, normal dU suppression implies that in our group the availability of B 12 and folate (and possibly PLP) was not limiting in the utilization of folate for DNA‐thymine synthesis. The marrow erythroid maturation defect remains unexplained.