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1 tion as a means to prevent pregnancy-induced megaloblastic anemia.
2 parable with those observed in patients with megaloblastic anemia.
3 en the S-phase accumulation and apoptosis in megaloblastic anemia.
4 thesis of thymidylate in the pathogenesis of megaloblastic anemia.
5 the metabolic disorder, thiamine-responsive megaloblastic anemia.
6 es explanations for the clinical findings in megaloblastic anemia.
9 f folate or vitamin B(12) (cobalamin) causes megaloblastic anemia, a disease characterized by pancyto
10 Mutations in THTR-1 cause thiamin-responsive megaloblastic anemia, a tissue-specific disease associat
15 inborn error of metabolism, characterized by megaloblastic anemia and/or pancytopenia, severe cerebra
19 data) for risk of deficiency on the basis of megaloblastic anemia as a hematologic indicator in perso
20 ary levels of the vitamin folate can lead to megaloblastic anemia, birth defects, impaired cognitive
21 normal erythropoiesis is a common feature of megaloblastic anemias, congenital dyserythropoietic anem
24 essive disorder defined by the occurrence of megaloblastic anemia, diabetes mellitus, and sensorineur
26 paired purine nucleotide metabolism, whereas megaloblastic anemia has been associated with impaired d
27 dies of impaired DNA synthesis and repair in megaloblastic anemia have concerned mainly the decreased
29 wed not only as a nutrient needed to prevent megaloblastic anemia in pregnancy but also as a vitamin
30 sm, the degree of uracil misincorporation in megaloblastic anemia is sufficient to increase the stead
31 blastic anemia (diabetes mellitus, deafness, megaloblastic anemia) lacking functional Slc19a2 has bee
32 -vitamin B12 receptor, results in hereditary megaloblastic anemia (MGA1), owing to vitamin B12 malabs
34 amage, accounting for the pathophysiology of megaloblastic anemia observed in vitamin B12 and folate
35 However, in patients with thiamin-responsive megaloblastic anemia, plasma thiamin levels are within n
36 and symptoms of vitamin B12 deficiency, e.g. megaloblastic anemia, precise evaluation and treatment i
37 Cubulin mutations cause a hereditary form of megaloblastic anemia secondary to vitamin B(12) deficien
40 isincorporated into the DNA of patients with megaloblastic anemia to levels detectable by nonradioact
41 lasts from patients with thiamine-responsive megaloblastic anemia (TRMA) syndrome with diabetes and d
42 y of the syndrome called thiamine-responsive megaloblastic anemia (TRMA) with diabetes and deafness.
43 iency disorders, such as thiamine-responsive megaloblastic anemia (TRMA), which is associated with sp
44 parents had diabetes mellitus, deafness, or megaloblastic anemia, which raised the possibility that
45 linical vitamin B12 deficiency can result in megaloblastic anemia, which results from the inhibition
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