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Elevated serum S -adenosylhomocysteine in cobalamin-deficient megaloblastic anemia

Abstract Impaired methylation due to accumulation of S -adenosylhomocysteine (SAH) may contribute to the pathophysiology of cobalamin-deficient anemia. We assayed serum S -adenosylmethionine (SAM), SAH, total homocysteine (tHcy), and methylmalonic acid (MMA) in 15 subjects with cobalamin-deficient m...

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Published in:Metabolism, clinical and experimental clinical and experimental, 2007-03, Vol.56 (3), p.339-347
Main Authors: Guerra-Shinohara, Elvira M, Morita, Olga E, Pagliusi, Regina A, Blaia-d'Avila, Vera L, Allen, Robert H, Stabler, Sally P
Format: Article
Language:English
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Summary:Abstract Impaired methylation due to accumulation of S -adenosylhomocysteine (SAH) may contribute to the pathophysiology of cobalamin-deficient anemia. We assayed serum S -adenosylmethionine (SAM), SAH, total homocysteine (tHcy), and methylmalonic acid (MMA) in 15 subjects with cobalamin-deficient megaloblastic anemia and compared results with those of 19 subjects with anemia/pancytopenia due to other causes. Cobalamin-deficient subjects had a median hematocrit level of 20% and mean cell volume of 111.7 fL. The median serum cobalamin level was 37 pg/mL, MMA 3030 nmol/L, and tHcy 62.0 μ mol/L. SAH was elevated in 13 of 15 subjects (median, 42 nmol/L) and the median SAM value was normal (103 nmol/L), but SAM/SAH ratio was low (2.5). The SAH was higher and SAM/SAH ratio was lower in cobalamin-deficient subjects compared with those with other anemias after excluding 4 patients with renal insufficiency. SAM concentrations were not low in cobalamin deficiency. Cobalamin injections corrected anemia, MMA, tHcy, SAM/SAH ratio, and SAH. Some hematologic variables were inversely correlated with SAH and cobalamin but not tHcy or MMA. In conclusion, serum SAH is elevated in cobalamin-deficient subjects with megaloblastic anemia and corrects with parenteral cobalamin therapy.
ISSN:0026-0495
1532-8600
DOI:10.1016/j.metabol.2006.10.009