Anemia Research Today is a free monthly online journal that collates and summarizes the latest research about Anemia, including details on symptoms, diagnosis, diet, treatment, causes.

Elevated serum S-adenosylhomocysteine in cobalamin-deficient megaloblastic anemia.

Guerra-Shinohara EM, Morita OE, Pagliusi RA, Blaia-d'Avila VL, Allen RH, Stabler SP

Department of Clinical and Toxicological Analysis, Pharmaceutical School, University of São Paulo, São Paulo 05508-900, Brazil.

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 micromol/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.

Published 12 February 2007 in Metabolism, 56(3): 339-47.
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