Vitamin B12 Deficiency Does Not Induce Homocysteine Increase in Transfusion-Dependent β-Thalassemia Major Patients Receiving Folic Acid Supplementation.

Abstract

Vitamin B₁₂ deficiency is a frequent but underdiagnosed complication in patients with transfusion-dependent β-thalassemia. Folic acid supplementation, commonly prescribed in this population, may mask hematological signs and alter homocysteine metabolism, complicating diagnosis. We conducted a cross-sectional study of 80 patients with transfusion-dependent β-thalassemia receiving daily folic acid supplementation (1 mg). Fasting serum vitamin B₁₂ and plasma homocysteine levels were measured, and the correlation between B₁₂ status and homocysteine was analyzed. Nineteen patients (23.8%) had biochemical vitamin B₁₂ deficiency (<200 pg/mL). However, the mean homocysteine concentration did not differ significantly between B₁₂-deficient and non-deficient patients (7.5 ± 4.2 vs. 6.39 ± 3.73 µmol/L; p = 0.420). No significant correlation was found between serum B₁₂ and homocysteine levels (r = -0.128, p = 0.267). In patients with transfusion-dependent β-thalassemia receiving folic acid supplementation, homocysteine may not reliably reflect vitamin B₁₂ deficiency, and normal levels should not be used to exclude deficiency. Routine screening with more specific markers, such as methylmalonic acid, may be necessary to prevent undetected B₁₂ deficiency and its neurological complications.