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

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.