Pyridoxine (vitamin B6) is necessary for synthesis of D-aminolevulinic acid, a precursor of heme. Pyridoxine-deficient patients develop anemia with microcytic-hypochromic RBCs that can simulate chronic iron deficiency. Both hereditary and acquired (secondary) forms exist. The hereditary form is rare and the acquired form is uncommon, with the most frequently mentioned secondary type being due to tuberculin therapy with isoniazid (INH).

Sideroblastic Anemias*

Alcoholism (most common etiology)
Lead poisoning
Drug induced (isoniazid, cycloserine, chloramphenicol)
Some patients with various diseases
Other hemolytic anemias
Megaloblastic anemia
Myeloproliferative and myelodysplastic disorders
Hypothyroidism or hyperthyroidism

*Marrow sideroblasts more than 20% of nucleated RBC.

Sideroblastic anemias. Pyridoxine deficiency anemia is included in the sideroblastic anemias. These conditions by definition have conversion of at least 20% of all bone marrow nucleated RBC to ringed sideroblasts. Ring sideroblasts are normoblasts with abnormal numbers of iron-stainable cytoplasmic granules that appear to form a ring around the nucleus when stained with iron stains. The sideroblastic anemia group includes the rare hereditary form that frequently responds to pyridoxine and a secondary or acquired category that includes various conditions that may be associated with sideroblastic marrows (see the box above). Of these, the most likely to have sideroblastic marrows are alcoholism, thalassemia, and some of the myelodysplastic syndromes. Hematologically, the sideroblastic anemias are characterized by hypochromic RBCs, sometimes predominant and sometimes coexisting with a minority or majority population of nonhypochromic RBC (“dimorphic” RBC population). If the hypochromic microcytic RBC are predominant, the MCV may be decreased. There typically is an elevated serum iron level with increased saturation of iron-binding capacity.