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Sideroblastic Anemia

Sideroblastic anemia, a group of heterogenous disorders, produce a common defect - failure to use iron in hemoglobin (Hb) synthesis, despite the availability of adequate iron stores. These anemias may be hereditary or acquired; the acquired form, in turn, can be primary or secondary.

Hereditary sideroblastic anemia often responds to treatment with pyridoxine. Correction of the secondary acquired form depends on the causative disorder; the primary acquired (idiopathic) form, however, resists treatment and usually proves fatal within 10 years after onset of complications or a concomitant disease.


Hereditary sideroblastic anemia appears to be transmitted by X-linked inheritance, occurring mostly in young males; females are carriers and usually show no signs of this disorder.

The acquired form may be secondary to ingestion of, or exposure to, toxins, such as alcohol and lead, or to drugs, such as isoniazid and chloramphenicol. It can also occur as a complication of other diseases, such as rheumatoid arthritis, lupus erythematosus, multiple myeloma, tuberculosis, and severe infections.

The primary acquired form, known as refractory anemia with ringed sideroblasts, is most common in elderly people. It's often associated with thrombocytopenia or leukopenia as part of a myelodysplastic syndrome.

In sideroblastic anemia, normoblasts fail to use iron to synthesize Hb. As a result, iron is deposited in the mitochondria of normoblasts, which are then called ringed sideroblasts.

Signs and symptoms

Sideroblastic anemia usually produce nonspecific clinical effects, which may exist for several years before being identified. Such effects include anorexia, fatigue, weakness, dizziness, pale skin and mucous membranes and, occasionally, enlarged lymph nodes.

Heart and liver failure may develop from excessive iron accumulation in these organs, causing dyspnea, exertional angina, slight jaundice, and hepatosplenomegaly. Hereditary sideroblastic anemia is associated with increased GI absorption of iron, causing signs of hemosiderosis. Additional symptoms in secondary sideroblastic anemia depend on the underlying cause.


Ringed sideroblasts on microscopic examination of bone marrow aspirate, stained with Prussian blue or alizarin red dye, confirm the diagnosis.

Microscopic examination of blood shows hypochromic or normochromic, and slightly macrocytic, erythrocytes. Red blood cell (RBC) precursors may be megaloblastic, with anisocytosis (abnormal variation in RBC size) and poikilocytosis (abnormal variation in RBC shape).

Unlike iron deficiency anemia, sideroblastic anemia lowers Hb and raises serum iron and transferrin levels. In turn, faulty Hb production raises urobilinogen and bilirubin levels. Platelet and leukocyte levels remain normal, but thrombocytopenia or leukopenia occasionally occurs.


Acquired sideroblastic anemia may be cured when the condition that causes it is treated or removed.

If the cause of a patient's anemia cannot be determined, blood transfusions may be necessary. Medications are prescribed to stimulate excretion or excess iron that accumulates as a result of these transfusions.

In rare instances, treatment with oral pyridoxine (a B-complex vitamin) benefits patients whose sideroblastic anemia was present at birth. This treatment improves the condition of some patients but does not cure the anemia.


Sideroblastic anemia of unknown origin may lead to leukemia. It may take as long as 10 years for this disease progression to take place.

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