What is the treatment for microcytic hypochromic anemia?

Treatment of Microcytic Hypochromic Anemia

The first-line treatment for microcytic hypochromic anemia is oral ferrous sulfate 200 mg three times daily for at least three months after hemoglobin normalizes to replenish iron stores, as this addresses iron deficiency—the most common cause of this anemia pattern. 1

Initial Diagnostic Confirmation

Before initiating treatment, confirm the diagnosis with specific testing:

• Measure serum ferritin as the most specific test for iron deficiency, with levels <15 μg/L indicating absent iron stores and <30 μg/L indicating low body iron stores; a cut-off of 45 μg/L provides optimal sensitivity and specificity. 1
• Evaluate transferrin saturation as a more sensitive test than hemoglobin alone for detecting iron deficiency. 1
• Use RDW to differentiate causes: A low MCV with RDW >14.0% suggests iron deficiency anemia, while RDW ≤14.0% suggests thalassemia minor. 1

Treatment Algorithm for Iron Deficiency Anemia

Standard Oral Iron Therapy

• Prescribe ferrous sulfate 200 mg (65 mg elemental iron) three times daily, taken separately from meals to maximize absorption. 1, 2
• Continue treatment for at least 3 months after hemoglobin normalizes to adequately replenish iron stores—stopping when hemoglobin normalizes leads to relapse. 1, 2
• Add ascorbic acid (vitamin C) to enhance iron absorption if needed. 1, 2
• Switch to alternative formulations (ferrous gluconate or ferrous fumarate) if ferrous sulfate is not tolerated due to gastrointestinal side effects. 1, 2

Response Monitoring

• Recheck CBC at 2 weeks to confirm response to therapy—a hemoglobin rise ≥10 g/L within 2 weeks confirms iron deficiency. 1, 2
• Monitor hemoglobin and red cell indices every 3 months for 1 year, then annually to detect relapse. 1, 2
• Provide additional oral iron if hemoglobin or MCV falls below normal during follow-up. 1

Intravenous Iron Indications

Switch to IV iron if oral therapy fails, specifically when: 1, 2

• Documented malabsorption exists
• True intolerance to all oral formulations occurs
• Blood losses exceed maximal oral replacement capacity
• Expect hemoglobin increase of at least 2 g/dL within 4 weeks of IV iron administration. 1

Treatment for Specific Genetic Causes

When iron deficiency is excluded or patients fail to respond to iron therapy, consider genetic disorders:

X-Linked Sideroblastic Anemia (ALAS2 Defects)

• Initiate pyridoxine (vitamin B6) 50-200 mg daily as initial treatment, with expected response in pyridoxine-responsive cases. 1, 3
• Maintain lifelong supplementation at 10-100 mg daily for responders to avoid neurotoxicity from excessive doses. 1, 3

SLC25A38 Defects

• Consider hematopoietic stem cell transplantation (HSCT) as the only curative option for severe cases. 1, 3
• Provide symptomatic treatment with erythrocyte transfusions and chelation therapy until definitive treatment. 1, 3

STEAP3 Defects

• Treat with erythrocyte transfusions in combination with erythropoietin (EPO), and manage systemic iron loading with chelation therapy. 1, 3

Iron-Refractory Iron Deficiency Anemia (IRIDA/TMPRSS6 Defects)

• Administer intravenous iron repeatedly (iron sucrose or ferric gluconate), as these patients show resistance to oral iron; hemoglobin and ferritin increase but rarely normalize completely. 1
• Monitor ferritin levels and avoid exceeding 500 mg/L to prevent iron overload risk, especially in children and adolescents. 1

Critical Pitfalls to Avoid

• Always investigate the underlying cause of iron deficiency—assume gastrointestinal blood loss until proven otherwise and perform stool guaiac testing; obtain detailed menstrual history in premenopausal women. 2
• Screen for combined deficiencies (iron with B12 or folate deficiency) that can coexist and complicate treatment. 1, 2
• Do not stop iron therapy when hemoglobin normalizes—continue for 3 months to replenish stores. 1, 2
• Consider thalassemia trait if persistent microcytosis occurs despite iron repletion, particularly with normal or low-normal RDW. 1, 2
• Evaluate for genetic disorders if failure to respond to adequate oral iron therapy occurs after 4 weeks, or if family history of microcytic anemia exists. 1, 2

Special Populations

Myelodysplastic Syndrome with Ring Sideroblasts (MDS-RS)

• Luspatercept is approved and effective for MDS-RS patients, especially those with SF3B1 mutation, achieving erythroid response rates up to 63% and red blood cell transfusion independence in 38% of patients. 3

Iron Overload Management

• Use phlebotomy as the preferred method when tolerated for managing iron overload in patients receiving chronic transfusions or with genetic iron loading disorders. 3
• Implement iron chelation therapy when phlebotomy is not tolerated or contraindicated. 3
• Consider MRI of the liver to detect toxic iron loading early in patients at risk. 1, 3