Management of Microcytic Hypochromic Anemia (RBC 6.7, MCV 72, MCH 25)
Start oral iron supplementation with ferrous sulfate 200 mg three times daily for at least three months after correction of anemia to replenish iron stores, as this is first-line treatment for microcytic hypochromic anemia. 1
Initial Diagnostic Workup
Before initiating treatment, confirm the diagnosis with specific testing:
- Measure serum ferritin first - this is the most specific test for iron deficiency, with levels <30 μg/L indicating low body iron stores, though a cut-off of 45 μg/L provides optimal sensitivity and specificity 1, 2
- Check transferrin saturation (TSAT) - this is more sensitive for detecting iron deficiency than hemoglobin concentration alone 1, 2
- Evaluate RDW (red cell distribution width) to differentiate causes: low MCV with RDW >14.0% suggests iron deficiency anemia, while low MCV with RDW ≤14.0% suggests thalassemia minor 1, 2
- Order hemoglobin electrophoresis if thalassemia is suspected based on RDW pattern 2
Treatment Algorithm
First-Line Oral Iron Therapy
- Prescribe ferrous sulfate 200 mg (65 mg elemental iron) three times daily for at least three months after anemia correction 1, 2, 3
- Add ascorbic acid (vitamin C) to enhance iron absorption 1, 2
- Alternative formulations include ferrous gluconate or ferrous fumarate if ferrous sulfate is not tolerated 1
- Expect a good response defined as hemoglobin rise ≥10 g/L within 2 weeks, which confirms iron deficiency 1, 2
For Non-Responders to Oral Iron
If the patient fails to respond after 2-4 weeks:
- Consider intravenous iron if malabsorption is present, with expected hemoglobin increase of at least 2 g/dL within 4 weeks 1, 2
- Re-evaluate for genetic disorders of iron metabolism or heme synthesis, including SLC11A2 defects, STEAP3 defects, SLC25A38 defects, ABCB7 defects, or ALAS2 defects 4, 1
- Test for thalassemia if RDW is normal or near normal 1
Special Genetic Conditions Requiring Alternative Management
- ALAS2 defects (X-linked sideroblastic anemia): Start pyridoxine 50-200 mg daily initially, then maintain lifelong supplementation at 10-100 mg daily if responsive 4, 1
- SLC11A2 defects: Treat with oral iron supplementation and/or erythropoietin (EPO) and/or erythrocyte transfusions based on individual needs 4, 1
- STEAP3 defects: Use erythrocyte transfusions combined with EPO, and manage systemic iron loading with chelation 4, 1
- SLC25A38 defects: Consider hematopoietic stem cell transplantation (HSCT) as the only curative option 4, 1
Monitoring Protocol
- Check hemoglobin and red cell indices at three-monthly intervals for one year, then after a further year 1, 2
- Provide additional oral iron if hemoglobin or MCV falls below normal 1, 2
- Monitor for iron overload in patients receiving multiple transfusions or long-term iron therapy 1
- Consider MRI of the liver in specific cases (particularly SLC11A2 defects) to detect toxic iron loading early, as normal serum ferritin does not exclude liver iron loading 4, 1
Critical Pitfalls to Avoid
- Do not overlook combined deficiencies - iron deficiency can coexist with B12 or folate deficiency, requiring evaluation of vitamin levels 2
- Do not assume normal hemoglobin excludes iron deficiency - hypochromic changes precede anemia development 2
- Do not miss the 7% of patients with both thalassemia trait and iron deficiency - check ferritin even when thalassemia is diagnosed 2
- Always investigate the source of iron loss in adults - occult gastrointestinal malignancy must be excluded 2
- Check compliance and dosage if iron stores are not replete at the end of treatment, and seek occult bleeding 5