Low MCH with Normal Hemoglobin and Normal RDW: Interpretation
A low MCH with normal hemoglobin and normal RDW most likely indicates early iron deficiency or thalassemia trait, and you should immediately order serum ferritin and transferrin saturation to distinguish between these two conditions. 1, 2
Primary Diagnostic Considerations
Iron deficiency in its earliest stages is the leading diagnosis when MCH is reduced but hemoglobin remains normal, because the bone marrow begins producing hypochromic red cells (low hemoglobin content per cell) before total hemoglobin concentration drops. 1, 2 The normal RDW indicates that red cell size variation has not yet become pronounced, which occurs later as iron stores become more depleted. 3, 2
Thalassemia trait (heterozygous thalassemia) characteristically presents with low MCH, normal or near-normal hemoglobin, and importantly, a normal or only mildly elevated RDW (typically ≤14.0%). 3, 4 This pattern reflects a uniform population of small, hemoglobin-poor cells rather than the mixed population seen in progressive iron deficiency. 3
Essential Confirmatory Testing
Order the following tests immediately to establish the diagnosis:
- Serum ferritin: A level <30 μg/L confirms iron deficiency in the absence of inflammation; use <100 μg/L as the cutoff when inflammation is present. 1, 2
- Transferrin saturation (TSAT): A value <15-20% supports iron deficiency and is less affected by inflammatory states than ferritin. 1, 5
- C-reactive protein (CRP): Measure this to interpret ferritin correctly, as ferritin rises as an acute-phase reactant and can mask true iron deficiency. 1, 2
- Complete MCV measurement: Confirm whether microcytosis is present (MCV <80 fL), which would further support either diagnosis. 3, 1
Distinguishing Iron Deficiency from Thalassemia Trait
If iron studies show ferritin <30 μg/L and TSAT <20%, diagnose iron deficiency and investigate the underlying cause (gastrointestinal blood loss in men and postmenopausal women, menstrual losses in premenopausal women, or dietary insufficiency). 1, 2
If iron studies are completely normal (ferritin >30 μg/L, TSAT >20%), strongly suspect thalassemia trait and order hemoglobin electrophoresis, particularly in patients of Mediterranean, African, Middle Eastern, or Southeast Asian descent. 1 Thalassemia trait patients should not receive iron supplementation and require genetic counseling if planning pregnancy. 1
Common Pitfalls to Avoid
- Do not assume normal hemoglobin excludes iron deficiency—MCH drops before total hemoglobin falls, making low MCH an early marker of iron-deficient erythropoiesis. 1, 6
- Do not rely solely on RDW to rule out iron deficiency—RDW remains normal in early iron deficiency and only rises as the deficiency progresses and red cell populations become more heterogeneous. 3, 2
- Do not overlook concurrent inflammation—ferritin cutoffs must be adjusted upward (<100 μg/L rather than <30 μg/L) when CRP is elevated, or you will miss iron deficiency in patients with chronic disease. 1, 2
- Do not give iron empirically to patients with suspected thalassemia trait—iron supplementation is contraindicated and potentially harmful in these individuals. 1
Clinical Significance
This laboratory pattern represents a critical window for early intervention. In iron deficiency, the bone marrow is already producing hemoglobin-poor red cells even though total hemoglobin concentration has not yet declined. 1, 2 Identifying and treating iron deficiency at this stage prevents progression to overt anemia and its associated morbidity (fatigue, impaired cognitive function, reduced exercise tolerance). 1
Monitoring Strategy
Once you confirm the diagnosis and initiate treatment:
- For iron deficiency: Start oral iron supplementation (ferrous sulfate 325 mg once to three times daily) and recheck CBC with iron studies in 4-8 weeks to confirm hemoglobin rise and MCH normalization. 1, 2
- For thalassemia trait: No treatment is needed; provide reassurance, genetic counseling if appropriate, and avoid unnecessary iron supplementation. 1