Management of Normocytic Anemia with Elevated Ferritin, Low Iron, and Thrombocytosis
This clinical presentation is consistent with anemia of inflammation (also called anemia of chronic disease), and management should focus on identifying and treating the underlying inflammatory or chronic disease process rather than iron supplementation. 1
Diagnostic Interpretation
Your patient's laboratory findings create a characteristic pattern:
Anemia of inflammation is diagnosed when serum iron is low despite adequate iron stores (ferritin not low) 1. Your patient has iron 35 (low) with ferritin 352 (elevated), which is the hallmark of this condition.
The elevated ESR (28) and thrombocytosis (469) further support an underlying inflammatory process 2, as reactive thrombocytosis commonly accompanies inflammatory states and iron deficiency.
Low albumin and low total protein indicate chronic inflammation or protein loss, which can contribute to anemia of chronic disease 1.
The normocytic MCV with stable hemoglobin 9.0 g/dL is typical for anemia of inflammation 1, 3, distinguishing it from iron deficiency anemia which would be microcytic.
Primary Management Strategy
Focus investigation on identifying the underlying inflammatory or chronic disease:
Evaluate for occult malignancy, particularly given the combination of anemia, elevated ferritin, thrombocytosis, and inflammatory markers 4. In adults with unexplained anemia and inflammatory markers, gastrointestinal malignancy must be excluded.
Screen for autoimmune conditions including rheumatoid arthritis, inflammatory bowel disease, and systemic lupus erythematosus, as these commonly cause anemia of inflammation 1.
Assess for chronic infections including endocarditis, osteomyelitis, or occult abscesses that could explain the inflammatory picture 1.
Consider chronic kidney disease given the elevated BUN/creatinine ratio (29.31), though CMP is otherwise unremarkable 3.
Why Iron Supplementation is NOT Indicated
Do not treat with iron supplementation despite the low serum iron 1. In anemia of inflammation, iron is sequestered in macrophages and unavailable for erythropoiesis due to elevated hepcidin levels. The ferritin of 352 ng/mL confirms adequate iron stores 4, 5.
Iron therapy would be ineffective and potentially harmful, as it cannot overcome the hepcidin-mediated iron sequestration and may contribute to oxidative stress 1.
Thrombocytosis Management
The thrombocytosis (469) is reactive and secondary to the underlying inflammatory process 2, 6. Reactive thrombocytosis associated with anemia and inflammation typically resolves when the underlying condition is treated 2.
Extreme thrombocytosis can occur with inflammatory states, and the correlation with elevated inflammatory markers (ESR 28) supports a reactive rather than clonal process 2, 6.
Critical Next Steps
Obtain a comprehensive evaluation for underlying disease:
Gastrointestinal evaluation with bidirectional endoscopy (EGD and colonoscopy) to exclude malignancy, particularly given age and unexplained anemia 4.
CT imaging of chest/abdomen/pelvis to evaluate for occult malignancy or inflammatory processes.
Autoimmune serologies including ANA, RF, anti-CCP, and inflammatory bowel disease markers.
Peripheral blood smear review to exclude primary hematologic disorders 3.
Common Pitfalls to Avoid
Do not misinterpret low iron as iron deficiency requiring supplementation - the elevated ferritin definitively excludes absolute iron deficiency 4, 5.
Do not attribute thrombocytosis to a primary myeloproliferative disorder without excluding reactive causes 2, 6. The combination with anemia and inflammation strongly suggests reactive thrombocytosis.
Do not delay investigation of the underlying cause - anemia of inflammation always has an underlying etiology that requires identification and treatment 1.
Treatment of Anemia
Treatment should target the underlying inflammatory condition 1. The anemia will improve as the underlying disease is controlled.
Recombinant human erythropoietin may be considered if anemia is symptomatic and the underlying condition cannot be rapidly controlled, though this is typically reserved for chronic kidney disease or specific malignancies 3.