Which parasites can cause iron deficiency (low iron) with elevated ferritin levels?

Parasites That Can Cause Low Iron with High Ferritin

No specific parasites directly cause the combination of low iron with high ferritin levels; rather, this pattern is typically seen in chronic inflammatory conditions where parasitic infections trigger inflammation-mediated changes in iron metabolism.

Mechanism of Parasite-Induced Iron Dysregulation

Parasitic infections can affect iron metabolism through two primary mechanisms:

1. Direct blood loss mechanism (causing true iron deficiency):

   • Hookworms (Necator americanus and Ancylostoma duodenale) - feed on blood in intestinal mucosa 1
   • Schistosoma species (S. haematobium, S. japonicum) - cause chronic blood loss 2, 3

2. Inflammation-mediated mechanism (causing functional iron deficiency with elevated ferritin):

   • Any chronic parasitic infection that triggers significant inflammatory response
   • Inflammation upregulates hepcidin production in the liver 4
   • Hepcidin reduces iron export from macrophages through reduction of ferroportin 4
   • This creates functional iron deficiency despite adequate or elevated iron stores

Laboratory Pattern Explanation

The pattern of low iron with high ferritin represents:

• Functional iron deficiency: Low transferrin saturation (<16%) with normal or elevated ferritin (>100 μg/L) 4, 5
• Anemia of chronic disease/inflammation: Characterized by impaired iron utilization despite adequate or increased iron stores 4

Parasites Most Commonly Associated with This Pattern

When chronic parasitic infections persist, they can trigger the anemia of chronic disease pattern:

1. Schistosomiasis (especially S. japonicum) 2, 3

   • Research shows increased iron stores correlate with worse disease outcomes
   • Hepcidin levels respond to changing iron status during infection
   • Can lead to fibrosis development around granulomas with increased iron availability

2. Chronic hookworm infections 1, 6, 7

   • Initially cause true iron deficiency through blood loss
   • With chronicity, can trigger inflammatory response
   • May present with mixed picture of iron deficiency and inflammation

Diagnostic Considerations

To differentiate between true iron deficiency and functional iron deficiency with inflammation:

• Basic workup: Complete blood count with MCV, reticulocytes, serum ferritin, transferrin saturation, and CRP 4

• Interpretation:

  • Ferritin <30 μg/L without inflammation = true iron deficiency 4, 5
  • Ferritin 30-100 μg/L with inflammation = possible combined iron deficiency and inflammation 4, 5
  • Ferritin >100 μg/L with transferrin saturation <16% and inflammation = anemia of chronic disease 4

• Additional helpful tests:

  • Soluble transferrin receptor (sTfR) - high in iron deficiency, normal/low in ACD 4
  • Reticulocyte hemoglobin content - more exact indicator of iron stores during inflammation 4
  • Hepcidin levels - more reliable indicator of iron deficiency than transferrin saturation in inflammation 4

Clinical Implications

• Parasitic infections may initially present with classic iron deficiency (low ferritin)
• With chronic infection and inflammation, the pattern shifts to functional iron deficiency (low iron, high ferritin)
• Iron supplementation in patients with functional iron deficiency and active inflammation may worsen outcomes 2
• Treatment should target the underlying parasitic infection first, then address iron status

Common Pitfalls

• Misinterpreting elevated ferritin as adequate iron stores in the presence of inflammation
• Failing to recognize that ferritin is an acute phase reactant that increases with inflammation
• Providing iron supplementation without addressing the underlying parasitic infection
• Not adjusting ferritin thresholds for diagnosing iron deficiency in the presence of inflammation (should use higher cutoff of up to 100 μg/L) 4, 5

Remember that the combination of low iron with high ferritin in parasitic infections represents a complex interplay between the host's iron metabolism and inflammatory response to the parasite, rather than a direct effect of the parasite itself.