Pathogenesis and causes
The adult human body contains 3–4 g of iron, the majority of which is part of hemoglobin. Deficiency occurs with a negative balance: when losses exceed intake or absorption.
Main etiological factors:
- Chronic blood loss: losing 10–15 ml of blood per day critically depletes iron stores.
- Alimentary factor: insufficient dietary intake.
- Malabsorption: impaired absorption due to small bowel pathology, achlorhydria, or post-gastrectomy.
Clinical manifestations
In addition to general signs of anemia, sideropenic syndrome develops, associated with a deficiency of iron-containing enzymes in tissues:
- Skin and nails: brittle nails and koilonychia (concave nail plate shape) are characteristic.
- GI tract: atrophic glossitis, angular stomatitis ("cheilitis"), and atrophic gastritis.
- Esophagus: dysphagia may occur due to mucosal fold deformation (Plummer–Vinson syndrome).
Diagnostics
Laboratory findings are characterized by decreased serum iron and ferritin levels. Peripheral blood smear shows microcytosis and hypochromia. In severe deficiency, annulocytes (ring-shaped erythrocytes) and ovalocytes appear.
Bone marrow staining with Prussian blue reveals an absence of hemosiderin stores, which is a key diagnostic criterion.
Briefly: answers to topical questions
Which serum biochemical markers change in iron-deficiency anemia (IDA)?
In iron-deficiency anemia, markers of store depletion and compensatory expansion of transport capacity change.
The following parameters decrease:
- Serum iron — drops below normal.
- Serum ferritin — the main indicator of tissue stores (drops below 10 µg/L).
- Transferrin saturation coefficient — 15% or less.
The following biochemical markers increase:
- Total iron-binding capacity of serum (TIBC).
- Latent iron-binding capacity (UIBC).
- Transferrin — the transport protein for free iron.
These parameters respond to iron deficiency in the early stages and change unidirectionally.
What stages are distinguished in the pathogenesis of iron deficiency development in the body?
Sources indicate that with a negative iron balance, the process of iron loss occurs sequentially, and on this basis, 4 stages of sideropenia are distinguished.
Confirmed sequence of iron deficiency development:
- First and foremost, tissue iron reserves are mobilized and depleted.
- Ferritin and hemosiderin levels decrease.
- The drop in hemoglobin iron levels, i.e., the manifestation of anemia, occurs only after the depot is completely emptied.
Iron deficiency also triggers two parallel pathological processes:
- Hematological pathway: slowed heme synthesis → inhibited hemoglobin formation → anemia → hypoxia and tissue/organ damage.
- Tissue pathway: impaired synthesis of iron-containing compounds, including enzymes and myoglobin → decreased antioxidant activity → intensified lipid peroxidation → tissue and organ damage.
Which specific tissue enzymes decrease in activity during sideropenic syndrome?
In sideropenic syndrome, the structure and activity of iron-containing enzymes and compounds are impaired. Sources indicate:
- Cytochromes.
- Catalase.
- Peroxidases, including glutathione peroxidases.
- Xanthine oxidase.
- Ribonucleotide reductase.
These disorders are associated with a deficiency of iron-containing enzymes and compounds, tissue hypoxia, decreased antioxidant activity, intensified lipid peroxidation, and tissue/organ damage.
"IDA is MHS: Microcytosis, Hypoplasia (nails/mucosa), Sideropenia" [Note: translated maintaining the clinical mnemonic sense].
Class and exam questions
How does anemia of chronic disease differ from iron-deficiency anemia?
In anemia of chronic disease, ferritin levels are normal or elevated, and iron is sequestered in macrophages, whereas in iron-deficiency anemia, iron stores are depleted.
What are ringed sideroblasts?
These are erythroblasts with excessive iron accumulation in mitochondria around the nucleus, characteristic of sideroblastic anemias rather than IDA.
Why does atrophic gastritis occur in IDA?
Atrophic gastritis can be both a cause (via achlorhydria) and a consequence of iron deficiency, creating a vicious cycle of malabsorption.
What else to study on this topic
- Differential diagnosis of microcytic anemias.
- Mechanisms of development of sideroblastic anemias.
- The role of transferrin in iron transport and atransferrinemia.
- Pathophysiology of anemia of chronic disease and tumors.
- Plummer–Vinson syndrome: morphological changes of the esophagus.
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