Iron Deficiency Anemia and Thrombotic Risk Factors

Iron deficiency anaemia (IDA) is the most prevalent form of anaemia worldwide, arising when iron stores are insufficient to sustain normal erythropoiesis. Characterised by reduced haemoglobin concentration, microcytic red cells and diminished oxygen‐carrying capacity, IDA triggers compensatory mechanisms that may predispose to thrombosis. Reactive thrombocytosis is frequently observed, driven by enhanced megakaryocyte differentiation and platelet production. Concurrently, alterations in coagulation balance—such as upregulated transferrin expression and increased formation of procoagulant complexes—promote a hypercoagulable state. Hypoxia‐inducible factors, inflammatory cytokines and endothelial dysfunction further amplify thrombotic risk by modulating platelet adhesion, activation of coagulation proteases and impairment of natural anticoagulant pathways. Globally, this interplay has profound implications for patients with inflammatory bowel disease, chronic kidney disease, cancer or hormonal therapies. Early recognition of IDA as a modifiable thrombotic risk factor and timely iron repletion can mitigate secondary thrombocytosis, restore haemostatic equilibrium and reduce the incidence of both arterial and venous thromboembolic events.

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Iron Deficiency Anemia and Thrombotic Risk Factors publication trend

The graph below shows the total number of articles in iron deficiency anemia and thrombotic risk factors across all publications each year (not limited to Nature Index journals).

Technical terms

Iron deficiency anaemia (IDA): A disorder characterised by low haemoglobin and depleted iron stores, leading to microcytic erythrocytes and reduced oxygen delivery.

Thrombocytosis: An elevated platelet count in peripheral blood, often reactive to iron deficiency and associated with increased thrombotic potential.

Hypercoagulability: A state in which the blood’s tendency to clot is enhanced, resulting from imbalances among coagulation factors, platelets and natural anticoagulants.

Transferrin: The principal iron-binding plasma glycoprotein that, beyond iron transport, interacts with coagulation proteases and inhibitors to regulate thrombin generation.

References

1. Platelet levels before and after iron replacement therapy in patients with iron deficiency anemia. Hematology (2025).
2. Iron-Deficiency and Estrogen Are Associated With Ischemic Stroke by Up-Regulating Transferrin to Induce Hypercoagulability. Circulation Research (2020).
3. Transferrin plays a central role in coagulation balance by interacting with clotting factors. Cell Research (2019).
4. Increased expression of HIF2α during iron deficiency–associated megakaryocytic differentiation. Journal of Thrombosis and Haemostasis (2015).