Impact of Anaemia and Dysregulated Iron Metabolism on COVID-19 Clinical Outcome – Review Article
Coronavirus disease-19 (COVID-19) is a disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that can manifest in a wide range of forms, but the most common symptoms are fever, headache, fatigue, respiratory problems, lost sense of smell and taste, sore throat, muscle pain and malaise.
In patients with COVID-19, the inflammatory response of the organism affects iron homeostasis. Severe COVID-19 infections may lead to a hyperinflammatory condition, characterised by elevated ferritin levels that correlate with the severity of the clinical course, prolonged intensive care unit (ICU) stay, development of acute respiratory distress syndrome and a fatal outcome. As a result of iron metabolism disorders in inflammation, decreased erythropoiesis and reduced biological activity of erythropoietin, the erythrocyte half-life is shortened, leading to anaemia of chronic inflammation. Cytokine IL-6 plays the most crucial role in regulating iron concentration. It affects iron metabolism by producing hepcidin via STAT 3. Hepcidin produces regulatory effects on iron by binding with ferroportin, the only known transmembrane iron exporter.
Anaemia has long been characterised as a significant risk factor contributing to increased mortality and poorer clinical outcomes for various infections. The most severe forms of COVID-19 infection result in pneumonia, causing a reduced supply of oxygen to the circulation, ultimately leading to ischemia of vital organs. Anaemia of chronic disease is more common in COVID-19 positive patients and is associated with a poorer clinical outcome. A higher ferritin/transferrin ratio indicates an advanced inflammatory condition and may be a predictive factor of ICU admission.