Review Article ​

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Year: 2020 I Volume: 2 I Issue: 4 I Pages I 8 - 16

 https://doi.org/10.46982/gjmt.2020.109

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Anemia of Chronic Disease: Epidemiology and Pathophysiological Mechanisms – Literature Review

 

Abdulrahman Ismaiel1,2*, Nahlah Al Srouji3

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1 Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.

2 2nd Department of Internal Medicine, Cluj-Napoca, Romania.

3 Leon Daniello Clinical Hospital of Pneumology, Cluj-Napoca, Romania 

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* Corresponding Author:

Abdulrahman Ismaiel, MD

Email: abdulrahman.ismaiel@yahoo.com

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Source of funding:  None

 

Conflict of interest: None

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Abstract

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Anemia of chronic disease (ACD), also known as anemia of inflammation (AI), is the term used to describe the hypoproliferative anemia. ACD was demonstrated in several conditions including systemic inflammation, acute and chronic infections of bacterial, viral, parasitic or fungal etiologies, cancer and hematological malignancies, chronic diseases such as chronic kidney disease and congestive heart failure, in addition to ageing, graft versus host disease after solid-organ transplantation, critical illness, and obesity. As a result of the possible different etiologies, the pathogenesis of ACD is complex with multiple pathways.

Although the relationship between anemia, chronic inflammation and iron was discovered decades ago, only recently did research describe the role of several pro-inflammatory cytokines, in addition to molecular pathways and the type II acute-phase protein hepcidin involving iron absorption and metabolism, helping in the understanding of new pathophysiological mechanisms which were not previously understood that can lead to ACD. Hence, our understanding of the molecular mechanism related to intestinal iron absorption and metabolism has improved significantly.

The pathophysiology of ACD is thought to be due to three main processes including a decreased erythrocyte survival that creates a demand for a mild increase in bone marrow production of erythrocytes, inability of the bone marrow to respond to the required increased demand due to an altered erythropoietin production or impaired ability to respond to erythropoietin by erythroid progenitor cells and alteration in iron stores’ mobilization through increased uptake and retention of iron in cells of the reticuloendothelial system.

Lately, research advances including hepcidin’s discovery contributed to our understanding regarding iron metabolism and pathophysiological mechanisms in ACD. However, future research remains essential in order to find potential therapeutic strategies, possibly targeting genes coding cytokines to discover optimal therapies in treating ACD more efficiently.

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