Journal of Blood Disorders & Transfusion

Chronic Illness Induced Anemia and Disrupted Iron Handling

Parvin Brown^* Department of Hematology, University of Western Australia, Perth, Australia
^*Correspondence: Parvin Brown, Department of Hematology, University of Western Australia, Perth, Australia, Email:

Received: 29-Jul-2025, Manuscript No. JBDT-25-30347; Editor assigned: 31-Jul-2025, Pre QC No. JBDT-25-30347 (PQ); Reviewed: 14-Aug-2025, QC No. JBDT-25-30347; Revised: 21-Aug-2025, Manuscript No. JBDT-25-30347 (R); , DOI: 10.4172/2155-9864.25.S15.071

Description

Anemia of inflammation is one of the most common forms of anemia encountered in clinical practice, particularly among individuals living with long-standing medical conditions. Its presentation is often subtle and patients may experience gradual changes in energy levels, reduced exercise tolerance and altered daily functioning. Although it shares features with other anemias, its development is shaped by persistent immune activation, disturbance of iron handling and impaired red blood cell production. Understanding how these elements interact is important for effective management, especially because this condition frequently coexists with chronic illnesses that already place considerable stress on overall health.

Chronic diseases such as autoimmune disorders, chronic kidney impairment, persistent infections, malignancies and metabolic abnormalities can all give rise to a prolonged inflammatory state. During this process, cytokines released from activated immune cells influence numerous physiological pathways. One of the main consequences is the alteration of iron regulation, leading to restricted availability of iron for erythropoiesis. Despite adequate or even increased iron stores, the body limits iron release to the bloodstream, thereby influencing the production of new red blood cells. This is a defining feature that differentiates anemia of inflammation from nutritional deficiencies.

Iron metabolism in anemia of inflammation differs significantly from the patterns seen in nutritional iron deficiency. Ferritin, an iron storage protein, tends to be elevated because it also functions as an acute-phase reactant. Serum iron and transferrin saturation are typically low, reflecting limited circulating iron. Total iron-binding capacity is often low or normal, in contrast to the elevated levels observed in classic iron deficiency anemia. These laboratory distinctions assist clinicians in determining whether anemia is caused by inadequate iron intake, impaired absorption, chronic disease activity, or a combination of factors. In many cases, both mechanisms may coexist, particularly in individuals with gastrointestinal disorders, chronic kidney conditions, or poor dietary intake [1-3].

The chronic activation of the immune system also alters macrophage function, affecting iron recycling. Normally, macrophages break down senescent red blood cells and release iron back into circulation. However, under persistent inflammatory influence, macrophages retain iron rather than releasing it. This retention is partly due to increased hepcidin activity and partly due to cellular responses that make macrophages less likely to mobilize stored iron. The result is a continuous reduction in circulating iron, even though total body iron stores may be normal or increased. This imbalance contributes to a persistent state of functional iron deficiency, where iron is present but unavailable for effective red blood cell development.

Patients with chronic illnesses may present with nonspecific symptoms that overlap with the manifestations of their underlying disease. Fatigue, shortness of breath, decreased exercise endurance and reduced concentration are common complaints. Because these symptoms are often attributed to the primary illness, anemia of inflammation can remain unrecognized unless laboratory assessments are performed. For this reason, routine blood tests play an important role in evaluating individuals with long-standing inflammatory or infectious conditions. Awareness of anemia patterns helps prevent misdiagnosis and ensures appropriate

Nutritional factors still matter, even though anemia of inflammation is not primarily caused by dietary iron deficiency. Adequate intake of iron, vitamin B12, folate and other nutrients supports red blood cell production. Patients with chronic illnesses may have altered diets, reduced appetite, or impaired nutrient absorption, making regular assessment of nutritional status valuable. Identifying coexisting deficiencies ensures that treatable factors are addressed and helps improve the overall management of anemia [4-7].

Monitoring is essential to guide treatment decisions. Regular evaluation of hemoglobin, ferritin, transferrin saturation, inflammatory markers and renal function allows clinicians to assess the effectiveness of interventions and detect changes in disease activity. Since anemia of inflammation often develops gradually, proactive monitoring helps prevent progression to more severe stages. Additionally, understanding individual patterns of inflammation and iron.

Collaboration among healthcare providers is essential for optimal management. Hematologists, nephrologists, rheumatologists, infectious disease specialists and primary care physicians all encounter patients with anemia of inflammation. Coordinated care ensures accurate diagnosis, appropriate testing, and individualized treatment plans. Shared decisionmaking between clinicians and patients helps define goals, discuss therapeutic options and address potential concerns related to long-term treatment strategies [8-10].

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