Journal of Blood Disorders & Transfusion

Chronic Therapy Associated Red Blood Cell Deficiency

Myura Soldin^* Department of Medicine and Clinical Sciences, University of Calgary, Calgary, Canada
^*Correspondence: Myura Soldin, Department of Medicine and Clinical Sciences, University of Calgary, Calgary, Canada, Email:

Received: 29-Jul-2025, Manuscript No. JBDT-25-30348; Editor assigned: 31-Jul-2025, Pre QC No. JBDT-25-30348 (PQ); Reviewed: 14-Aug-2025, QC No. JBDT-25-30348; Revised: 21-Aug-2025, Manuscript No. JBDT-25-30348 (R); Published: 28-Aug-2025, DOI: 10.4172/2155-9864.25.S15.072

Description

Therapeutic Plasma Exchange (TPE) is an established procedure used to remove pathogenic substances such as autoantibodies, immune complexes, or toxins from the blood. It is commonly applied in conditions including autoimmune disorders, neurological diseases and certain hematologic illnesses. While TPE can be highly effective in controlling disease activity and preventing organ damage, patients undergoing chronic or repeated sessions often develop hematologic alterations. Among these, anemia represents a frequent and clinically significant complication. Understanding the mechanisms, clinical implications and management strategies for anemia in this population is important for optimizing patient care and minimizing morbidity.

Patients receiving chronic TPE often undergo treatments at regular intervals over weeks, months, or even years. Each session involves removal of plasma and replacement with fluids such as albumin, plasma, or a combination of both. While this process efficiently reduces circulating pathogenic substances, it can also lead to losses of red blood cells, iron and other essential components. Even though TPE is generally considered safe, repeated procedures can cumulatively affect hematologic parameters. Monitoring hemoglobin, hematocrit and iron status becomes particularly important in long-term therapy.

Several mechanisms contribute to anemia in patients undergoing chronic TPE. Direct removal of red blood cells during the procedure is one factor. Although TPE primarily targets plasma, some erythrocytes are unavoidably removed along with plasma, especially when replacement fluids alter blood viscosity or volume. Over time, these small losses can accumulate, resulting in decreased total red blood cell mass. The magnitude of this effect depends on factors such as the frequency of treatments, the volume exchanged per session and the type of replacement fluid used.

Iron deficiency represents another mechanism underlying anemia in this setting. Plasma exchange can reduce circulating iron bound to transferrin, while repeated removal of plasma proteins may also reduce available iron stores indirectly. In addition, patients with chronic diseases requiring TPE often experience inflammation, which can alter iron metabolism and inhibit erythropoiesis. Elevated levels of inflammatory cytokines stimulate hepcidin production, restricting iron release from storage sites and further limiting its availability for red blood cell production. As a result, functional iron deficiency can develop even in patients with adequate iron stores.

Chronic illness itself contributes to anemia in this population. Many patients undergoing TPE have underlying autoimmune or systemic conditions that independently suppress red blood cell production. Inflammatory cytokines interfere with erythropoietin signaling and inhibit the maturation of erythroid precursors. Kidney involvement in some conditions can reduce erythropoietin synthesis, compounding the effect of chronic blood losses. In these circumstances, anemia is multifactorial, arising from both procedural losses and disease-related suppression of erythropoiesis.

Hemolysis, though less common, can also contribute. Mechanical stress during plasma exchange, particularly in procedures that use filtration techniques, can lead to red blood cell damage. Hemolysis may be subtle, detectable only by laboratory markers such as elevated lactate dehydrogenase, indirect bilirubin, or reticulocyte count. Even low-grade hemolysis over repeated sessions can cumulatively reduce red blood cell mass. Awareness of this possibility is important, particularly in patients with pre-existing hematologic vulnerabilities or fragile erythrocytes.

Transfusion support remains an important option for patients with severe or symptomatic anemia. Red blood cell transfusions provide immediate correction of hemoglobin levels, improving oxygen delivery and alleviating fatigue and dyspnea. However, repeated transfusions carry risks including alloimmunization, iron overload and volume-related complications. Therefore, transfusion decisions should be individualized, balancing the benefits against potential adverse effects. Integrating transfusion strategies with ongoing TPE requires careful planning to maintain stable hematologic status.

In conclusion, anemia is a common and significant complication in patients undergoing chronic therapeutic plasma exchange. Its development results from a combination of procedural effects, iron metabolism alterations, chronic inflammation and underlying disease factors. Recognition, monitoring, and proactive management are essential to prevent symptomatic anemia, support red blood cell production and maintain quality of life. Therapeutic strategies including iron supplementation, erythropoiesis-stimulating agents, procedural optimization and transfusion support offer effective approaches to address anemia. Long-term observation and coordinated care enhance the ability to manage this complication while preserving the benefits of plasma exchange. By integrating laboratory monitoring, patient education and individualized therapeutic approaches, clinicians can effectively address anemia in patients receiving chronic TPE, ensuring that treatment goals are met without compromising hematologic stability.