Development of iron deficiency anemia in patients undergoing extracorporeal photopheresis: Comparison of the UVAR and CELLEX instruments

Abstract

Introduction: Extracorporeal photopheresis (ECP) is a procedure used to influence T-cell activity in patients suffering from immune-mediated cellular damage secondary to activated lymphocytes. Although well-tolerated, iron deficiency anemia (IDA) has been described. The goal herein is to describe IDA in patients who received extracorporeal photopheresis (ECP) treatment using UVAR (Therakos Inc) and CELLEX (Therakos Inc) instruments. Design and Methods: Patients treated with ECP from 2015 to 2019 were retrospectively analyzed. IDA was defined by a decrease in hemoglobin following treatment with concomitant decrease in mean cell volume, mean corpuscular hemoglobin concentration, increased RBC distribution width, and/or iron studies compatible with IDA. Results: During the four-year study period, thirty-four patients received ECP. Thirteen (38%) underwent treatment with the previous UVAR device while 21 (62%) received treatment on the newer CELLEX instrument. Nineteen (56%) of the cohort developed clinical and laboratory evidence of IDA with an average of 3.2 g/dL decrease in hemoglobin. Patients who developed IDA treated on the CELLEX instrument experienced a significantly greater drop in hemoglobin (P = .04) than those treated on the UVAR. Examining the CELLEX-treated patients, those who received the procedure at greater frequency experienced significantly greater drops in hemoglobin (P = .03). Conclusions: IDA is a risk of chronic ECP therapy and is likely secondary to retained blood components in the instrument. The temporal relationship between anemia and ECP treatment has a direct correlation with the treatment schedule. Patients undergoing ECP treatment should be closely monitored for the development of IDA.

Impact of extracorporeal photopheresis on blood and coagulation parameters

“…In 56% of patients studied, IDA could be detected over time. 9 In the present study, the number of patients with a pathological decrease in hemoglobin levels roughly doubled compared to baseline levels with a total incidence of 25% over time. This relatively low incidence compared to the studies discussed above may be explained by differences in the patient population.…”

“…However, the correlation of decreases in hemoglobin, MCV, and hematocrit indicate that iron deficiency was likely the cause of anemia in most cases. [8][9][10] In addition, particularly changes in lymphocyte and leucocyte counts could also be explained, at least in part, by concomitant immunosuppressive therapies (e.g., immunosuppressants) and/or exacerbated by the underlying disease (e.g., GvHD) without any influence by ECP. [8][9][10] Nevertheless, the acute changes observed 24 h after the first cycle of ECP indicate that the procedure may have a direct impact on blood parameters.…”

“…By contrast, Quaglino et al 12 observed an incidence of only 6% ECP‐treated CTLC patients who developed anemia ( n = 51). Recently, Moosavi et al 9 studied 34 patients of which most patients had GvHD ( n = 19). Interestingly, they determined that the mean drop of hemoglobin under ECP treatment significantly differed between the CELLEX and the UVAR XTS techniques (3.3 vs. 2 g/dl, respectively) 9 .…”

“…A decrease in platelet count may occur as a consequence of heparin‐induced thrombocytopenia 13 . Anemia has been observed in long‐term ECP patients, after incomplete reinfusion, or, rarely, due to hemolysis 7–12 . Kuhn et al 8 studied 123 ECP patients with GvHD, CTCL, solid organ transplant rejection, or other indications.…”

“…As limitation for the assessment of anemia in this retrospective study, determination of exact causes, such as iron deficiency remains unresolved. However, the correlation of decreases in hemoglobin, MCV, and hematocrit indicate that iron deficiency was likely the cause of anemia in most cases 8–10 . In addition, particularly changes in lymphocyte and leucocyte counts could also be explained, at least in part, by concomitant immunosuppressive therapies (e.g., immunosuppressants) and/or exacerbated by the underlying disease (e.g., GvHD) without any influence by ECP 8–10 .…”