# Twenty Years of Therapeutic Leukocytapheresis in Newly Diagnosed Acute Myeloid Leukemia: Insights From A Single Center

**Authors:** Vojtech Latal, Ivana Skoumalova, Miroslava Palova, Tomas Szotkowski, Martin Cernan, Jana Navratilova, Helena Urbankova, Zuzana Pikalova, Ludek Raida, Edgar Faber, Tomas Papajik

PMC · DOI: 10.1002/jca.70111 · Journal of Clinical Apheresis · 2026-03-16

## TL;DR

This study examines the use of leukocytapheresis in treating high white blood cell counts in newly diagnosed AML patients, showing it is safe and effective as a bridge to further treatment.

## Contribution

The study provides long-term clinical insights into the safety and efficacy of leukocytapheresis for hyperleukocytosis in AML.

## Key findings

- Leukocytapheresis effectively reduced white blood cell counts without significant adverse events.
- Median overall survival was 5.9 months, with better outcomes in therapy-eligible patients.
- Leukocytapheresis was particularly beneficial as a bridge to definitive therapy for symptomatic patients.

## Abstract

Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy, and 5%–20% of newly diagnosed patients present with hyperleukocytosis (HL). HL, most often defined as WBC > 100 000/μL, is a hematologic emergency associated with severe complications, early mortality, and poor prognosis, requiring immediate intervention. From November 2005 to September 2025, 65 newly diagnosed AML patients with HL underwent leukocytapheresis (LCP) at University Hospital Olomouc. Clinical data were retrospectively collected from medical records. The primary objective was to evaluate the procedural efficacy and safety. Clinical and laboratory data were analyzed. Survival outcomes were assessed by Kaplan–Meier analysis and compared using the log‐rank test. Median age at diagnosis was 57 years. Dyspnea (60.0%), neuropsychiatric symptoms (31.7%), and visual impairment (6.2%) were the most common leukostasis manifestations. LCP effectively reduced WBC counts without significant adverse events, median of 2.2 TBV was treated, and 52.3% of the patients requiring more than one session. FLT3‐ITD and NPM1 mutations were detected in 26/46 (56.5%) and 17/43 (39.5%), respectively, KMT2A rearrangements were present in 5/57 (8.8%). Intensive chemotherapy was feasible in 56.9% of patients, with 26.2% undergoing allo‐HSCT. Median OS was 5.9 months (95% CI: 1.3–8.4), significantly longer in therapy‐eligible patients, but outcomes remained poor, highlighting HL as an unmet clinical need. LCP remains a valuable therapeutic option for patients with HL in newly diagnosed AML. Our long‐term experience supports its safety and efficacy, particularly in symptomatic patients, as a bridge to definitive therapy regardless of treatment intensity eligibility.

## Linked entities

- **Genes:** NPM1 (nucleophosmin 1) [NCBI Gene 4869], KMT2A (lysine methyltransferase 2A) [NCBI Gene 4297]
- **Diseases:** acute myeloid leukemia (MONDO:0015667)

## Full-text entities

- **Genes:** VCAM1 (vascular cell adhesion molecule 1) [NCBI Gene 7412] {aka CD106, INCAM-100}, TET2 (tet methylcytosine dioxygenase 2) [NCBI Gene 54790] {aka IMD75, KIAA1546, MDS}, ITGB3 (integrin subunit beta 3) [NCBI Gene 3690] {aka BDPLT16, BDPLT2, BDPLT24, CD61, FMAIT1, GP3A}, ETV6 (ETS variant transcription factor 6) [NCBI Gene 2120] {aka TEL, TEL/ABL, THC5}, ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}, MME (membrane metalloendopeptidase) [NCBI Gene 4311] {aka CALLA, CD10, CMT2T, NEP, SCA43, SFE}, CD24 (CD24 molecule) [NCBI Gene 100133941] {aka CD24A}, NPM1 (nucleophosmin 1) [NCBI Gene 4869] {aka B23, NPM}, MECOM (MDS1 and EVI1 complex locus) [NCBI Gene 2122] {aka AML1-EVI-1, EVI1, KMT8E, MDS1, MDS1-EVI1, PRDM3}, ITGA2B (integrin subunit alpha 2b) [NCBI Gene 3674] {aka BDPLT16, BDPLT2, CD41, CD41B, FMAIT2, GP2B}, ITGAX (integrin subunit alpha X) [NCBI Gene 3687] {aka CD11C, SLEB6}, FUT4 (fucosyltransferase 4) [NCBI Gene 2526] {aka CD15, ELFT, FCT3A, FUC-TIV, FUTIV, LeX}, CD22 (CD22 molecule) [NCBI Gene 933] {aka SIGLEC-2, SIGLEC2}, CD33 (CD33 molecule) [NCBI Gene 945] {aka CD33rSiglec, SIGLEC-3, SIGLEC3, p67}, SELE (selectin E) [NCBI Gene 6401] {aka CD62E, ELAM, ELAM1, ESEL, LECAM2, selectin-e}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, CD19 (CD19 molecule) [NCBI Gene 930] {aka B4, CVID3}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, CEBPA (CCAAT enhancer binding protein alpha) [NCBI Gene 1050] {aka C/EBP-alpha, CEBP}, DNTT (DNA nucleotidylexotransferase) [NCBI Gene 1791] {aka TDT}, TFRC (transferrin receptor) [NCBI Gene 7037] {aka CD71, IMD46, T9, TFR, TFR1, TR}, GYPA (glycophorin A (MNS blood group)) [NCBI Gene 2993] {aka CD235a, GPA, GPErik, GPSAT, HGpMiV, HGpMiXI}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, CD7 (CD7 molecule) [NCBI Gene 924] {aka GP40, LEU-9, TP41, Tp40}, MPO (myeloperoxidase) [NCBI Gene 4353], CD34 (CD34 molecule) [NCBI Gene 947], KMT2A (lysine methyltransferase 2A) [NCBI Gene 4297] {aka ALL-1, ALL1, CXXC7, GAS7, HRX, HTRX}, KRT20 (keratin 20) [NCBI Gene 54474] {aka CD20, CK-20, CK20, K20, KRT21}, KIT (KIT proto-oncogene, receptor tyrosine kinase) [NCBI Gene 3815] {aka C-Kit, CD117, MASTC, PBT, SCFR}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, CBFB (core-binding factor subunit beta) [NCBI Gene 865] {aka CLCD2, PEBP2B}, FLT3 (fms related receptor tyrosine kinase 3) [NCBI Gene 2322] {aka CD135, FLK-2, FLK2, STK1}, ABL1 (ABL proto-oncogene 1, non-receptor tyrosine kinase) [NCBI Gene 25] {aka ABL, BCR-ABL, CHDSKM, JTK7, bcr/abl, c-ABL}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CD14 (CD14 molecule) [NCBI Gene 929], CD2 (CD2 molecule) [NCBI Gene 914] {aka LFA-2, SRBC, T11}, CD5 (CD5 molecule) [NCBI Gene 921] {aka LEU1, T1}, FCGR1A (Fc gamma receptor Ia) [NCBI Gene 2209] {aka CD64, CD64A, FCG1, FCGR1, FCRI, FcgammaRI}, TXK (TXK tyrosine kinase) [NCBI Gene 7294] {aka BTKL, PSCTK5, PTK4, RLK, TKL}, ANPEP (alanyl aminopeptidase, membrane) [NCBI Gene 290] {aka AP-M, AP-N, APN, CD13, GP150, LAP1}, DNMT3A (DNA methyltransferase 3 alpha) [NCBI Gene 1788] {aka DNMT3A2, HESJAS, M.HsaIIIA, TBRS}, CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}
- **Diseases:** microvascular obstruction (MESH:D017566), headache (MESH:D006261), Leukostasis (MESH:D018921), or pulmonary complications (MESH:D008171), Dyspnea (MESH:D004417), hypocalcemia (MESH:D006996), Philadelphia chromose (MESH:D010677), neuropsychiatric disorders (MESH:D001523), inv(16) (MESH:C580205), epileptic seizures (MESH:D004827), intracranial hemorrhage (MESH:D020300), Myeloid (MESH:D007951), AML (MESH:D015470), death (MESH:D003643), Leukemia (MESH:D007938), DIC (MESH:D004211), septic shock (MESH:D012772), leukocytosis (MESH:D007964), dizziness (MESH:D004244), bleeding (MESH:D006470), infection (MESH:D007239), respiratory insufficiency (MESH:D012131), impaired consciousness (MESH:D003244), XL (MESH:D000080345), Coma (MESH:D003128), myocardial ischemia (MESH:D017202), endothelial damage (MESH:D014652), hematologic malignancy (MESH:D019337), seizures (MESH:D012640), inflammation (MESH:D007249), GvL (MESH:D006086), thromboembolic (MESH:D013923), TLS (MESH:D015275), confusion (MESH:D003221), vision impairment (MESH:D014786), tissue injury (MESH:D017695), retinal hemorrhage (MESH:D012166), MODS (MESH:D009102), positive (MESH:D000377), clonal disorder of hematopoiesis (MESH:C536227), APL (MESH:D015473)
- **Chemicals:** dexamethasone (MESH:D003907), AZA (MESH:D001379), gilteritinib (MESH:C000609080), idarubicin (MESH:D015255), GO (MESH:D000079982), fludarabine (MESH:C024352), azacitidine (MESH:D001374), calcium (MESH:D002118), BM medium (-), ATRA (MESH:D014212), cytarabine (MESH:D003561), venetoclax (MESH:C579720), sorafenib (MESH:D000077157), HU (MESH:D006918), mitoxantrone (MESH:D008942), midostaurin (MESH:C059539), dasatinib (MESH:D000069439)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

52 references — full list in the complete paper: https://tomesphere.com/paper/PMC12993091/full.md

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Source: https://tomesphere.com/paper/PMC12993091