• Vol. 34 No. 3, 229–234
  • 15 April 2005

Therapeutic Leukapheresis in Hyperleukocytic Leukaemias—The Experience of a Tertiary Institution in Singapore

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ABSTRACT

Introduction: Hyperleukocytic leukaemias are associated with early mortality due to respiratory or neurological complications. They result from endothelial damage secondary to leukostasis. Leukapheresis, which aims to lower the white blood cell (WBC) count, has been used in certain patients to reduce the threat from leukostasis. However, there are very few published clinical investigations on the most appropriate use of leukapheresis in hyperleukocytosis. Materials and Methods: We performed a retrospective analysis of 14 patients with hyperleukocytic leukaemia who presented to our institution and underwent therapeutic leukapheresis. We compare their clinical and biological characteristics and investigate the impact of leukapheresis on early mortality and long-term prognosis. Results: The median presenting WBC count was 439 x 103 / mm3 . Although patients with acute myeloid leukaemia (AML) had the lowest median presenting WBC counts, they constituted the largest group of patients with symptomatic hyperleukocytosis. Leukapheresis was highly effective, with the mean absolute and percentage reduction in WBC after each cycle being 126 x 103 /mm3 and 31.9% respectively. Four patients with AML died within 2 weeks of presentation despite prompt and effective leukapheresis. Conclusion: The interaction between the leukaemic cells and the vascular environment, a mechanism that none of the current therapies directly address, is probably more important in causing leukostasis than the absolute cell count itself.


Hyperleukocytic leukaemia is conventionally defined as leukaemia with an initial white blood cell (WBC) count or blast count greater than 100,000/mm3 . 1 It has a dramatic clinical presentation and represents a very challenging therapeutic problem due to the high early mortality. The many early complications and deaths are directly attributed to hyperleukocytosis and its resultant microcirculatory dysfunction, a phenomenon known as leukostasis,2,3 where the sludging of leukaemic blasts in capillary vessels and their adhesive interactions give rise to deleterious effects. Symptoms may arise from the involvement of any organ system, but intraparenchymal brain haemorrhage and respiratory failure account for the majority of deaths. The rapid destruction of leukaemic cells in response to chemotherapy also causes metabolic disturbances (tumour lysis syndrome).

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