The Leukemoid Reaction

The Leukemoid Reaction (LR) represents a profound, non-neoplastic, and transient elevation of the white blood cell (WBC) count, conventionally defined by levels exceeding $50 \times 10^9$ cells/L, occurring in response to severe physiological stimuli or underlying disease states.1 The clinical significance of this syndrome stems from its ability to dramatically mimic hematologic malignancies, primarily Myeloproliferative Neoplasms (MPNs) such as Chronic Myeloid Leukemia (CML). Pathologically, LR is characterized by robust neutrophilia with a marked left shift, reflecting accelerated myelopoiesis driven by circulating colony-stimulating factors (CSFs).1 Critical morphological findings, including toxic granulation and Döhle bodies, confirm the reactive nature of the process.4 The diagnostic challenge is resolved through laboratory differentiation utilizing the Leukocyte Alkaline Phosphatase (LAP) score, which is typically elevated in LR but low in CML, and definitively through the absence of the $BCR$-$ABL$ fusion gene.5 Etiologically, severe infections (e.g., sepsis, C. difficile), profound trauma, and paraneoplastic phenomena are the most frequent triggers.7 Paraneoplastic Leukemoid Reaction (PLR), driven by tumor-secreted granulocyte colony-stimulating factor (G-CSF), warrants special attention as it indicates an aggressive tumor phenotype and confers a grave prognosis.9 Management focuses entirely on identifying and eliminating the underlying stimulus, with intensive supportive care, including aggressive hydration and potential cytoreduction, reserved for cases presenting with symptomatic hyperleukocytosis.1