The development of myeloid leukocytosis in leukemia patients during antileukemic treatment requires a differential diagnosis between myeloid leukemoid reaction and leukemia progression. We herein report the case of an 80-year-old Japanese man with chronic myelomonocytic leukemia (CMML) who developed marked myeloid leukocytosis (36.3 × 10⁹/L) with 32.5% monocytes and 48% neutrophils about 4 weeks after the initial 5-azacitidine (AZA) treatment. The leukocytosis was unlikely to be attributed to infection and adverse drug reaction. As it resolved in a few days without any interventions, the transient myeloid leukocytosis was confirmed to be a myeloid leukemoid reaction. After four cycles of AZA treatment, leukemic blasts in the bone marrow decreased and the patient became transfusion-independent. Interestingly, levels of serum G-CSF showed a similar trend to the myeloid leukocytosis, while those of serum GM-CSF and IL-17 were undetectable throughout the clinical course, suggesting that a differentiation response to AZA treatment might lead to the myeloid leukemoid reaction. Our case implies that a marked but transient myeloid leukemoid reaction mimicking CMML progression can develop during AZA treatment, which requires careful clinical monitoring and differential diagnosis.

白血病患者在抗白血病治疗期间出现髓样白细胞增多症需要在髓样白血病反应和白血病进展之间进行鉴别诊断。我们在此报告了一名患有慢性粒单核细胞白血病 (CMML) 的 80 岁日本男子的病例，他出现明显的髓系白细胞增多症 (36.3 × 10 ⁹/L) 在最初的 5-阿扎胞苷 (AZA) 治疗后约 4 周，单核细胞为 32.5%，中性粒细胞为 48%。白细胞增多不太可能归因于感染和药物不良反应。由于在几天内没有任何干预就消失了，短暂的髓系白细胞增多被证实是一种髓系白血病反应。经过四个周期的 AZA 治疗后，骨髓中的白血病母细胞减少，患者不再需要输血。有趣的是，血清 G-CSF 水平显示出与髓样白细胞增多相似的趋势，而血清 GM-CSF 和 IL-17 的水平在整个临床过程中检测不到，这表明对 AZA 治疗的分化反应可能导致髓样白血病反应.