病例报告:非小细胞肺癌中的嗜酸性粒细胞增多症

Hyunwoo Kwon , Mingjia Li , Jesse D Sheldon , Nicholas Jones , Nicolas Gallastegui Crestani , Zihai Li , Dwight H Owen
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引用次数: 0

摘要

背景嗜酸性粒细胞过多症的定义是嗜酸性粒细胞绝对计数≥1,500 个/微升,可能是原发性(克隆性)血液病的结果,也可能是过敏原、寄生虫感染、药物或癌症引起的炎症的继发反应。对该病的评估需要进行全面的病史、体格检查和实验室检查,以确定潜在的病因,并评估终末器官损伤的证据,以防出现嗜酸性粒细胞过多综合征。病例介绍 一位 60 岁的白种男性吸烟者,既往有脑血管意外和射血分数降低的心力衰竭病史,出现急性脑病,随后发展为多系统器官衰竭。外周血涂片和其他血液学检查未提示克隆性血液恶性肿瘤。外周血、下呼吸道和脑脊液的广泛感染检查结果均为阴性。查阅近期病历,未发现任何可能致病的药物。定位胸腔积液的诊断性胸腔穿刺术显示为分化较差的非小细胞肺癌,这被认为是其严重的高嗜酸性粒细胞增多症的根本病因。他的脑病和其他内脏器官损伤的症状和体征被认为不太可能是由嗜酸性粒细胞过多症直接引起的。我们的病例报告强调了副肿瘤病因是不明原因的高嗜酸性粒细胞增多症患者的一个重要诊断考虑因素。文献综述显示,非小细胞肺癌和其他实体恶性肿瘤患者的嗜酸性粒细胞增多症与疾病进展迅速和预后不良有关,但其潜在机制仍不清楚。有趣的是,非小细胞肺癌患者嗜酸性粒细胞过多的病例报告表明,其发病率偏向男性。有必要对嗜酸性粒细胞在调节抗肿瘤免疫中的作用及其性别差异进行研究。
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Case report: Hypereosinophilia in non-small cell lung cancer

Background

Hypereosinophilia, as defined by the absolute eosinophil count ≥ 1,500 cells per microliter, can be a consequence of primary (clonal) hematologic disorders or secondary response to inflammation from allergens, parasitic infections, medications or cancer. Its evaluation requires comprehensive history and physical as well as laboratory studies to identify the underlying cause and assess for evidence of end-organ damage in concern for hypereosinophilia syndrome. Here, we report a rare case of paraneoplastic hypereosinophilia with an absolute eosinophil count exceeding 70,000 cells per microliter in the setting of a newly diagnosed metastatic non-small cell lung cancer.

Case presentation

A 60-year-old Caucasian male smoker with past medical history of cerebrovascular accidents and heart failure with reduced ejection fraction presented with acute encephalopathy and later developed multi-system organ failure. Peripheral blood smear and other hematologic studies were not suggestive of clonal hematologic malignancy. Extensive infectious work-up of peripheral blood, lower respiratory tract and cerebrospinal fluid was negative. Review of recent medical record did not identify any potentially causative drugs. Diagnostic thoracentesis of the loculated pleural effusion showed poorly differentiated non-small cell lung cancer, which was deemed as the underlying etiology of his profound hypereosinophilia. His encephalopathy and other signs and symptoms of end organ damage were thought less likely to be directly driven by hypereosinophilia. Progressive critical illness unfortunately precluded disease-directed therapy and his family opted for comfort care to mitigate suffering.

Conclusions

Our case report highlights paraneoplastic etiology as an important diagnostic consideration in a patient with unexplained hypereosinophilia. Review of the literature shows that hypereosinophilia in patients with non-small cell lung cancer and other solid malignancies correlates with rapid disease progression and poor prognosis, though the underlying mechanisms remain unclear. Interestingly, case reports of hypereosinophilia in non-small cell lung cancer suggest a male-biased incidence. Investigation of the role of eosinophils in modulating anti-tumor immunity and its sex difference is warranted.

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