A 75-year-old woman presented to the emergency department with progressive abdominal pain, fever, and diarrhea after taking levofloxacin for a respiratory tract infection. On evaluation, she was in clinical shock, with blood pressure 88/58 mmHg and heart rate 122 beats per minute. A complete blood count provided by the Sysmex XN-1000 analyzer showed leukocytosis (13.8 × 10⁹/L, 95% neutrophils) and thrombocytopenia (22 × 10⁹/L). She had acidosis, renal impairment, coagulopathy, and elevated C-reactive protein level. Because of the thrombocytopenia, an examination of a peripheral-blood smear was performed in the hematology laboratory, which showed vacuolated neutrophils that contained phagocytized platelets. Of 200 neutrophils examined, 161 (80%) contained between one and six platelets (Figure 1). These findings indicated spurious thrombocytopenia. The emergency department staff were notified by the laboratory that the patient's platelet count was normal. Subsequently, she underwent internal jugular-vein catheterization for fluid resuscitation without oozing or hematoma. Pseudomembranous colitis was diagnosed on the basis of a positive Clostridioides difficile stool test. She was treated with metronidazole and vancomycin, but her course was complicated by renal failure necessitating hemodialysis. Eventually, she made a full recovery. During hospitalization, multiple routinely prepared films from EDTA-anticoagulated blood consistently demonstrated platelet phagocytosis but with the resolution of the colitis, the phenomenon became progressively less pronounced. The automated platelet count became normal within 30 days.

A peripheral-blood smear should always be examined in new cases of thrombocytopenia or whenever the platelet count is unexpectedly low, in order to confirm the thrombocytopenia. The blood smear may be requested by physicians or initiated by laboratory staff [1]. As seen here, a laboratory-initiated blood smear, is particularly valuable because it may permit earlier recognition of pseudothrombocytopenia. The incidence of pseudothrombocytopenia is 1.9% among hospitalized patients and 0.15% in the outpatient setting [2]. Falsely low counts may be the result of small clots, platelet clumping, platelet satellitism, or abnormally large platelets. Phagocytosis of platelets by neutrophilic granulocytes is a rare cause of pseudothrombocytopenia, often seen in association with platelet satellitism [2]. Ordinarily, “flags” produced by automated blood-count analyzers are very useful for detecting errors in platelet enumeration. In this patient, however, the flagging system did not detect an error, suggesting that phagocytosis of platelets by neutrophils cannot be detected by the automated flagging systems.

Phagocytosis of platelets by neutrophilic granulocytes is an in vitro phenomenon occurring only in EDTA-anticoagulated blood [2, 3]. It is not reproduced if blood is drawn into a citrated tube or smears are made directly from capillary blood. The underlying mechanism is not fully understood, but might be related to IgG autoantibodies directed against the glycoprotein IIb/IIIa complex of platelets and the Fcγ-receptor III of neutrophils. The working hypothesis is that at room temperature, the chelation of calcium ions by EDTA alters the glycoprotein IIb/IIIa molecule and the neutrophil Fcγ-receptor exposing epitopes for the IgG autoantibody, which forms a bridge between platelets and neutrophils. Neutrophil–platelet adherence is followed by platelet phagocytosis [2, 3]. Platelet activation may also play a part. On activation by inflammatory triggers, platelets express P-selectin on their surfaces, which facilitates platelet adherence to neutrophils [4].

In contrast to platelet clumping which frequently occurs in routine blood counts, platelet phagocytosis is seen mainly during severe illness such as infection, thrombosis, and malignant hypertension [3]. Our patient's case is, to our knowledge, the first report of pseudothrombocytopenia occurring in pseudomembranous colitis.

This case illustrates an important cause of spurious thrombocytopenia in the acutely ill patient. Awareness of this phenomenon can prevent unnecessary measures such as platelet transfusions, postponement of invasive interventions, or discontinuation of medications.

一名 75 岁女性在服用左氧氟沙星治疗呼吸道感染后，因进行性腹痛、发热和腹泻到急诊科就诊。经评估，她处于临床休克状态，血压 88/58 mmHg，心率 122 次/分。Sysmex XN-1000 分析仪提供的全血细胞计数显示白细胞增多（13.8 × 10⁹/L，95% 中性粒细胞）和血小板减少症（22 × 10⁹/L）。她有酸中毒、肾功能损害、凝血功能障碍和 C 反应蛋白水平升高。由于血小板减少症，在血液学实验室进行了外周血涂片检查，显示空泡中性粒细胞含有吞噬血小板。在检查的 200 个中性粒细胞中，161 个 （80%） 包含 1 到 6 个血小板（图 1）。这些发现表明假性血小板减少症。实验室通知急诊科工作人员，患者的血小板计数正常。随后，她接受了颈内静脉导管插入术进行液体复苏，无渗出或血肿。根据艰难梭菌粪便试验阳性诊断为伪膜性结肠炎。她接受了甲硝唑和万古霉素治疗，但她的病程因肾功能衰竭而复杂化，需要进行血液透析。最终，她完全康复了。在住院期间，来自 EDTA 抗凝血的多个常规制备的胶片一致显示血小板吞噬作用，但随着结肠炎的消退，这种现象逐渐变得不那么明显。自动血小板计数在 30 天内恢复正常。

在新发血小板减少症病例或血小板计数意外偏低时，应始终检查外周血涂片，以确认血小板减少症。医生可能要求进行血涂片检查，也可能由实验室工作人员发起 [1]。如图所示，实验室发起的血涂片特别有价值，因为它可能允许早期识别假性血小板减少症。假性血小板减少症的发病率在住院患者中为 1.9%，在门诊患者中为 0.15% [2]。假性低计数可能是小凝块、血小板聚集、血小板沙地炎或血小板异常大的结果。中性粒细胞对血小板的吞噬作用是假性血小板减少症的罕见原因，常与血小板satellitia有关[2]。通常，自动血细胞计数分析仪产生的“标志”对于检测血小板计数中的错误非常有用。然而，在该患者中，标记系统未检测到错误，这表明自动标记系统无法检测到中性粒细胞对血小板的吞噬作用。

中性粒细胞对血小板的吞噬作用是一种体外现象，仅发生在 EDTA 抗凝血中 [2， 3]。如果将血液抽入柠檬酸盐管或直接从毛细血管血制成涂片，则不会重现。其潜在机制尚不完全清楚，但可能与针对血小板糖蛋白 IIb/IIIa 复合物和中性粒细胞 Fcγ 受体 III 的 IgG 自身抗体有关。工作假设是，在室温下，EDTA 对钙离子的螯合会改变糖蛋白 IIb/IIIa 分子和中性粒细胞 Fcγ 受体暴露 IgG 自身抗体的表位，从而在血小板和中性粒细胞之间形成桥梁。中性粒细胞-血小板粘附之后是血小板吞噬作用 [2， 3]。血小板活化也可能起作用。在炎症触发物激活后，血小板在其表面表达 P-选择素，这有助于血小板对中性粒细胞的粘附 [4]。

血小板吞噬作用主要见于感染、血栓形成和恶性高血压等严重疾病，而血小板吞噬作用则常见于感染、血栓形成和恶性高血压等严重疾病中。据我们所知，我们患者的病例是假膜性结肠炎中发生的假性血小板减少症的首次报告。

该病例说明了急症患者假性血小板减少症的重要原因。意识到这种现象可以防止不必要的措施，例如血小板输注、推迟侵入性干预或停药。