大血小板影响光学法与电阻抗法血小板计数差异的比较分析

目的：单纯大血小板如何影响电阻抗法和光学法血小板计数的差异,为光学法血小板计数的合理应用和有效提高血小板计数的准确性提供支持。方法采用 Sysmex-XE5000全自动血液分析仪电阻抗法和光学法对132例红细胞参数正常的血常规标本进行研究分析,按照 P-LCR 分为大血小板组和正常血小板组。采用非配对 t 检验比较两组间的红细胞参数和血小板参数,采用配对 t 检验比较组内电阻抗法和光学法血小板计数结果。结果两组血小板参数存在极显著差异,大血小板组的 P-LCR、MPV、PDW 和 IPF％均明显高于正常血小板组,而红细胞参数无明显差异。大血小板组电阻抗法和光学法血小板计数差异有统计学意义（P ＜0．05）,电阻抗法计数结果偏低,而正常血小板组则无明显差异。结论大血小板比率升高与未成熟血小板的增加有关。电阻抗法仅根据颗粒大小进行区分,容易将体积较大的大血小板排除,造成血小板计数减低。因此,当大血小板比率升高时,应采用光学法进行血小板计数,避免电阻抗法引起的假性减低。     

血小板计数准确性研究及对策

目的：探讨临床常规血小板（PLT）计数不准确的原因,并提出纠正措施。方法收集PLT计数异常标本180例,分为4组,分别为低值 PLT 组（PLT≤20×109/L）72例,小红细胞组54例,大 PLT 组33例,PLT 聚集组21例,分别采用光学法（PLT-O）、阻抗法（PLT-I）、手工镜检法（PLT-M）3种方法同时计数 PLT,用配对 t 检验进行分析。结果低值 PLT 组、小红细胞组、大 PLT 组光学法与 PLT 计数 PLT-M 法比较差异无统计学意义（P ＞0．05）,而 PLT-I 法与 PLT-M 法 PLT 计数比较差异有统计学意义（P ＜0．05）。PLT 聚集组的标本,PLT-I 法和 PLT-O 法计数结果比较,PLT-O 法结果更接近真实值。结论PLT-I法 PLT 计数的影响因素很多,主要有小红细胞干扰导致计数偏高,大 PLT 漏检导致 PLT 结果偏低,PLT 聚集等,当 PLT 计数结果异常时应根据复检规则复检,采用手工 PLT-M 法或者 PLT-O 法纠正,必要时重新采血测定。     

Relationship of the platelet distribution width/platelet count ratio with thyroid antibody levels in patients with Hashimoto's thyroiditis

ObjectiveI investigated whether the platelet distribution width/platelet count (PDW/PC) ratio, which is an inexpensive and simple test performed for almost all patients, is applicable in the follow-up of patients with Hashimoto’s thyroiditis and examined the relationship of this ratio with thyroperoxidase and thyroglobulin antibody levels.Materials and methodsThe study groups consisted of 67 patients with Hashimoto’s thyroiditis and 17 controls. All participants were aged 20 to 75 and treated the Internal Medicine outpatient clinic of my institution. The PDW/PC ratio and thyroid antibody levels were retrospectively evaluated in patients with normal liver and renal function and normal white blood cell counts, hemoglobin levels, and hematocrit levels.ResultsThyroid antibody levels were significantly higher in patients with Hashimoto’s thyroiditis than in controls. PC was higher in patients with Hashimoto’s thyroiditis, whereas the PDW/PC ratio was lower. However, these differences were not statistically significant.ConclusionIn this study, I did not find a statistically significant relationship between thyroid antibody levels and PDW/PC. However, a weak correlation between these variables was identified.     

Mean platelet volume/platelet count ratio predicts severe pneumonia of COVID‐19

BackgroundAlthough platelet mean volume/platelet count ratio (MPR) is considered to be a crucial marker of inflammatory and infectious diseases, the relationship between MPR and novel coronavirus infectious disease 2019 (COVID‐19) remains unclear.MethodsIn this retrospective study, 85 patients with confirmed COVID‐19 were enrolled and divided into low and high MPR group. Data from repeated measures were compared by the generalized estimating equations. Cox regression analyses were performed to assess the impact of MPR on the incidence of severe pneumonia (SP), with inverse probability of treatment weighting (IPTW) used to reduce confounding bias. The primary outcome is the incidence of SP of COVID‐19.ResultsDuring follow‐up, 17 (20.0%) patients were developed to SP. Compared with mild patients, patients with SP developed showed a higher MPR level at baseline, day 1, day 2, and day 3 after admission (P = .005, P = .015, P = .009, and P = .032, respectively). Kaplan‐Meier method showed a higher incidence of SP in the high MPR group than the low MPR group (log‐rank test = 10.66, P = .001). After adjustment, high MPR was associated with an elevated incidence of SP (HR, 5.841, 95% CI, 1.566‐21.791, P = .009). The IPTW method also suggested that MPR was a significant factor related to the incidence of SP (HR, 8.337, 95% CI, 4.045‐17.182, P < .001).ConclusionHigh MPR level is an independent risk factor for severe pneumonia in patients with COVID‐19.     

XE-5000血细胞分析仪血小板计数性能评价

目的评价Sysmex XE-5000血细胞分析仪对血小板(PLT)的检测性能。方法对XE-5000分别用电阻抗法和荧光法对血小板计数进行精密度、线性测试及干扰试验进行评估,并与显微镜计数法作对比试验。运用SPSS12.0对数据进行分析。结果平均批内精密度为PLT-I 1.30%、PLT-O 1.40%;批间精密度为PLT-I1.87%、PLT-O2.39%;携带污染率范围为PLT-I 0.00%~1.32%、PLT-O0.00%~1.17%;平均为PLT-I 0.44%和PLT-O0.33%;在线性稀释试验中低、中、高值与理论值的相关系数(r)分别为,PLT-I 0.991、0.997、0.997,PLT-O0.997、0.998、0.992;在RBC碎片干扰试验中,PLT-O对低值样本显示出较强的抗干扰能力(t=1.14,P>0.05),PLT-I与PLT-O测定血小板结果与PLT-M结果相关性良好。结论 Sysmex XE-5000对血小板计数具有精密度好、抗干扰能力强、重复性好、检测速度快等优点,是常规实验室测定血小板的较理想仪器。     

阻抗法与镜检法检测低值血小板结果比较分析及对临床血小板输血判断的影响

目的分析、比较三台血液分析仪阻抗法与显微镜手工法计数低值血小板结果,并探讨其对血小板输血阈值判断的影响。方法选择本实验室三台血液分析仪（LH750、CD-3700和Sysmex-xt1800i）分别计数低值血小板患者274例,PLT均小于100×109/L,以显微镜手工法为参考,按检测结果将血小板分为0〈PLT≤5×109/L,5×109/L〈PLT≤10×109/L,10×109/L〈PLT≤20×109/L,20×109/L〈PLT〈100×109/L四组,并与手工法结果进行比较分析。结果三台血液分析仪与镜检法计数在PLT≤20×109/L时相关系数（γ）均〈0.8。当20〈PLT〈100×109/L时相关系数（γ）均≥0.8.从ROC曲线分析,三台血液分析仪分别在0〈PLT≤5×109/L和5×109/L〈PLT≤10×109/L两组中AUC均小于0.90,在10×109/L〈PLT≤20×109/L组中AUC均大于0.90（分别为0.913,0.904,0.947）。结论三台血液分析仪计数PLT≤20×109/L的样本与镜检法相关性较低或无直接相关性,故对低值血小板,考虑需要血小板输血时,应慎重对待仪器检测的结果。由ROC曲线可知Sysmex-xt1800i对不同输血阈值的判断要优于LH750和CD-3700。     

光学法与电阻抗法血小板计数差异及仪器报警信息分析

目的：以手工显微镜计数法为参考,比较光学法与电阻抗法计数血小板的差异,并对仪器报警信息进行分析。方法应用SysmexXE‐2100全自动血液分析仪,同时采用光学法、电阻抗法检测468例患者的血小板计数（PLT‐O、PLT‐I）,并与手工显微镜计数法检测的血小板计数（PLT‐M）进行比较,同时镜检观察红细胞与血小板的数量及形态,并记录仪器的红细胞和血小板的报警信息。结果非血液病组中,PLT‐M、PLT‐I、PLT‐O差异无统计学意义（P＝0．071）。血液病组中,PLT‐I与PLT‐M、PLT‐O差异均有统计学意义（P＜0．05）,PLT‐M与PLT‐O差异无统计学意义（P＞0．05）。血液病组仪器出现血小板报警信息者149例,出现红细胞报警信息者127例,与镜检结果较符合。结论当血小板计数低于正常参考范围内时,PLT‐I计数误差较大,需PLT‐M和PLT‐O方法复检或校正;当出现血小板或红细胞报警信息时,均需涂片复检。     

Reduction of linezolid-associated thrombocytopenia by the dose adjustment based on the risk factors such as basal platelet count and body weight

The aim of the present study was to evaluate the efficacy of dose modification based on the risk factor for linezolid-induced thrombocytopenia. A multivariate logistic regression analysis performed in the observational study showed that low body weight of <55 kg (odds ratio [OR]: 33.2, 95% confidence interval [CI]: 2.16–510.1, P = 0.012) and the baseline platelet count of <200 × 10³/mm³ (OR: 24.9, 95% CI: 1.53–404.7, P = 0.024) were found to be risk factors for linezolid-induced thrombocytopenia. In the subsequent intervention study, in which daily dose of linezolid was set to 20 mg/kg in patients with either one of the risk factors or 1200 mg in those without any risk factor, the onset of thrombocytopenia was significantly prolonged in the intervention study group (P = 0.043), without reducing clinical efficacy. These findings suggest that dose adjustment of linezolid is effective in preventing thrombocytopenia without reducing its clinical efficacy in patients having risk factors.     

红细胞分布宽度与血小板计数比值、中性粒细胞计数与血小板计数比值对严重烧伤患者的预后评估

目的 观察严重烧伤患者的血小板计数(PLT)变化趋势、红细胞分布宽度(RDW)/PLT比值(RPR)、中性粒细胞计数(N)/PLT比值(NPR)水平及其对预后的评估价值.方法 选取2017年1月至2019年8月杭州市江干区人民医院收治的烧伤面积大于总体表面积30％的患者101例作为研究对象,记录入院后PLT开始减少的时...     

The circulating platelet count is not dictated by the liver,but may be determined in part by the bone marrow: analyses from human liver and stem cell transplantations

Summary. Background: The platelet count varies considerably between individuals, but within an individual the platelet count is remarkably stable over time. Mechanisms controlling the platelet count are not yet established. Objective: In the present study, we tested the hypothesis that the liver is important in controlling the circulating platelet count, as the liver is the main producer of thrombopoietin. Methods: We compared the platelet count prior to and after liver transplantation in > 250 patients transplanted for familial amyloidotic polyneuropathy (FAP). In contrast to most patients undergoing liver transplantation, patients with FAP have normal liver function before transplantation. Furthermore, we compared platelet counts in 89 living liver donors with the platelet count in the recipients of these grafts. Finally we compared platelet counts in donor‐recipient pairs of hematopoietic stem cells. Results and conclusions: The platelet count prior to transplantation correlated with the platelet count at 3 or 12 months after transplantation in patients with FAP (r = 0.48, P < 0.0001 at 3 months, r = 0.39, P < 0.0001 at 12 months), whereas the platelet count in a living liver donor did not correlate with the platelet count in the recipient at 3 or 12 months after transplantation (r = 0.16, P = 0.26 at 3 months, r = 0.11, P = 0.30 at 12 months). The platelet count of related donors of hematopoietic stem cells correlated with the platelet count in the recipient after transplantation (r = 0.25, P = 0.011). Conclusions: These results suggest that the liver, in spite of being the prime producer of thrombopoietin, does not dictate the circulating platelet count, whereas the bone marrow does appear to play a role.     

CD40 ligand shedding is regulated by interaction between matrix metalloproteinase‐2 and platelet integrin αIIbβ3

Summary. Background: CD40 ligand (CD40L, CD154) in the circulatory system is mainly contained in platelets, and surface‐expressed CD40L on activated platelets is subsequently cleaved by proteolytic activity to generate soluble CD40L (sCD40L). However, the enzyme responsible for the shedding of CD40L in activated platelets has not been clearly identified yet. We have recently found that molecular interaction of matrix metalloproteinase‐2 (MMP‐2) with integrin α_IIbβ₃ is required for the enhancement of platelet activation. Objectives: To elucidate the biochemical mechanism of MMP‐2‐associated sCD40L release. Methods: Localization of MMP‐2 and CD40L in platelets was analyzed by flow cytometry and fluorescence microscopy. The release of sCD40L from activated platelets was measured by enzyme‐linked immunosorbent assay. MMP‐2 binding to α_IIbβ₃ was analyzed by immunoprecipitation and western blotting. Recombinant hemopexin‐like domain and MMP‐2‐specific inhibitor were used to characterize the nature of MMP‐2 binding and catalytic activity. Results: It was revealed that interaction of MMP‐2 with α_IIbβ₃ is required for effective production of sCD40L in activated human platelets. Platelet activation and release of sCD40L were significantly affected by inhibition of platelet‐derived MMP‐2 activity or by inhibition of binding between the enzyme and the integrin. It was also found in platelet‐rich plasma that MMP‐2 activity is responsible for generating sCD40L. Conclusions: The results presented here strongly suggest that MMP‐2 interacts with α_IIbβ₃ to regulate the shedding of CD40L exposed on the surfaces of activated human platelets.     

A Thrombelastograph whole blood assay for clinical monitoring of NSAID-insensitive transcellular platelet activation by arachidonic acid

Optical platelet aggregation (OPA) with platelet-rich plasma (PRP) was compared with a Thrombelastograph (TEG) whole blood assay for monitoring arachidonic acid (AA)-induced platelet activation. Assays were performed on 47 interventional cardiology and 24 general surgery patients receiving aspirin therapy for cardiovascular disease, as well as 48 volunteers asked to take nonsteroidal anti-inflammatory drugs (NSAIDs) or 12 volunteers on chronic NSAID therapy unrelated to diagnosed cardiovascular disease. Whole blood TEG monitoring of NSAID inhibition detected NSAID-insensitive AA activation of platelets in a significantly higher number of cardiology (23%) and surgery (25%) patients and normal volunteers on chronic NSAID (25%) therapy relative to normal subjects not on chronic NSAID therapy (0%). Whole blood NSAID insensitivity was observed with cyclooxygenase-I inhibitors, such as aspirin and ibuprofen; was not affected by Celebrex, a cyclooxygenase-II inhibitor; but was completely inhibited by thromboxane-receptor antagonists. This was not due to platelet NSAID insensitivity, because complete inhibition of AA-activation responses in PRP was observed with either TEG or OPA assays. We confirmed that thromboxane B(2) formation in PRP from NSAID-insensitive subjects was completely inhibited by NSAIDs. However, significant amounts were formed in whole blood from NSAID-insensitive subjects, but not in whole blood from NSAID-sensitive subjects. Thromboxane formation after AA addition was not found in washed blood cells with 90% reduced platelet counts or in leukocyte-rich buffy coat fractions, but could be restored by addition of PRP. NSAID-insensitive activation was inhibited by nordihydroguaiaretic acid, with an IC(50) of 30 micromol, implicating 12- and/or 15-lipoxygenases in this transcellular pathway.