阿米卡星在EDTA依赖性假性血小板减少的探讨

目的探讨乙二胺四乙酸盐(EDTA-K2)抗凝血在检测时出现假性血小板减少的临床解决思路。方法 5例假性血小板减少的患者分别采集2管EDTA-K2抗凝血标本和1管枸橼酸钠(1∶9)抗凝血标本,其中1管EDTA-K2抗凝血标本在采血0.5h后加入阿米卡星,然后用全自动血细胞分析仪分别检测不同时间段各管抗凝血标本的血小板计数,并做血涂片染色镜检。结果 4例患者的EDTA-K2抗凝血标本加入阿米卡星后,血小板计数结果正常且聚集的血小板解离;1例患者的EDTA-K2抗凝血标本加或未加入阿米卡星,血小板计数结果都会随着时间的延长恢复到正常水平;枸橼酸钠(1∶9)抗凝血在采血10min内检查血小板计数结果正常,但随时间延长会出现聚集导致血小板减少。结论阿米卡星可以解离EDTA-K2抗凝血中的血小板聚集,避免患者重复抽血检查。但加入阿米卡星后效果不明显时,需重新抽取枸橼酸纳(1∶9)抗凝血10min内进行检测,以获得准确的血小板计数结果。     

EDTA依赖性假性血小板减少的实验室解决思路

目的探讨乙二胺四乙酸(EDTA)依赖性假性血小板减少的临床解决思路。方法采集5例EDTA依赖性假性血小板减少患者的EDTA及枸橼酸钠抗凝血,每位患者的EDTA-K2抗凝血均在不同时间段分别加入6.5 mg/mL阿米卡星,并依次采用血液分析仪检测及血涂片检查。结果 3例患者在抽血前或抽血后1.5 h内在其EDTA抗凝血中加入阿米卡星后能在不影响其它血细胞形态和分布的情况下解离凝集血小板,其血小板计数能在室温下4 h之内维持稳定。余下2例患者,加或不加阿米卡星,其血小板数均会随着时间的延长逐渐增加,最终基本恢复正常水平,阿米卡星起到加速作用。结论添加阿米卡星的血小板检测结果在4 h保持稳定,结果明显优于更换枸橼酸钠抗凝剂。该药在医院抗菌药物中使用普遍,且在临床实际工作中,可以减少患者重复采血,缩短报告等候时间。阿米卡星可作为处理EDTA依赖的假性血小板减少的一线方法在临床普及。     

EDTA依赖性假性血小板减少研究进展

EDTA依赖性血小板假性减少是由于使用抗凝剂乙二胺四乙酸引起的体外血小板聚集,使血小板计数呈假性减少的一种现象,发生率低,临床易误诊误治。本文就其发生及纠正作一综述。     

7例EDTA依赖性假性血小板减少

目前,以乙二胺四乙酸二钾（EDTA—K2）为抗凝剂的真空负压采血管广泛用于临床,但EDTA—K2的使用会引起血小板的聚集,导致血小板假性减少。有文献报道部分人群血小板有EDTA依赖性聚集,造成仪器检测结果假性降低,这种现象称为EDTA依赖性假性血小板减少症（PTCP）,发生率为0．07％～0．21％。     

阿米卡星在1例多抗凝剂依赖性假性血小板减少症中的应用研究

目的 :研究阿米卡星在多抗凝剂依赖性假性血小板减少症中抑制血小板聚集的机制。方法 :采集1例乙二胺四乙酸(edathamil,EDTA)依赖性假性血小板减少症患者的乙二胺四乙酸二钾(EDTA-K2)及枸橼酸钠抗凝血,在不同时间段分别加入阿米卡星,依次用血细胞分析仪进行血小板计数,并行血涂片镜检,用流式细胞仪检测血小板膜表面标志物CD61、CD42b、PAC-1、CD62p的表达率。结果:采血后1 h内在EDTA-K2抗凝血中加入阿米卡星,能在不影响其他血细胞形态和分布的情况下,抑制血小板的聚集并解离聚集血小板,同时抑制血小板膜表面标志物CD62p活化,且血小板计数能在室温下4 h内维持稳定。枸橼酸钠抗凝血则随时间延长,血小板计数结果明显下降。结论:阿米卡星能纠正多抗凝剂依赖性假性血小板减少症患者的血小板计数,起到抑制血小板聚集并解离聚集血小板的作用,其机制可能与抑制了血小板膜表面标志物CD62p的表达有关。     

EDTA依赖性假性血小板减少症

对22例假性血小板减少症患者的相关资料进行回顾性分析。结果EDTA抗凝血会诱发血小板聚集,导致仪器法计数血小板假性减少伴白细胞假性增高,且临床无出血征及凝血功能检查正常。     

EDTA依赖性假性血小板减少误诊1例

患者,男,86岁,2010年7月于我院血液科就诊。主诉外院多次血常规检查示血小板计数于(3～15)×109/L间波动,且多次针对治疗均无效,故临床初步诊断为血小板减少症。患者既往身体健康,无血液病病史。体格检查:全身皮肤黏膜未见明显出血点或瘀斑,各项基本体征正常。外院骨髓检查报告示:有核细胞增生活跃,巨核细胞系分布正常。     

EDTA依赖性假性血小板减少1例

血小板减少为临床常见症状,表现为由于各种原因导致的血小板计数结果低于参考值下限。当血小板减少时可出现一系列症状,如皮肤淤血、鼻出血、口腔黏膜出血等,严重者可出现内脏出血、脑出血甚至危及生命。乙二胺四乙酸二钾(EDTA-K2)为血液分析的常用抗凝剂,但有时会引起血小板聚集,使血小板计数假性减少,临床诊断为EDTA依赖性假性血小板减少症(EDTA-PTCP)。赤壁市蒲纺医院(同济赤壁医院)于2019年12月16日收治1例血小板减少的患者,前后两次血常规检测所得血小板计数结果出现较大偏差,使用EDTA-K2抗凝管检测血常规时,患者的血小板数值低于正常参考值下限(26×10^9/L);改用肝素抗凝管检测时,患者的血小板数值在正常值参考范围内。经血小板人工计数及血涂片复片染色检查等手段复检后,均显示患者血小板数值在正常值参考范围内,证实了该例患者为EDTA-PTCP。     

EDTA依赖性假性血小板减少症1例

EDTA依赖性假性血小板减少症(EDTA-depen-dent pseudo thrombocytopenia,PTCT)就是由于EDTA盐作为抗凝剂的抗凝血在全自动血细胞计数仪上检测时,发生血小板聚集而引起的假性血小板减少的现象。我科近期在血常规检测中发现1例PTCT的典型病例,现报告如下。1材料与方法1.1病例摘要患者XXX,女,28岁,在我院进行产前检查的孕妇,PT、APTT、TT和Fg均在正常范围内,牙龈、皮肤、胃肠道等处无紫癜、出血现象。     

EDTA依赖性假性血小板减少症1例

EDTA依赖性假性血小板减少症（EDTA-depen-dent pseudo thrombocytopenia,PTCT）就是由于EDTA盐作为抗凝剂的抗凝血在全自动血细胞计数仪上检测时,发生血小板聚集而引起的假性血小板减少的现象。我科近期在血常规检测中发现1例PTCT的典型病例,现报告如下。     

丁胺卡那霉素对EDTA依赖性凝集血小板的解离及其机制

目的研究丁胺卡那霉素对EDTA抗凝剂依赖的聚集血小板的解离作用和机制,为血常规标本中血小板凝聚提供可靠的解决方法。方法在EDTA依赖的假性血小板减少症(PTCP)患者的EDTA-K2抗凝血样本中,于不同时间段加入不同浓度丁胺卡那霉素进行凝集血小板的解离试验,通过血小板计数和涂片观察解离效果;用流式细胞仪检测血小板膜表面CD41、CD61、CD62p、PAC-1和IgG的表达百分率。结果抽血后1h内加入丁胺卡那霉素对血小板凝集的解离作用明显,血小板计数可恢复到即时检测的水平,血小板CD62p、PAC-1和IgG的表达量被显著抑制,而CD41和CD61未受明显影响。结论PTCP患者血常规样品抽血后1h内加入丁胺卡那霉素能有效解离凝集的血小板,作用机制可能与抑制患者血小板膜表面CD62p、PAC-1和IgG的表达有关;此法有助于解决EDTA所致的血小板计数的假性减少。     

Inherited thrombocytopenia caused by ANKRD26 mutations misdiagnosed and treated as myelodysplastic syndrome: report on two cases

Essentials

• Thrombocytopenia 2 (THC2) is an inherited thrombocytopenia (IT) with dysmegakaryopoiesis.
• Physicians often do not suspect the genetic origin of thrombocytopenia in patients with THC2.
• We report two THC2 patients misdiagnosed with myelodysplasia and treated with chemotherapy.
• IT should be always considered in patients with isolated thrombocytopenia and dysmegakaryopoiesis.

     

β内酰胺类抗生素联用阿米卡星治疗医院获得性肺炎的疗效观察

目的探讨β内酰胺类抗生素联合阿米卡星治疗医院获得性肺炎患者的临床疗效。方法将43例医院获得性肺炎患者分为治疗组（22例）和对照组（21例）。治疗组患者给予β内酰胺类抗生素联合阿米卡星注射液抗感染,对照组患者单用β内酰胺类抗生素抗感染治疗。比较两组患者的治疗效果、住院时间及不良反应。结果两组患者治疗效果的比较差异无统计学意义（P〉0．05）。治疗组患者住院时间较对照组明显缩短（P〈0．05）。除治疗组中有1例患者发生药物过敏,其余患者均未发生不良反应。结论β内酰胺类抗生素联合阿米卡星注射液治疗医院获得性肺炎虽然不能提高药物疗效,但可明显缩短患者住院时间。     

丁胺卡那霉素对血小板聚集和凝血功能的抑制作用

目的 观察丁胺卡那霉素对血小板聚集和凝血功能试验的抑制作用,探讨其对止血功能的影响及相关作用机制.方法 将不同浓度丁胺卡那霉素分别与献血者富血小板血浆和乏血小板血浆作用,分为4组:0 mg/L组、30 mg/L组、91 mg/L组和910 mg/L组.以血小板聚集分析仪检测ADP诱导的血小板最大聚集率,以流式细胞仪检测活化血小板P-选择素、GPⅡb/Ⅲa及Fg-R表达水平,以血液凝固分析仪测定PT、APTT、TT及Fg水平.以前述4种浓度丁胺卡那霉素以及62.5 U/ml肝素钠和109 mmoL/L柠檬酸钠分别与新鲜全血作用,测定CT及血浆Ca2+浓度.分别检测10例急性下呼吸道感染患者在丁胺卡那霉素常规剂量治疗前和治疗后30 min ADP诱导的血小板最大聚集率、P-选择素、GPⅡb/Ⅲa及Fg-R表达水平,并测定PT、APTT、CT和血浆Ca2+浓度.结果 30 mg/L组血小板最大聚集率、P-选择素和Fg-R分别为(65.8±3.9)%、(9.2±1.0)%和(12.6±1.7)%,显著低于0 mg/L组的(88.0±4.6)%、(16.1±1.3)%和(31.0±2.5)%,差异均有统计学意义(t值分别为9.442、8.432和9.993,P均＜0.01);30 mg/L组APTT(80.5±6.8)s和CT(857±66)s明显高于0 mg/L组的(33.0±3.6)s和(447±35)s,差异均有统计学意义(t值分别为11.312和13.211,P均＜0.01);丁胺卡那霉素浓度与血小板最大聚集率呈显著负相关,与聚集的抑制率呈显著正相关,与APTT呈显著正相关[r值分别为-0.832、0.939和(＞0.870),P均＜0.05];30 mg/L组,91 me/L组和910 mg/L组呈剂量依赖性抑制P-选择素和Fg-R表达及使CT增加[F组间=21.44、26.24和(＞29.81),P均＜0.01].0 mg/L组、30mg/L组、91 mg/L组和910 mg/L组PT值分别为(14.7±1.9)s、(15.2±1.7)s、(15.6±1.5)s、(22.1±2.1)s,差异有统计学意义(F=8.21,P＜0.05),而GPⅡb/Ⅲa、TT、Fg以及血浆Ca2+浓度在4组间差异无统计学意义(P均＞0.05).丁胺卡那霉素治疗后患者血小板最大聚集率(51.6±10.1)%、P-选择素(6.8±1.8)%和Fg-R(20.1±5.8)%明显低于治疗前的(66.8±11.4)%、(10.9±3.1)%和(28.5 ±7.4)%,APTT(49.8±5.9)s和CT值(660±59)s则明显高于治疗前的(26.9±3.8)s和(410±45)s,差异均有统计学意义(t值分别为5.456、8.875、7.423、10.012和11.322,P均＜0.01).治疗前、后GPⅡb/Ⅲa、PT和Ca2+浓度变化无统计学意义(P＞0.05).结论 丁胺卡那霉素通过抑制血小板纤维蛋白原受体活化和释放反应途径抑制血小板聚集,可能通过抑制内源凝血系统因子途径而抑制凝血功能,从而对止血功能有抑制作用;应用丁胺卡那霉素抗感染治疗可能有发生出血的危险.     

Evaluation of pretest clinical score (4 T''s) for the diagnosis of heparin-induced thrombocytopenia in two clinical settings

BACKGROUND: Heparin-induced thrombocytopenia (HIT) is a prothrombotic adverse drug reaction caused by heparin. As thrombocytopenia is common in hospitalized patients receiving heparin, it would be useful to have a clinical scoring system that could differentiate patients with HIT from those with other reasons for thrombocytopenia. AIM: To compare prospectively the diagnostic utility of a clinical score for HIT in two different clinical settings. METHODS: The pretest clinical scoring system, the '4 T's', was used to classify 100 consecutive patients referred for possible HIT in one hospital (Hamilton General Hospital, HGH) into high, intermediate, and low probability groups. This system was also used to classify likewise 236 patients by clinicians in Germany referring blood for diagnostic testing for HIT in Greifswald (GW). The clinical scores were correlated with the results of laboratory testing for HIT antibodies using the serologic criteria for HIT with high diagnostic specificity. RESULTS: In both centers, patients with low scores were unlikely to test positive for HIT antibodies [HGH: 1/64 (1.6%), GW: 0/55 (0%)]. Patients with intermediate [HGH: 8/28 (28.6%), GW: 11/139 (7.9%)] or high scores [HGH: 8/8 (100%), GW: 9/42 (21.4%)] were more likely to test positive for clinically significant HIT antibodies. The positive predictive value of an intermediate or high clinical score for clinically significant HIT antibodies was higher at one center (HGH). CONCLUSIONS: A low pretest clinical score for HIT seems to be suitable for ruling out HIT in most situations (high-negative predictive value). The implications of an intermediate or high score vary in different clinical settings.     

Killing activity of meropenem in combination with amikacin against VIM- or KPC-producing Enterobacteriaceae that are susceptible,intermediate, or resistant to amikacin

Amikacin is administered with a carbapenem to treat serious infections caused by carbapenem-resistant Enterobacteriaceae (CRE). The varying degrees of activity of the individual agents correspond to differences in activity of the 2 in combination. Amikacin and meropenem are not bactericidal against amikacin-resistant CRE.     

原发免疫性血小板减少症的规范化诊治

原发免疫性血小板减少症(primary immune thrombocytopenia, ITP)是一种获得性免疫介导的血小板减少性疾病,其发病机制为免疫失耐受导致的血小板破坏过多及巨核细胞产生血小板不足。临床表现主要为血小板减少性的出血及疲劳等症状。ITP的诊断无特异性指标,需排除其他的血小板减少性疾病。治疗目的为维持血小板在安全水平,预防出血,并提高患者生活质量。治疗指征为血小板≤30×10⁹/L和(或)有出血表现,对于老年患者、重体力劳动者、有高血压等出血风险较高的合并症患者以及需抗血小板、抗凝治疗患者等,可适当放宽治疗指征。一线治疗为糖皮质激素及静脉注射人免疫球蛋白;二线治疗包括促血小板生成药物、利妥昔单抗及脾切除等治疗;对于难治性ITP患者,可考虑维A酸等三线治疗。     

小儿血液透析后假性动脉瘤形成的预防及护理

目的:探讨小儿血液透析后假性动脉瘤的预防和护理措施。方法:选择2001年1月~2005年6月136例行血液透析患儿,通过规范穿刺技术、准确使用抗凝剂治疗、切实有效压迫动脉穿刺处、积极控制高血压、勤观察同时做好家长、患儿的心理支持等措施来加以预防。结果:136例患儿中有5例并发假性动脉瘤,其中4例治愈,1例行外科手术修复。其余均顺利实施血液透析,无并发症发生。结论:精心的预防护理对防范小儿血液透析后假性动脉瘤的形成至关重要。     

Use of plasma exchange in patients with heparin-induced thrombocytopenia: a report of two cases and a review of the literature

Heparin-induced thrombocytopenia (HIT), which is characterized by thrombocytopenia and potentially serious thromboses, may develop in patients exposed to heparin anticoagulation. HIT is caused by antibodies to the heparin/platelet factor 4 (PF4) complex. Management of HIT involves discontinuation of heparin and anticoagulation with a nonheparin alternative such as a direct thrombin inhibitor (DTI). This poses a challenge in the management of patients who need to undergo cardiopulmonary bypass surgery (CPB), because CPB requires anticoagulation with heparin and standardized protocols for use of DTIs are not widely available. We report two patients with HIT who underwent successful CPB with heparin anticoagulation following plasma exchange (PE) to reduce heparin/PF4 antibody titers. Case 1 is a 46-year-old male with cardiac amyloidosis who needed urgent placement of a left ventricular assist device. Case 2 is a 34-year-old woman with acute myocarditis who needed placement of a biventricular assist device. Both patients had positive enzyme-linked immunosorbent assay assays for heparin/PF4 antibodies and clinical evidence of HIT before PE. Following PE and subsequent CPB, neither patient had clinical or laboratory evidence of HIT. The literature regarding the use of PE for the treatment of complications of HIT and as prophylaxis before CPB is reviewed.     

A randomized clinical trial of ceftriaxone and amikacin versus piperacillin tazobactam and amikacin in febrile patients with hematological neoplasia and severe neutropenia

Goal of work We compared the efficacy of ceftriaxone (CA regimen) and piperacillin-tazobactam (PTA regimen) in association with amikacin in the treatment of febrile episodes in severely neutropenic hematological patients.Patients and methods A total of 252 febrile episodes in 224 patients were randomized.Main results The CA regimen was effective in 62/122 evaluable episodes (50.8%), and the PTA regimen was effective in 64/121 (52.9%; P>0.2). Median time to failure was 4 and 5 days (P>0.1). Further infections developed in 21/122 episodes (17.2%) with the CA regimen and in 12/121 (9.9%) with the PTA regimen (P=0.06). The overall mortality at the end of the febrile episode was 11/243 (4.5%); seven deaths were considered to be related to infection.Conclusions Patients treated with piperacillin-tazobactam and amikacin tended to become afebrile sooner and to suffer a lower rate of further infections, even though our data did not show any statistically significant differences between the two groups.