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1.
1例57岁男性患者因行溶栓术,给予尿激酶200 000 U,1次/6 h泵入;肝素钠12 500 U入0.9%氯化钠注射液50 ml进行24 h微量泵泵入。溶栓治疗当日血小板计数为126×109/L,第3天为99×109/L,第4天降至65×109/L。考虑为肝素诱导血小板减少症,停用肝素钠,改为阿加曲班抗凝,并继续应用尿激酶行第2次溶栓术。停用肝素钠后血小板计数即回升,第2、4天分别为93×109/L、113×109/L,第5天恢复到术前水平。  相似文献   

2.
肝素诱导的血小板减少症   总被引:2,自引:0,他引:2  
赵彬  梅丹  李拥军  管珩 《中国药师》2007,10(8):822-824
近年来临床药师在与医师查房中,常见某些患者血小板减少无法解释,而部分患者发生血小板(Plt)减少前曾使用过肝素,检索相关文献发现肝素会导致血小板减少。肝素是临床最常用的抗凝药之一,成份为硫酸氨基葡聚糖,属酸性粘多糖,多由牛肺或牛肠、猪肠、羊肠中提取,因其最初得自于肝脏故名肝素。20世纪40年代首次用于临床,60多年以来肝素广泛用于抗凝治疗。  相似文献   

3.
肝素诱导血小板减少症   总被引:1,自引:0,他引:1  
郭涛 《医药导报》1999,18(6):391-392
目的 :阐明肝素诱导血小板减少症及血栓形成。方法 :对该病的概念、机制及治疗作一综述。结果 :使用牛肝素发病率较猪肝素高。结论 :肝素诱导血小板减少症应引起人们重视 ,建议确需使用肝素的患者尽可能使用猪肝素。  相似文献   

4.
李静  李坚  温浩 《中国医院药学杂志》2018,38(12):1302-1306
目的:分析急性冠脉综合征(ACS)患者发生低分子肝素诱导血小板减少症(HIT)的相关危险因素。方法:收集某院2011年1月-2017年11月出院的ACS且使用低分子肝素抗凝治疗的患者资料,调查血小板减少的发生情况,并通过单因素和多因素Logistic回归分析,得出肝素诱导的HIT的独立危险因素。结果:共纳入190例患者(HIT组48例,对照组142例)。年龄≥ 70岁(t=4.274,P=0.042)、血小板基础值(t=6.442,P=0.000)、肾功能肌酐水平(t=-4.080,P=0.000)、血红蛋白水平(t=3.337,P=0.001)、肝功能谷丙转氨酶(t=-2.253,P=0.025)、联合使用抗菌药物(t=27.023,P=0.000)以及联合使用替罗非班(t=4.656,P=0.031)在HIT组与对照组之间差异有显著性。对以上指标进一步进行多因素Logistic回归分析,得到高龄(OR=0.183,P=0.008)、血小板基础值低(OR=0.960,P=0.000)、肾功能肌酐水平高(OR=1.023,P=0.005)、联合使用抗菌药物(OR=0.191,P=0.003)、联合使用替罗非班(OR=3.500,P=0.041)是HIT发生的独立危险因素。结论:ACS患者在使用低分子肝素时应警惕HIT的发生,尤其年龄≥ 70岁、血小板基础值低、肾功能肌酐值高、联合使用抗菌药物及联合使用替罗非班的患者。  相似文献   

5.
患者,男,85岁,因外伤后右髋关节活动障碍1d入院。查体:右下肢外旋畸形,大转子部叩击痛明显,髋关节活动障碍。骨盆正位X线片示右股骨颈骨折头下型。临床诊断:右股骨颈骨折。入院后拟行人工股骨头置换术。术前查血小板:150×10^9/L,术前1d应用低分子肝素钠5000U皮下注射,次日手术顺利,术中出血约650ml。  相似文献   

6.
患者,男,85岁,因外伤后右髋关节活动障碍1d入院.查体:右下肢外旋畸形,大转子部叩击痛明显,髋关节活动障碍.骨盆正位X线片示右股骨颈骨折头下型.临床诊断:右股骨颈骨折.入院后拟行人工股骨头置换术.术前查血小板:150×109/L,术前1d应用低分子肝素钠5000U皮下注射,次日手术顺利,术中出血约650ml.术后6h皮下注射低分子肝素钠2500U,此后每天1次皮下注射5000U.术后6d查血小板40×109/L停用低分子肝素钠并应用激素治疗,术后7d查血小板20×109/L继续应用激素及1个单位血小板治疗,术后8d查血小板10×109/L,患者出现喘憋、皮肤淤斑,肺部CT广泛肺栓塞,出现呼吸功能衰竭,最终因多器官功能衰竭死亡.  相似文献   

7.
目的探讨冠状动脉介入治疗(PCI)患者使用肝素发生血小板减少症和血栓形成的危险性及处理原则。方法对1例PCI患者围手术期间使用肝素发生血小板减少症和血栓形成的原因、临床表现、实验室指标进行分析。结果由于诊断及时,处理得当,患者病情得到控制,痊愈出院。结论拟行PCI术的患者,尤其对于高龄患者,应用肝素时需要全面的评估利弊;同时,还要严密监测实验室指标,以便及时防治不良反应出现。  相似文献   

8.
例1为24岁男性患者,因急性心肌梗死,给予阿司匹林300mg、氯吡格雷300mg口服和普通肝素10000U静脉推注,并行冠状动脉造影、经皮冠状动脉腔内成形术及支架植入术。患者术前血小板计数为228.0×109/L,术后1h降至36.2×109/L。考虑为肝素诱导的血小板减少,遂停用肝素,给予阿加曲班0.5~2μg·kg-1·min-1静脉滴注。第3天患者血小板升至101×109/L,第4天恢复正常。例2为69岁男性冠状动脉粥样硬化性心脏病患者,在冠状动脉造影术中静脉推注普通肝素3000U。之后,行冠状动脉搭桥术,术前连续7d给予低分子肝素(1mg·kg-1·12h-1)皮下注射,术中给予普通肝素7000U静脉滴注。术前患者血小板计数197.0×109/L,术后降至19.2×109/L。停用肝素,给予阿加曲班0.5~1.5μg·kg-1·min-1静脉滴注,血小板计数升至146.0×109/L。  相似文献   

9.
10.
范鸣 《药学进展》2007,31(3):143-143
在美国,肝素钠注射剂产品的标签上最近补充了一则警告语,提示肝素致血小板减少症(HIT)可能延迟发生,进一步建议用此类产品时应密切监测不同程度的血小板减少症出现,若血小板计数跌至100000/mm3以下或血栓形成复发,则此肝素产品应立即停用,考虑改用其他抗凝药。先前肝素产品标签上也有关于致血小板减少症的警告语,而此次修订的新警告语还强调,HIT为一种抗体介导的严重不良反应,由不可逆的血小板凝聚所致,并可进而发展为静脉和动脉血栓形成,即所谓肝素致血小板减少与血栓形成(HITT)。这些新警告语已在近期的美国FDA MedWatch网站公布。…  相似文献   

11.
Argatroban is a direct thrombin inhibitor approved for anticoagulation in heparin-induced thrombocytopenia (HIT; in several countries) and in patients with or at risk of HIT undergoing percutaneous coronary intervention (PCI; in the USA). HIT is a relatively common extreme prothrombotic condition. When HIT is reasonably suspected, an alternative anticoagulant should be promptly initiated. In historical controlled studies, argatroban reduced new thrombosis, mortality from thrombosis and the composite of death, amputation or thrombosis, without increasing bleeding. With intravenous infusion, advantages include short half-life, easy monitoring and elimination primarily by hepatobiliary (rather than renal) means. In patients undergoing PCI, argatroban with or without glycoprotein IIb/IIIa inhibition leads to high rates of procedural success with low bleeding risk. Herein we review argatroban therapy for HIT and for PCI.  相似文献   

12.
Background: Heparin-induced thrombocytopenia (HIT) is a rare but severe prothrombotic adverse effect of heparin treatment. The underlying cause is the formation of highly immunogenic complexes between negatively charged heparin and positively charged platelet factor 4 (PF4). Resulting antibodies against these PF4/heparin complexes can activate platelets via the platelet FcγIIa receptor, leading to thrombin generation and thus to the paradox of a prothrombotic state despite thrombocytopenia and application of heparin. Prompt diagnosis of HIT is important in order to change treatment to prevent severe thromboembolic complications. However, this is often difficult as thrombocytopenia is frequent in hospitalized patients and the commercially available laboratory tests for HIT antibodies have a high negative predictive value but only a poor positive predictive value. This leads to overdiagnosis and overtreatment of HIT, which also bear the risk for adverse outcomes.

Areas covered: This review aims at resuming recent data on HIT, thereby focusing on the role of new anticoagulants and providing a framework for diagnosis and treatment. Furthermore, it provides some insights into the pathogenesis of this peculiar adverse drug reaction and ventures a guess at its future relevance in clinical practice.

Expert opinion: New drugs which are strongly negatively charged should be assessed for their capacity to form complexes with PF4. If they do so, they bear the risk of inducing a HIT-like immune response. The immunology of HIT is still largely unresolved. Understanding HIT might provide insights into other immune and autoimmune response mechanisms.  相似文献   

13.
Background: Heparin-induced thrombocytopenia (HIT) is a serious, life-threatening complication which occurs in 1 – 3% of patients receiving heparin. Patients with untreated HIT have an up to 50% risk of developing life- and limb-threatening thromboembolic complications. Treatment is based upon clinical suspicion, stopping heparin therapy and initiation of anticoagulation with a rapidly acting alternative non-heparin anticoagulant, such as argatroban – a hepatically excreted direct thrombin inhibitor which is effective in the treatment of HIT. Objective: To summarize the pharmacological and clinical data, and discuss the impact of argatroban in the current treatment of HIT. Methods: A literature search was performed with the aid of Pubmed and Google. Search parameters of ‘argatroban’, ‘heparin-induced thrombocytopenia’ and ‘treatment’ were input into both search engines. Conclusion: Argatroban is a safe and effective treatment for HIT. In patients taking other hepatically cleared medications, lower initial doses may have to be used to avoid over-anticoagulation.  相似文献   

14.
Heparin-induced thrombocytopenia (HIT) is an antibody-mediated syndrome associated with heparin exposure, a falling platelet count and a high risk of thrombosis. Cardiovascular patients are at increased risk of HIT due to wide use of heparin in this population. Should HIT be suspected, heparin must be avoided in most situations, and anticoagulation with an alternative anticoagulant should be instituted. Preferred agents include the direct thrombin inhibitors argatroban and lepirudin, whilst bivalirudin or desirudin (other direct thrombin inhibitors) can be used in some situations. The indirect thrombin inhibitors, danaparoid and fondaparinux, can also be considered at times. These agents and their use in cardiac patients, including patients with acute coronary syndrome, percutaneous coronary interventions, acute ST elevation myocardial infarction or cardiac surgery, will be reviewed.  相似文献   

15.
16.
目的 为临床药师参与肝素诱导血小板减少症(HIT)治疗提供参考.方法 临床药师参与1例普通肝素诱导重度血小板减少患者的诊断与治疗,包括肝素相关的血小板减少的危急情况下急救处理、后续抗凝药物选择,并给予患者全程化的药学监护.结果 患者病情好转出院,出院时血小板已经恢复至正常值,住院期间患者未见明显出血.结论 临床药师可以协助医师处理药品严重不良反应,保证患者临床用药的安全、减少临床药品不良事件的发生.  相似文献   

17.
利奈唑胺相关血小板减少的危险因素分析   总被引:4,自引:0,他引:4  
目的探讨利奈唑胺相关血小板减少的危险因素。方法收集2011年1月至2012年7月在复旦大学附属中山医院因感染应用利奈唑胺的162例住院患者的临床资料并进行回顾性分析,根据用药后是否出现血小板减少,将患者分为血小板减少组和血小板正常组。主要分析指标为患者性别、年龄、体重,应用利奈唑胺前血小板计数、血清肌酐清除率(Ccr)、白蛋白、血红蛋白、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平,应用利奈唑胺的剂量、给药途径和持续时间,以及合并用药情况等。对影响血小板计数的相关变量分别进行t检验、Mann-Whitney U检验和Kruskal-Wallis H检验,对筛选出的危险因素进行逐步Logistic回归统计分析,计算比值比(OR)及95%置信区间(CI)。结果 162例患者中男113例,女49例,年龄19~96岁,平均年龄(57.2±16.1)岁;用药方法均为静脉滴注,600 mg/次,2次/d。应用利奈唑胺的时间为1~46 d,中位时间6 d。血小板正常组115例,血小板减少组47例。47例患者用药后出现血小板减少的中位时间为4.5 d,血小板计数平均为(53±29)×109/L,其中轻、中、重度分别为25、10、12例。逐步Logistic回归分析显示,用药前Ccr<50 ml/min的OR为6.75,95%CI为2.93~15.58,P=0.000;血小板计数<100×109/L的OR为4.54,95%CI为1.53~13.50,P=0.006;应用利奈唑胺时间>14 d的OR为4.00,95%CI为1.40~11.39,P=0.009;用药前AST>75 U/L的OR为2.73,95%CI为1.07~6.99,P=0.036。结论应用利奈唑胺前Ccr、血小板计数低于正常、AST高于正常和应用利奈唑胺时间>14 d可能为利奈唑胺相关血小板减少的危险因素。  相似文献   

18.
ABSTRACT

Introduction: Heparin-induced thrombocytopenia (HIT) is a drug-mediated, prothrombotic disorder caused by immunization against platelet factor 4 (PF4) after complex formation with heparin or other polyanions. A subset of anti-PF4/heparin antibodies are capable of intravascular platelet activation by cross-linking Fcgamma receptor IIA leading to platelet count decrease and/or thrombosis. HIT can be potentially associated with devastating complications such as life-threatening thrombosis making it one of the most serious adverse drug reactions. Diagnosis of HIT based on clinical information is often difficult.

Area covered: This review highlights the pathophysiology of HIT, emphasizing characteristic clinical features and the role of laboratory assays in the diagnosis of HIT. In addition, a summary of current therapeutic options for patients with HIT will be provided.

Expert opinion: A combination of clinical pretest scoring system and laboratory investigation is usually necessary to diagnose HIT. If HIT is strongly suspected, all sources of heparin must be stopped and an alternative non-heparin anticoagulant should be started to prevent new thromboembolic complications. However, heparin alternative anticoagulants bear a considerable bleeding risk, especially if given to patients with thrombocytopenia due to other reasons than HIT. A better understanding of clinical and laboratory features of HIT may help developing strategies to avoid complications induced by this serious adverse reaction against heparin.  相似文献   

19.
Fondaparinux as a treatment option for heparin-induced thrombocytopenia   总被引:1,自引:0,他引:1  
Heparin-induced thrombocytopenia (HIT) is an immune-mediated complication that can occur after exposure to heparin products. Because patients with HIT are at increased risk for thrombosis, anticoagulation is warranted. The direct thrombin inhibitors lepirudin and argatroban are approved by the United States Food and Drug Administration (FDA) for this indication. Bivalirudin, another direct thrombin inhibitor, is approved for use in patients with HIT who must undergo percutaneous coronary intervention. The synthetic pentasaccharide fondaparinux lacks FDA approval for treating patients with HIT; however, a few published reports describe its use. Furthermore, various small-scale, in vitro studies have demonstrated a lack of cross-reactivity between fondaparinux and HIT antibodies. Large, in vivo comparison trials must be performed before fondaparinux can become a standard treatment option in the setting of HIT.  相似文献   

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