万古霉素鞘内注射与静脉滴注治疗颅内感染临床疗效及安全性的Meta分析

目的评价万古霉素鞘内注射与静脉滴注治疗颅内感染的临床疗效及安全性。方法计算机检索Pub Med、Medline、中国知网(CNKI)、维普网(VIP)、万方数据知识服务平台等数据库,检索时间为建库至2016年6月,筛选有关万古霉素鞘内注射与静脉滴注治疗颅内感染临床疗效及安全性的随机对照研究,其中鞘内注射组患者予以万古霉素鞘内注射治疗,静脉滴注组患者予以万古霉素静脉滴注治疗;采用Rev Man 5.2软件进行Meta分析。比较两组患者临床疗效、细菌清除率、肾毒性发生率、临床治疗时间。结果共纳入8篇文献,包括513例患者。Meta分析结果显示,鞘内注射组患者临床疗效[相对危险度(RR)=1.24,95%CI(1.16,1.33),P0.000 01]优于静脉滴注组、细菌清除率[RR=1.16,95%CI(1.03,1.30),P=0.02]高于静脉滴注组、肾毒性发生率[RR=0.11,95%CI(0.02,0.46),P=0.003]低于静脉滴注组、临床治疗时间[标准均数差(MD)=-11.18,95%CI(-12.71,-9.64),P0.000 01]短于静脉滴注组。结论万古霉素鞘内注射治疗颅内感染的临床疗效优于静脉滴注,有利于提高细菌清除率、减少肾毒性、缩短临床治疗时间,且安全性较高。     

17例RhD血型不相合血小板输注的回顾性分析与策略

目的:通过回顾性分析RhD血型不相合血小板输注的患者，总结RhD不相合血小板输注的经验和应对策略。方法:利用医院六级电子病历和临床输血管理系统，获取2014至2021年血型为RhD阴性且符合研究纳入标准的17例患者，收集其基本信息、检验结果、血液输注的情况并进行统计分析。结果:17例患者ABO血型A型、B型、O型、AB型占比分别为2例(11.76%)、5例(29.41%)、9例(52.94%)、1例(5.88%);输注血小板总计51个治疗量，其中2个治疗量为RhD阴性，49个治疗量为RhD阳性；输注血小板后随访时间为28～167 d;均未见输血不良反应；不规则抗体筛查结果阴性，未见RhD及其他同种免疫反应。结论:RhD血型不相合血小板输注可有效改善患者出血及凝血相关指标，且不会引起严重的输血不良反应及免疫反应，为血小板减少症和出血患者带来益处，保障临床血小板治疗的及时性和有效性。     

慢性肝病患者血小板减少发生机制及治疗

正血小板减少是慢性肝病常见的并发症。不同原因导致的肝硬化均可伴发血小板减少症。在我国引起肝硬化的各种原因中,尤以慢性病毒性乙型及丙型肝炎、慢性血吸虫病、酒精性及非酒精性脂肪性肝病、自身免疫性肝病多见。慢性肝病并发血小板减少症与肝病严重程度及预后相关,并导致患者临床常规检查及治疗变得比较棘手。正确处理好血小板减少症对改善肝病患者的预后具有重要意义。     

老年重症感染患者应用万古霉素的疗效及安全性

目的探析万古霉素治疗老年重症感染患者的临床疗效和安全性。方法观察34例老年重症感染患者应用万古霉素治疗后的临床有效率、细菌清除率、药物不良反应发生率、治疗前后的肝、肾功能指标。结果万古霉素治疗总有效率为85.3%,细菌清除率76.4%,不良反应发生率为5.9%,治疗前后肝、肾功能指标无显著变化(P0.05)。结论万古霉素治疗敏感细菌引起的老年重症感染效果显著,相对安全,但治疗过程中应严格监测肝肾功能。     

利奈唑胺、万古霉素治疗MRSA致VAP的研究

目的探讨利奈唑胺对比万古霉素治疗耐甲氧西林金黄色葡萄球菌(MRSA)致呼吸机相肺炎(VAP)的临床疗效、安全性及其对血清C反应蛋白(CRP)的影响。方法我科收治的MRSA所致VAP 64例作为研究对象,采用随机数字表法分为试验组33和对照组31例。试验组给予利奈唑胺0.6 g ivgtt bid,7 d;对照组给予万古霉素1g ivgtt bid,7 d。比较两组患者治疗前后临床有效率、细菌清除率、药物相关不良反应及血清学指标有无差别。结果试验组临床有效率、细菌清除率均显著高于对照组(P0.05);两组患者药物相关不良反应无明显差别(P0.05);治疗后两组患者WBC、血小板、CRP及PCT均较治疗前明显下降(P0.05),但试验组下降更为显著(P0.05)。结论利奈唑胺治疗MRSA致呼吸机相肺炎用的临床有效率较高,不良反应轻微。     

长期服用阿司匹林致血小板减少20例临床分析

目的 探讨临床长期服用阿司匹林致血小板减少的临床诊断治疗及发病机制。方法 选取20例住院病人确诊有心脑血管病后开始服用阿司匹林后血小板计数减少者为研究对象，采取停药或服用泼尼松，严重者予甲泼尼松龙，使血小板计数恢复正常。结果 20例立即停用阿司匹林，10例较轻病人于15d内血小板恢复正常，10例症状较重病人给予拨尼松15d后血小板恢复正常。结论 部分病人服用阿司匹林后可因免疫机制、药物毒副反应使血小板减少，与服用时间及剂量相关性不大，治疗预后良好，临床工作应高度警惕。     

替罗非班引起的血小板减少症相关分析

抗血小板药物的应用是冠心病治疗的重要一环。替罗非班是一种血小板糖蛋白IIb/IIIa受体拮抗剂,可抑制血小板的活化,已广泛应用于急性冠状动脉综合征和经皮冠状动脉介入治疗中,以预防血栓形成和减少缺血事件的发生。临床实践中,血小板减少是血小板糖蛋白Ⅱb/Ⅲa受体拮抗剂常见的不良反应,尽管大多数不危及生命,但也会导致肺泡出血等严重并发症。文章就1例经皮冠状动脉介入治疗术中应用替罗非班后出现血小板减少的病例为引,就替罗非班导致的PCI围手术期血小板减少诊断、鉴别、治疗及预后作一综述。     

基因重组人白细胞介素-11防治化疗所致血小板减少的临床研究

目的观察巨和粒(基因重组人白细胞介素-11,rhIL-11)预防和治疗化疗所致血小板减少的疗效和不良反应。方法对2003-05~2004-05期间沈阳军区总医院肿瘤科42例接受GC方案化疗的非小细胞肺癌患者采用双盲安慰剂对照、自身交叉研究方法,比较rhIL-11和安慰剂对化疗后血小板最低值的影响及毒性。rhIL-11在化疗药给药结束后24h开始用药,25μg/kg皮下注射,连续用药7~14d,血小板高于300×109/L时停药。结果rhIL-11可明显升高化疗中血小板最低值,减少输血的次数。rhIL-11的不良反应主要是轻度水肿、乏力及感冒样症状等。结论rhIL-11对化疗所致血小板降低有明显的防治作用,疗效安全、确实,不良反应轻微。     

万古霉素-利奈唑胺序贯治疗老年关节置换假体周围MRSA感染的效果

目的回顾性分析万古霉素-利奈唑胺序贯治疗对老年关节置换假体周围耐甲氧西林金黄色葡萄球菌(MRSA)感染的临床效果。方法老年关节置换术后假体周围MRSA感染患者11例接受手术治疗的同时,应用万古霉素-利奈唑胺序贯治疗,观察治疗效果及不良反应。结果应用万古霉素-利奈唑胺序贯治疗假体周围MRSA感染,治愈率为81.8%,治愈患者红细胞沉降率、C反应蛋白、白细胞计数及中性粒细胞百分比在治疗后1、3个月均较治疗前明显下降,且降至正常范围;1例出现复发情况,1例治疗失败。万古霉素、利奈唑胺的不良反应率分别为9.1%、18.2%。结论万古霉素-利奈唑胺序贯治疗老年假体周围MRSA感染效果显著。     

他汀类药物药理作用、临床应用及不良反应的研究进展

他汀类药物是3-羟基-3甲基戊二酰辅酶A(HMG-COA)还原酶抑制剂,具有明确的降低血脂、抗炎、改善内皮功能、抗血小板聚集等作用,目前其临床应用主要集中在心血管疾病一级预防方面。近年来随着该类药物临床应用的愈加广泛,其不良反应也越来越受到关注,尤其是肌毒性和肝毒性方面,因此如何正确、合理应用他汀类药物以及如何减少其不良反应仍是亟待解决的热点问题。     

Thrombocytopenia Induced by Vancomycin-Dependent Platelet Antibody

Background and objectives: Many drugs are associated with thrombocytopenic purpura through immune-mediated platelet destruction. The case of a woman who suffered lifethreatening thrombocytopenia during vancomycin treatment for Staphylococcus aureus septicemia is reported. Materials and methods: Conventional clinical and laboratory methods, including flow cytometry. Results: After treatment of septicemia with vancomycin, severe thrombocytopenia and bleeding occurred, without detection of drug-dependent platelet antibodies (DDPA). This was followed by vegetative endocarditis, whereupon antibiotics were withdrawn so as to isolate the organism. The thrombocytopenia was corrected. On day 34, antibiotics including vancomycin were reinstituted, and three days later thrombocytopenia recurred. With a change in antibiotics, the platelet count corrected itself within four days. Conclusions: Vancomycin may induce potentially severe immunological thrombocytopenia.     

Acute vancomycin-dependent immune thrombocytopenia as an anamnestic response

Drug-related thrombocytopenia is a well-described but relatively rare complication of antibiotic therapy. In this entity, platelet destruction is immune-mediated, often resulting in a precipitous drop in platelet count over a short period of time. Most of these cases of thrombocytopenia are drug-dependent, as discontinuation of the offending agent frequently results in a timely return to baseline, pre-exposure platelet levels. We report the case of a 61-year-old male patient receiving vancomycin and ceftazidime for lower extremity wet gangrene who experienced a marked, acute reduction in platelet count 12 to 15 hours after starting antibiotic therapy. There was no readily apparent clinical or laboratory explanation for his thrombocytopenia. Pre- and post- antibiotic serum samples were preserved and sent for drug-dependent platelet antibody analysis. The pre-exposure specimen revealed the presence of IgG vancomycin-dependent platelet antibodies, while the post-exposure specimen demonstrated both IgG and IgM vancomycin-dependent platelet antibodies. Ceftazidime-dependent platelet antibodies were not identified in either sample. These findings indicate prior sensitization to vancomycin, with subsequent acute production of IgM anti-platelet antibodies after re-exposure to the antibiotic. The patient's antibiotics were held after the acute-onset of thrombocytopenia with subsequent restoration of normal platelet counts within 4 days of drug withdrawal, and the patient at no time experienced significant adverse bleeding events. Antibiotic therapy with vancomycin is a rare and perhaps overlooked cause for new-onset thrombocytopenia in hospitalized patients. This case illustrates that the development of severe thrombocytopenia within hours of vancomycin administration does not rule out drug-related immune clearance, as the rapid platelet destruction may indicate an anamnestic antibody response to the drug after previous exposure. In such a scenario, immediate discontinuation of vancomycin is recommended to improve platelet counts. From a laboratory perspective, retrieval of serum both pre- and post-administration of vancomycin is most helpful in determining a patient's drug-immunization status and can help guide safe drug use during future infections.     

Vancomycin-induced thrombocytopenia

Vancomycin-induced thrombocytopenia has only been reported once previously in the medical literature. We describe a patient in whom sudden severe reversible thrombocytopenia developed on two separate occasions after exposure to vancomycin hydrochloride. A 54-year-old man was admitted to the hospital for bilateral swelling and erythema of his extremities. At the time of admission he received 2 days of vancomycin therapy without incident. On day 14 he was reexposed to vancomycin and thrombocytopenia developed, with a nadir value of 17 x 10(9)/L. On day 30, a single dose of vancomycin was administered, and thrombocytopenia once again developed, with a nadir value of 11 x 10(9)/L. Hematologic cytopenias are infrequent adverse effects of vancomycin therapy. It is postulated that these effects may be due to an immunologically mediated mechanism. With the increasing use of vancomycin due to the emergence of methicillin-resistant Staphylococcus aureus, this case should alert clinicians to this rare but potentially lethal manifestation of vancomycin.     

Vancomycin-dependent antibodies associated with thrombocytopenia and refractoriness to platelet transfusion in patients with leukemia

Two patients with leukemia experienced profound thrombocytopenia and refractoriness to platelet transfusion during vancomycin treatment. In one patient, withdrawal of drug and administration of platelet transfusions restored platelet counts to near normal levels (approximately 100 x 10(9)/L), however, subsequent challenge with vancomycin due to recurring infection again precipitated severe thrombocytopenia (platelets less than 10 x 10(9)/L) and life-threatening hemorrhagic symptoms. Potent vancomycin-dependent antiplatelet antibodies were detected in the serum of both patients during the refractory period using staphylococcal protein A rosette formation. Employing a monoclonal antibody-antigen capture enzyme-linked immunosorbent assay (ELISA), the patients were found to have vancomycin-dependent IgG antibodies that bound specifically to platelet glycoproteins (GP) IIb and/or IIIa. One of these antibodies failed to react with platelets deficient in GPIIb/IIIa obtained from an individual with Glanzmann's thrombasthenia. These findings provide the first major evidence for drug-dependent antibodies in association with severe thrombocytopenia and refractoriness to platelet transfusion in alloimmunized leukemia patients and, further, provide the first demonstration of vancomycin-dependent antibodies reactive with platelets.     

Thrombocytopenia in a patient on peritoneal dialysis

Adverse reactions to drugs occur in up to 6% of hospitalized patients and are an important cause of increment in morbimortality. The widely-prescribed antibiotics beta-lactams and sulfamides are the most frequently associated to adverse reactions and hypersensitivity. Vancomycin is a glycopeptidic antibiotic used to treat infections caused by Staph. coagulasa positive (S. aureus) and Staph. coagulasa negative. Nowadays its extensive use is a consequence of bacterial resistance to classical antibiotics such as beta-lactams. In Nephrology Units, vancomycin is the antibiotic of first choice to treat staphylococcal infections related to central venous catheters for hemodialysis, as well as for the treatment of peritonitis in patients undergoing peritoneal dialysis. Toxicity due to vancomycin includes the "red man syndrome", ototoxicity and hematological toxicity. The most common sign of haematological toxicity is mild neutropenia; less frecuent are leukocytosis, eosinophilia, agranulocytosis and thrombocytopenia.     

Effects of vancomycin on platelets, plasma proteins and hepatitis B surface antigen.

The antibiotic vancomycin shares many similarities with ristocetin, an agent noted for its effects on platelets and plasma fibrinogen. Vancomycin did not aggregate platelets as ristocetin, but platelets were incorporated into precipitates induced by vancomycin. Fibrinogen and factor VIII were precipitated from plasma at low concentrations of vancomycin. The precipitated fibrinogen remained clottable. Hepatitis B surface antigen was selectively precipitated from serum and could be recovered from the precipitate. Rabbits receiving bolus intravenous injections of high doses of vancomycin developed hypofibrinogenemia and thrombocytopenia within minutes and often went on to die. Studies with 125I-vancomycin revealed little stable binding of the antibiotic to platelets or fibrinogen. A relationship is suggested between the potent protein precipitating effects and phlebitis at the infusion site commonly associated with vancomycin therapy.     

Unfractionated heparin compared with low-molecular-weight heparin as related to heparin-induced thrombocytopenia

PURPOSE OF REVIEW: Heparin-induced thrombocytopenia is a severe side effect of treatment with unfractionated heparin. The relation of low-molecular-weight heparin to heparin-induced thrombocytopenia is less well understood. This review will summarize what is known about the similarities and differences between thrombocytopenia induced by low-molecular-weight heparin and that induced by unfractionated heparin. RECENT FINDINGS: The pathophysiology of unfractionated heparin-induced thrombocytopenia, caused by the development of antibodies to heparin/platelet factor 4 complexes, holds true for low-molecular-weight heparin because the molecules of the latter are of the same saccharidic structure as those of unfractionated heparin. Owing to their smaller size, however, low-molecular-weight heparin does not interact with platelet factor 4 and platelets as efficiently as does unfractionated heparin. This translates to a two- to threefold lower risk of immune sensitization (antibody generation and occurrence of clinical heparin-induced thrombocytopenia). Low-molecular-weight heparin-induced thrombocytopenia antibodies are more often immunoglobulin A and immunoglobulin M, in contrast to the immunoglobulin G antibodies generated with unfractionated heparin-induced thrombocytopenia, which tend to be more often associated with clinical heparin-induced thrombocytopenia. The clinical expression of low-molecular-weight heparin-induced thrombocytopenia is generally similar to that of unfractionated heparin-induced thrombocytopenia but can have a slower onset, more severe thrombocytopenia, and slower platelet count recovery. Given that low-molecular-weight heparin, of itself, is linked with heparin-induced thrombocytopenia pathophysiology and it can interact with most preexisting heparin-induced thrombocytopenia antibodies generated after exposure to unfractionated heparin, treatment of heparin-induced thrombocytopenia patients with low-molecular-weight heparin is contraindicated. SUMMARY: The risk of the development of heparin-induced thrombocytopenia with low-molecular-weight heparin treatment is reduced relative to the frequency of unfractionated heparin-induced thrombocytopenia, but it is not eliminated, and platelet counts should be monitored with treatment.     

An unusual case of vancomycin-related systemic reaction accompanied with severe thrombocytopenia mimicking pacemaker-related infective endocarditis: a case report and review of literature

Vancomycin is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive resistant bacteria. In recent years, several cases of vancomycin-associated immune thrombocytopenia have been presented as case reports, but the real incidence of this side effect is still unknown. In this report, we would like to present a case during which we confronted with a great dilemma: urgent removal of whole defibrillator system due to highly suspected infective endocarditis or leaving the defibrillator in place and simply switching vancomycin to another antibiotic agent and wait.     

Successful treatment of right-sided native valve methicillin-resistant Staphylococcus aureus endocarditis and septicaemia with teicoplanin and rifampicin: a case report

Vancomycin is the drug of choice in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) infection. However, the presence of certain clinical complications like renal failure alters vancomycin pharmacokinetics, leading to drug accumulation and toxicity. This highlights the need to identify an effective substitute for treating MRSA infections when vancomycin cannot be used. We report the case of a 57-y-old Indian male diagnosed with tricuspid valve endocarditis with septicaemia and a right upper lobe cavity caused by MRSA. The patient also presented with renal failure, which precluded the use of vancomycin for treatment. A 6-week regimen of teicoplanin and rifampicin was used instead, and the infection was successfully treated. This case report provides evidence of the effectiveness of teicoplanin and rifampicin in the treatment of MRSA bacteraemia in situations where the use of vancomycin is contraindicated.     

Efficacy and safety of linezolid in liver transplant patients

S. Radunz, B. Juntermanns, G.M. Kaiser, J. Treckmann, Z. Mathe, A. Paul, F.H. Saner. Efficacy and safety of linezolid in liver transplant patients
Transpl Infect Dis 2011: 13: 353–358. All rights reserved Abstract: Bacterial infections are the main cause of death within the first year after liver transplantation, and the increased incidence of multidrug‐resistant gram‐positive pathogens has created a major challenge in the treatment of these patients. Linezolid, the first US Food & Drug Administration‐approved oxazolidinone, offers a valuable novel treatment option for serious gram‐positive infections. Linezolid is relatively non‐toxic but prolonged treatment with linezolid was associated with thrombocytopenia. Here we report on the experience of linezolid treatment in adult liver transplant patients, who are at an increased risk for thrombocytopenia because of hypersplenism. From November 2003 until December 2009, we evaluated the clinical course of 46 liver transplant patients (27 male/19 female) in our surgical intensive care unit. For proven or probable gram‐positive infection, all patients received linezolid 600 mg intravenously every 12 h. On clinical improvement, treatment was changed to oral linezolid 600 mg twice daily. Treatment duration was 11 ± 7 days. Treatment indications were pneumonia (n=8), blood stream infection (n=30), and surgical site/abdominal infection (n=3). Clinical cure was achieved in 43 out of 46 patients. During the course of treatment, no cases of severe thrombocytopenia occurred and a statistically significant platelet count increase was seen from day 1 (110 ± 73/nL) to day 7 (165 ± 116/nL) and day 14 (180 ± 140/nL). We did not observe any further adverse events, especially no severe neurological complications (e.g., serotonin syndrome) or signs of lactate acidosis. Two patients died from uncontrolled vancomycin‐resistant Enterococcus faecium sepsis with septic shock and one due to uncontrolled methicillin‐resistant Staphylococcus aureus pneumonia. These deaths were considered to be unrelated to linezolid treatment, and linezolid was regarded as the optimal treatment choice in these patients. A subgroup analysis of patients treated for >14 days revealed no statistically significant differences when compared with patients on shorter treatment. In particular, no cases of thrombocytopenia occurred during longer treatment. In conclusion, linezolid is a safe and effective treatment for adult liver transplant patients with gram‐positive infections.