新生儿先天性巨细胞病毒感染12例报告

巨细胞病毒(CMV)是新生儿婴儿病毒感染最常见的病原之一．新生儿CMV感染率为0．5％．国外报道先天性CMV感染为0．5～2．5％，其中造成临床异常者占15-33％。我科于1993年11月以来．收治12例先天性CMV感染的患儿．现报道如下．     

更昔洛韦治疗新生儿先天性巨细胞病毒感染的临床观察

目的 探讨更昔洛韦治疗新生儿先天性巨细胞病毒感染的临床效果.方法 收集2012年2月～2013年4月来本院进行治疗的先天性巨细胞病毒感染的新生儿62例,按照随机数字表法分为观察组和对照组各31例.两组患儿均给予对症支持治疗,观察组采用更昔洛韦注射液治疗,对照组采用利巴韦林注射液治疗,比较两组的临床疗效及实验室指标的改善情况.结果 观察组患儿治愈率为77.42％、好转率为9.68％、黄疸消退率为87.10％,均明显高于对照组的48.39％、19.35％、67.74％,两组差异有统计学意义（P＜0.05）.观察组的总胆红素（TBiL）、谷丙转氨酶（ALT）、谷草转氨酶（AST）水平较对照组明显低,差异有统计学意义（P＜0.05）.观察组患儿没有发现明显的不良反应.结论 更昔洛韦治疗新生儿先天性巨细胞病毒感染效果满意,值得临床推广应用.     

新生儿人巨细胞病毒感染的临床分析

目的探讨新生儿人巨细胞病毒感染的临床分析。方法 2008年3月—2011年1月收治人巨细胞病毒感染新生儿126例,进行总结。结果 26例人巨细胞病毒感染新生儿经10～14d为一疗程治疗后复查血CMV-IgM、尿CMV-DNA110例患儿症状及实验室指标明显改善。16例症状及实验室指标无明显改善,其中5例疗程未进行完死亡,11例3个月后症状及实验室指标恢复。结论新生儿人巨细胞病毒感染具有严重的后果,应加强对孕妇产前检查,以达到早期证实人巨细胞病毒感染,积极进行预防,明确诊断后应有更昔洛韦进行治疗,有良好的效果。     

孕产妇及新生儿巨细胞病毒感染236例分析

人巨细胞病毒(human cytomegalovirus,HCMV)是目前引起孕产妇宫内感染的最常见病毒,孕妇感染率很高,据曾蔚越报道,孕妇抗巨细胞病毒抗体阳性率可达94.6％。孕妇感染HCMV,几乎不表现出明显症状,但病毒仍可通过胎盘、产道致胎儿宫内感染,从而引起新生儿畸形、死胎、流产、早产、IUGR等。为了解我院孕产妇及新生儿HCMV感染情况,我们用酶联免疫吸附试验(ELISA)对236例孕产妇及新生儿进行特异性抗体HCMV-IgM检测,结果如下。     

新生儿人巨细胞病毒感染的实验室诊断研究进展

新生儿巨细胞病毒性疾病是一种新生儿常见疾病,因其发病隐匿,故临床上以实验室检测为诊断疾病的关键。本文综述了实验室常用的检测方法,比较了各种检测方法的利弊及临床的应用状况和前景,为医生合理地诊断新生儿巨细胞病毒性疾病提供参考。     

巨细胞病毒感染诊治进展

人巨细胞病毒（Human cytomegalovirus,HCMV）归属于人疱疹病毒科、β疱疹病毒亚科,为双链DNA病毒,是人类疱疹病毒中基因组最大的DNA病毒。HCMV通过密切接触感染者的体液（尤其是尿液、唾液、血液和生殖器分泌物）在人群中传播,人对HCMV普遍易感。     

新生儿巨细胞病毒感染致血液系统损害30例

目的:本文针对巨细胞病毒感染对30例新生儿的血液系统产生的损害进行分析讨论.方法:选取我院30例正常新生儿进行血液系统检测,为常规组;然后选取30例巨细胞病毒感染的新生儿进行血液系统的检测,通过对患儿是否贫血、血小板是否减少、白细胞改变以及患感染性并发症的人数这几个方面进行对照分析.结果:常规组中新生儿出现贫血的人数为1例,其它均没有改变;而对照组中出现贫血的患儿有29例,占总人数的96.7％,而出现其它血小板减少以及白细胞数目改变和出现并发症的概率都明显高于对照组,表面新生儿如果出现巨细胞病毒感染将会影响其血液系统,导致出现紊乱或者使患者免疫力下降造成其它血液并发症.通过对数据进行分析计算,所得P＜0.05,具有统计学意义.常规组中出现病症的概率计算使的P＞0.05,不具有统计学意义.值得临床分析研究.结论:新生儿巨细胞病毒感染将会使患者出现贫血、血小板减少、白细胞改变以及其它血液并发症,正常儿出现贫血的原因不由巨细胞病毒感染引起,并且根据以上两组新生儿所得结果分析了解出现的并发症原因并对此选择合适治疗方案.     

小儿巨细胞病毒感染致病特点及诊治进展

小儿巨细胞病毒性疾病是由巨细胞病毒(cytomegalovirus,CMV)感染小儿机体引起的疾病,简称CMV病.CMV感染在我国流行广泛.小儿机体阻抑CMV的入侵能力极弱,故很容易受感染,尤其是胎儿及免疫力低下的婴儿更易受其侵害.肝脏和肺部是CMV感染的主要靶器官.此外,还可侵犯神经、血液及泌尿系统等,可引起致死性或致残性的严重感染.     

不孕症妇女单纯疱疹病毒和巨细胞病毒感染的检测与分析

目的探讨不孕症妇女单纯疱疹病毒(HSV)和巨细胞病毒(CMV)感染情况。方法采用酶联免疫斑点技术对不孕症妇女血清进行HSV和CMV特异性IgM、IgG抗体检测,并与同期早妊妇女作对照。结果不孕组血清HSV和CMV特异性IgM、IgG抗体阳性率分别为6.75%、97.47%,4.22%、96.62%;早妊组阳性率分别为1.81%、95.02%,0.90%、98.19%。不孕组HSV-IgM、CMV-IgM抗体阳性率明显高于早妊组,差异有统计学意义(P<0.01,P<0.05),两组HSV-IgG、CMV-IgG抗体阳性率差异无统计学意义(P均>0.05)。结论 HSV、CMV活动性感染与不孕症密切相关,可能是导致女性不孕的原因之一。     

婴儿巨细胞病毒感染听力损伤及更昔洛韦的治疗作用

目的 研究巨细胞病毒(CMV)感染患儿的听力损伤情况,探讨更昔洛韦治疗婴儿CMV感染的疗效.方法 将68例CMV感染婴儿分为治疗组(38例,加用更昔洛韦)与对照组(30例,仅用护肝利胆等对症治疗).治疗前后进行尿CMV-DNA及脑干听觉诱发电位(BAEP)检测.结果 治疗组治疗后尿CMV-DNA阴转率高于对照组(P<0.05).BAEP测试:与对照组相比,治疗后除了Ⅲ-Ⅴ波峰间期(IPL)外各波潜伏期(PL)及IPL均较前减少(P<0.05).Ⅴ波听反应阈:治疗组治疗后听力损伤率(13.1%)低于对照组(26.6%)(P<0.05).结论 BAEP检测可早期发现CMV感染患儿听力障碍的程度和性质.加用更昔洛韦治疗近期可减少尿中CMV排毒及消除病毒血症,远期可降低听力异常的发病率.     

药品分类管理的现状和措施

20世纪50年代，美国反思“药毒事件”，率先建立了药品分类管理制度；20世纪80年代，世界卫生组织的《阿拉木图宣言》建议各国将分类管理作为药品政策的立法议题；2001年，《中华人民共和国药品管理法》明确规定“国家对药品实行处方药与非处方药分类管理制度”，并计划到2005年建立起具有中国特色的药品分类管理体系。     

44例巨细胞病毒感染婴儿脑干听觉诱发电位分析

目的 观察婴儿期巨细胞病毒(CMV)感染后脑干听觉诱发电位(BAEP)的变化,探讨CMV感染对其听力的影响.方法 将44例巨细胞病毒感染患儿(CMV感染组)和36例正常体检儿童(对照组)进行BAEP检测,并分析BAEP各波峰潜伏期(PL)、峰间期(IPL)及Ⅴ波听阈值的差异.结果 CMV感染组BAEP异常率为40.9%,Ⅰ、Ⅴ波PL及Ⅰ-Ⅲ、Ⅰ-Ⅴ波IPL延长;Ⅴ波听反应阈值增高,与对照组比较,差异有统计学意义(P＜0.05).结论 CMV感染婴儿的听觉传导通路有不同程度的损害,BAEP监测有助于临床早期发现听力损害.     

Current status and opportunities for therapeutic drug monitoring in the treatment of tuberculosis

Introduction: Tuberculosis remains a global health problem and pharmacokinetic variability has been postulated as one of the causes of treatment failure and acquired drug resistance. New developments enable implementation of therapeutic drug monitoring, a strategy to evaluate drug exposure in order to tailor the dose to the individual patient, in tuberculosis treatment.

Areas covered: Literature on pharmacokinetics and pharmacodynamics of anti-tuberculosis drugs was explored to evaluate the effect of drug exposure in relation to drug susceptibility, toxicity and efficacy. New, down-sized strategies, like dried blood spot analysis and limited sampling strategies are reviewed. In addition, molecular resistance testing of Mycobacteria tuberculosis, combining a short turn-around time with relevant information on drug susceptibility of the causative pathogen was explored. Newly emerging host biomarkers provide information on the response to treatment.

Expert opinion: Therapeutic drug monitoring can minimize toxicity and increase efficacy of tuberculosis treatment and prevent the development of resistance. Dried blood spot analysis and limited sampling strategies, can be combined to provide us with a more patient friendly approach. Furthermore, rapid information on drug susceptibility by molecular testing, and information from host biomarkers on the bacteriological response, can be used to further optimize tuberculosis treatment.     

Current management strategies for the prevention and treatment of cytomegalovirus infection in pediatric transplant recipients

Cytomegalovirus (CMV) is a significant cause of morbidity and mortality following transplantation, especially in the pediatric population, who remain at high risk of primary infection. The availability of effective antiviral therapy has led to dramatic improvements in the outcome of CMV infection in patients undergoing transplantation. In recent years, three major strategies have been developed for the prevention of CMV disease in this population: reduction of risk of viral acquisition or reactivation by management of risk factors; prophylaxis of all 'at-risk' patients using prophylactic strategies for a defined period of time, initiated at or near the time of transplant; and pre-emptive treatment with ganciclovir of selected 'at-risk' patients, guided by either laboratory markers indicative of subclinical infection or the presence of specific risk factors. In general, well designed comparative studies of one or more antiviral agents for the prevention of CMV have not been carried out. While ganciclovir appears to be more effective than aciclovir, its tolerability profile is less optimal. The use of foscarnet avoids myelosuppresions, but is associated with significant nephrotoxicity. Its use should be reserved for patients unable to tolerate ganciclovir or with ganciclovir-resistant CMV disease. Similar to foscarnet, the high frequency of nephrotoxicity associated with the use of cidofovir limits its use to clinical scenarios suggestive of ganciclovir resistance. Newer options, such as valaciclovir and valganciclovir, are currently under investigation and preliminary experience has been promising. Finally, passive immunoprophylaxis has been shown to prevent CMV disease after solid organ transplantation, but its use in bone marrow transplantation is controversial. Essentially, pre-emptive strategies have relied on the quantitation in the peripheral blood of CMV phosphoprotein pp65 antigen and/or the polymerase chain reaction assay. Strict guidelines for the use of those assays as a guide to pre-emptive therapy have not been standardized. Prospective trials comparing pre-emptive therapy using either intravenous or oral ganciclovir, and now oral valganciclovir or valaciclovir, are necessary to determine the relative cost effectiveness and efficacy of these alternative strategies. Finally, it remains controversial as to whether prophylaxis or pre-emptive therapy is the optimal strategy for preventing CMV disease. While a growing body of literature describes these approaches in adult transplant recipients, published experience in children has been much more limited.     

Outcome assessment: functional status measures as therapeutic endpoints for heart failure

The role of measures of patients' functional status during chronic heart failure is to bridge the outcome information gap between physiologic assessments and the goal of medical care, which is to prolong the patient's life with minimal disability due to the syndrome and subsequent health care. The methods of rigorously developing and applying patient questionnaires as outcome measures will be unfamiliar to many health care providers. Many health care providers trained with different perspectives probably have an incredulous view of patient evaluations. What have we accomplished, though, if patients cannot perceive a net benefit from our services? In the final analysis, the patients' outcome assessments, collected in a systematic and unbiased manner, rather than the proxy measures used by health care providers, are the bottom line.     

革兰阴性杆菌感染现状及应对措施

细菌感染已经成为临床不可忽视的问题。在感染菌谱中,革兰阴性杆菌感染具有明显加剧趋势,且耐药现象日趋严重,严重影响了药物的疗效和疾病的预后。本文就革兰阴性杆菌感染现状、耐药状况、耐药机制以及应对措施进行综述,为临床合理选择抗生素提供依据。     

Current status and perspectives on the development of therapeutic agents for Alzheimer's disease

Acetylcholinesterase inhibitors have beneficial effects to improve the cognitive impairment in patients with mild to moderate Alzheimer's disease (AD). In addition, a channel blocker of N-methyl-D-aspartate receptor, memantine hydrochloride, was approved as a therapeutic agent for patients with moderate to severe AD in both EU countries in 2002 and USA in 2003, while the clinical development is still ongoing in Japan. In contrast, the pharmacotherapy for a prime cure against AD is not available in the market, although there has been a worldwide search for novel compounds. The most plausible mechanism for the treatment of AD is the reduction of the amyloid beta-peptide (Abeta) plaques, one of the pathological markers of AD, in the brain. For this purpose, the inhibitors of beta-secretase and gamma-secretase, which cleave amyloid precursor protein (APP) to release Abeta, has been developed to interfere with APP processing. The beta-sheet breaker and metal chelators for the breakdown of aggregated Abeta have also been synthesized as well as the immunotherapeutic approach using Abeta vaccine. On the other hand, some nonsteroidal anti-inflammatory drugs, such as ibuprofen and sulindac, noncompetitively inhibited Abeta production but not Notch cleavage. The development of Abeta-lowering drugs is highly expected for the treatment of AD.     

Non-steroidal anti-inflammatory drugs. Current status and rational therapeutic use

Aspirin (acetylsalicylic acid), the first of the NSAIDs (introduced in 1899), was initially never referred to as an anti-inflammatory agent. It was the advent of cortisone in 1949 that demonstrated dramatically that corticosteroids had anti-inflammatory properties and the term 'non-steroidal anti-inflammatory drug' was first used when phenylbutazone was introduced 3 years later. Since then, the NSAIDs have proliferated. There is to date no good evidence that they halt progression of rheumatoid disease, but by easing pain and diminishing swelling they make life much easier in osteoarthrosis, rheumatoid arthritis and many other types of arthritis, and are the drugs of first choice in acute gout. Their mode (or modes) of action are obscure and though inhibition of cyclo-oxygenase (prostaglandin synthetase) is clearly important, other mechanisms are also involved. The assessment of the anti-inflammatory action of these agents has received considerable attention in clinical trials because, whatever their action may be in experimental animal models, their action in inflamed joints in human patients must be ascertained, since there may be little parallel between the two. Different experimental animal models give different results with various agents and often bear little relation to their therapeutic action in man. No attempt has been made here to review in depth all the NSAIDs that have appeared since 1952. All have anti-inflammatory and analgesic activity and all can cause gastrointestinal side effects, though effectiveness and toxicity vary from drug to drug and patient to patient, there being very great interpatient variability. Non-reactors, patients who apparently fail to respond to certain agents, need further study, for it seems that these subjects may metabolise these agents differently from others. Considerable ingenuity has been shown not only in evolving new NSAIDs but in finding new ways of administering them. The number and variety of NSAIDs in their various forms varies greatly from country to country, depending largely on the regulatory bodies of those countries. In the meantime, the search for a better, less toxic compound continues with the hope that one may be found which has a deeper and more basic action on the underlying disease process.