α干扰素联合丙种球蛋白注射液治疗小儿特发性血小板减少性紫癜的疗效观察

目的探讨α干扰素联合丙种球蛋白注射液治疗小儿特发性血小板减少性紫癜的临床疗效。方法选取我院2013年1~9月门诊收治的78例特发性血小板减少性紫癜患儿做为研究对象。随机分为治疗组40例与对照组38例,对照组患儿应用丙种球蛋白注射液治疗,治疗组患儿在对照组患儿用药的基础上联合使用α干扰素治疗,对比两组患儿的临床治疗效果及患儿的血液指标。结果治疗组患儿的治疗总有效率显著高于对照组,差异具有统计学意义(P0.05)。治疗组患儿的治疗后的BAFF、PAIgG、PAIgM、PAIgA低于对照组,PLT计数高于对照组,差异具有统计学意义(P0.05)。结论应用α干扰素联合丙种球蛋白注射液治疗小儿特发性血小板减少性紫癜治疗效果显著,提高机体免疫力,值得临床推广应用。     

归脾丸联合西药治疗儿童慢性特发性血小板减少性紫癜的效果

目的研究归脾丸联合西药治疗儿童慢性特发性血小板减少性紫癜的临床效果。方法随机抽取214例慢性特发性血小板减少性紫癜患儿,随机分为参照组和试验组,各107例。参照组采用甲基泼尼松龙、维生素C治疗,试验组则联合归脾丸治疗。观察记录两组患者治疗效果、不良反应发生情况及临床症状消失时间,对患者血小板计数、特异性抗血小板有关抗体PAIgA、PAIgG、PAIgM等指标进行测定。结果 (1)试验组治疗总有效率与参照组相比要低,不良反应发生率与参照组相比要低,差异有统计学意义(P 0.05)。(2)试验组临床症状消失时间(2.16±0.51)d,参照组临床症状消失时间(3.45±0.26)d,差异有统计学意义(P 0.05)。(3)测定结果显示,试验组血小板计数指标与参照组相比要高,PAIgG、PAIgM指标与参照组相比要低,差异有统计学意义(P 0.05)。而两组PAIgA指标比较,差异无统计学意义(P 0.05)。结论归脾丸联合西药治疗儿童慢性特发性血小板减少性紫癜的临床效果显著,值得应用于临床推广。     

血小板表面相关抗体检测对ITP的诊断作用研究

目的 研究血小板表面相关抗体检测对特发性血小板减少性紫癜(ITP)的诊断作用研究.方法 选取2012年1月至2013年1月收治的ITP患者50例(A组),非免疫性血小板减少患者20例(B组),其他自身免疫性疾病患者20例(C组),另征集20名健康志愿者作为D组.测定4组血小板膜糖蛋白Ⅱb-Ⅲa(PAC-1)以及血小板相关抗体PAIgG、PAIgA、PAIgM水平,对ITP患者进行病情分级,并对治疗后进行疗效评定,统计各个分级的ITP患者及不同疗效患者血小板相关抗体阳性率.结果 4组PLT、PAC-1、PAIgA、PAIgG、PAIgM水平差异有统计学意义(P＜0.05).A组PAIgA、PAIgG、PAIgM均明显高于其他3组患者(P＜0.05).ITP 1、2、3级患者PAIgA、PAIgG、PAIgM阳性率差异有统计学意义(P＜0.05).且随着ITP分级升高,患者PAIgA阳性率呈升高趋势(r值分别为0.712、0.614、0.732,P＜0.05).显效、进步、无效组患者PAIgA阳性率差异有统计学意义(P＜0.05),且随着治疗效果的改善,PAIgA阳性率呈降低趋势(r=0.642,P＜0.05).显效、进步、无效组患者PAIgG、PAIgM阳性率差异有统计学意义(P＜0.05).且随着疗效改善,患者PAIgG阳性率呈升高趋势(r值分别为0.723和0.721,P＜0.05).结论 ITP患者血小板表面相关抗体较正常人有所升高,且血小板相关抗体高低与病情程度有一定的相关性,有助于临床ITP的诊疗.     

血小板相关抗体检测在血小板减少性疾病中的临床价值

目的通过检测血小板相关抗体（PAIg）,探讨血小板减少性疾病与血小板相关抗体的临床意义。方法应用ELISA方法对140例血小板减少性疾病患者和40例健康体检者（正常对照组）进行PAIgG、PAIgM、PAIgA3项联合检测。结果特发性血小板减少性紫癜（ITP）伴血小板减少的系统性红斑狼疮（SLE）PAIg阳性率均明显高于正常组,血液肿瘤组和肝病患者组PAIg阳性略高于正常对照组。ITP、SLE的PAIgG、PAIgA、PAIgM值均高于正常对照组,差异有统计学意义（P〈0.05）;血液肿瘤组和肝病患者组则与正常对照组无显著差异（P〉0.05）。结论 PAIg的检测有助于了解血小板减少症的发生机制,必要时也可作为血小板减少性疾病的筛查手段。     

升血小板胶囊联合重组人血小板生成素治疗特发性血小板减少性紫癜的疗效观察

目的观察升血小板胶囊联合重组人血小板生成素注射液治疗特发性血小板减少性紫癜(ITP)的临床疗效。方法选取2016年1月—2016年10月在信阳市中心医院住院治疗的ITP患者68例,随机分为对照组和治疗组,每组各34例。对照组皮下注射重组人血小板生成素注射液,300 U/(kg·d),1次/d。治疗组在对照组的基础上口服升血小板胶囊,1.8 g/次,3次/d。两组患者均治疗14 d。评价两组患者临床疗效,同时比较治疗前后两组患者血小板计数和血清相关血小板抗体(PAlgG)升高例数差异。结果治疗后,对照组临床总有效率为70.59%,显著低于治疗组的91.18%,两组比较差异具有统计学意义(P0.05)。治疗后,两组血小板计数均明显升高,同组比较差异具有统计学意义(P0.05);且治疗组患者血小板计数水平显著高于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,治疗组血清PAIgG水平大于108 ng/10PA的例数显著少于对照组,两组比较差异具有统计学意义(P0.05)。结论血小板胶囊联合重组人血小板生成素能显著缩短ITP患者血小板恢复的时间,提高临床效果,具有一定的临床推广应用价值。     

槐杞黄颗粒联合重组人血小板生成素治疗特发性血小板减少性紫癜的临床研究

目的 探讨槐杞黄颗粒联合重组人血小板生成素治疗特发性血小板减少性紫癜的临床疗效。方法 选取2017年1月-2018年2月青岛市市立医院（集团）收治的特发性血小板减少性紫癜患者84例为研究对象,按照随机数字表法分为对照组和治疗组,每组各42例。对照组皮下注射重组人血小板生成素注射液,15 000 U/次,1次/d。治疗组在对照组基础上温水冲服槐杞黄颗粒,1袋/次,2次/d。两组连续治疗14 d。观察两组的临床疗效,比较两组的血小板相关抗体、血小板计数、T淋巴细胞亚群。结果 治疗后,对照组和治疗组的总有效率分别为73.81%、90.48%,两组比较差异有统计学意义（P<0.05）。治疗后,两组血小板相关免疫球蛋白G（PAIgG）、血小板相关免疫球蛋白A（PAIgA）、血小板相关免疫球蛋白M（PAIgM）水平明显降低,而血小板计数明显升高,同组治疗前后比较差异有统计学意义（P<0.05）;且治疗组这些观察指标明显优于对照组,两组比较差异具有统计学意义（P<0.05）。治疗后,两组CD3⁺、CD4⁺、CD4⁺/CD8⁺水平明显升高,而CD8⁺水平明显降低,同组治疗前后比较差异有统计学意义（P<0.05）;且治疗组这些观察指标明显优于对照组,两组比较差异具有统计学意义（P<0.05）。结论 槐杞黄颗粒联合重组人血小板生成素治疗特发性血小板减少性紫癜具有较好的临床疗效,能降低血小板相关抗体,改善机体免疫功能,降低不良反应的发生,具有一定的临床推广应用价值。     

血必净注射液联合重组人血小板生成素治疗脓毒症相关性血小板减少症的临床研究

目的研究血必净注射液联合重组人血小板生成素注射液治疗脓毒症相关性血小板减少症的临床疗效。方法选取2017年12月—2019年12月在天津市中医药研究院附属医院治疗的70例脓毒症相关性血小板减少症患者,将所有患者随机分为对照组和治疗组,每组各35例。对照组静脉滴注重组人血小板生成素注射液,300 U/kg,1次/d,患者在用药过程中待血小板绝对值升高≥50×109/L或血小板100×109/L即应停用。治疗组在对照组基础上静脉滴注血必净注射液,50 mL/次,2次/d。两组患者均持续治疗14 d。观察两组临床疗效,比较两组血小板水平动态变化、血清Toll4受体(TLR4)、血小板第4因子(PF4)和内源性血小板生成素(TPO)水平及血清血管性血友病因子(vWF)、肿瘤坏死因子-α(TNF-α)、可溶性CD40配体(s CD40L)水平。结果治疗后,治疗组总有效率为94.29%,对照组总有效率为82.86%,治疗组总有效率显著高于对照组(P0.05)。治疗3、5、7、10 d后,治疗组血小板水平均高于同期对照组(P0.05)。治疗后,两组患者血清TLR4、PF4和TPO水平明显降低(P0.05);且治疗组血清TLR4、PF4和TPO水平降低较明显(P0.05)。治疗后,两组血清v WF、TNF-α和s CD40L水平均显著降低(P0.05);并且治疗组患者血清v WF、TNF-α和s CD40L水平降低较明显(P0.05)。结论血必净注射液联合重组人血小板生成素注射液治疗脓毒症相关性血小板减少症具有较好的治疗效果,可降低血清TLR4、PF4、TPO水平和vWF、TNF-α和s CD40L水平。     

重组人血小板生成素对难治性特发性血小板减少性紫癜患者血清炎症因子及Th1/Th2影响研究

目的探讨重组人血小板生成素对难治性特发性血小板减少性紫癜患者血清炎症因子及Th1/Th2的影响。方法选取2017年1月至2021年1月我院难治性特发性血小板减少性紫癜患者60例,随机分2组,各30例。对照组采用环孢素,观察组在此基础上采用重组人血小板生成素,持续治疗3个月。比较两组治疗前后血小板计数(Platelet count,PLT)、血小板体积分布宽度(Platelet volume distribution width,PDW)、血小板比容(Platelet specific volume,PCT)、血小板平均体积(Mean platelet volume,MPV)和白介素-2(Interleukin-2,IL-2)、白介素-4(Interleukin-4,IL-4)及IL-2/IL-4。结果与治疗前比较,两组治疗后PLT、PCT均升高,PDW、MPV均降低,且观察组治疗后PLT、PCT高于对照组,PDW、MPV低于对照组,差异有统计学意义(P<0.05)。与治疗前比较,两组治疗后血清IL-2、IL-2/IL-4均降低,血清IL-4升高,且观察组治疗后血清IL-2、IL-2/IL-4低于对照组,血清IL-4高于对照组,差异有统计学意义(P<0.05)。两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论重组人血小板生成素对难治性特发性血小板减少性紫癜患者的疗效确切,能改善血小板参数,与纠正Th1/Th2失衡有关。     

重组人血小板生成素和免疫球蛋白治疗脓毒症相关性血小板减少症的临床研究

目的比较性研究重组人血小板生成素和免疫球蛋白治疗脓毒症相关性血小板减少症的临床疗效。方法收集2012年1月—2014年3月天津市第一中心医院、天津市南开医院脓毒症合并血小板减少症患者67例,随机分为对照组(35例)和治疗组(32例)。治疗组在对症治疗的基础上sc重组人血小板生成素注射液300 U/kg,1次/d。对照组在对症治疗的基础上静脉点滴人免疫球蛋白400 mg/kg,1次/d。两组患者血小板计数恢复至100×109/L时或血小板计数绝对值升高≥50×109/L时即停用升血小板药。观察治疗前,治疗第1、2、3、5、7、9天两组患者血小板计数、Toll4受体(TLR4)、血小板第4因子(PF4)、内源性血小板生成素(TPO)的变化。随访28 d记录两组血液制品的使用情况。结果自用药后第2天开始,两组患者血小板计数均进行性升高,同组治疗前后差异有统计学意义(P0.05);治疗组较对照组升高的幅度更大(P0.05)。从治疗第1天开始,两组TLR4、PF4均较治疗前显著降低(P0.05),TPO显著升高,自治疗第5天后对照组TLR4、PF4下降趋势明显高于治疗组(P0.05);自治疗第2天开始,治疗组TPO显著高于对照组(P0.05)。治疗组输注血小板、血浆、红细胞均低于对照组(P0.05)。结论重组人血小板生成素和免疫球蛋白治疗脓毒症相关性血小板生成素均有临床疗效,但重组人血小板生成素能在较短时间内提升患者血小板计数从而降低了患者早期出血的风险。     

甘露聚糖肽口服液联合人免疫球蛋白治疗特发性血小板减少性紫癜的临床研究

目的探讨甘露聚糖肽口服液联合人免疫球蛋白治疗特发性血小板减少性紫癜的临床疗效。方法选取2014年8月—2015年8月在上海市浦东医院接受治疗的特发性血小板减少性紫癜患者74例,随机分为对照组和治疗组,每组各37例。对照组iv静注人免疫球蛋白(pH4),0.4 g/kg,1次/d。治疗组在对照基础上口服甘露聚糖肽口服液,1支/次,3次/d。两组患者均治疗4周。观察两组的临床疗效,比较治疗前后两组T淋巴细胞亚群、血小板相关抗体、血小板计数(PLT)、白细胞介素-4(IL-4)、止血时间和血小板数量达正常时间的情况。结果治疗后,对照组和治疗组的总有效率分别为78.38%、94.59%,两组比较差异有统计学意义(P0.05)。治疗后,两组患者CD~(3+)和CD~(4+)的水平及CD~(4+)/CD~(8+)的比值均显著升高,而CD~(8+)的水平显著下降,同组治疗前后差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者血小板相关免疫球蛋白G(PA IgG)、血小板相关免疫球蛋白A(PA IgA)和血小板相关免疫球蛋白M(PA IgM)的水平均明显降低,同组治疗前后差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者PLT及IL-4水平均明显升高,同组治疗前后差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,治疗组止血时间和血小板数量达正常时间均早于对照组,两组比较差异均具有统计学意义(P0.05)。结论甘露聚糖肽口服液联合人免疫球蛋白治疗特发性血小板减少性紫癜具有较好的临床疗效,可提高患者机体免疫功能,加快止血,具有一定的临床推广应用价值。     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Polymorphisms in genes involved in neurotransmission in relation to smoking

Smoking behavior is influenced by both genetic and environmental factors. The genetic contribution to smoking behavior is at least as great as its contribution to alcoholism. Much progress has been achieved in genomic research related to cigarette-smoking within recent years. Linkage studies indicate that there are several loci linked to smoking, and candidate genes that are related to neurotransmission have been examined. Possible associated genes include cytochrome P450 subfamily polypeptide 6 (CYP2A6), dopamine D₁, D₂, and D₄ receptors, dopamine transporter, and serotonin transporter genes. There are other important candidate genes but studies evaluating the link with smoking have not been reported. These include genes encoding the dopamine D₃ and D₅ receptors, serotonin receptors, tyrosine hydroxylase, trytophan 2,3-dioxygenase, opioid receptors, and cannabinoid receptors. Since smoking-related factors are extremely complex, studies of diverse populations and of many aspects of smoking behavior including initiation, maintenance, cessation, relapse, and influence of environmental factors are needed to identify smoking-associated genes. We now review genetic polymorphisms reported to be involved in neurotransmission in relation to smoking.     

Tramadol concentrations in blood and in cerebrospinal fluid in a neonate

Based on blood and cerebrospinal fluid samples collected in a full-term neonate, the penetration of tramadol in the central nervous system is described. Following intravenous administration of tramadol, a lag time of about 4 h was observed until full blood–brain equilibration was achieved. This pharmacokinetic observation is in line with a recent pharmacodynamic evaluation of the central opioid effects of tramadol in adults.     

Disease control in asthmatic children seen in private practice in Switzerland

ABSTRACT

Background: Asthma is the most common chronic childhood disease in Switzerland with a prevalence of 10%. Asthma has a high economic burden accounting for high medical costs. Assessment of disease control is likely to be of help in the implementation of strategies to improve asthma. Therefore, we aimed to evaluate asthma control and therapy regimens among children in private practice.

Methods: We assessed asthma control as well as therapy regimens in 575 asthmatic children in an experience programme in Switzerland by using an abbreviated questionnaire based on the asthma control questionnaire and the child health questionnaire on Visit 1 and Visit 2.

Results: Good asthma control at Visit 1 was only present in 25.7% of asthmatic children. Occasional asthma symptoms, limitation of physical activity, nocturnal awakening and anxiety of the parent was present in 80.5%, 41.2%, 46.8% and 57% of the children, respectively. After adjustment of therapy regimens at Visit 1, mainly by adding a leukotriene receptor antagonist, asthma control was reported to be much better in 53.4% of the children at Visit 2.

Conclusions: As asthma control is inadequately achieved within a major portion of asthmatic children, it is imperative to find measures to improve asthma control and hence, to reduce the burden of disease.