木糖醇注射液与两种抗生素配伍的稳定性研究

目的考察头孢他啶、甲磺酸培氟沙星在木糖醇注射液中的稳定性.方法模拟临床用法用量,对配伍溶液在6h之内的外观、pH值及含量的变化进行研究.结果配伍溶液的各项指标均无显著性变化.结论两种抗生素均可与木糖醇注射液配伍使用.     

Imatinib accelerates progenitor cell‐mediated liver regeneration in choline‐deficient ethionine‐supplemented diet‐fed mice

Severe chronic hepatic injury can induce complex reparative processes. Ductular reaction and the appearance of small hepatocytes are standard components of this response, which is thought to have both adverse (e.g. fibrosis, carcinogenesis) and beneficial (regeneration) consequences. This complex tissue reaction is regulated by orchestrated cytokine action. We have investigated the influence of the tyrosine kinase inhibitor imatinib on a regenerative process. Ductular reaction was induced in mice by the widely used choline‐deficient ethionine‐supplemented diet (CDE). Test animals were treated daily with imatinib. After 6 weeks of treatment, imatinib successfully reduced the extent of ductular reaction and fibrosis in the CDE model. Furthermore, the number of small hepatocytes increased, and these cells had high proliferative activity, were positive for hepatocyte nuclear factor 4 and expressed high levels of albumin and peroxisome proliferator‐activated receptor alpha. The overall functional zonality of the hepatic parenchyma (cytochrome P450 2E1 and glucose 6 phosphatase activity; endogenous biotin content) was maintained. The expression of platelet‐derived growth factor receptor beta, which is the major target of imatinib, was downregulated. The anti‐fibrotic activity of imatinib has already been reported in several experimental models. Additionally, in the CDE model imatinib was able to enhance regeneration and preserve the functional arrangement of hepatic lobules. These results suggest that imatinib might promote the recovery of the liver following parenchymal injury through the inhibition of platelet‐derived growth factor receptor beta.     

Poor responses to tyrosine kinase inhibitors in a child with precursor B‐cell acute lymphoblastic leukemia with SNX2‐ABL1 chimeric transcript

In addition to BCR, various rare fusion partners for the ABL1 gene have been reported in leukemia. We have identified the fusion gene SNX2‐ABL1 in a pediatric case of acute lymphoblastic leukemia (ALL), which has only once previously been reported in an adult patient. Cytogenetic analysis detected this fusion gene arising from a t(5;9)(q22;q34) translocation. ALL cells carrying a SNX2‐ABL1 fusion exhibited a BCR‐ABL1+ ALL‐like gene expression profile. The patient poorly responded to dasatinib but partially responded to imatinib. Treatment using tyrosine kinase inhibitors requires further investigation to optimize the genotype‐based treatment stratification for patients with SNX2‐ABL1 fusion.     

安定配合硬膜外阻滞镇痛分娩的临床研究

目的:探讨产程活跃期应用安定加低浓度、小剂量、局麻药甲磺酸罗哌卡因及舒芬太尼实施自控镇痛泵镇痛分娩方法及对产程和母婴的影响。方法:实验组采取活跃期安定缓慢静脉推注联合低浓度、小剂量的1.192%甲磺酸罗哌卡因复合舒芬太尼实施硬膜外阻滞,微量自控泵给药的镇痛分娩;对照组自然分娩;两组比较分析。结果:实验组产妇第一产程平均时间(186.46±8.52)min、自然分娩率增91.25%、剖宫产率6.25%。产妇身心状态评估:宫缩时表情自然73例,心率、血压平稳,宫缩无影响。对照组产妇第一产程平均时间(270.68±12.34)min、自然分娩率66.25%、剖宫产率28.75%,产妇身心状态评估表情自然12例(P<0.01);心率、血压增快,具有统计学意义(P<0.05)。结论:安定配合硬膜外阻滞镇痛分娩的效果好,能缩短产程,降低剖宫产率,保持产妇良好的心态,提高产科质量,是比较理想的分娩镇痛方法。     

甲磺酸阿帕替尼片用于标准治疗失败后卵巢癌治疗的有效性和安全性

目的:观察甲磺酸阿帕替尼用于标准治疗失败后卵巢癌的有效性和安全性，为多线耐药的卵巢癌患者提供一种治疗方式。方法:选取2015年6月至2018年3月二线及二线后化疗失败的晚期卵巢癌患者26例，口服甲磺酸阿帕替尼后观察疗效及毒副反应。结果:1例患者CR，17例患者PR,2例患者SD,6例患者PD，客观有效率69%，疾病控制率77%，中位PFS达4.3个月。患者总体耐受性良好，常见的不良反应为1-3级的胃肠道反应，包括腹痛、恶心及呕吐，其中以腹痛最为常见。结论:对于经标准治疗失败后的晚期卵巢癌患者，阿帕替尼具有良好的疗效和安全性。     

注射用甲磺酸齐拉西酮对双相Ⅰ型障碍躁狂发作急性激越症状的疗效和安全性

目的分析注射用甲磺酸齐拉西酮治疗双相Ⅰ型障碍躁狂发作急性激越症状的疗效和安全性。方法选取2019年4月至2020年4月本院收治的60例双相Ⅰ型障碍躁狂发作急性激越症状患者,按治疗方式的不同分为两组,各30例。对照组采用氟哌啶醇注射液治疗,研究组采用甲磺酸齐拉西酮注射液治疗。比较两组不良反应发生率、阳性与阴性症状量表兴奋因子(PANSS-EC)评分、临床疗效总评量表-病情程度(CGI-SI)评分等。结果治疗后,研究组CGI-SI评分略低于对照组,但差异无统计学意义;治疗前及治疗后2、6、24、48、72 h两组PANSSEC评分比较差异无统计学意义;研究组不良反应总发生率为6.67%,低于对照组的43.33%,差异有统计学意义(P<0.05)。结论与氟哌啶醇注射液比较,临床采用注射用甲磺酸齐拉西酮药物治疗双相Ⅰ型障碍躁狂发作急性激越症状,虽疗效基本相当,但给药安全性更高,对疾病治疗有利。     

Tyrosine kinase inhibitor imatinib (STIS71) as an anticancer agent for solid tumours

Imatinib mesylate, also known as ST1571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R). It binds to the ATP-binding site of the target kinase and prevents the transfer of phosphate from ATP to the tyrosine residues of various substrates. At oral doses of 300 mg or greater, the vast majority of patients with chronic myeloid leukaemia achieve a haematological response and this is usually associated with limited toxicity. Imatinib also has substantial activity in Philadelphia chromosome-positive acute lymphoblastic leukaemia expressing the BCR-ABL fusion protein. Gastrointestinal stromal tumours (GISTS) have also been evaluated for clinical activity of imatinib. About 90% of malignant GISTs harbour a mutation in c-kit leading to KIT receptor autophosphorylation and ligand-independent activation. According to initial clinical studies, more than 50% of GISTs respond to therapy within a few months, and only about 10-15% progress. The potential for cure and the optimal length of treatment are currently not known. Several other human cancers may over-express KIT or PDGF-R, and clinical trials to evaluate the role of imatinib in the treatment of such cancers are currently ongoing. Imatinib is an example of a specifically designed, highly targeted cancer therapy, which poses novel requirements for both pathology laboratories and clinicians in terms of identifying the major molecular mechanisms involved in tumour growth.     

First case of immune-mediated haemolytic anaemia associated to imatinib mesylate

Imatinib mesylate is a specific inhibitor of protein tyrosine kinase activity secondary to bcr-abl, mostly indicated for the treatment of patients with Philadelphia chromosome positive chronic myeloid leukaemia (CML). Generally, the undesirable effects of imatinib administration observed in clinical trials were of mild-to-moderate degree, and no haemolysis has been associated with this drug. We report here a case of immune-mediated haemolytic anaemia associated to imatinib mesylate successfully treated with prednisone in a patient with CML. Laboratory investigation showed anaemia [haemoglobin (Hb) of 59 g/L], reticulocyte of 61 x 10(9)/L and a positive direct antiglobulin test. Anti-drug in vitro studies revealed a positive result with gel microcolumn assay by an adsorption mechanism. Seventy-four days after prednisone therapy, the patient's Hb level was of 110 g/L with negative direct antiglobulin test and drug in vitro studies. This case demonstrated that patients treated with imatinib mesylate can present immune-mediated haemolysis and adequate management of this event can be done maintaining the drug and associating corticosteroids.