静脉输注卡铂致过敏的报道及药学服务

目的:为临床安全使用卡铂提供药学信息和药学服务。方法:报告卡铂化疗中出现的3例不良反应,包括2例胸闷憋气、血压下降和1例严重的过敏性休克。结合案例对卡铂过敏的报道进行文献检索分析。结果:根据病例及文献汇总,分析卡铂过敏反应的发生特点、机制、危险因素、预防方式以及后续治疗方法,总结卡铂过敏反应的相关药学信息和药学服务要点。结论:药师通过临床治疗实践,获得积累卡铂过敏反应的相关知识和经验并为临床治疗选择提供药学服务。     

紫杉醇治疗妇科恶性肿瘤的护理

目的探讨应用紫杉醇联合卡铂治疗妇科肿瘤的毒副反应与护理对策,进一步提高护理质量,减轻患者痛苦。方法对41例妇科恶性肿瘤患者进行化疗前预处理,行紫杉醇卡铂联合化疗,过程中专人守护,对毒副反应进行观察与护理。结果本组41例患者,40例患者完成全部化疗。只有1例因过敏反应而更改化疗方案。结论做好紫杉醇卡铂联合化疗患者中的护理,是减轻化疗中毒副反应、减少患者痛苦的重要手段。     

妇科肿瘤卡铂化疗所致过敏反应的中国专家共识（2022年版）

铂类药物广泛应用于妇科恶性肿瘤的化疗。卡铂作为顺铂的衍生物，属于第二代铂类抗癌药，具有“等效、低毒”的特点。过敏反应是卡铂化疗过程中的常见并发症，严重急性过敏反应可危及患者生命。预防卡铂过敏、及时诊断并给予规范治疗，对于提高妇科肿瘤治疗效果、降低患者死亡风险具有重要意义。本共识的制定，旨在为妇科肿瘤医师提供借鉴和指引。     

结直肠癌患者奥沙利铂过敏4例回顾性分析

奥沙利铂(oxaliplatin,L-OHP)又名草酸铂,属第三代铂类抗肿瘤药物。奥沙利铂由Kidani在1978年首先合成,它最显著的特点是不与顺铂、卡铂发生交叉耐药性或交叉度低,其与5-氟尿嘧啶/亚叶酸联合应用是治疗结直癌最常用化疗方案之一。它的剂量限制性毒性反应是神经系统毒性反应。除了神经系统累积毒性,过敏反应也限制了奥沙利铂的临床应用,其中1%过敏患者可能发生致命性过敏反应。     

临床药师参与1例奥沙利铂过敏反应患者后续化疗方案制定的药学实践

过敏反应(hypersensitivity)是奥沙利铂常见的不良反应,奥沙利铂引起过敏反应的识别、处理及后续化疗方案的制定是临床必须要解决的问题,尤其对于以铂类药物化疗为主的妇科肿瘤患者。本文介绍了临床药师参与1例奥沙利铂过敏卵巢癌复发患者后续化疗方案制定的药学实践,协助医师制定患者后续化疗方案并实施药学监护,最终患者顺利完成全部化疗周期。充分体现了临床药师在肿瘤患者个体化治疗中的作用,同时为临床处理此类药物不良反应提供了参考。     

临床药师参与1例奥沙利铂过敏反应患者后续化疗方案制定的药学实践

过敏反应(hypersensitivity)是奥沙利铂常见的不良反应,奥沙利铂引起过敏反应的识别、处理及后续化疗方案的制定是临床必须要解决的问题,尤其对于以铂类药物化疗为主的妇科肿瘤患者。本文介绍了临床药师参与1例奥沙利铂过敏卵巢癌复发患者后续化疗方案制定的药学实践,协助医师制定患者后续化疗方案并实施药学监护,最终患者顺利完成全部化疗周期。充分体现了临床药师在肿瘤患者个体化治疗中的作用,同时为临床处理此类药物不良反应提供了参考。     

奥沙利铂致过敏危险因素分析

目的分析奥沙利铂致结直肠癌患者过敏的危险因素。方法回顾分析185例接受奥沙利铂化疗的结直肠癌患者,分析人口学特征,既往过敏史,实验室检查,化疗方案和抗过敏预防措施的使用等。结果奥沙利铂所致过敏反应者23例,其中17例患者发生Ⅰ/Ⅱ度过敏反应,6例患者发生Ⅲ/Ⅳ度过敏反应。与无过敏反应组相比,过敏反应组患者奥沙利铂化疗间断率高,其中Ⅰ/Ⅱ度过敏反应组患者化疗次数较多。结论化疗次数增多和奥沙利铂化疗曾有间断与发生过敏反应相关。     

1例奥沙利铂致过敏反应患者的药学监护

目的:探讨临床药师在对奥沙利铂致过敏反应进行药学监护中的作用。方法:临床药师参与1例奥沙利铂致过敏反应患者的药学监护,在患者出现过敏反应时建议停用奥沙利铂,给予地塞米松注射液5 mg,之后减缓奥沙利铂滴注速度。结果:医师采纳临床药师建议,给予地塞米松注射液5 min后,患者过敏反应减轻;在严密监测下继续治疗,患者未再出现类似过敏反应。结论:奥沙利铂为常用抗肿瘤药物,医务人员应熟悉其不良反应的预防、诊断与治疗,对含奥沙利铂的化疗方案提前进行评估,筛查患者过敏的高危因素。临床药师参与药物治疗的药学监护,有利于药品不良反应监测,可促进临床更加安全、合理用药。     

快速脱敏疗法在卡铂过敏患者中的应用研究

目的评价快速脱敏治疗在卡铂过敏患者中应用的安全性及疗效。方法收集2016年7月至2017年12月在我院妇科肿瘤病房接受卡铂快速脱敏治疗患者的临床资料,回顾性分析其临床特征、治疗效果及安全性。结果共有16例患者接受卡铂快速脱敏治疗,其中有14例患者完成全部预定治疗,2例患者在首次脱敏治疗中出现重度反应,经治疗后再次出现,放弃治疗。完成治疗的14例患者共进行了72次脱敏治疗,其中共出现22次过敏反应,16次轻度反应,6次重度反应。81.8%的过敏反应出现在患者的前2次脱敏治疗中。45.5%的过敏反应发生在溶液1输注过程中,9%发生在溶液2输注中,45.5%发生在溶液3输注中。过敏反应的频率和严重程度随后续疗程而降低。结论卡铂快速脱敏治疗方法安全有效,可由具备相关专业知识的医护人员完成。     

吉西他滨联合卡铂双周方案治疗晚期非小细胞肺癌护理

目的吉西他滨联合卡铂双周方案治疗晚期非小细胞肺癌的临床疗效、毒副作用观察及护理。方法选择晚期NSCLC32例,以GEM加卡铂方案进行化疗,吉西他滨1．25g／m^2,第1、15d静滴30min;卡铂按AUC=5计算,第1、15天各静滴一半,28d为1个周期,每例至少治疗2个周期。结果全部患者均完成2个周期以上化疗,未出现过敏反应和心脏损害,无治疗相关性死亡。经治疗和护理后,所有不良反应均逐渐缓解,无1例发生严重并发症。结论选择吉西他滨联合卡铂治疗晚期NSCLC的同时,采取积极有效的护理措施,可以明显减轻不良反应的发生,提高患者的生存质量,使治疗顺利完成。     

妇科恶性肿瘤紫杉醇化疗所致过敏反应诊治的中国专家共识（2023年版）

紫杉醇类已广泛应用于妇科恶性肿瘤的化疗。过敏反应是紫杉醇化疗过程中的常见不良反应,严重者甚至会危及患者生命。预防紫杉醇过敏、及时诊断并给予规范治疗,对于提高妇科肿瘤治疗效果、降低患者死亡风险具有重要意义。本共识对紫杉醇化疗过敏反应的分级、诊断、治疗及预防等方面的内容进行了制定,旨在为妇科恶性肿瘤紫杉醇化疗所致过敏反应的规范化预防和诊治提供参考。     

Rapid desensitization of hypersensitivity reactions to chemotherapy agents

All chemotherapy agents can cause hypersensitivity reactions, which have limited the used of critical drugs in very sick patients for fear of inducing a more severe reaction and possibly death. The choice of an alternative chemotherapy regimen is often limited by tumor sensitivity and, because of the increasing number of cancer survivors, exposure to multiple courses of the same or similar chemotherapy agents. Increased exposures lead to sensitization and to hypersensitivity reactions in an increasing patient population. The need to offer first line therapy after cancer recurrence has spurred the clinical development of rapid desensitizations, which allow patients to be treated with medications to which they have presented hypersensitivity reactions. Desensitization protocols are available to treat hypersensitivity reactions to most chemotherapy agents including taxenes, platinums, doxorubicin, monoclonal antibodies and others, by gradual re-introduction of small amounts of drug antigens up to full therapeutic doses. Candidate patients include those who present mild to severe type I hypersensitivity, mast cell/IgE dependent, reactions during the chemotherapy infusion or shortly after. Symptoms include pruritus, flushing, urticaria, angioedema, respiratory and gastrointestinal distress, changes in blood pressure including hypotension, and shock with anaphylaxis. Associated musculoskeletal symptoms and pain can be present in patients reacting to taxenes as in anaphylactoid reactions, in which mast cell/IgE mechanisms cannot be demonstrated. There is now strong evidence that anaphylactoid reactions are amendable to treatment with the same rapid desensitization protocols as for type I hypersensitivity reactions. Initial rapid desensitizations should only be performed in settings with one on one nurse-patient care and where resuscitation personnel and resources are readily available. Temporary tolerization is achieved in a few hours. After the first desensitization, standard protocols are available for safe, repeated desensitizations in outpatient settings with similar conditions, which not only provides flexibility, but allows patients to remain in clinical studies. Breakthrough symptoms are less severe than the initial hypersensitivity reaction in all series reviewed, and deaths have not been reported. The aim of this review is to familiarize the medical community with the type of hypersensitivity reactions amendable to rapid desensitization and to review protocols for chemotherapy desensitization that can be used for most chemotherapy agents. Few studies have measured the cancer response to the chemotherapy agents delivered through rapid desensitizations. One patient population in which 26 patients were desensitized to carboplatin and 16 to paclitaxel had similar rates of remission as for non-desensitized patients. Education of nurses, pharmacists, oncology and allergy specialists will lead to the universal use of rapid desensitization protocols for all cancer patients with hypersensitivity reactions to chemotherapy agents. Basic research is needed to uncover the cellular and molecular mechanisms underlying the temporary tolerization induced by rapid desensitization, so that pharmacological interventions can improve its safety and efficacy.     

Carboplatin: a new cisplatin analog

Carboplatin, a new antineoplastic agent with a spectrum of antitumor activity similar to cisplatin, has shown appreciable activity in patients with ovarian carcinoma, head and neck cancer, and small-cell lung cancer. This platinum complex is less nephrotoxic, ototoxic, and neurotoxic than cisplatin. Myelosuppression may be severe and dose-limiting. Carboplatin distributes into a volume approximating total body water, and is slowly bound to plasma proteins; its elimination is a biphasic process. Renal clearance of free platinum from carboplatin correlates highly with creatinine clearance in patients with normal or impaired renal function. The recommended iv dose of carboplatin as a single agent in previously untreated patients is 400-500 mg/m2; dosage must be reduced in patients with decreased renal function, low initial platelet count, or extensive prior chemotherapy or radiation therapy. Carboplatin will be most useful in patients with decreased renal function and those who cannot tolerate high-volume hydration regimens. Patients at higher risk for development of cisplatin-related ototoxicity or neurotoxicity (e.g., patients expected to receive cumulative cisplatin doses exceeding 600-800 mg/m2) may be ideal candidates for carboplatin as initial therapy. Large-scale comparative trials are needed before carboplatin can be recommended as a replacement for cisplatin.     

紫杉醇脂质体与传统紫杉醇治疗晚期鼻咽癌的疗效分析

目的比较紫杉醇脂质体和传统紫杉醇联合卡铂一线治疗晚期鼻咽癌的疗效及毒性。方法回顾性分析2010年1月-2011年12月我院晚期鼻咽癌的一线治疗患者临床资料,72例晚期鼻咽癌患者被分为实验组和对照组,实验组（35例）应用紫杉醇脂质体,而对照组（37例）应用普通紫杉醇,每次剂量均为135-175mg/m2;两组均联合卡铂,采用AUC=5。每21d为1个周期,每2个周期评价疗效1次。结果 72例患者共接受341个周期化疗,所有患者均可评价疗效。实验组总有效率为71.4%,对照组为70.3%,两者之间无统计学差异。两组血液学及消化道毒性相似,而在由溶媒所产生的相关毒性方面,紫杉醇（对照组）明显高于紫杉醇脂质体（实验组）。结论与传统紫杉醇联合卡铂一线治疗晚期鼻咽癌相比,紫杉醇脂质体联合卡铂方案疗效相似,但由溶媒所产生的毒性更低,且使用方便,值得临床推广应用。     

Dose response of carboplatin-induced nephrotoxicity in rats

Abstract: Carboplatin, a second-generation platinum-containing anticancer drug, is currently being used against a variety of cancers. High-dose carboplatin chemotherapy can cause renal tubular injury in cancer patients. However, the biochemical mechanism of carboplatin-induced renal injury has not been well studied. This study investigated the dose response of carboplatin-induced changes in endogenous antioxidants, lipid peroxidation and platinum content in rat kidney. Male Wistar rats (250-300 g) were divided into five groups and treated as follows: (1) control (saline, intraperitoneally); (2) carboplatin (64 mg/kg, intraperitoneally); (3) carboplatin (128 mg/kg, intraperitoneally); (4) carboplatin (192 mg/kg, intraperitoneally); and (5) carboplatin (256 mg/kg, intraperitoneally). The animals were sacrificed four days after treatment. The blood and kidneys were isolated and analyzed. Plasma creatinine and blood urea nitrogen levels were increased significantly in response to carboplatin in a dose-dependent manner. Renal superoxide dismutase and catalase activities were decreased significantly due to carboplatin at dosages of 128 mg/kg and above. The protein expressions of renal copper/zinc-superoxide dismutase and manganese-superoxide dismutase significantly depleted after carboplatin. Carboplatin (192 and 256 mg/kg) significantly increased lipid peroxidation (malondialdehyde concentration) in rat kidneys. Carboplatin dose-dependently increased the renal platinum concentration, with significance at dosages of 128 mg/kg and above. Carboplatin (256 mg/kg) significantly increased renal xanthine oxidase activity, while ratio of reduced to oxidized glutathione depleted significantly. The data suggested that carboplatin caused dose-dependent oxidative renal injury, as evidenced by renal antioxidant depletion, enhanced lipid peroxidation, platinum content, plasma creatinine and blood urea nitrogen levels in rats.     

A case of glassy cell carcinoma of the uterine cervix effectively responding to chemotherapy with paclitaxel and carboplatin

Glassy cell carcinoma (GCC) of the uterine cervix is a highly malignant tumor and has a poor prognosis. As yet, no effective systemic chemotherapy to this tumor has been reported. Here we describe a case of recurrent GCC that responded to paclitaxel and carboplatin combination treatment. The patient, a 32-year-old woman, with clinical staging FIGO IB1 disease had a radical hysterectomy and postoperative radiotherapy. Three months after initial treatment, she had a relapse as peritoneal dissemination, which was confirmed in the second surgery (adnectomy) and which did not respond to platinum-based conventional chemotherapy (cisplatin, adriamycin, cyclophosphamide and carboplatin, etoposide). The recurrent peritoneal tumors responded well to paclitaxel and carboplatin combination treatment. An elevated serum concentration of carcinoembryonic antigen (672 ng/ml) was reduced to 14.4 ng/ml by six such courses. Peritoneal histopathology confirmed a complete response in the third surgery (ileostomy) for adhesive ileus by the radiotherapy. This is the first report of effective systemic chemotherapy with paclitaxel and carboplatin to recurrent GCC of the uterine cervix.     

Dose Response of Carboplatin‐Induced Nephrotoxicity in Rats

Abstract: Carboplatin, a second‐generation platinum‐containing anticancer drug, is currently being used against a variety of cancers. High‐dose carboplatin chemotherapy can cause renal tubular injury in cancer patients. However, the biochemical mechanism of carboplatin‐induced renal injury has not been well studied. This study investigated the dose response of carboplatin‐induced changes in endogenous antioxidants, lipid peroxidation and platinum content in rat kidney. Male Wistar rats (250–300 g) were divided into five groups and treated as follows: (1) control (saline, intraperitoneally); (2) carboplatin (64 mg/kg, intraperitoneally); (3) carboplatin (128 mg/kg, intraperitoneally); (4) carboplatin (192 mg/kg, intraperitoneally); and (5) carboplatin (256 mg/kg, intraperitoneally). The animals were sacrificed four days after treatment. The blood and kidneys were isolated and analyzed. Plasma creatinine and blood urea nitrogen levels were increased significantly in response to carboplatin in a dose‐dependent manner. Renal superoxide dismutase and catalase activities were decreased significantly due to carboplatin at dosages of 128 mg/kg and above. The protein expressions of renal copper/zinc‐superoxide dismutase and manganese‐superoxide dismutase significantly depleted after carboplatin. Carboplatin (192 and 256 mg/kg) significantly increased lipid peroxidation (malondialdehyde concentration) in rat kidneys. Carboplatin dose‐dependently increased the renal platinum concentration, with significance at dosages of 128 mg/kg and above. Carboplatin (256 mg/kg) significantly increased renal xanthine oxidase activity, while ratio of reduced to oxidized glutathione depleted significantly. The data suggested that carboplatin caused dose‐dependent oxidative renal injury, as evidenced by renal antioxidant depletion, enhanced lipid peroxidation, platinum content, plasma creatinine and blood urea nitrogen levels in rats.     

卡铂前体脂质体的制备及安全性的初步评价

目的：制备卡铂前体脂质体,并对用药安全性进行初步评价.方法：采用薄膜挤压法制备卡铂脂质体,加入冻干支持剂冷冻干燥后得到卡铂前体脂质体.对豚鼠全身用药的过敏性、家兔全身用药的血管刺激性以及溶血性进行考察.结果：制备所得的卡铂前体脂质体水合后的包封率为72.0%,载药量为24.0%,平均粒径为125.1 nm.卡铂前体脂质体不引起豚鼠过敏反应,不引起家兔溶血和红细胞凝集反应,静脉注射对家兔血管无刺激性.结论：制备所得的卡铂前体脂质体有较高的包封率和载药量,水合后粒径均匀,形态圆整,且具有较好的用药安全性.