贝伐珠单抗治疗脑转移瘤难治性瘤周水肿的疗效分析

目的 观察贝伐珠单抗治疗恶性肿瘤脑转移瘤难治性瘤周水肿的疗效及不良反应。方法 回顾性分析于本院接受贝伐珠单抗治疗的14例伴难治性瘤周水肿的恶性肿瘤脑转移瘤患者的临床资料,包括乳腺癌脑转移7例、肺癌5例、食管癌1例、右上颌窦腺样囊性癌1例。所有患者均为甘露醇、地塞米松等常规治疗无效的难治性脑水肿病例。评估患者在贝伐珠单抗治疗前后的临床症状、生活质量评分及MRI显示的水肿体积,并详细记录治疗相关不良反应。结果 全组患者接受贝伐珠单抗治疗的中位剂量为4.76 mg/kg。全组14例患者中,11例患者在贝伐珠单抗给药后头晕、头痛症状明显减轻,3例患者症状改善不明显。全组14例患者贝伐珠单抗治疗后瘤周水肿体积较治疗前明显减少［（38 804±14 859）mm3 vs.（80 100±28 338）mm3,P=0.02］,水肿指数较治疗前有降低的趋势（15.38±7.12 vs. 26.40±16.52,P＞0.05）,但差异无统计学意义。14例患者中有1例于第2次贝伐珠单抗治疗后出现上颌窦创面大量出血死亡,3例患者出现可控制的高血压,未出现蛋白尿、贫血、口腔炎等其他并发症。结论 贝伐珠单抗可控制恶性肿瘤脑转移的难治性瘤周水肿,为严重脑水肿患者争取放疗机会,但应谨慎掌握适应证,警惕严重不良反应。     

贝伐珠单抗治疗肺腺癌脑转移瘤伴难治性脑水肿效果观察

目的探讨贝伐珠单抗治疗肺腺癌脑转移瘤伴难治性脑水肿的效果及对血清血管内皮生长因子(VEGF)的影响。方法回顾性分析2015年7月至2018年12月青岛市中心医院收治的25例肺腺癌脑转移伴难治性脑水肿患者的临床资料,既往经甘露醇联合糖皮质激素脱水降颅压治疗无效。患者分为单用贝伐珠单抗组和联用贝伐珠单抗组。给予贝伐珠单抗(5 mg/kg)治疗后评估患者临床症状、功能状态评分(KPS)、瘤周水肿程度以及血清VEGF水平的变化。结果治疗后19例患者症状明显减轻,6例患者症状改善不明显;所有患者KPS评分高于治疗前,瘤周水肿指数较治疗前下降,差异均具有统计学意义(均P<0.05)。治疗后血清VEGF水平较治疗前降低,且联用贝伐珠单抗组血清VEGF水平低于单用贝伐珠单抗组,差异均有统计学意义(均P<0.05)。治疗中出现高血压3例,便血及咯血各1例,经对症处理后好转,无严重不良反应发生。结论贝伐珠单抗治疗肺腺癌脑转移伴难治性瘤周水肿具有一定疗效,可以改善患者生命质量,且可有效降低患者血清VEGF水平,提示VEGF有可能成为判断疗效及疾病进展的重要指标之一。     

贝伐珠单抗联合地塞米松治疗脑胶质瘤放疗后瘤周脑水肿效果的初步对照研究

目的比较贝伐珠单抗联合地塞米松治疗脑胶质瘤放疗后瘤周脑水肿(PTBE)临床效果。方法选取我院2020年3月至2022年12月收治的54例脑胶质瘤放疗后PTBE患者进行回顾性研究, 将患者按随机数字表法随机分为两组, 各27例。对照组采用地塞米松治疗, 研究组在此基础上加用贝伐珠单抗治疗。比较两组疗效, QLQ-C30与MoCA评分, 脑水肿带的平均宽度、指数、体积和不良反应。结果治疗6周后, 研究组总有效率高于对照组(85.19%∶59.26%, P<0.05)。研究组QLQ-C30与MoCA评分高于对照组[(30.61±4.21)分∶(17.23±3.79)分与(24.32±2.78)分∶(16.45±2.71)分, 均P<0.05], NIHSS评分、脑水肿带平均宽度、指数、体积低于对照组[(6.54±1.23)分∶(9.04±1.11)分、(2.87±0.41)cm∶(3.24±0.37)cm、(5.53±1.51)分∶(7.35±1.47)分、(130.02±39.89)cm3∶(231.46±42.71)cm3, 均P<0.05]。两组不良反应总发生率相近(...     

贝伐珠单抗在恶性脑水肿治疗中的应用

以贝伐珠单抗为主的抗血管生成药物通过减少血管通透性和血脑屏障破坏,能有效减轻恶性脑水肿,缓解临床症状,改善患者生命质量。贝伐珠单抗在治疗恶性脑水肿方面取得了积极的疗效,因此被认为是治疗恶性脑水肿的一种安全、有效的治疗手段。     

贝伐珠单抗联合紫杉醇治疗复发性卵巢癌疗效分析

目的 观察贝伐珠单抗联合紫杉醇治疗复发性卵巢癌的疗效和不良反应.方法 35例复发性卵巢癌患者应用贝伐珠单抗联合紫杉醇作为二线或多线治疗.结果 35例患者均可进行疗效评价,有效率为54.29%,疾病控制率为82.86%.不良反应主要有骨髓抑制、恶心呕吐、高血压、蛋白尿等,大多为轻度.结论 贝伐珠单抗联合紫杉醇治疗复发性卵巢癌安全有效,患者可耐受,是复发性卵巢癌可选择的治疗方案之一.     

贝伐珠单抗治疗放射性脑坏死研究进展

放射性脑坏死是原发性或继发性脑肿瘤以及头颈部肿瘤放疗后的严重晚期、不可逆的并发症,尚无有效的治疗方法。近几年来,贝伐珠单抗越来越多地被用于放射性脑坏死的治疗,并确定有一定疗效,可以改善患者生存,但关于最佳治疗时机、方案等一直存在争议,缺乏基本共识,本文就这方面研究进展进行简要回顾。     

贝伐珠单抗治疗放射性脑坏死研究进展

放射性脑坏死是原发性或继发性脑肿瘤以及头颈部肿瘤放疗后的严重晚期、不可逆的并发症,尚无有效的治疗方法。近几年来,贝伐珠单抗越来越多地被用于放射性脑坏死的治疗,并确定有一定疗效,可以改善患者生存,但关于最佳治疗时机、方案等一直存在争议,缺乏基本共识,本文就这方面研究进展进行简要回顾。     

贝伐珠单抗治疗恶性腹腔积液的研究进展

恶性腹腔积液是晚期肿瘤患者常见的并发症,不仅严重影响患者的生活质量,还提示预后较差.目前针对恶性腹腔积液的全身治疗有限盐利尿、补充白蛋白、治疗原发肿瘤等,还有在此基础上进行腹腔穿刺引流及腹腔药物灌注等局部治疗.血管内皮生长因子(VEGF)是恶性腹腔积液形成的关键介质,其主要通过调节血管生成,增加血管通透性来诱导腹腔积液...     

贝伐珠单抗治疗脑胶质瘤及放射性脑坏死

贝伐珠单抗作为全球第一个抗血管生成的单克隆抗体,获得美国食品和药物管理局批准用于胶质母细胞瘤的挽救治疗,之后贝伐珠单抗治疗恶性胶质瘤成为研究的焦点,但最新研究结果并不支持其在恶性胶质瘤的一线治疗中应用.另外,该药在放射性脑坏死的治疗上也取得令人鼓舞的效果,确切疗效有待进一步证实.     

一氧化氮与脑膜瘤瘤周水肿的关系

目的　探讨一氧化氮 (NO )在脑膜瘤组织中的含量及其与影像学上瘤周水肿的相互关系。方法　采用Griess试剂间接测定 2 6例脑膜瘤患者瘤组织中NO含量 ,根据CT扫描结果估计瘤周水肿的程度。结果　脑膜瘤中NO含量明显高于对照组 ,P <0 .0 1;NO含量与瘤周水肿程度呈正相关关系 ,r =0 .45 3 ,P <0 .0 5。结论　NO在脑膜瘤中高水平表达 ,与瘤周水肿的形成有关 ,与脑膜瘤的生物学特征紧密相关。     

Low-dose bevacizumab as an effective pre-treatment for peri-tumoral brain edema prior to CyberKnife radiosurgery: A case report

A 75-y-old Chinese female patient diagnosed with lung adenocarcinoma with brain metastasis suffered severe nausea and vomiting, and these symptoms were contraindications for CyberKnife treatment. Neither mannitol, nor dexamethasone, relieved the symptoms. However, after the patient received a single dose of bevacizumab (200 mg, 2.9 mg/kg), the patient's symptoms were significantly relieved. The patient subsequently completed a successful CyberKnife treatment. In addition, the patient received an oral treatment of gefitinib. At 15 months post treatment, the patient's brain tumor was controlled. Thus, administration of bevacizumab at a low dose (2.9 mg/kg) may significantly alleviate peri-tumoral brain edema and its symptoms, thereby facilitating radiosurgery treatment.     

奥希替尼联合贝伐珠单抗治疗14例EGFR突变型肺腺癌脑转移的疗效观察

目的:观察和评估奥希替尼联合贝伐珠单抗治疗14例EGFR突变型肺腺癌脑转移患者的疗效及安全性.方法:回顾性分析2017年1月至2019年12月广州市胸科医院收治的伴有EGFR突变的肺腺癌脑转移患者共14例,所有患者均给予奥希替尼及贝伐珠单抗联合治疗,每3周为1个周期,观察其脑转移病灶疗效并评估不良反应.结果:14例患者...     

A feline model for experimental studies of peritumor brain edema

Summary An in vivo model for correlative imaging studies of intracerebral glial tumors and peritumor brain edema has been developed. Adult male and female cats implanted with 1 × 10⁶ or 5 × 10⁵ 9L glioma cells had parietal tumors of 4 mm or greater in diameter and showed signs of increased intracranial pressure 13.7±1.9 days or 19.2±1.3 days after implantation. No immunosuppression was required and the success rate for tumor growth after implantation was 88%. Histologically, the tumor resembles a malignant astrocytoma.The tumor contained the highest water content (85.94%); peritumor white matter was more edematous (73.01%) than white matter in the contralateral hemisphere (69.04%), sham-operated (69.41%) and control brain (68.76%). There was no correlation between the size of the tumor and water content in tumor or white matter. Increased tissue albumin in peritumor white matter indicated blood-brain barrier dysfunction within the tumor and confirmed the vasogenic origin of the edema.Proton magnetic resonance imaging provided good spatial and contrast resolution with increased signal intensity in edematous white matter, decreasing with distance from the tumor. The large brain of this animal model allows the use of serial imaging and regional correlative biochemical measurements in a single animal. Other advantages of this model are its predictability and the short time required to produce tumors with marked peritumor edema.     

抗血管生成药物治疗恶性脑水肿的研究进展

抗血管生成药物通过减少血管通透性和血脑屏障破坏,能有效减轻恶性脑水肿,缓解临床症状,改善患者生命质量。目前多种抗血管生成药物在治疗恶性脑水肿方面取得了积极的疗效,因此被认为是较糖皮质激素治疗恶性脑水肿更为安全、有效的治疗手段。     

超选择性颅内动脉灌注贝伐珠单抗治疗复发恶性脑胶质瘤的疗效及安全性

目的:观察超选择性颅内动脉灌注贝伐珠单抗治疗复发恶性脑胶质瘤的疗效及安全性。方法:纳入2017年10月至2020年11月在我院神经外科接受超选择性颅内动脉灌注贝伐珠单抗治疗的11例复发恶性脑胶质瘤患者,观察治疗后的无进展生存期、Karnofsky评分及不良反应,随访终点为肿瘤再次出现复发或转移。结果:经2个周期治疗后,11例复发恶性脑胶质瘤患者的疾病控制和客观反应人数分别为10例和8例,患者Karnofsky评分较治疗前显著提高(P<0.05)。中位无进展生存时间为6个月,11例患者中有1例出现皮肤过敏,1例患者出现白细胞减少。结论:采用超选择性颅内动脉灌注贝伐珠单抗治疗复发恶性脑胶质瘤安全、有效,值得临床进一步推广应用。     

Effects of glucocorticoid and chemotherapy on the peritumoral edema and astrocytic reaction in experimental brain tumor

To study the effects of glucocorticoids and chemotherapeutic agents on the pathophysiology of the tumor-induced brain edema, the site of Evans blue-albumin extravasation, the distribution of extravasated serum albumin, and the extent of local astrocytic reaction were examined in a rat model of implanted brain tumor. Experimental brain tumors were produced by implanting small pellets of Walker 256 carcinosarcoma into the cerebral cortex of Wistar rats. In the steroid group, rats were administered with intraperitoneal methylprednisolone succinate (15 mg/kg) daily on and after the 6th day postimplantation, and sacrificed on the 14th day. In the chemotherapy group, rats were given an intravenous injection of cyclophosphamide (30 mg/kg) on the 14th day, and sacrificed on the 21st day. Rats in the untreated group were sacrificed on the 14th day without any therapy. Each animal was sacrificed by the transcardiac perfusion with paraformaldehyde 30 min after intravenous injection of Evans blue. Firstly, coronal blocks of the brain were examined for Evans blue staining macroscopically. Paraffin embedded sections were studied for the Evans blue fluorescence and for the immunohistochemical reaction to serum albumin and GFAP. The examination of Evans blue demonstrated that the origin of extravasation of serum albumin was the tumor and the adjacent brain with dense tumor cell infiltration in any group of rats. The extravasated serum albumin distributed widely and the astrocytic reaction was prominent in the brain of the untreated group. A positive correlation was observed between the intensity of albumin immunoreaction and the degree of astrocytic proliferation. Chemotherapy effectively decreased the size of tumor and reduced the extravasation of serum albumin. The astrocytic reaction was however, not reduced. In the steroid group, the size of tumor was not significantly affected but the albumin extravasation as well as astrocytic reaction was markedly reduced. It was concluded that glucocorticoid is an effective drug against tumor-induced brain edema, which not only reduces the extravasation of serum components but also prevents histologic alterations of the brain.