Neuro-Behçet's disease (NBD) is a rare and potentially severe manifestation of Behçet's disease, frequently associated with poor neurological outcomes. Management relies on high-dose corticosteroids and immunosuppressive agents, yet a subset of patients develops rapidly progressive and treatment-refractory disease. We report the case of a 39-year-old man with Behçet's disease who presented with progressive neurological deterioration. Brain magnetic resonance imaging (MRI) revealed multiple inflammatory lesions involving the brainstem and cerebral hemispheres, with subsequent radiological progression despite intensive immunosuppressive therapy. Tocilizumab, an interleukin-6 receptor antagonist, was introduced as salvage treatment in the context of rapid disease worsening. Follow-up MRI demonstrated a striking regression of inflammatory lesions. However, this radiological improvement was not accompanied by clinical recovery, and the patient ultimately died due to severe systemic complications. This case illustrates a marked dissociation between radiological response and clinical outcome in severe, refractory neuro-Behçet's disease. While the imaging findings suggest a potential effect of IL-6 blockade on inflammatory brain lesions, they also underscore the limitations of radiological improvement as a surrogate marker of clinical benefit. This observation highlights the complexity of disease progression in NBD and the critical importance of early intervention and comprehensive systemic management.

2026-03-03·ESC Heart Failure

Immune checkpoint inhibitor myocarditis: when profound troponin elevation diverges from unremarkable imaging

Article

作者: Eijsvogels, Thijs M H ; van Rosendael, Philippe J ; Biesbroek, P Stefan ; Driessen, Roel S ; Slaats, Jeroen ; Selder, Jasper L ; Niessen, Hans W ; Lameris, Roeland ; Labots, Mariette ; Götte, Marco J

Abstract:

Background:

Immune checkpoint inhibitors (ICI) have revolutionized cancer treatment but are associated with serious immune-related adverse effects. Myocarditis is particularly concerning due to its unpredictable presentation, challenging diagnostics and high mortality.

Case Presentation:

An 82-year-old male with stage 3 melanoma developed pulmonary metastases and started treatment with an immune checkpoint inhibitor targeting PD-1. Two weeks later, he presented with progressive muscle weakness, diplopia, and respiratory difficulties. Laboratory tests revealed profoundly elevated cardiac troponin levels and electrocardiography showed new conduction abnormalities, which led to the diagnosis of ICI myocarditis. Together with his myositis and myasthenic crisis, the triple M syndrome was established. Echocardiography and cardiac magnetic resonance imaging (MRI) demonstrated preserved left ventricular function without clear signs of myocardial inflammation or fibrosis. Various potential causes of falsely elevated cardiac troponin results were carefully evaluated and excluded. Despite noninvasive ventilation and intensive immunosuppressive treatment, including high-dose corticosteroids, intravenous immunoglobulin, and an interleukin-6 receptor inhibitor, the patient’s condition deteriorated, resulting in respiratory failure and death 12 days after admission. Post-mortem examination revealed histologic confirmation of immune mediated myocarditis with small foci of myocardial inflammation and necrosis not detected on imaging.

Conclusions:

This case highlights the complexity of diagnosing ICI myocarditis, particularly when biomarker elevations do not correlate with imaging findings. It raises critical considerations about the interpretation of cardiac biomarkers in immune-related adverse events and challenges the current interpretation of cardiac MRI for diagnosing ICI myocarditis. A multidisciplinary approach is essential for optimal patient care in this emerging area of cardio-oncology.

2026-03-01·DRUGS & AGING

Switching from Originator Tocilizumab to Biosimilar in Giant Cell Arteritis: Evaluation of Effectiveness and Safety in a Multicenter Cohort of 38 Patients

Article

作者: Silva-Díaz, María Teresa ; Labrador, Eztizen ; Molina-Collada, Juan ; Sánchez-Lucas, Marina ; Nieto, Juan Carlos ; Loricera, Javier ; Ferraz-Amaro, Iván ; Moya, Patricia ; Blanco, Ricardo

BACKGROUND:

Tocilizumab (TCZ) is an interleukin-6 receptor inhibitor approved for the treatment of giant cell arteritis (GCA). Biosimilars of TCZ, such as TYENNE™, are biologic agents which are similar to the originator (RoACTEMRA™) in structure, efficacy, and safety. Many indications, including GCA, are extrapolated from pivotal trials in rheumatoid arthritis (RA), supported by pharmacological similarity and immunogenicity data.

OBJECTIVE:

The objective was to evaluate the effectiveness and safety of switching from originator TCZ (RoACTEMRA™) to biosimilar TCZ (TYENNE™) in patients with GCA managed in routine clinical practice.

METHODS:

This observational, retrospective, multicenter, real-world study included patients with GCA who switched from RoACTEMRA™ to TYENNE™. Outcomes assessed included clinical and laboratory parameters of disease activity, complete remission, glucocorticoid burden, and safety profile. Comparisons were performed at baseline, 3 months, and 6 months. Linear mixed models and mixed-effects logistic regression were used to assess differences across follow-up visits.

RESULTS:

A total of 38 patients (68.4% female; mean age 74.1 years) were included. GCA phenotypes comprised cranial (n = 14; 36.8%), extracranial (n = 14; 36.8%), and mixed presentation (n = 10; 26.3%). Prior exposure to RoACTEMRA™ averaged 36.3 ± 28.4 months. Subcutaneous TCZ was administered in 32 patients (84.2%), while 6 received intravenous therapy. At the time of switch, 92.1% were clinically asymptomatic and 81.6% met criteria for complete remission. TYENNE™ was used as monotherapy in 34 patients (89.5%) and in combination with methotrexate in 4 patients (10.5%). Treatment regimens were preserved in all but one patient who was receiving originator TCZ at a dose of 4 mg/kg every 6 weeks, in whom the dosing interval was spaced from 6 to 8 weeks. After a mean follow-up of 8.2 ± 3.1 months, no significant differences were found in complete remission rates, daily prednisone dose, or inflammatory markers respect to baseline. Retention of biosimilar TCZ was 94.7%. TCZ dosing intervals were extended in four patients (10.5%), and treatment was discontinued in one patient owing to sustained remission. No disease relapses occurred. One patient developed herpes zoster, and another discontinued biosimilar TCZ following diagnosis of diverticulosis.

CONCLUSIONS:

Switching from originator TCZ (RoACTEMRA™) to biosimilar TCZ (TYENNE™) appears to be safe and effective in patients with GCA in routine clinical practice.

项与 Interleukin-6 receptor(Tosoh Corp.) 相关的新闻（医药）

2026-04-08

·网易号

从瘫痪在床到再获行走：一例NMOSD患者经萨特利珠单抗维持治疗实现功能重塑

*仅供医学专业人士阅读参考NMOSD快速进展，在2个月内致患者四肢瘫痪，如何通过维持治疗来阻断复发、挽救功能？视神经脊髓炎谱系疾病（neuromyelitis optica spectrum disorders, NMOSD）是一种自身免疫介导的以视神经和脊髓受累为主的中枢神经系统炎症性疾病。其发病机制与水通道蛋白-4的自身抗体免疫球蛋白G（AQP4-IgG）密切相关[1]。该病以视神经炎和纵向延伸的长节段横贯性脊髓炎为典型临床特征，具有复发率高、致残率高的特点。NMOSD的每一次临床发作均可能导致不可逆性神经损伤，反复发作后神经功能缺损的逐步累积可导致患者严重残疾[1]。因此，患者一经确诊，应尽早启动以预防复发为目的的序贯治疗，并坚持长期规范管理[1]。本期报告一例29岁女性患者的诊疗过程。该患者以右手麻木起病，在2个月内快速进展为四肢无力、无法站立。经系统检查确诊为AQP4-IgG阳性的NMOSD。在急性期，经大剂量激素冲击联合免疫球蛋白治疗后，病情得到部分控制；为预防复发、避免残疾进展，后续使用了萨特利珠单抗进行维持治疗。随访1年，患者不仅未再复发，神经功能得到显著改善，从无法站立恢复至可独立行走300米，基本恢复至正常生活，印证了高效靶向维持治疗在改善NMOSD患者远期预后中的重要价值。病例介绍基本信息：患者女，29岁。主诉：右手麻木2月余，四肢麻木无力2月。现病史：患者2月余前无明显诱因出现右手麻木，不伴肢体无力。2月前，症状迅速进展，出现四肢麻木无力，右侧为著，右手精细活动差，右下肢无力进行性加重，勉强站立，搀扶下可行走，胸部以下感觉减退，束带感明显。1月余前，病情进一步恶化，出现站立不能，右上肢持物困难。就诊于外院，MRI检查显示脊髓内较广泛异常信号，中枢神经系统脱髓鞘疾病自身抗体4项检查显示AQP4-IgG 1:320+，诊断为“视神经脊髓炎”。给予人免疫球蛋白、大剂量激素冲击治疗后，四肢无力症状较前稍缓解。发病以来，患者精神状态差，小便正常，便秘。图1 患者在外院行颈椎及胸椎增强MRI显示，枕骨大孔-颈2椎体水平、颈4-胸腰髓内见条片状稍长T2信号，增强扫描颈5椎体水平脊髓病变内见条片状轻中度强化，余部分病灶未见强化既往史及家族史：无高血压、糖尿病等特殊病史，家族史无特殊。入院检查：查体显示，患者神志清楚，高级神经活动正常，颅神经阴性。左上肢肌力4级，左下肢肌力3级，右上肢肌力3+级，右下肢肌力2级，双下肢肌张力增高。双上肢腱反射稍减弱，双下肢腱反射亢进，双侧巴氏征及Chadock征阳性。胸6平面以下感觉减退。无法独立行走。扩展残疾状态量表（EDSS）评分：8分。治疗方案：在激素减量过程中，启动萨特利珠单抗治疗，在第0、2和4周进行前三次皮下注射给药，每次120mg，之后每4周给予一剂120mg维持剂量。随访结果：应用萨特利珠单抗1年内，患者未再出现复发，且无药物相关不良反应。神经功能逐步改善。4个月后肢体麻木无力明显减轻，可独立行走100米。1年后可独立行走300米，基本恢复至正常工作生活。查体示双上肢及左下肢肌力5-级，右下肢肌力4+级，双小腿及双足感觉稍减退。AQP4-IgG滴度降至1:32，EDSS评分降至4.5分。图2 患者启动萨特利珠单抗维持治疗后EDSS评分变化病例讨论NMOSD的急性脊髓炎可造成严重的运动、感觉及自主神经损害，且每一次发作都可能带来不可逆的神经功能累积性损伤[1]。研究表明，女性、育龄期、脊髓长节段受累、AQP4抗体阳性、血清白细胞介素-6（IL-6）水平升高等因素，提示患者未来复发风险较高[2]。本例患者为育龄期女性，AQP4抗体滴度高达1:320，脊髓病变累及多个节段，且病程进展极为迅速，2个月内即从单侧手部麻木进展至四肢瘫痪、无法站立，EDSS评分达8分，属于高活动性、高复发风险人群。因此，尽早启动序贯治疗并坚持长期维持，对于延缓疾病进展、预防不可逆残疾具有重要意义。基础研究表明，细胞因子IL-6在NMOSD的发病机制中扮演了关键角色，阻断IL-6信号通路成为控制疾病活动的关键策略[3]。作为一种抗IL-6R单克隆抗体，萨特利珠单抗可以全面、精准、高效、持久地抑制NMOSD的核心关键环节，阻断IL-6介导的异常自身免疫激活，包括初始T细胞向辅助性T细胞17（Th17）分化所致的Th17/调节性T细胞（Treg）失衡、B细胞分化为浆母细胞以及致病性AQP4抗体的产生，还能有效遏制血脑屏障与血眼屏障的破坏、中枢神经系统炎性细胞浸润及脱髓鞘等关键病理过程[4]。长期随访研究（SAkuraMoon）结果显示，AQP4抗体阳性的NMOSD患者接受萨特利珠单抗维持治疗，456周（8.8年）时年复发率（ARR）仅有0.07（95%CI：0.05-0.10），89%的患者（95%CI：80%-94%）无严重复发，82%（95%CI：72%–89%）保持无持续EDSS恶化[5]。在该研究中，萨特利珠单抗中位暴露时间长达6.9年，为患者接受萨特利珠单抗治疗的最长时间超过11年，这也是迄今为止NMOSD靶向生物制剂领域中随访时间最长的临床试验，为萨特利珠单抗的长期应用提供了有力支持。本例患者在急性期治疗后，于激素减量过程中平稳过渡至萨特利珠单抗维持治疗。随访1年，患者不仅未再复发，神经功能亦获得显著改善，AQP4-IgG滴度大幅下降，EDSS评分从8分降至4.5分。这一结果充分说明，对于AQP4抗体阳性NMOSD患者，早期启用萨特利珠单抗进行维持治疗，可通过有效预防复发、避免新发神经功能缺损的累积，为神经功能的稳定与改善提供关键保障。专家述评本例患者病程进展迅速，从单侧手部麻木发展至四肢瘫痪、无法站立，仅历时2个月，EDSS评分高达8分。此类患者若仅依赖急性期激素及免疫球蛋白治疗，虽可暂时控制病情，但复发风险极高，且每一次复发均可能导致不可逆的神经功能累积性损害。该病例的诊疗过程具有重要的临床借鉴意义。在急性期治疗后，及时、平稳地序贯至靶向药物维持治疗，是实现减少复发、改善预后的关键。本病例中，萨特利珠单抗的启用时机合理，与激素减量过程良好衔接。随访1年显示，患者不仅无复发，神经功能亦从无法站立恢复至独立行走300米，EDSS评分下降3.5分。这表明，通过萨特利珠单抗有效预防复发，避免了新发神经功能缺损的累积，为神经功能的稳定与改善创造了良好条件。萨特利珠单抗作为一种抗IL-6R单克隆抗体，其机制优势在于从源头抑制IL-6介导的异常免疫激活，全面减少AQP4抗体的产生。长期随访数据证实其具有持久的疗效与良好的安全性，为NMOSD患者提供了可靠的维持治疗选择。本病例的实践也进一步提示，对于AQP4-IgG阳性且疾病活动性较高的患者，早期启用萨特利珠单抗，有助于实现“预防复发、避免残疾累积”的治疗目标，为患者的长期功能维持与生活质量改善带来切实获益。专家简介刘洪波教授郑州大学一附院神经内科副主任二级教授主任医师医学博士博士生导师中华医学会神经病学分会神经免疫学组委员中国医师协会神经内科分会神经免疫学组委员中国免疫学会神经免疫分会常务委员中国卒中学会免疫分会常务委员中国神经科学学会神经免疫学分会委员河南省免疫学会神经免疫分会主任委员河南省研究型医院学会神经免疫与感染分会副主任委员专家简介刘举教授郑州大学第一附属医院，神经内科，博士、副主任医师中国医药教育协会神经免疫专委会委员河南省免疫学会神经免疫专业委员会常委兼秘书河南省医学会神经病学神经免疫学组委员河南省医师协会神经免疫学组委员河南省研究型医院学会神经免疫与感染专委会委员河南省卒中学会神经免疫分会秘书调研问题参考文献：[1]中华医学会神经病学分会神经免疫学组.中国视神经脊髓炎谱系疾病诊断与治疗指南（2025版）[J]. 中华神经科杂志, 2025, 58(7): 687-703.[2] Ma X, Kermode AG, Hu X, et al. Risk of relapse in patients with neuromyelitis optica spectrum disorder: Recognition and preventive strategy. Mult Scler Relat Disord. 2020 Nov;46:102522.[3]Meher BR, Mohanty RR, Dash A. Review of Satralizumab for Neuromyelitis Optica Spectrum Disorder: A New Biologic Agent Targeting the Interleukin-6 Receptor. Cureus. 2024 Feb 27;16(2):e55100.[4]Fujihara K, Bennett JL, de Seze J,et al. Interleukin-6 in neuromyelitis optica spectrum disorder pathophysiology. Neurol Neuroimmunol Neuroinflamm. 2020 Aug 20;7(5):e841.[5]Bennett JL, Fujihara K, Saiz A, et al. Long-Term Efficacy and Safety of Satralizumab in Patients With Neuromyelitis Optica Spectrum Disorder From the SAkuraMoon Open-Label Extension Study. Neurol Neuroimmunol Neuroinflamm. 2025 Sep;12(5):e200450.*“医学界”力求所发表内容专业、可靠，但不对内容的准确性做出承诺；请相关各方在采用或以此作为决策依据时另行核查。

100 项与 Interleukin-6 receptor(Tosoh Corp.) 相关的药物交易

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