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[How long should treatment with tocilizumab be carried out for giant cell arteritis and how should it be ended (discontinue/taper off)?]
[对于巨细胞动脉炎,应该进行多长时间的托珠单抗治疗,应该如何结束 (停止/逐渐减少)?]
- 影响因子:25.02
- DOI:10.1007/s00393-020-00947-4
- 作者列表:"Henes J
- 发表时间:2021-03-01
Abstract
:The revised S2 guidelines for treatment of giant cell arteritis have recently been published. Glucocorticosteroids remain the standard first line treatment. For severe or relapsing courses of the disease, the IL‑6 antagonist tocilizumab, a potent antibody, is now available as a therapeutic option; however, how long this treatment should be continued after having achieved a stable remission remains a matter of discussion. For patients with a complicated course and a high risk of relapse, a continuous treatment would be the safest way; however, with a milder course of disease for approximately half of the patients, treatment without relapse can be discontinued again. ZUSAMMENFASSUNG:Gerade eben wurden die neuen S2-Leitlinien zur Behandlung der Riesenzellarteriitis publiziert. Weiterhin bleibt die Glukokortikosteroidtherapie Standardtherapie. Bei schwereren Verläufen und Rezidiven steht uns mit dem IL(Interleukin)-6-Antagonisten Tocilizumab eine potente Antikörpertherapie zur Verfügung. Wie lange diese Therapie nach Erreichen einer stabilen Remission allerdings fortgesetzt werden muss/soll, ist bis jetzt nicht geklärt. Bei komplikativen Verläufen und hohem Rezidivrisiko sollte eine Dauertherapie durchgeführt werden. Bei milderem Verlauf kann jedoch bei knapp der Hälfte der Patienten die Therapie ohne Rezidiv auch wieder beendet werden.
摘要
: 最近发布了经修订的S2巨细胞动脉炎治疗指南。糖皮质激素仍然是标准的一线治疗。对于严重或复发的疾病,il-6拮抗剂tocilizumab是一种有效的抗体,现在可以作为一种治疗选择; 然而,在达到稳定缓解后,这种治疗应该持续多久仍然是一个讨论的问题。对于病程复杂且复发风险高的患者,连续治疗将是最安全的方式; 然而,对于大约一半的患者,病程较轻,可以再次停止无复发的治疗。 ZUSAMMENFASSUNG: 杰拉德·埃本·沃登·迪恩·S2-Leitlinien·祖尔·贝汉德隆来自雷森泽拉动脉炎。Weiterhin bleibt死Glukokortikosteroidtherapie标准疗法。6-对抗Tocilizumab eine anti kö rpertherapie zurf ü gung.Wie lange diese Therapie nach Erreichen einer stabilen Remission allerdings fortgesetzt werden muss/soll, ist bis jetzt nicht geklärt.Bei komplikativen Verläufen und hohem Rezidivrisiko sollte eine Dauertherapie durchgeführt werden.Bei milderem Verlauf kann jedoch bei knapp der Hälfte der Patienten die Therapie ohne Rezidiv auch wieder beendet werden.
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METHODS::Purpose: To report on ocular Vogt-Koyanagi-Harada (VKH)-like syndrome under vemurafenib treatment for metastatic melanoma.Design: A case report.Method: Description of clinical and imaging manifestations including fundus photography, fluorescein, and indocyanine green angiography.Results: A 46-year-old Thai female was diagnosed with metastatic melanoma of the skin and had been treated with multiple surgical excisions, radiotherapy, and vemurafenib (initial dose 480 mg orally twice daily, subsequently increased to maximum dose of 960 mg twice daily). After 6 months of vemurafenib use, she complained of bilateral redness and photophobia and was diagnosed with bilateral anterior uveitis, which was topically treated. Two weeks later, her visual acuity (VA) sharply deteriorated to 20/80 and counting fingers. Ocular examination at that stage stronly resembled acute VKH disease. She exhibited intraocular inflammation, and her fundus examination revealed bilateral optic disc swelling and serous retinal detachment. Fluorescein angiogram showed disc leakage and multiple pinpoint hyperfluorescence leakage spots and indocyanine green demonstrated multiple hypofluorescent spots. Oral prednisolone 30 mg/day was commenced while vemurafenib medication was ceased. Three weeks later, her vision improved, and serous retinal detachment subsided. However, her cutaneous melanoma recurred.Conclusions: Vemurafenib, a potential adjunct treatment for metastatic melanoma, was complicated by the development of panuveitis, papillitis, and multiple serous detachments. These ocular symptoms were similar to the presentation of acute VKH syndrome.
METHODS::Comprehensive reviews of the clinical characteristics and pathogenesis of Aicardi-Goutières syndrome (AGS), particularly its contextualization within a putative type I interferonopathy framework, already exist. However, recent reports of attempts at treatment suggest that an assessment of the field from a therapeutic perspective is warranted at this time. Here, we briefly summarize the neurological phenotypes associated with mutations in the seven genes so far associated with AGS, rehearse current knowledge of the pathology as it relates to possible treatment approaches, critically appraise the potential utility of therapies, and discuss the challenges in assessing clinical efficacy. WHAT THIS PAPER ADDS: Progress in understanding AGS disease pathogenesis has led to the first attempts at targeted treatment. Further rational therapies are expected to become available in the short- to medium-term.
METHODS::Purpose: To report the efficacy of adalimumab in a case of chronic Vogt-Koyanagi-Harada (VKH) disease refractory to conventional corticosteroids and immunosuppressive therapy and complicated by central serous chorioretinopathy (CSC).Case report: A 66-year-old woman diagnosed with VKH was treated with intravenous corticosteroids followed by oral corticosteroids and cyclosporine. However, systemic corticosteroids could not be tapered because of recurrent ocular inflammation and systemic complications (diabetes mellitus, moon face, bone weakness), while CSC appeared in both eyes. A diagnosis of chronic VKH resistant to medications complicated by corticosteroid-induced CSC was made. Systemic corticosteroids and cyclosporine were tapered and adalimumab initiated. Bilateral ocular inflammation and CSC were gradually reduced and visual acuity improved without any adverse effect. Twelve months after starting adalimumab monotherapy, no signs of active VKH and CSC were present.Conclusions: Adalimumab is one of the effective therapeutic options for refractory VKH disease complicated with corticosteroid-induced adverse effects.
神经系统自身免疫性疾病是以自身免疫细胞、免疫分子等攻击神经系统为主要致病机制的自身免疫性疾病。在免疫反应中,作用于神经系统自身抗原的致病抗体统称为神经系统自身抗体。