阿达单抗继发于溃疡性结肠炎患者的凸出性蛛网膜下腔出血。

Lucrecia Bandeo, Astrid Rausch, Miguel Saucedo, Anibal Chertcoff, Luciana Leon Cejas, Claudia Uribe Roca, Sol Pacha, Manuel Fernandez Pardal, Ricardo Reisin, Pablo Bonardo
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引用次数: 0

摘要

TNF-α拮抗剂是用于治疗溃疡性结肠炎(UC)的药物。非外伤性蛛网膜下腔出血是一种罕见的非动脉瘤性蛛网膜下腔出血亚型,主要由可逆性脑血管收缩综合征(RCVS)、脑淀粉样血管病和后路可逆性脑病综合征(PRES)引起。我们报告一位26岁的女性患者,诊断为UC服用阿达木单抗。她在因急性严重UC恶化入住我院的同一天接受了最后一次剂量。在治疗中加入了类固醇。入院5天后,患者出现雷击式头痛、畏光、恶心和呕吐。MRI显示左侧额部蛛网膜下腔出血,t2加权和FLAIR序列显示位于双枕叶、左小脑半球和脑干的高强度病变。数字血管造影无显著差异。停用阿达木单抗,但仍坚持类固醇治疗。患者症状完全消退,出院时进行了正常的神经学检查。两个月后,她无症状,MRI显示继发于cah的浅表性铁质沉着,白质高信号消退。本例患者的凸出性蛛网膜下腔出血可能继发于PRES或RCVS。在这两种综合征中可以观察到类似的MRI表现,以及类似的临床和血管造影表现。这表明这两种情况可能反映了相同病理的不同表现,其中血管张力和内皮功能障碍起主要作用。据我们所知,这是首例与阿达木单抗相关的严重UC和凸出性蛛网膜下腔出血患者的报告。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Convexity Subarachnoid Hemorrhage Secondary to Adalidumab in a Patient with Ulcerative Colitis.

Convexity Subarachnoid Hemorrhage Secondary to Adalidumab in a Patient with Ulcerative Colitis.

Convexity Subarachnoid Hemorrhage Secondary to Adalidumab in a Patient with Ulcerative Colitis.

Convexity Subarachnoid Hemorrhage Secondary to Adalidumab in a Patient with Ulcerative Colitis.

The TNF-α antagonists are the drugs used for the treatment of ulcerative colitis (UC). Nontraumatic convexity subarachnoid hemorrhage is an infrequent nonaneurysmal subtype of subarachnoid bleeding caused mainly by reversible cerebral vasoconstriction syndrome (RCVS), cerebral amyloid angiopathy, and posterior reversible encephalopathy syndrome (PRES). We present a 26-year-old female patient with a diagnosis of UC taking Adalimumab. She received her last doses the same day she was admitted to our hospital for an acute severe UC exacerbation. Steroids were added to the treatment. Five days after admission she presented a thunderclap headache with photophobia, nausea, and vomiting. An MRI was performed showing left frontal convexity subarachnoid hemorrhage and hyperintense lesions on T2-weighted and FLAIR sequences located in both occipital lobes, left cerebellar hemisphere, and brainstem. Digital angiography was unremarkable. Adalimumab was discontinued but persisted on treatment with steroids. The patient evolved with complete resolution of her symptoms and was discharged with a normal neurological exam. Two months later, she was asymptomatic and her MRI revealed superficial siderosis secondary to cSAH with resolution of white matter hyperintensities. Convexity subarachnoid hemorrhage in our patient could be secondary to PRES or to RCVS. Analogous MRI findings can be observed in both syndromes, along with similar clinical and angiographic findings. This suggests that both conditions may reflect different manifestations of the same pathology, in which vascular tone and endothelial dysfunction play a major role. To our knowledge, this is the first report of a patient with severe UC and convexity subarachnoid hemorrhage associated with Adalimumab.

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