Staunton H, Stafford F, Leader M, O'Riordain D
Department of Neurosciences, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin.
Arch Neurol. 2000 Apr;57(4):581-4. doi: 10.1001/archneur.57.4.581.
Failure of response of giant cell arteritis (GCA) to corticosteroid therapy has invariably been attributed to the delay in diagnosing the disease or the use of inadequate corticosteroid dosage. Following our observation of progressive deterioration following the introduction of prednisolone use in a patient, we examined the possibility that worsening of the condition might be due to corticosteroid therapy rather than coincidence.
To determine whether corticosteroid therapy may exacerbate GCA. DESLGN: Case report and an analysis of similar cases reported in the medical literature.
A 64-year-old man had a 3-month history of headache, night sweats, malaise and general weakness, and anorexia and weight loss and a more recent history of jaw claudication, dysphagia, and hoarseness. Clinical findings included prominent temporal arteries with absent pulsation, abnormal saccades to the right, and eyelid retraction. Laboratory findings included an elevated erythrocyte sedimentation rate and platelet count. Results of a biopsy of the temporal artery confirmed GCA. Magnetic resonance imaging scans showed ischemic cerebellar lesions and a mature infarct in the left anterior occipital, posteroparietal region. Following corticosteroid therapy commencement, the patient's condition deteriorated steadily for 5 days with clinical signs suggestive of an evolving vertebrobasilar stroke. Following treatment with high-dose intravenous dexamethasone sodium phosphate and heparin sodium, his symptoms improved.
The review included analysis of autopsy-based reports in which clinical details are provided and clinical reports in which major visual or cerebral complications are described. Significant complications occurred in many cases shortly following the introduction of corticosteroid therapy. In many of these cases, the symptoms indicated that GCA had been present for a significant period prior to corticosteroid therapy.
Progressively evolving occlusive strokes may occur following corticosteroid therapy in patients with GCA. In cerebrovascular complications, vascular occlusion occurs at sites of active vasculitis, usually within the vertebrobasilar system. It is not certain that the worsening of the condition following corticosteroid therapy is always coincidental, and an alternative possibility, namely a functional relationship between the initiation of corticosteroid therapy and clinical deterioration, should be borne in mind.
巨细胞动脉炎（GCA）对皮质类固醇治疗无反应一直被归因于疾病诊断延迟或皮质类固醇剂量不足。在我们观察到一名患者使用泼尼松龙后病情逐渐恶化后，我们研究了病情恶化可能是由于皮质类固醇治疗而非巧合的可能性。
确定皮质类固醇治疗是否会加重GCA。
病例报告及对医学文献中报道的类似病例的分析。
一名64岁男性，有3个月的头痛、盗汗、不适、全身无力、厌食和体重减轻病史，近期有下颌跛行、吞咽困难和声音嘶哑病史。临床检查发现颞动脉明显且搏动消失、右眼异常扫视和眼睑回缩。实验室检查结果包括红细胞沉降率和血小板计数升高。颞动脉活检结果证实为GCA。磁共振成像扫描显示小脑缺血性病变以及左枕叶前部、顶叶后部的陈旧性梗死。开始皮质类固醇治疗后，患者病情持续恶化5天，临床体征提示椎基底动脉卒中进展。经大剂量静脉注射地塞米松磷酸钠和肝素钠治疗后，他的症状有所改善。
该综述包括对提供临床细节的尸检报告以及描述主要视力或脑部并发症的临床报告的分析。许多病例在开始皮质类固醇治疗后不久就出现了严重并发症。在许多这些病例中，症状表明在皮质类固醇治疗之前GCA已经存在了相当长的时间。
GCA患者在接受皮质类固醇治疗后可能会发生进行性发展的闭塞性卒中。在脑血管并发症中，血管闭塞发生在活动性血管炎部位，通常在椎基底动脉系统内。皮质类固醇治疗后病情恶化不一定总是巧合，应考虑另一种可能性，即皮质类固醇治疗的开始与临床恶化之间存在功能关系。
