Durable medication-free remission of sarcoidosis following discontinuation of anti-tumor necrosis factor-α therapy

医学 中止 结节病 内科学 肿瘤坏死因子α 疾病 回顾性队列研究 抗体 皮质类固醇 免疫学 外科 胃肠病学
作者
Arthur M.F. Yee
出处
期刊:Respiratory Medicine [Elsevier]
卷期号:206: 107055-107055 被引量:3
标识
DOI:10.1016/j.rmed.2022.107055
摘要

Background Monoclonal antibodies against tumor necrosis factor-alpha (TNF-α) have been used successfully in the treatment of sarcoidosis, but optimal duration of their use is unclear. Published studies have consistently suggested that withdrawal of therapy typically results in prompt disease relapse. The aim of this study is to identify and characterize patients with sarcoidosis in whom medication-free disease remissions were induced and sustained following treatment with and subsequent discontinuation of anti-TNF-α antibodies. Methods A retrospective chart review was conducted to identify patients satisfying three criteria: (1) histopathological documentation of sarcoidosis; (2) disease remission induced by anti-TNF-α antibodies, since discontinued; and (3) subsequent maintained clinical, radiological, and laboratory remission for at least one year without ongoing immunomodulatory medications. Results Eight patients whose sarcoidosis remained in medication-free remissions were identified. The duration of remissions ranged from 22 to 132 months. All patients had previously had inadequate response to corticosteroid therapy and at least one steroid-sparing agent, prompting the use of anti-TNF-α antibodies. Before anti-TNF-α therapy was discontinued, all eight patients had been able to remain off systemic corticosteroid therapy for at least a year (range 12–130 months). Conclusions These observations suggest that in select sarcoidosis patients, anti-TNF-α antibodies may induce prolonged medication-free remissions. The sustained capacity to remain off corticosteroids during anti-TNF-α therapy may be a favorable prognostic indicator for maintained disease remission. These findings may help to develop principles for optimal utilization of these agents and to shed light onto the potential pathogenic role of TNF-α in this disease.
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