• Use of Tocilizumab led to symptomatic improvement in neuropathic pain, numbness and dysautonomia • Tocilizumab stopped the progression of debilitating SFN symptoms that continued with prior therapies • Tocilizumab may be useful in S-SFN patients who are refractory or intolerant to standard care Sarcoidosis-associated small fiber neuropathy (S-SFN) is frequently associated with chronic pain and poor quality of life. Tocilizumab is an anti-IL-6 receptor monoclonal antibody used to treat rheumatological conditions; however, its utility in S-SFN remains uncertain. This study aims to describe the clinical outcomes of three patients with S-SFN treated with tocilizumab. A retrospective chart review was conducted for three patients with S-SFN who were treated with tocilizumab at the Neurosarcoidosis Center at Johns Hopkins Hospital between 2014 and 2024. Demographic and clinical data were extracted and described. IRB approved the patient's chart review. Patient 1 : 54-year-old male with S-SFN causing severe refractory neuropathic pain and dysautonomia. No response shown to methotrexate and infliximab. Intolerance to IVIG due to aseptic meningitis. Subcutaneous tocilizumab was initiated at 162 mg every 7 days with improved pain. Patient 2 : 67-year-old female with S-SFN causing paresthesia and numbness in extremities and dysautonomia. Adalimumab was discontinued after anti-adalimumab antibody development; IVIG was suspended after superior mesenteric artery thrombosis. Subcutaneous tocilizumab was initiated at 162 mg every 14 days, improving numbness, neuropathic and gastrointestinal symptoms. Patient 3 : 61-year-old female with S-SFN causing neuropathic pain and dysautonomia. No response to corticosteroids, TNF-alpha inhibitors, mycophenolate, and methotrexate. Tocilizumab was initiated at 162 mg every 7 days, improving systemic symptoms, gastrointestinal dysmotility, and neuropathic pain. Tocilizumab may improve pain, gastrointestinal, and sensory symptoms in patients with S-SFN refractory to standard sarcoidosis immunosuppressive therapies. IL-6 may play a role in the underlying pathophysiology of S-SFN .
Aguilera-Pena et al. (Wed,) studied this question.
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