Abstract
We thank Dr. Avasarala for the questions on our article.1 The defining feature of sarcoidosis is granulomatous inflammation, a very different pathology than in multiple sclerosis (MS). As discussed in our article, tumor necrosis factor (TNF)-α is important for granuloma formation and maintenance, including in humans with sarcoidosis.2 Inhibition of TNF-α by infliximab is the postulated mechanism for its benefit in sarcoidosis and neurosarcoidosis. Differentiating suspected inflammatory-demyelinating lesions from granulomatous pathologies in the CNS is based on clinical phenotype, MRI appearance, and clinical context. TNF-α inhibitors have been shown to increase relapse risk in established MS3 and may be associated with CNS inflammatory-demyelinating events in rare instances.4
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