LAUSR

GA: granuloma annulare ILCS: intralesional corticosteroids JAK: Janus kinase NF-kB: nuclear factor kB NL: necrobiosis lipoidica p: phosphorylated STAT: signal transducer and activator of transcription INTRODUCTION Necrobiosis lipoidica (NL) is an idiopathic granulomatous disorder that causes plaques on the lower part of the legs that commonly ulcerate. Histologically, NL shows palisaded granulomatous inflammation horizontally layered within degenerated collagen and an associated lymphoplasmacytic infiltrate. Little is known about the molecular pathogenesis of NL, and no reliably effective therapies exist. In autoimmune granulomatous disorders, macrophage recruitment and activation appear to depend on T-cellederived cytokines including interferon gamma. Interference with such cytokine signals via blockade of the downstream Janus kinase (JAK) esignal transducer and activator of transcription (STAT) signaling pathway is a promising new treatment approach in disorders characterized by excessive macrophage activation. We and others have recently shown that JAK inhibitors are effective in treating sarcoidosis and granuloma annulare (GA). In 2018, Lee and English reported that a patient with ulcerative NL in the setting of polycythemia vera had marked improvement in the ulcerative component of her NL with ruxolitinib, a JAK1/2 inhibitor. Although provocative, it remains unclear how reproducible this effect is and whether JAK-STAT is activated in other cases of NL.