INTRODUCTION
Granuloma annulare (GA) is a benign, non-infectious cutaneous granulomatous disease with an estimated prevalence of up to 0.06% in the United States.1 It typically presents as skin colored to erythematous papules or plaques of circinate or annular configuration.2 There are multiple variants including localized, generalized, perforating, patch, and subcutaneous subtypes.2 The pathogenesis of the disease remains elusive. Current theories involve immunologic and cytokine receptor signaling responses. Newer research highlights GA as an immunologically driven condition elucidating the involvement of both Th1 and Th2 pathways as well as Th17 and Th22 axes and the Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathway.3,4 However, it is important to note that emerging studies may not consistently concur, and larger studies are needed to investigate the pathogenic arms involved in the disease process with the ultimate goal of streamlining treatment.
There are currently no Food and Drug Administration-approved therapies specifically for GA. Intralesional or topical cortico-steroids are considered first-line options.2 However, even our first-line treatment options do not offer consistent efficacy for all patients, and thus we must turn to second-line and third-line options whose efficacy are typically not supported by large, ran-domized controlled trials but rather anecdotal reports or trials with small sample sizes. These include, but are not limited to, biologic therapy, phosphodiesterase-4 inhibition, antimalari-als, antimicrobials, isotretinoin, methotrexate, pentoxifylline, phototherapy, sulphasalazine, and more recently, JAK inhibi-tors.2 Indeed, both oral and topical tofacitinib have recently been reported to be efficacious in treating GA, underscoring the immunologic mechanisms at play in the pathogenesis of the disease.3,5,6,7 Given the recent evidence implicating these immu-nologic mechanisms, including Th1, Th2, and Th17 pathways, in the pathogenesis of GA, we hypothesized that treatment with tapinarof cream 1% may improve GA symptoms.
Case Study
There are currently no Food and Drug Administration-approved therapies specifically for GA. Intralesional or topical cortico-steroids are considered first-line options.2 However, even our first-line treatment options do not offer consistent efficacy for all patients, and thus we must turn to second-line and third-line options whose efficacy are typically not supported by large, ran-domized controlled trials but rather anecdotal reports or trials with small sample sizes. These include, but are not limited to, biologic therapy, phosphodiesterase-4 inhibition, antimalari-als, antimicrobials, isotretinoin, methotrexate, pentoxifylline, phototherapy, sulphasalazine, and more recently, JAK inhibi-tors.2 Indeed, both oral and topical tofacitinib have recently been reported to be efficacious in treating GA, underscoring the immunologic mechanisms at play in the pathogenesis of the disease.3,5,6,7 Given the recent evidence implicating these immu-nologic mechanisms, including Th1, Th2, and Th17 pathways, in the pathogenesis of GA, we hypothesized that treatment with tapinarof cream 1% may improve GA symptoms.
Case Study
A 49-year-old healthy female presented with a long-standing history of GA with concomitant pruritus. The patient reported that the condition had been biopsy-proven in the past and had been present for a few years. Previous treatments included several courses of topical corticosteroids. These treatment courses provided intermittent relief, but she continued to experience frequent flares on the dorsal surface of her hand (Figure 1). She expressed interest in topical non-steroidal treatment due
