INTRODUCTION
Tofacitinib is a Janus kinase (JAK) 1-3 inhibitor first U.S. Food and Drug Administration (FDA) approved in 2012 for rheumatoid arthritis, with subsequent approval for psoriatic arthritis, ulcerative colitis, polyarticular course juvenile idiopathic arthritis, and ankylosing spondylitis in 2017, 2018, 2020, and 2021, respectively.1,2 In the last several years, oral tofacitinib has become an increasingly utilized treatment option for immune-mediated skin conditions such as alopecia areata (AA), vitiligo, plaque psoriasis, and atopic dermatitis; however, it is not FDA approved for these diseases.3,4 These conditions’ pathophysiology involves an interplay of cytokines and interleukins in which the JAK-signal transducer and activation of transcription (STAT) signaling pathway has a role.5
AA and vitiligo are largely TH1 and interferon-gamma driven diseases.6 In AA, CD8+ T cells produce interferon-gamma which leads to collapse of immune privilege and increased production of IL-15, propagating autoimmune destruction of the hair follicle.6 In vitiligo, an autoimmune disease in which melanocytes are destroyed resulting in de-pigmentation, interferon-gamma induces expression of the C-X-C motif in chemokine-10 (CXCL10) in immune cells, leading to melanocyte destruction and depigmentation.7 Notably, interferon-gamma mediates its effects through the JAK-STAT pathway.5,8 Due to the relationship between AA and vitiligo with interferon gamma and the JAK-STAT pathway, JAK inhibitors, such as tofacitinib, are an appropriate choice for targeted therapy of these conditions. In this case report, we present a patient with concomitant AA and non-segmental vitiligo who was treated with oral tofacitinib. The autoimmune components of both diseases and similar pathophysiology cause AA and vitiligo to occur together more often than one would expect by chance; with approximately 3-8% of patients with AA having concomitant vitiligo.9 The patient in this report attempted multiple different treatment regimens with minimal improvement, however, upon initiation with tofacitinib, had moderate to significant improvement in both her AA and vitiligo, with no reported side effects.
AA and vitiligo are largely TH1 and interferon-gamma driven diseases.6 In AA, CD8+ T cells produce interferon-gamma which leads to collapse of immune privilege and increased production of IL-15, propagating autoimmune destruction of the hair follicle.6 In vitiligo, an autoimmune disease in which melanocytes are destroyed resulting in de-pigmentation, interferon-gamma induces expression of the C-X-C motif in chemokine-10 (CXCL10) in immune cells, leading to melanocyte destruction and depigmentation.7 Notably, interferon-gamma mediates its effects through the JAK-STAT pathway.5,8 Due to the relationship between AA and vitiligo with interferon gamma and the JAK-STAT pathway, JAK inhibitors, such as tofacitinib, are an appropriate choice for targeted therapy of these conditions. In this case report, we present a patient with concomitant AA and non-segmental vitiligo who was treated with oral tofacitinib. The autoimmune components of both diseases and similar pathophysiology cause AA and vitiligo to occur together more often than one would expect by chance; with approximately 3-8% of patients with AA having concomitant vitiligo.9 The patient in this report attempted multiple different treatment regimens with minimal improvement, however, upon initiation with tofacitinib, had moderate to significant improvement in both her AA and vitiligo, with no reported side effects.
CASE REPORT
A 49 year-old female presented to the clinic with a diagnosis of alopecia areata affecting her scalp, eyebrows, eyelashes, and body hair; as well as vitiligo affecting her left peri-oral area, left malar area, midline chest, bilateral forearms, and bilateral dorsal hands (approximately 10% BSA). She developed AA at the age of 21 and by the age of 32 had complete hair loss on her scalp. Since that time, she had cyclical flares of regrowth and complete hair loss, every two years. At her initial visit, hydrocortisone 2.5% cream daily, triamcinolone 0.1% cream
