Treatment of Concomitant Alopecia Areata and Crohn's Disease in a Young Child With Tofacitinib: Case Report

Background:
TNF-α antagonists are often used to treat inflammatory bowel disease (IBD) such as Crohn’s disease (CD) and Ulcerative colitis (UC) and have been proven to have high efficacy rates. However, they have been implicated in the development of several adverse reactions including alopecia areata (AA), the effects of which can be both clinical and psychosocial especially in children. There have been multiple reports of patients developing AA with infliximab therapy. Some of which describe significant improvement or resolution of symptoms following the discontinuation of infliximab and initiation of topical treatment. Tofacitinib, a Janus kinase 3 inhibitor have been shown to block the downstream pathways in production of inflammatory cytokine in patients with AA. However there is a knowledge gap in efficacy of tofacitinib in children who have CD and AA. We present the youngest patient with CD and AA who responded well to tofacitinib. The aim of this case report is to describe that Janus Kinase 3 inhibitor can be used to not only treat the Alopecia Areata but also Crohn’s disease in children.
Methods:
This case reports describes a 12 yr old with ileocolonic CD who developed AA of the scalp secondary to infliximab treatment. The patient was diagnosed with CD at 9 years of age in May 2021 and started on infliximab infusions 5 mg/kg/day with good clinical response. Drug levels were within normal range with no antibody to infliximab. After 6 infusions every 8 weeks, the patient had some hair loss which has eventually progressed rapidly to bold spots in 6 months. She was diagnosed with AA by dermatologist. She had bald spots throughout the crown of scalp, R temporal and occipital areas. Her alopecia did not respond to topical treatments with fluocinonide for the scalp, followed by Clobetasol.
Results:
At the recommendation of her dermatologist, patient was transitioned from infliximab to tofacitinib 5 mg twice daily. Almost immediately, patient’s alopecia began to improve. She saw significant hair regrowth after 1 month and experienced complete resolution by 8 months. Her CD continued to be in clinical remission. She underwent upper and lower endoscopy with biopsies in 12/2023 which were normal.
Conclusions:
AA is an autoimmune disease mediates by cytotoxic T cell driven inflammation targeting hair follicles. Pediatric AA is the severe form of AA. Oral tofacitinib is a successful treatment for AA in adults and pediatric patients. Both Infliximab and CD itself may have precipitated AA in our patient. The development of AA following infliximab treatment and the timeline of the patient’s symptom resolution suggests that the patient’s alopecia likely developed secondary to her infliximab infusions. To our knowledge this is the youngest patient with concomitant CD and AA who responded well to tofacitinib. This case shows that tofacitinib should be considered for AA and CD in pediatric patients.