JAK inhibitors are helping patients with alopecia areata, eczema/atopic dermatitis, psoriasis, and vitiligo. JAK inhibitors: A newer type of medication Find out how you can enjoy summer while reducing flare-ups. The sun, heat, and humidity can all trigger rosacea and lead to flare-ups. Hairstyles that pull can cause hair lossįeatured Reduce summertime rosacea flare-ups.Central centrifugal cicatricial alopecia.Although the sustainability of this treatment’s effects is still unknown,( 9) this is the first report of effective tofacitinib therapy in a patient with alopecia universalis in Korea.Diseases & conditions Everyday care Darker Skin Tones Cosmetic treatments Public health programs Find a dermatologist Go to AAD Homeĭermatologists team up to improve patient care Type I and II IFNs signal through cell surface receptors that initially activate JAKs, specifically JAK1 and either tyrosine kinase 2 (TYK2) or JAK2, respectively.( 4) Recently, an open-label clinical trial showed that the JAK inhibitor ruxolitinib, which has relative selectivity for JAK1 and JAK2, reversed the disease in three patients with moderate-to-severe AA.( 7) Another case report showed that treatment of alopecia universalis and psoriasis using tofacitinib resulted in a clinical response.( 5) JAK-family protein kinases are downstream effectors of the IFN receptor in keratinocytes their signalling mediates interlukin 15 activation of T-cells, which explains the effectiveness of JAK inhibitors for the treatment of AA.( 8) This class of drugs offers the convenience of being orally bioavailable when compared with biologic inhibitors of IFNs.( 4) JAK inhibitors are a promising class of drugs for treatment of AA. AA is known as a prominent abnormality in the IFN pathway. Small-molecule JAK inhibitors have been developed as novel therapeutic agents and are currently available for the treatment of myelofibrosis, rheumatoid arthritis and psoriasis. ![]() Photographs show (a) the patient’s scalp before treatment (b) some improvement with partial hair growth after two weeks of tofacitinib treatment (c) near complete regrowth of hair after six weeks of therapy and (d) full regrowth of hair after 32 weeks of therapy. The patient did not report any side effects such as herpes zoster. Laboratory monitoring showed no abnormalities in serum creatinine, electrolytes, glucose, complete blood count, hepatic function and lipid profiles. Following tofacitinib treatment, the patient had complete hair growth on her scalp, with no signs of recurrence of alopecia universalis. Scalp hair had fully regrown by 32 weeks of treatment ( Fig. Two weeks after starting treatment, the patient experienced a remarkable improvement in hair regrowth. The patient began treatment with tofacitinib 5 mg twice daily. The results of laboratory evaluations, including antinuclear antibody, rheumatoid factor, anti-Ro antibody, anti-La antibody and anti-double stranded DNA antibody, were all negative. On examination, she was found to have scant scalp hair with no eyebrows or facial hair, and no hair on her arms, legs, torso, axillae and groin. ![]() The patient’s medical history was unremarkable and she denied a family history of alopecia. Treatment with minoxidil, methotrexate and platelet-rich plasma injection had not been effective. She reported a history of AA, which started at about 20 years of age and progressed to alopecia universalis within three years. ![]() Recent research conducted in human subjects has identified several genes underlying AA.( 2, 3) Jabbari et al identified a prominent interferon (IFN) signature in AA, which signals through Janus kinase (JAK) molecules.( 4) Tofacitinib citrate, a novel small-molecule selective JAK 1/3 inhibitor for the treatment of moderate-to-severe rheumatoid arthritis, was approved by the Food and Drug Administration in late 2012.( 5) JAK inhibitors are emerging as potential therapies for many autoimmune conditions, including AA.( 6) We report a case of significant hair regrowth following treatment with oral tofacitinib citrate for alopecia universalis.Ī 28-year-old woman presented to us for management of alopecia universalis. Severe AA is known as alopecia universalis.( 1) AA may be secondary to an autoimmune reaction involving antibodies, T-cells and cytokine-mediated losses. Alopecia areata (AA) is a nonscarring form of alopecia that affects approximately 1.7% of the population.( 1) In this condition, loss of hair may be localised or widespread.
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