Alopecia areata

Management Strategy

There are presently no FDA-approved treatments for AA. Approach to management depends on a variety of factors, including patient age, extent and duration of hair loss, and impact on quality of life. Traditional therapeutic options include topical, intralesional and systemic corticosteroids, topical immunotherapy, and systemic immunomodulatory medications. While mild patchy disease often improves with topicals and/or intralesional corticosteroids, more severe AA is less likely to respond to these treatments. Janus kinase (JAK) inhibitors have recently emerged as an effective treatment for AA, and large clinical trials are presently underway.

Intralesional corticosteroids , most commonly triamcinolone acetonide, are considered first-line therapy for adult patients with limited, patchy AA. There is evidence that 2.5 mg/mL has similar efficacy to 5 mg/mL and 10 mg/mL concentrations. Injections are typically performed at 4–6-week intervals, with up to 40 mg administered per session. Side effects include skin atrophy, which is usually transient.

For patients who are unable to tolerate intralesional therapy, topical corticosteroids may provide some benefit. Superpotent topical corticosteroids such as clobetasol propionate are applied twice daily to affected areas and may be followed by an eventual taper once there has been regrowth.

Topical immunotherapy with contact sensitizers, including squaric acid dibutyl ester (SADBE) and diphenylcyclopropenone ( DPCP , also called diphencyprone), induces allergic contact dermatitis, which likely works by changing the immune milieu of the hair follicle. DPCP is a more stable compound than SADBE and more widely utilized. Patients are first sensitized with 2% DPCP to a localized area (e.g., 2 cm ² area on the buttock or hip) followed by weekly applications of increasing concentrations typically ranging from 0.001% to 0.1% until the patient develops mild erythema and pruritus, which is then maintained with repeated application of the same concentration solution. Side effects include generalized dermatitis and lymphadenopathy.

Janus kinase (JAK) inhibitors are an emerging treatment for patients with AA, with efficacy now described in numerous case reports, retrospective series, and open-label clinical trials. These small molecules, which variably target the JAK family of enzymes, disrupt signaling of IFN-γ and IL-15, which appear to be integral cytokines to AA pathogenesis. Tofacitinib and ruxolitinib have been most commonly used, with larger studies reporting that 50%–75% of patients experienced >50% scalp hair regrowth and 20%–66% patients experienced near-complete or complete regrowth. In adult patients, we typically start with tofacitinib 5 mg twice daily and consider increasing to 10 mg twice daily if there is not at least 25% scalp hair regrowth by 3–6 months. While JAK inhibitors are generally well tolerated, potential adverse events include serious infection, malignancy, and blood clots and therefore a thorough discussion of potential risks is important prior to initiating treatment. Large, placebo-controlled clinical trials investigating a variety of JAK inhibitors are now underway. While there have been reports of successful use of topical JAK inhibitors for AA, clinical trials have failed to show efficacy. Compounded topical preparations of tofacitinib or ruxolitinib in 1%–2% concentrations may be considered for the treatment of limited areas, such as the eyebrow regions or small areas on the scalp, or for patients in whom avoidance of systemic therapy is desired or appropriate.

Systemic corticosteroids are sometimes effective for the treatment of AA; however, there are significant risks associated with long-term treatment and relapse is common after discontinuation, and so routine use is not recommended. Pulsed therapy may be associated with less morbidity and may be useful for some patients experiencing rapidly progressive hair loss. Monthly doses of prednisone 5 mg/kg (maximum 300 mg) for 4–6 months may be considered; however, patients need to be counseled that hair growth may not be sustained.

Oral minoxidil monotherapy has been shown to lead to significant scalp hair regrowth in 18% of patients and may be synergistic with oral JAK inhibitors, and we use it commonly in the treatment of our patients, both as monotherapy and in combination with other treatments. The minoxidil dose we typically use is 2.5–5 mg once or twice daily. Topical minoxidil 5% is unlikely to yield improvement in AA when used as monotherapy, but it may be useful as an adjunctive therapy, such as with intralesional or topical corticosteroids or topical JAK inhibitors.