US Pharm. 2024;49(5):39-44.

ABSTRACT: Alopecia areata (AA), a nonscarring autoimmune-based hair disorder, has a lifetime incidence rate of up to about 2% and may affect psychological, emotional, and social realms. How AA occurs has not yet been fully elucidated, and currently no cure for this condition exists. Pharmacologic treatment options include oral Janus kinase inhibitors, intralesional or topical corticosteroids, topical minoxidil, anthralin, and contact immunotherapy. Pharmacists can play a role in AA management by participating in medication optimization and selection, evaluating regimens for potential drug-drug or drug-disease interactions, monitoring laboratory values, and assisting with dosing parameters; they can also counsel patients on appropriate use of medications.

Hair disorders extend beyond the commonly identified androgenetic alopecia. Alopecia is categorized as scarring (cicatricial), nonscarring, and structural. Scarring alopecia, an inflammatory scalp condition, leads to permanent hair loss because of the follicular damage it causes. Fragile or brittle hair that breaks easily or gives the appearance of failure to grow is structural alopecia. Alopecia areata (AA) is a form of autoimmune-mediated nonscarring alopecia that does not result in hair-follicle destruction. AA has a lifetime incidence of 1.7% to 2.1%, appears to increase linearly with age, and affects males and females at a similar rate.^1,2 In the United States, AA prevalence ranges from 0.199% to 0.22% overall and 0.09% for moderate-to-severe disease.^3-6

The impact of AA on health-related quality of life (QOL) may be significant, affecting psychological, emotional, or social realms. Assessment tools specific to AA have been validated.⁷ Factors affecting the impact of AA on QOL include stress, stress preceding onset of AA, age of onset, changes in social status (family stress and job changes), changes in physical appearance, and female sex.^2,8,9 The prevalence of depression and anxiety ranges from 25% to 60%.^2,8 In a study investigating stigmas surrounding individuals with alopecia, an evaluation of 2,017 completed surveys revealed that 45.8% of respondents had never heard of AA.¹⁰ Respondents identified persons with severe hair loss as sick (29.8%), unattractive (27.2%), contagious (9.9%), not intelligent (3.9%), and dirty (3.9%).¹⁰

HAIR CYCLE

Hair undergoes constant regeneration through a three-phase process that consists of the following (TABLE 1): anagen (growth), catagen (regression), and telogen (rest).^11,12 Up to 85% to 90% of the 80,000 to 150,000 hair follicles located in the scalp are in the anagen phase. The remaining follicles may be in the catagen phase (<1%) or in the telogen phase (≤10%).¹¹ Multiple immune modulators are involved in pigmentation and hair cycling. These include transforming growth factor (TGF)-beta, alpha–melanocyte-stimulating hormone (alpha-MSH), neurotrophins, melanocortins, nerve growth factor, and hepatocyte factor. Other factors involved include sex hormones (estrogens and androgens), stress mediators (cortisol, substance P, prolactin, and adrenocorticotropic hormone), and thyroid hormones.¹¹

Owing to inflammation, the telogen phase becomes more prominent in AA.¹³ How AA occurs has not yet been fully elucidated. One proposed mechanism is dysregulation of immune function at the hair follicle. Inhibition of TGF-beta and alpha-MSH may lead to secretion of interferon (IFN)-gamma and interleukin (IL)-15, which affect regulatory T-cell function and promote natural killer cell and T-cell proliferation, affecting the hair bulb.¹⁴

HAIR-LOSS EVALUATION

Given the multitude of hair-loss causes, the patient interview is important in evaluation and diagnosis. Pertinent information includes duration, rate, progression, location, and pattern of hair loss. Many types of alopecia are asymptomatic, with no itching, burning, pain, or tenderness noted. Washing frequency, chemical applications to the hair (e.g., bleaching or hair dye), and traction (ponytails, tight braids) can affect the hair shaft.¹²

Medical and family history may also play a role in hair loss. A genetic component has been postulated based on findings of a concordance rate of 10% in dizygotic twins and 42% in identical twins.¹⁵ Medical disorders that cause undue stress, such as major illness or surgery, can cause hair loss. Medications and significant dietary restrictions can affect hair loss or growth. Proposed environmental factors include psychological and physiologic stressors, infection, vaccinations, hormone fluctuations, and nutrition.¹⁶

A visual inspection should be performed to determine whether the alopecia is scarring or nonscarring and to determine scalp-hair distribution and density. The hair-shaft assessment will differentiate between androgenetic and structural hair loss. A handheld magnifier used to evaluate the scalp and hair (trichoscopy) may assist in determining the alopecia type. If scarring alopecia or structural alopecia is a concern, a confirmatory scalp biopsy may be performed.¹²

CLINICAL FEATURES OF ALOPECIA AREATA

Asymptomatic hair loss that presents as one or more oval or round skin-colored patches that are well demarcated and smooth is typical of AA.^13,14,16,17 Exclamation-point hairs are often found on the peripheral edge of the patch and occur primarily in acute versus chronic AA. Exclamation point hairs are shorter in length (3-4 mm) than regular hairs, and their proximal end is narrower than the distal end. Trichoscopy may identify yellow dots, black dots, and broken hairs.¹⁶ Subtypes of AA include alopecia totalis, in which hair loss affects the whole scalp, and alopecia universalis, which describes loss of all body hair. AA may involve a single occurrence of limited patchy hair loss or may be recurrent for long periods of time and progress through acute, subacute, and chronic stages.^13,14,16,17 Nail involvement is present in 7% to 66% of patients with AA. Nail pitting is most common, and the degree of involvement is higher in severe AA.^13,14,18

Scalp biopsies are not usually needed for diagnosis but may be performed for diagnostic confirmation. Guidelines do not specifically recommend any laboratory tests; however, thyroid-stimulating hormone, 25-hydroxyvitamin D, and ferritin levels may be useful in combination with a CBC to guide further evaluation and rule out other hair-loss disorders.¹³

PROGNOSIS

Spontaneous remission may occur within 1 year in up to 34% to 50% of patients, although many will experience multiple occurrences. Progression to alopecia totalis or universalis occurs in 14% to 25% of individuals, and <10% recover.^13,19 Factors that affect prognosis and increase the risk of poor prognosis include younger age of onset, severity and duration, nail involvement, family history, ophiasis (posterior and lateral scalp-hair loss), atopy, and concurrent autoimmune disorders.^13,14,16 Comorbid conditions seen with AA include atopy (allergic rhinitis, asthma, eczema), contact dermatitis, mental health disorders (anxiety and depression most common), hyperlipidemia, hypertension, anemia, gastroesophageal reflux disease, thyroid disease, diabetes mellitus, irritable bowel disease, systemic lupus erythematosus, rheumatoid arthritis, psoriasis/psoriatic arthritis, and vitiligo.^8,20

Treatment

At present, no cure exists for AA. Decisions on whether or not to treat and the type of treatment are often guided by severity, age, risk versus benefit, and patient preference. Although currently there is no definition of disease severity, the parameters >50% (severe) or <50% (limited, patchy) of scalp-hair loss are frequently used.^21,22 Nonpharmacologic options include camouflage with hairpieces such as wigs, toupees, demiwigs, and cascades. Hair extensions, braiding, hair additions, concealing powders, hair-thickening fibers, and styling products may also be used. Semipermanent options include scalp micropigmentation, and tattooing is a permanent option.²³

This article will focus on pharmacotherapy options for scalp AA. Pharmacologic options include topical and systemic therapies. Corticosteroids, contact immunotherapy, minoxidil, anthralin, cyclosporin, methotrexate, azathioprine, and sulfasalazine have been studied for AA, and more recently Janus kinase (JAK) inhibitors have been approved. There is a paucity of robust literature supporting the use of pharmacologic interventions for the treatment of AA. However, a 2023 meta-analysis found that JAK inhibitors such as baricitinib were effective in achieving ≥75% short-term and long-term hair regrowth compared with placebo, but the efficacy of other treatments was unclear.²⁴

Corticosteroids

Corticosteroids act by suppressing T cell–mediated attacks on the hair follicles.²⁵ Therapy options include intralesional, topical, and systemic corticosteroids, which are discussed below.

Intralesional Corticosteroids: This option is the mainstay of therapy for limited AA. Triamcinolone acetonide 2.5 mg/mL to 10 mg/mL at a volume of 0.1 mL may be injected into the dermis and/or subcutis of each patch of scalp AA, with a maximum total dosage of 10 mg to 20 mg per session. Injections should be separated by 1 cm. Hair-tuft growth of about 0.5 cm in diameter is anticipated to occur, and clinical improvement is expected within 2 to 6 weeks.^21,26,27 Sessions should occur no more than every 4 to 6 weeks, and treatment should be discontinued once growth is complete (or after 6 months if there is no response). Possible side effects include minor discomfort, scalp atrophy, and hypopigmentation.^21,22,26,27 Studies evaluating the efficacy of intralesional corticosteroid therapy indicate that up to 62% of patients will achieve hair regrowth; however, many studies have been small in size and of short duration.^{16,21,22,25,26,28}

Topical Corticosteroids: Topical scalp therapy with once-daily potent or ultrapotent corticosteroids can achieve hair regrowth in 6 weeks to 3 months in 30% to 57% of patients.^16,21 Topical corticosteroids should be considered in patients who cannot tolerate intralesional corticosteroids, and they are considered first-line therapy in children aged ≤12 years.^22,27 Beard and eyelash areas should be avoided because of concerns about skin atrophy.^22,27 Side effects include folliculitis, telangiectasia, local atrophy, and rare hypothalamic-pituitary-adrenal axis suppression.^21,22

A single-center, randomized, blinded, two-arm, parallel-group superiority trial was conducted in 42 children aged 2 to 16 years with AA affecting ≥10% of scalp surface area who were treated with clobetasol propionate 0.05% cream or hydrocortisone 1% cream.²⁹ Compared with hydrocortisone cream, clobetasol propionate demonstrated a statistically significant decrease in area of hair loss (P <.001) at 12, 18, and 24 weeks when applied two times daily for two cycles of 6 weeks on/6 weeks off. At 24 weeks, 85% of the clobetasol group versus 33.3% of the hydrocortisone group achieved at least 50% reduction in hair-loss surface area.²⁹ In a small investigator-blinded, parallel-group study of 61 adults with hair loss of <26%, the hair-regrowth rate with betamethasone valerate foam versus betamethasone dipropionate lotion applied two times daily for 12 weeks was evaluated.³⁰ The hair-regrowth rate was based on the regrowth score, with a range of 0 (<10% regrowth) to 4 (>75% regrowth). The regrowth rate was 3.1 ± 1.5 and 1.8 ± 1.6 for foam and lotion, respectively (P <.01).³⁰

Systemic Corticosteroids: Systemic corticosteroids are typically reserved for severe AA based on concerns regarding long-term side effects and high relapse rates upon therapy cessation.^21,22,27 Daily administration is optimal, and prednisone or prednisolone is preferred.²⁷ Most studies investigating the efficacy and safety of oral corticosteroids in AA management are small and provide insufficient data. Studies conducted to examine the use of pulsed oral or IV corticosteroid therapy with prednisolone, methylprednisolone, and dexamethasone have demonstrated hair regrowth, but their sample sizes have been small.^21,22,31-35

JAK Inhibitors

JAK inhibitors are among the newest therapies for AA. The oral agents baricitinib (Olumiant) and ritlecitinib (Litfulo), which were approved for AA treatment in 2022 and 2023, respectively, are summarized in TABLE 2.^36,37 JAK inhibitors modulate the immune-mediated response that causes hair loss. JAK inhibitors block the cytokine-induced regulatory signaling pathway, activating signal transducers and activators of transcription by inhibiting JAK phosphorylation. This inhibition blocks IFN-gamma and multiple cytokines (IL-2, -4, -7, -9, -15, -21, and -23) and inhibits the production of inflammatory helper T cells, stimulating hair growth. Additionally, hair-follicle stem cells are activated, restoring anagen.^36-38

Baricitinib: The inhibitory effects of baricitinib are specific to JAK1, JAK2, JAK 3, and tyrosine kinase (TYK) 2, with less inhibitory effect at JAK3.³⁶ The phase II portion of BRAVE-AA1, a randomized, placebo-controlled trial of baricitinib in patients with ≥50% scalp hair loss (N = 110), found that baricitinib doses of 2 mg and 4 mg were effective in achieving a Severity of Alopecia Tool (SALT) score of ≤20 compared with placebo.³⁹ SALT scores comprise a range of 0 (no scalp-hair loss) to 100 (complete scalp-hair loss).³⁹ The subsequent BRAVE-AA1 (phase III portion) and phase III BRAVE-AA2 randomized, placebo-controlled trials evaluated baricitinib’s efficacy in treating severe AA in adult patients (N = 654 and N = 546, respectively) with SALT scores of ≥50 and a current AA episode lasting 6 months to 8 years without spontaneous improvement in the preceding 6 months.⁴⁰ At week 36, the proportion of patients with a SALT score of ≤20 was 35.9% to 38.8% with baricitinib 4 mg, 19.4% to 22.8% with baricitinib 2 mg, and 2.2% to 6.2% with placebo. The percentage-point change between each dose and placebo was statistically significant (P <.001).⁴⁰

Ritlecitinib: This medication inhibits JAK3 and the TYK expressed in the hepatocellular carcinoma kinase family.³⁷ The efficacy of ritlecitinib for the treatment of AA was assessed in ALLEGRO, a 48-week phase IIb/III, randomized, double-blind, placebo-controlled multicenter trial involving 718 patients aged ≥12 years with scalp-hair loss of ≥50%.^41,42 Seven treatment regimens were used. All ritlecitinib dosing groups were found to have a higher likelihood (14%-31%) of achieving SALT scores of ≤20 versus placebo (2%).^41,42 A post hoc analysis of the ALLEGRO trial revealed that ritlecitinib was effective regardless of hair-loss profile (presentation and location).⁴³

Adverse Effects: The most common adverse effects reported in clinical trials of baricitinib and ritlecitinib include upper respiratory infection, headache, acne, and nasopharyngitis. Instances of elevated creatinine phosphokinase were identified, typically with higher doses.^36,37,39-42 A long-term safety analysis of 1,303 subjects (median 532 exposure days) in the BRAVE-AA1 (both phases) and BRAVE-AA2 trials revealed that infections such as herpes zoster (n = 34), nasopharyngitis (n = 85), and upper respiratory tract infection (n = 129) were most common, and the investigators concluded that baricitinib’s safety profile in AA was consistent with its overall safety profile.⁴⁴

Topical Minoxidil

Minoxidil acts by promoting hair growth rather than mediating an immune or inflammatory response. Studies evaluating topical minoxidil in AA have been limited in size, with many having ≤60 patients and conflicting results regarding efficacy. Topical minoxidil may be applied in conjunction with other agents or used as monotherapy, and it may exert a dose-dependent response in limited AA.^{22,26,27,45,46}

Anthralin

Anthralin, a scalp irritant that creates irritant contact dermatitis of the scalp, has been used for several decades to treat AA. Anthralin has been shown effective for producing hair regrowth, but studies have been limited and small in size.^21,26 No consensus regarding anthralin use was reached by the Alopecia Areata Consensus of Experts (ACE study).²⁷ Anthralin 0.5% to 2% may be applied to the scalp for 10 to 30 minutes daily, then rinsed with lukewarm water and the scalp shampooed. Contact time may be increased by 10 minutes every 2 weeks until dermatitis is achieved or 1 hour is reached.^21,22 Side effects include scalp irritation, erythema, and scaling (desired reaction). Anthralin may stain cloth, hair, and skin.^21,22,26

Contact Immunotherapy

The mechanism of action by which squaric acid dibutylester (SADBE) and diphenylcyclopropenone (DPCP) affect hair regrowth is unknown. It is posited that these compounds modulate immune response, affecting hair-follicle inflammatory infiltrate. Other theories are that it induces lymphocyte apoptosis and/or exerts an effect on lymphocyte type and function in the inflammatory infiltrate.^16,21,22,26 The ACE study did not address the use of contact immunotherapy.²⁷ Reported response rates vary widely (9%-87%).^16,21,26

Contact immunotherapy may be used in patients with ≥50% scalp-hair loss or refractory AA. Contact immunotherapy creates a mild irritant or allergic dermatitis lasting 36 to 48 hours. Sensitization with DPCP or SABDE begins with application of a 2% solution to a small area. Two weeks later, a 0.001% dose is applied to affected scalp areas that may be rinsed in 24 to 48 hours (DPCP) or 24 hours (SABDE). The dose is then titrated to response in weekly increments.^21,27

Oral Immunosuppressants

Methotrexate, cyclosporin, azathioprine, and sulfasalazine may have a role in refractory AA. However, owing to the possibility of significant side effects, potential toxicities, and limited data regarding efficacy, the use of these medications is limited, and close monitoring is necessary.^21,26,27

CONCLUSION

Many pharmacotherapy options exist for AA. However, the majority of studies demonstrating efficacy are limited and small in size, with variable results. The recently approved JAK inhibitors baricitinib and ritlecitinib show promise for treatment. Drug selection should be based on patient preference, AA severity and location, risk versus benefit of medication use, and potential effectiveness. Pharmacists can play a role in AA management by participating in medication optimization and selection, evaluating regimens for potential drug-drug or drug-disease interactions, monitoring laboratory values, and assisting with dosing parameters. Pharmacists can also recommend nonpharmacologic options and counsel patients on appropriate medication use.

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