Intralesional corticosteroid therapy is recommended as the first option for adults with mild to moderate AA. Additionally, it can be used as an adjuvant in patients with severe disease. This route of administration crosses the epidermal barrier, making the drug available directly to the inflamed area.22–24 This minimizes the possible adverse effects of systemic corticosteroid therapy and provides greater drug penetration when compared to the topical route.24 Patients with isolated, small-sized alopecia patches (<3 cm) occupying less than 25% of the scalp are the best candidates for intralesional injection.8,22,25,26

Approximately 60% to 75% of patients with AA patches who undergo corticosteroid injection experience hair growth, a rate that varies with disease severity, and the clinical response is generally perceived six weeks after starting treatment.25,27,28 Intralesional corticosteroid therapy can be applied to the scalp, eyebrows, beard, and other hairy areas of the body.8,22 Although it is an important pillar of AA treatment, the ideal concentration and total dose of the drug to be applied are still being debated.29

Triamcinolone acetonide (TAc) is the most widely used injectable synthetic corticosteroid worldwide.7,30 In Brazil, the available TAc is restricted in the package insert to intraocular use and, therefore, the most widespread form has become triamcinolone hexacetonide (TH), its less soluble derivative and with a greater risk of skin atrophy.24 Classically, a concentration of 2.5 to 10 mg/mL of triamcinolone is used for the scalp and 2.5 to 5 mg/mL for the face and other body areas.31,32 A pilot study demonstrated that lower concentrations, such as 2.5 mg/mL, were as effective as higher concentrations and with a lower risk of atrophy.33 Another study showed that the best risk-benefit would be the use of 5 mg/mL on the scalp and lower doses for areas with a greater risk of atrophy.34 An alternative option to TH in the intralesional treatment of AA is betamethasone (betamethasone dipropionate 5 mg/mL + betamethasone disodium phosphate 2 mg/mL). To achieve dose equivalence with 2.5 mg/mL of triamcinolone, 0.05 mL of betamethasone should be diluted in 0.95 mL of 0.9% saline solution.24 A good response has also been reported with hydrocortisone acetate 25 mg/mL.22

Infiltration of 0.02 to 0.1 mL per point is performed in the dermis or upper portion of the subcutaneous tissue, with spacing of 0.5–1 cm between punctures and an interval of four to six weeks between sessions.7,13,27 The number of applications required for hair regrowth varies; a significant response is generally observed after three sessions. More sessions, at the physician discretion, may be necessary to achieve complete hair regrowth. Dilution with saline or glucose solution is recommended, which may or may not be mixed with lidocaine.24 Adding lidocaine may increase the risk of drug flocculation if the anesthetic contains methylparaben, propylparaben, or phenol as components of its vehicle, increasing the chance of atrophy.24 The amount of corticosteroid applied per session should not exceed 40 mg of triamcinolone or equivalent.33

Pain is a limiting factor, especially in children or patients with extensive forms of AA.7,28 The use of topical anesthetics, vibration, or local cooling before application may be useful to minimize discomfort during the procedure.35 Needle-free devices are also an option, but the device must be sterilized before use.7 These complementary measures may allow infiltration in children and even in adults who initially reject intralesional therapy. Treatment should be discontinued if no improvement is observed after six months of starting the infiltrations.7,36 Patients who do not respond to corticosteroids may show resistance due to low expression of thioredoxin-reductase 1 in the external root sheath of the hair follicle.30,36

Adverse effects include pain and hemorrhage at puncture sites, headache, local skin atrophy, dyschromia, systemic absorption and, much more rarely, anaphylaxis.13,23 Skin atrophy is common and usually reversible, but there is a risk of permanent damage. To minimize its risk, the suggestion is apply small volumes of the drug, more diluted concentrations, more spaced punctures and avoid superficial injections outside the correct plane of drug administration.36 Increased intraocular pressure and cataracts have been reported in patients undergoing multiple sessions of intralesional corticosteroid therapy for AA of the eyebrows.22

Topical corticosteroid therapy is widely used in the treatment of all forms of AA, although its clinical efficacy is controversial due to limited evidence.7 It is usually used alone only in mild AA since its efficacy is apparently lower in more advanced forms of the disease.25 However, its use and possible benefits encompass all AA subtypes. The authors recommend topical corticosteroid therapy in patients who refuse intralesional therapy and in children, including in combination with systemic therapy in extensive cases.

Different local corticosteroids have been used in AA with variable responses.36 Comparative studies, however, have shown that very high-potency corticosteroids, such as clobetasol, are significantly more effective than lower-potency ones, such as hydrocortisone.28,37 Among the advantages of this therapeutic modality are the fewer side effects compared to the systemic route and the possibility of its use in different vehicles.31 Clobetasol has already shown positive results when used in foam, cream or, ointment.27,31 When applied under occlusion, its efficacy seems to be increased, with reports of some promising results even in severe forms of the disease, such as total and universal AA, although it may increase the chance of side effects.27,30

The most common adverse effects are folliculitis, local skin atrophy, stretch marks, acneiform rash, telangiectasia, dyschromia and, rarely, adrenal suppression.7,36 Washing the site 12 hours after application is recommended to reduce the incidence of folliculitis and a dosage of up to five times a week seems to prevent the appearance of atrophy.7

The action mechanism by which minoxidil stimulates the hair follicle has not yet been fully clarified. Vasodilation, angiogenesis, opening of potassium channels and stimulation of the proliferation of follicular dermal papilla cells are some of the proposed mechanisms.38,39 By increasing the duration of the hair cycle anagen phase, minoxidil seems to have a reasonable application as soon as hair regrowth begins, with the aim of increasing the thickness and length of the newly regrown hair.

A meta-analysis found minoxidil to be 5% superior to placebo when used in patch AA. This evidence was classified as having moderate quality.40 The concomitant use of topical anthralin or intralesional corticosteroid therapy seems to provide superior results to single-therapy treatments.41 The expected side effects are hypertrichosis, contact dermatitis, and pruritus.36

Although controversial, topical minoxidil has been widely used in clinical practice as an adjuvant therapy in AA. It can be used mainly in localized forms that already present partial hair regrowth. The usual concentration for use in adults is 5%, in one or two daily applications.

Topical immunotherapy (TIT) is performed with agents that trigger allergic contact dermatitis. They are used in AA treatment with the aim of reducing the lymphocytic inflammation in the anagen follicle. The mechanism is not well understood, but it is believed to be related to the diversion of the inflammatory process from the bulb to the site where the new inflammatory process is being induced by the medication. Thus, the follicle is able to recover.42,43

Upon contact with patient skin, the sensitizer triggers a delayed hypersensitivity reaction (type IV), producing memory lymphocytes. Thus, after new exposure to the same agent, the immune system will produce a T-cell-mediated inflammatory response.

In Brazil, the most commonly used sensitizing agent for this purpose is diphencyprone, available only in compounding pharmacies. It must be formulated in acetone, which is highly volatile and must be kept in containers protected from light (amber-colored vials).

After the initial exposure to diphencyprone, the entire immunological cascade to elicit memory takes between two and three weeks. Only after this period will the substance be recognized as an allergen, causing dermatitis. The satisfactory clinical response can vary between 30%-48%, but if any response is considered, it can reach up to 72.2%.42,44,45 Substance use is divided into three phases: sensitization, follow-up, and maintenance. Each phase has its own peculiarities that will be discussed below.

The use of anthralin also aims to divert the inflammatory process away from the bulb, but it causes irritant contact dermatitis, not allergic contact dermatitis. In Brazil, anthralin is only available through compounding, and like diphencyprone, it is often difficult to find. Its concentration can vary from 0.5‒2.0% diluted in cream. It causes hair regrowth in 71% of cases of patch alopecia46 and the average time for the initial response is three months, with full results after 15 months.46

The medication is applied to the affected area, penetrating up to 1 cm into the apparently healthy area. The patient is instructed to wash the area and remove the product thoroughly after 30 minutes. The procedure is repeated daily. The time of contact with the skin is increased by 15 minutes, every three days. In other words, it starts with 30 minutes, then increases to 45 minutes, 60 minutes, 75 minutes and so on, up to a maximum time of two hours. The aim is to cause mild eczema. If there is no reaction after two hours, the contact time can be extended, in some cases, to all night long.

Anthralin is a dark brown substance with a characteristic odor. With frequent applications, it ends up pigmenting the follicular ostia, simulating blackheads. However, dermoscopy clearly shows the difference between a black dot in the center of the ostium and the brown pigmentation regularly distributed around the edge of the follicular ostium caused by anthralin. One of the signs of therapeutic failure can be seen when no pigmentation of the ostia is observed, which can have three main causes: irregular application, short contact time with the scalp, or inadequate quality of the medication.

This is a safe therapy, but some precautions must be taken to avoid complications. Since the goal is to cause local irritation, the order of increasing the time the medication is in contact with the skin must be systematically followed, avoiding exacerbated irritation. The use of anthralin leads to hyperpigmentation of the treated area, but the color will return to normal after the treatment is interrupted. The use of corticosteroids is antagonistic to the effect of anthralin and diphencyprone because they reduce the inflammation anthralin and diphencyprone stimulate.

Anthralin is an option for children due to the absence of systemic side effects. It can be used as a second or third line of treatment for adults with mild AA, and even as an adjuvant in the treatment of severe AA.

Several forms of systemic administration of corticosteroids have been described for the treatment of AA. Since 1975, pulse corticosteroid therapy has been introduced in the treatment of AA, aiming at reducing side effects of long-term corticosteroid therapy and increasing therapeutic efficacy. Since then, several types of corticosteroid pulses have been described, especially for rapid rescue of severe and acute forms of AA.36

Oral mini-pulse dexamethasone was evaluated in a prospective cohort that used a mean dose of 2.7 mg/day, two days a week, in patients resistant to topical therapy. Approximately 51% of patients achieved SALT-50 after nine months of treatment. The daily dose used and treatment duration were associated with a higher frequency of side effects due to corticosteroid therapy. Hypothyroidism and early age of disease onset were predictors of lack of response to treatment.47

Oral pulse methylprednisolone was evaluated in two studies. In the first study, a mega dose of 15 mg/kg was evaluated in three different dosing regimens: three consecutive days every two weeks, two consecutive days every three weeks, and three consecutive days every three weeks, for 24 weeks. Regrowth rate was similar between the groups (>25%); however, the groups with shorter intervals had a higher frequency of side effects.48 The second study evaluated oral mini-pulse methylprednisolone 16 mg/day for two consecutive days per week. Forty percent of the participants showed satisfactory growth after three months, while more than 82% of the patients achieved the same results after six months.49

Mini-pulse prednisolone in severe AA was evaluated in a study that included 32 patients with SALT > 40 or persistent AA. Initially, the participants received a monthly pulse of 300 mg of prednisolone for four months. This dosage was effective for multifocal AA, with mild side effects. Refractory patients or those with universal AA responded with a pulse of 1000 mg/month. Females, disease duration greater than two years, and alopecia universalis were associated with poor or no response to treatment.50 Oral pulse prednisolone 200 mg/week for three months in patients with more than ten patches or with SALT ≥ 0 showed a response rate of approximately 34%.51 Other regimens have been described for patients with rapid progression or resistance, such as prednisolone 80 mg/day for three consecutive days every three months, and also the mega pulse of 15 mg/kg for two days every three weeks.48

There is no consensus in the literature on the dose and duration of daily oral corticosteroid therapy in AA. Prednisone can be used in doses ranging from 0.1 to 1 mg/kg/day. It is suggested to start with higher doses (0.5 to 1 mg/kg/day) and gradually reduce the dose (over six to 12 weeks) after hair regrowth is achieved.

Although it is not described in the guidelines for AA and has a higher cost, deflazacort has a more favorable safety profile. The drug has a high therapeutic index, with potency ranging from 70% to 90% of prednisone, and has a lower impact on calcium metabolism than any other synthetic corticosteroid. Moreover, it has a comparatively small effect on carbohydrate metabolism, water retention, and hypokalemia.52 It is suggested to start with a daily dose of 0.75 mg/kg for both adults and children and to reduce it slowly after hair regrowth.

Long-acting corticosteroids can be administered through the intramuscular or intravenous route as an alternative to oral use. The application of 40 mg of intramuscular TAc once a month for six months was shown to be superior to prednisolone pulse therapy (80 mg for three consecutive days every three months) and dexamethasone (0.5 mg/day for six months) in a randomized comparative clinical trial.53

As for intralesional use, TAc is also recommended over TH for intramuscular use due to the greater risk of developing atrophy and telangiectasias in the long term.54 The authors suggest, as a second option, replacement by the combination of betamethasone dipropionate 5 mg/mL (short-acting) with betamethasone disodium phosphate 2 mg/mL (long-acting).24Table 4 shows the dose equivalence of the different corticosteroids.55

Response rates with daily, intramuscular, or mini-pulse systemic corticosteroids are high, but many patients show recurrence when the dose is reduced or soon after the medication is discontinued. They are especially useful in controlling cases with rapid progression or in extensive cases with signs of activity. For those who respond to corticosteroids but become corticosteroid-dependent, the association of another systemic medication is necessary to spare its use.

Attention to the risk of side effects is essential for all types of long-term corticosteroid therapy. Endocrinological monitoring, bone densitometry assessment, and calcium and vitamin D supplementation are important measures to attenuate the risk of more severe adverse effects.55–58

JAKi were evaluated in double-blind, randomized, controlled, multicenter trials and were the first drugs officially approved for the treatment of severe AA. They inhibit the IFN-γ and IL-15 signaling pathways, which activate and perpetuate CD8+ cytotoxic T cells, responsible for autoimmune inflammation against the hair follicle.59

Baricitinib (JAK 1/2 inhibitor) and ritlecitinib (JAK 3/TEC inhibitor) are currently the two drugs approved in Brazil by Anvisa for the treatment of severe AA in patients aged ≥ 18 years and ≥ 12 years, respectively.

Baricitinib efficacy was demonstrated in two randomized phase 3 clinical trials involving 1,200 patients with severe AA (SALT > 50).5 At week 36, 38.8% of patients treated with baricitinib 4 mg/day achieved SALT < 20 in comparison with 22.8% of patients treated with 2 mg/day and 6.2% of patients receiving placebo. Extension studies with continuous baricitinib use for up to 104 weeks showed that efficacy continues to increase after 52 weeks and there is a high rate of maintenance of clinical results.60

In the phase 2b-3 study of ritlecitinib, patients with SALT > 50 were randomized to receive oral ritlecitinib or placebo with or without a four-week loading dose (200 mg loading dose followed by 50 mg or 200 mg loading dose followed by 30 mg, and 50 mg, 30 mg, 10 mg doses).6 At week 24, 31% of the patients in the ritlecitinib 200 mg/50 mg group, 23% of the patients in the ritlecitinib 50 mg group, and 2% of the patients in the placebo group achieved SALT ≤ 20. At week 48, 40% of the 200 mg/50 mg group and 43% of the 50 mg group achieved SALT ≤ 20, showing that the long-term outcome is similar between the two regimens.61

Other JAKi have shown efficacy in non-controlled studies and are considered options for off-label use, such as tofacitinib (JAK 1/3 inhibitor) at a dose of 5 mg twice daily, ruxolitinib (JAK 1/2 inhibitor) at a dose of 20 mg twice daily, and upadacitinib (JAK 1 inhibitor) at a dose of 30 mg/day. Topical preparations have not shown to be effective.62,63 Deuruxolitinib was approved for the treatment of AA in 2024 by the FDA, and ivarmacitinib has a review application for approval.64,65

To date, the use of JAKi in AA is considered safe. Adverse events that occurred more frequently than with a placebo were upper respiratory tract infections, urinary tract infections, nasopharyngitis, acne, increased transaminase levels, headache, and nausea. Adverse effects are generally mild and transient, and there was no increased risk of severe adverse effects when compared to placebo.62,63

All JAK inhibitors have safety information in their package inserts from the tofacitinib safety study (ORAL Surveillance) carried out in patients with rheumatoid arthritis aged ≥ 50 years with one or more cardiovascular risks, which showed an increased risk of adverse cardiovascular events, venous thromboembolism, severe infections, malignant neoplasms, and death compared with TNF inhibitors, which have a cardioprotective effect.66 This risk was not observed in patients with immune-mediated dermatological diseases, including AA.67 However, until further studies are available, the treatment of elderly patients, smokers, or those at increased risk of these conditions should be evaluated with caution.68 Recommendations for the use of JAK inhibitors are summarized in Table 5 and pretreatment precautions in Table 6.

Methotrexate (MTX) is a competitive inhibitor of dihydrofolate reductase. Its use at low doses in inflammatory diseases such as AA requires folic acid supplementation. Among the independent pathways, suppression of the JAK/STAT signaling pathway seems to be the main action mechanism.69

Initial doses of 5 to 10 mg/week are progressively increased, in four to six weeks, up to 20–25 mg. Since oral MTX at doses above 15 mg may show erratic absorption, the injectable option should be considered in these cases. The combination of oral and intralesional corticosteroids has been reported. In most cases, a minimum dose of MTX, ranging from 7.5 to 12.5 mg/week, is required for maintenance.70,71

Better responses are observed in men, patients over 40 years of age, with less than five years of disease duration, who reached cumulative doses of 1000 to 1500 mg, and who received corticosteroids in addition to MTX.71,72 Recurrence may occur during treatment and after discontinuation of the medication and long-term use is necessary.

MTX in combination with low doses of prednisone has shown terminal hair regrowth in up to 96% of patients with AA.70 Total regrowth has been demonstrated in 15% to 64% of the patients.72

Pancytopenia is the most feared toxicity when using low-dose MTX, but it is uncommon.73 Patients with renal failure, and hypoalbuminemia, who use erroneously high doses or use other medications that interact with MTX (e.g., anti-inflammatory drugs) are at greater risk.74,75 Interstitial pneumonitis and altered liver function have been reported.72 Folic acid supplementation reduces the side effects of MTX, especially gastrointestinal ones. Different doses and frequencies of administration have been described, ranging from 5 mg per week to 1–5 mg/day. Even in daily doses, folic acid does not interfere with MTX efficacy.76 Folinic acid supplementation is reserved for drug toxicity cases.76

It is suggested that a chest X-ray, serology for hepatitis B, C, and HIV, complete blood count, beta-HCG, and renal and liver function tests be performed before starting the treatment. Complete blood count, renal and liver function tests, and beta-HCG should be repeated at day 30 and after 60 to 90 days according to clinical evaluation.

Cyclosporine is an immunosuppressive agent capable of inhibiting the activation of helper T-cells and suppressing the production of interferon-gamma, reducing the perifollicular inflammatory infiltrate. The efficacy of cyclosporine was proven in a controlled, double-blind, and randomized study.77 A dose of 2 mg/kg/day divided into three doses is initially used, with a progressive increase up to 5 mg/kg/day.78 Hair regrowth varies from 25% to 76.6% when associated with systemic and intralesional corticosteroids.78,79

Although effective, its use is limited by side effects, especially nephrotoxicity, immunosuppression, and arterial hypertension. Nephrotoxicity, generally due to prerenal vasoconstriction, although reported, was reversible in patients with AA.78,79 The duration of cyclosporine use is limited and should be monitored. In severe cases, this can be challenging since when treatment is discontinued, AA tends to recur.

Azathioprine is an antimetabolite with few reports on its use in AA and low therapeutic response. Initial doses of 0.5‒1 mg/kg/day can be increased to 2‒3 mg/kg/day according to patient tolerance.80 At a dose of 2.5 mg/kg/day, it can be considered in recalcitrant AA. Some hair regrowth was observed in 43% of patients after four to six months.80 Gastrointestinal effects, elevated liver enzymes, pancreatitis, and bone marrow suppression are the most commonly reported side effects.

Better responses may be observed in combination with systemic or injectable corticosteroids or even MTX. The combination with MTX should be performed with caution, considering the increased side effects.81

The benefits of oral minoxidil in AA include anagen induction, aid in the treatment of coexisting androgenetic alopecia, and possible immunomodulation.82 The use of oral minoxidil in AA was first reported in the literature in 1987, in monotherapy with a dose of 5 mg, twice daily. Satisfactory hair regrowth occurred in 18% of the patients.83 Despite the high dose, facial hypertrichosis was observed in only 17% of the patients.

It was observed in a non-comparative study that oral minoxidil may have an additive effect when associated with JAK inhibitors.84 This association may benefit partial responders or even allow the use of lower doses of JAKi.

Oral minoxidil has been studied as monotherapy or adjunctive treatment in 363 patients with AA, including 42 children. Treatment duration ranged from four to 20 months. Daily doses ranged from 0.03 mg/day to 15 mg/day. Hypertrichosis was the most commonly reported adverse effect in all AA studies to date, ranging from 11.5% (0.99 mg) to 50% (2.5 and 5 mg for women and men, respectively). Mild cardiovascular adverse effects, including postural hypotension, palpitations, and peripheral edema, were less common. Severe cardiovascular adverse effects (pericardial effusion, tamponade, and angina pectoris) were not reported in any of these studies.82

Despite the limited evidence of results in monotherapy, oral minoxidil may be an interesting option as an adjunctive therapy, especially in extensive cases on systemic therapy.

The most studied light-based therapies in AA are excimer laser and 308-nm excimer light, which have immunosuppressive properties, possibly by inducing T-cell apoptosis. A review included eight clinical trials and case reports, with a total of 94 treated individuals, with an efficacy of 36.9% to 100%, with regrowth equal to or greater than 50%.85 A meta-analysis that included only four controlled studies using excimer laser on previously untreated AA patches confirmed the efficacy of the treatment.86 The main side effects of the therapy are mild erythema, pain during application, hyperpigmentation, blistering, pruritus, and desquamation.87 The high cost is the main disadvantage of the treatment. Excimer laser and excimer light may be treatment alternatives for mild and moderate refractory cases, especially when there is corticosteroid-induced atrophy or contact dermatitis due to other therapies.

Cosmetic camouflage options should be encouraged. Although few studies have quantified the benefit in the patients quality of life, the use of these resources is considered good practice even during treatment periods.88,89 There are numerous options for partial or total hair prostheses, and removable or fixed extensions and hairpieces.

Camouflage may be presented as hair fibers, sprays, waxes, and pigmented powders. Tricopigmentation may be performed on the scalp and eyebrow area. Eyelashes, false nails, and eyebrow prostheses may also be used.

AA is a common cause of hair loss in childhood and adolescence. Up to 60% of cases begin in the first two decades of life.90 In children, especially in mild cases, topical corticosteroids, preferably medium to high-potency ones (mometasone 1% to clobetasol 0.05%), are usually employed as the first therapeutic option. When possible, occlusion should be performed at night (e.g., using a shower cap, swimming cap, or plastic wrap). When there is a contraindication or lack of response to topical corticosteroids, anthralin (0.5–1%), diphencyprone, or minoxidil may be used in combination.46,91 Although effective, intralesional corticosteroid therapy is limited by the intolerance to pain and fear of needles that are common in this age group.

The administration of systemic medications may be considered in extensive cases or in cases of evident activity. The only medication with package insert approval for the systemic treatment of AA in the pediatric population is ritlecitinib, from 12 years of age.

The off-label use of JAK inhibitors in children under 12 years of age with severe AA has been described in case reports and small retrospective studies.92 To date, the literature suggests a good safety profile for the use of this category of medications in children. In a phase III clinical trial with 483 patients, baricitinib was shown to be safe and effective for the treatment of atopic dermatitis in children and adolescents between two and 18 years of age.93 Only 0.6% of the patients discontinued treatment due to adverse effects – none of them severe, compared to 1.6% of patients in the placebo group.93 Other studies evaluating the efficacy and safety of JAKi in childhood are ongoing, including a clinical trial with ritlecitinib for children aged six to 12 years with extensive/severe alopecia areata (Clinical Trial NCT05650333).

Among the other options available for systemic treatment, the authors prefer systemic corticosteroids and MTX (at a dose of 0.2 to 0.4 mg/kg/week). It is important to take into account the child stage of life and development and to be aware of possible adverse effects, especially changes in growth, metabolism, and immune competence.

The beard is the second most frequently affected area by AA, second only to the scalp.8 There are no randomized controlled clinical trials evaluating specific treatments for this region. The most common approach is the use of local therapies, starting with topical corticosteroids, followed by intralesional ones, or the direct use of intralesional corticosteroids, a therapy that has the greatest evidence of efficacy for localized and short-term AA.94 The dose of 2.5 mg/mL of triamcinolone is the most appropriate for treating the face. Although effective, the use of corticosteroids carries a greater risk of atrophy in this area. Minoxidil can be used as adjuvant therapy.

The involvement of the eyebrows and eyelashes has a major impact on quality of life, as it directly interferes with physiognomy. Alopecia in these specific areas is a factor that increases severity and may indicate systemic treatments. With baricitinib, approximately one-third of the patients with severe eyebrow and eyelash loss achieved normal or near-normal hair growth within 36 weeks of treatment, and with ritlecitinib, approximately 23% of patients with eyebrow or eyelash loss achieved normal or near-normal hair growth within 24 weeks.95 Topically, the only agents indicated for hypotrichosis or alopecia in the eyelash region, regardless of its etiology, are prostaglandin analogs, especially bimatoprost 0.03% solution.96,97 Some studies have tested the drug in adult and pediatric patients, with variable results, which is probably due to different severity of the conditions and, therefore, different AA prognoses.98 It seems to be a safe and potentially effective agent for the treatment of the region. It is important to be aware of the risk of eyelid hyperpigmentation and darkening of the iris.

In addition to the possibility of using bimatoprost 0.03% for the eyebrows, it is also possible to use topical and intralesional corticosteroids.96 Preferably use medium-potency corticosteroids, taking care not to drip onto the eyelids and eyes (a cream vehicle should be preferred rather than a solution). Intralesional infiltration of triamcinolone should be performed at a dose of 2.5 mg/mL to minimize the risk of skin atrophy. The association with topical minoxidil is also an option, similar to the scalp.

Dupilumab was the first biological drug approved for the treatment of moderate to severe atopic dermatitis, and some studies have reported improvement in AA symptoms in patients who received it, raising the hypothesis that it is a useful drug for patients with both conditions. However, there are also reports of worsening AA symptoms or even the emergence of the disease in patients undergoing treatment, which leaves its benefit as an uncertain possibility.99