Introduction

Vitiligo is an acquired skin disease characterized by depigmented, white macules and patches affecting one or several areas of the body and affecting approximately 0.5% to 1% of the population (Figure 1).^1-4 The condition often presents in childhood, with approximately half of patients affected before 20 years of age.^2,5 While the exact etiology of vitiligo is unknown, it is thought to involve autoimmune targeting of melanocytes, leading to loss of pigmentation in the skin. Loss of melanocytes in hair follicles with areas of involvement may also trigger leukotrichia, with loss of pigment in the hair (Figure 2). A combination of genetics, oxidative stress, inflammation, and environmental triggers are believed to play a role in this process.^1,6-8

Vitiligo can be divided into several subtypes based on distribution; these include the general, focal, segmental, acrofacial, mucosal, and universal subtypes. In children, generalized, focal, and segmental vitiligo are the most common (Figure 3). Furthermore, vitiligo can be bilateral, unilateral, symmetric, or asymmetric. Skin involvement can progress for the first 2 years but then tends to stabilize.^8,9 Though usually asymptomatic, vitiligo can have devastating impacts on quality of life, mental health, and social development, which often lead patients and families to explore available therapies.^10-13

Standard treatment for vitiligo includes topical corticosteroids, topical calcineurin inhibitors, oral corticosteroids, phototherapy, and laser, among other treatments, though response to treatment is variable and dependent on disease activity, severity, subtype, and patient preference. While partial repigmentation is often attainable, full repigmentation is challenging, especially in patients with more extensive involvement. Additionally, certain areas on the body such as the head and neck tend to respond better to treatment than other areas such as the acral sites.^8,9,14,15 Newer therapies targeting the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway have proven to be well tolerated and effective for vitiligo, though additional studies are warranted to establish long-term safety. Here, we provide an overview of current treatments for pediatric vitiligo.^9,15

Topical therapies

For mild disease, twice-daily application of a mid- to high-potency topical corticosteroid (eg, mometasone furoate, triamcinolone acetonide) or topical calcineurin inhibitor (eg, tacrolimus ointment, pimecrolimus cream) has been shown to be an effective monotherapy, with 40% to 90% of pediatric patients showing response to treatment over a 6-month period. To minimize the possibility of adverse effects associated with topical steroids (eg, skin atrophy, systemic absorption), many providers suggest limiting use to 15 days per month. For this reason, topical calcineurin inhibitors are usually the agents of choice for sensitive areas such as the face, underarms, or groin; they can be used in combination with corticosteroids and are safe to use continuously. Topical vitamin D analogs are also used for pediatric vitiligo but have fallen out of favor due to the higher likelihood of skin irritation.^3,9,14,16-18

More recently, the topical JAK 1/2 inhibitor ruxolitinib (Opzelura; Incyte Dermatology) was FDA approved for patients with nonsegmental vitiligo affecting less than 10% of the body and who are at least 12 years of age. Ruxolitinib was shown to result in greater than 75% improvement from baseline in half of patients over a 1-year period. Though uncommon, mild adverse effects include acne and pruritus.¹⁵

Narrowband UV-B

Because skin repigmentation can be stimulated by exposure to UV light, narrowband UV-B (nbUV-B) is usually the treatment of choice when topicals are ineffective or if there is more extensive skin involvement.¹⁹ Treatment is often administered in combination with topical agents or systemic therapy, given the improved response observed with 2 modalities compared with 1. NbUV-B is the most common form of phototherapy used for pediatric vitiligo, primarily due to its increased safety when compared with psoralen and UV-A. Standard treatment involves a few minutes of phototherapy exposure 2 to 3 times weekly, starting with a relatively low dose and increasing gradually until mild erythema is observed. It is important to administer phototherapy with caution, as higher doses can result in burning and further depigmentation due to the Koebner phenomenon.^20,21 If there has not been a good response after 6 months of treatment, nbUV-B can be stopped.

Systemic therapies

Systemic therapy is usually reserved for rapidly progressive disease or for more extensive disease that has not responded to skin-directed therapies.^9,14 Low-dose oral corticosteroids are still the mainstay of treatment for vitiligo that is spreading quickly over weeks to months. Oral prednisone 5 to 10 mg per day for no longer than 2 weeks is the standard treatment regimen. For patients with severe disease, concomitant treatment with nbUV-B therapy is also recommended.

For more extensive vitiligo that is stable—defined as no increase in size of existing lesions and absence of new lesions in the previous 3 to 6 months—mini pulses of oral methylprednisolone on 2 consecutive days weekly and low-dose oral methotrexate are also safe and effective treatments. Other systemic treatment options include minocycline, cyclosporine, apremilast, and certain supplements.^9,14,15 Once again, administering these medications in combination with topical agents or nbUV-B has been shown to be more effective than treating with systemic therapy alone.

Data for the use of oral JAK inhibitors (tofacitinib, baricitinib, and oral ruxolitinib) in children consist primarily of case series and case reports.¹⁵ While near complete repigmentation with oral JAK inhibitors has been reported in some areas of vitiligo, loss of response has been reported when treatment is ultimately discontinued. This is important, because the long-term safety of newer JAK inhibitors has not yet been established and has significant implications when considering starting these medications in childhood. Additionally, serious adverse effects including infection, malignancy, gastrointestinal perforations, and hyperlipidemia have been reported previously with use of oral JAK inhibitors.¹⁵

Laser therapy

The 308-nm monochromatic excimer laser (UV-B range) can be used to treat localized vitiligo. Similar to the response to nbUV-B, the sites that respond best to excimer laser are the face and neck. In one study of patients with stable vitiligo, more than 50% of patients showed more than 75% repigmentation with excimer laser therapy.²² Given the discomfort associated with laser therapy and need for multiple treatment sessions, excimer laser is typically reserved for older school-aged children and adolescents who are better able to understand their diagnosis and the potential impact of treatment.

Conclusion

Treatment for vitiligo is broad and includes topical corticosteroids, topical calcineurin inhibitors, oral corticosteroids, phototherapy, laser, and both topical and oral JAK inhibitors, though response to treatment is highly variable and dependent on disease activity, location, severity, and subtype. Less common treatments include alternative systemic agents, surgical skin grafting, platelet-rich plasma, medical tattooing, and camouflage.¹⁵ Camouflage with makeup can be helpful during treatment, especially when lesions involve exposed areas like the face, neck, and hands, or for patients who do not wish to medically treat their vitiligo. In general, combination therapy is more effective than monotherapy but may not be warranted in mild cases that respond well to topicals alone. Importantly, patients with vitiligo should be diligent about sun protection, as depigmented lesions are more prone to sunburns.

References:

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