Amanda F. Nahhas, DO1,2; Taylor L. Braunberger2, MD; Iltefat H. Hamzavi2, MD

1Department of Dermatology, Beaumont-Farmington Hills, Detroit, MI, USA
2Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA

Conflict of interest:
Dr. Hamzavi is an investigator for Incyte Corporation, Clinuvel, Bayer, Estée Lauder, Unigen Inc., and Ferndale Laboratories. Dr. Nahhas and Dr. Braunberger are former sub-investigators for Ferndale Laboratories, Bayer, Estée Lauder, and Unigen Inc., with grants that were paid to the institution.

Vitiligo is an acquired, autoimmune disease characterized by depigmented macules and patches on the skin, which occur secondary to melanocyte destruction. Available therapeutic options are broadly divided into medical, surgical and phototherapy, though treatment of vitiligo can be challenging. Early diagnosis and management can maximize treatment efficacy. The purpose of this discussion is to review updates in the management of vitiligo, including existing and emerging therapies.

Key Words:
medical management, phototherapy, treatment, vitiligo


Vitiligo is an acquired, autoimmune disease characterized by depigmented macules and patches on the skin, which occur secondary to melanocyte destruction. Focal and segmental vitiligo patterns involve ≤10% body surface area (BSA) and are considered stable patterns. Generalized vitiligo typically involves ≥10% BSA, appears bilaterally in a symmetric distribution, and generally follows a relapsing and remitting disease course.

Treatment can be challenging, though available modalities of therapy include pharmacologic, surgical, and phototherapy. Appropriate characterization of vitiligo type, consideration of disease extent and duration, and efficacy of prior therapies can guide management and maximize treatment efficacy.

Medical Management

In early, stable, localized disease (≤12 months since onset), topical corticosteroids, topical immunomodulators, targeted narrowband ultraviolet B (NB-UVB) phototherapy, or a combination can be effective. In generalized, stable disease, topical corticosteroids or immunomodulators in combination with NB-UVB phototherapy are the mainstay of therapy. In patients with generalized, rapidly progressive vitiligo, a 3-month trial of pulsed oral corticosteroids may help induce stabilization.1

Topical Therapies

Topical corticosteroids are effective agents in vitiligo due to their immunosuppressive and anti-inflammatory properties. Super-potent or potent corticosteroids are appropriate for treating the trunk and extremities, whereas mid-potency topical corticosteroids (or topical calcineurin inhibitors) are better suited for the face, neck, or intertriginous regions and in children. Cyclical application (1 week on and 1 week off for 6 months or for 5 days on and 2 days off ) can help avoid the cumulative adverse effects of topical corticosteroids, including skin atrophy, telangiectasias, and steroid-induced acne.1 Treatment should not exceed 14 days in a month per package insert.2

Topical calcineurin inhibitors, such as tacrolimus (0.1%) or pimecrolimus (1%), are immunomodulatory, steroid-sparing agents that may be used anywhere with the exception of mucous membranes, and are nearly as effective as topical corticosteroids but more favorable with steroid-sparing properties.3 Twice daily use can promote disease stabilization and twice weekly applications may be considered for maintenance therapy.4 Topical calcineurin inhibitors may be used in combination with topical corticosteroids on ‘off’ days. Although tacrolimus poses a theoretical, long-term risk of carcinogenicity due to its immunosuppressive properties, no cases in humans have been reported.1,5 In a mouse model investigating dermal photocarcinogenicity, topical 0.1% tacrolimus was associated with the development of lymphoma. An intra-individual left-right comparison study by Ostovari et al. involving 9 patients with generalized vitiligo found that repigmentation was optimized when topical calcineurin inhibitors were combined with UVB (308 nm excimer laser) exposure in all patients, whereas no repigmentation was observed on the side treated with topical 0.1% tacrolimus alone.6

Vitamin D analogs, such as topical calcipotriene, used in combination with phototherapy, may reduce time to repigmentation and the overall cumulative dose delivered.7

Oral Therapies

In progressive vitiligo, oral minipulse corticosteroid therapy (OMP) may be used to promote disease stabilization through immunosuppression. A typical regimen includes low-dose oral betamethasone or dexamethasone taken on 2 consecutive days per week for 3 to 6 months.1 Lack of disease stabilization after 3 months of combination therapy (OMP plus NB-UVB phototherapy) warrants discontinuation of the OMP only and reevaluation at 3-month intervals.1 Alternatively, upon failure of OMP, daily dosing with 20 mg of oral prednisone may be considered until disease progression has halted.8 In an early study published in 1993, 40 patients with extensive or rapidly progressive vitiligo were treated with 5 mg of betamethasone/ dexamethasone as a single oral dose on consecutive days weekly. Within 1 to 3 months, disease progression was arrested in 89% of the patients. In 2 patients, the dose was increased to 7.5 mg per day in order to halt disease progression. Within 2 to 4 months of treatment, 80% of patients noted increased spontaneous repigmentation that was maintained with continued therapy. Side effects consistent with oral corticosteroid use were observed in 42.5% of patients.9 In a study published in 2001, 29 patients with either progressive (n = 25) or stable (n = 4) vitiligo received 10 mg of oral dexamethasone on consecutive days weekly for 24 weeks. After an average of 18.2 ± 5.2 weeks, 88% (22 of 25) of patients with progressive vitiligo had arrest in disease activity. Side effects associated with oral corticosteroid use were observed in 69% of the patients studied.10 In a more recent study published in 2013, 444 patients with progressive vitiligo were treated with 2.5 mg of oral dexamethasone on consecutive days weekly. Using this regimen, arrest of disease progression was noted in 91.8% of these patients, with some repigmentation noted within 16.1 ± 5.9 weeks on average. Disease relapse occurred in 12.25% of patients, though the average disease-free survival until first relapse was 55.7 ± 26.7 weeks. Adverse effects consistent with oral corticosteroid use were observed in 9.2% of patients.11 Side effects associated with any oral corticosteroid use (i.e., acne, weight gain, headache, nausea, and lethargy) should be reviewed with patients. There is evidence to suggest that confetti-like macules and koebnerization are good physical markers of instability.12 These are markers the authors may use when deciding to initiate oral corticosteroid therapy.

Minocycline, through its anti-inflammatory, immunomodulatory, antioxidant, direct free radical scavenging, and anti-apoptotic properties, may be an effective therapy to arrest progression of vitiligo as well as induce repigmentation.13-14 In a study involving patients with gradually progressive vitiligo (majority being of the generalized vitiligo type), patients were instructed to take 100 mg of oral minocycline daily. Of the 32 patients included in the study, 29 showed arrest of disease progression, with onset as early as 4 weeks after initiation of treatment in 10 of the 29 patients. Seven of 32 patients showed moderate to marked repigmentation.15 A randomized trial comparing 6-month treatment with oral dexamethasone (5 mg weekly, 2.5 mg given on 2 consecutive days per week) versus oral minocycline (100 mg daily) in 50 patients with unstable, generalized vitiligo showed there were no statistically significant differences in vitiligo disease activity scores and Vitiligo Area Scoring Index between groups.16 Another study compared 3-month treatment of oral minocycline (100 mg daily) with NB-UVB phototherapy (twice weekly) in 42 patients with unstable vitiligo and found a statistically significant improvement in repigmentation in the group treated with NB-UVB.17

Use of methotrexate, an immunomodulating systemic agent, has been shown to improve vitiligo in 1 of 3 patients with rapidly progressive, generalized vitiligo when administered in an uptitrating dose of 12.5-25 mg per week, as reported in a recently published case series. Repigmentation was noted as early as 6 weeks to 14 months in this patient, who had previously failed to respond to topical calcineurin inhibitors and phototherapy.18 A prospective, randomized trial was performed comparing 24-week treatment with oral methotrexate (10 mg weekly) versus OMP (dexamethasone, 5 mg weekly, 2.5 mg given on 2 consecutive days per week) in 50 patients with unstable vitiligo. New lesions developed in 6 of 25 patients in the methotrexate group and 7 of 25 patients in the OMP group, though the difference was not statistically significant. Both groups demonstrated similar reductions in vitiligo disease activity scores.19 Due to the limited availability of studies supporting its superior efficacy compared to other available treatments, use of methotrexate can be considered as a steroid-sparing agent in patients with vitiligo refractory to topical treatment and phototherapy.

The role of antioxidants in the treatment of vitiligo remains controversial. Based upon a systematic review of the literature performed by Speeckaert et al., the oxidative stress pathway is deregulated in patients with vitiligo, although it is not considered disease specific, but rather consistent with findings that are expected in an immune-mediated skin disorder. Furthermore, it was noted that increased oxidative stress in non-lesional skin may be specific to vitiligo.20

Among the antioxidant therapies, oral Polypodium leucotomos (PL) extract has been studied in patients with generalized vitiligo due to its notable antioxidant and immunomodulatory properties. In a 26-week randomized clinical trial, patients received NB-UVB phototherapy (twice weekly) combined with either oral PL (250 mg thrice daily) (n = 25) or placebo (n = 24). Improvement in repigmentation was greatest in the group receiving oral PL and NB-UVB phototherapy and most prominent on the head and neck, which was statistically significant.21 A pilot, randomized, placebo-controlled clinical trial evaluated the effects of oral PL plus psoralen ultraviolet A (PUVA) versus placebo plus PUVA in 19 patients. Greater than 50% repigmentation was observed more frequently in the PL plus PUVA group compared to the placebo plus PL group.22

Ginkgo biloba extract has been shown to have some antioxidant and anti-inflammatory properties and may help induce stabilization of vitiligo. In a placebo-controlled, double-blind study evaluating the efficacy of Ginkgo biloba extract in patients with gradually progressive vitiligo, 40 mg of oral Ginkgo biloba extract was administered to 24 patients 3 times daily for 6 months, while 18 patients received the placebo. Twenty patients in the active treatment and 8 patients in the placebo-controlled group had arrest in progression of disease, which was statistically significant. Ten patients in the active treatment group showed marked to complete repigmentation, compared to 2 patients in the placebo-controlled group.23 A separate 12-week pilot clinical trial involving 11 patients showed that twice daily administration of 60 mg of oral Ginkgo biloba extract resulted in improved total Vitiligo Area Scoring Index measures and spreading as noted by Vitiligo European Task Force scores, with trends toward improvement of vitiligo lesion area and staging on Vitiligo European Task Force scores.24 More clinical trials with larger cohorts are needed to better evaluate the efficacy of antioxidants, including Polypodium leucotomos and Ginkgo biloba extracts.


NB-UVB is recommended in rapidly spreading vitiligo or extensive generalized vitiligo involving >5% to 10% of BSA.1 Its immunosuppressive effects and ability to induce differentiation of melanocytes and production of melanin makes it an effective therapy.25 A starting regimen of 200 mJ, delivered twice or thrice weekly, is appropriate in all phototypes, as it avoids risk of phototoxic reactions.26 Once asymptomatic, when light pink erythema lasting less than 24 hours (the treatment endpoint) is no longer observed, the dose can be escalated in 10% to 20% increments until this endpoint is reestablished.26 Patients should be warned of the risk of phototoxicity, and if this occurs, the next dose should be decreased or skipped, depending on the severity of the reaction. Alternatively, a fixed dosing schedule may be used that considers skin phototype differences in minimum erythema dose,27 but this is only recommended in darker skin phototypes due to the increased risk of phototoxic reactions.26

In patients with limited BSA of vitiligo (<10%) or in early, segmental disease, targeted phototherapy (excimer lasers and excimer lamps), is appropriate.28,29 This approach avoids the generalized skin tanning effect induced by NB-UVB, although it does not address disease stabilization since clinically unaffected skin is not treated.1

Either twice or thrice weekly phototherapy may be prescribed, as available comparison studies have not demonstrated superior efficacy in the final degree of repigmentation.30,31 In studies using excimer laser, onset of repigmentation was observed earlier with thrice weekly dosing and repigmentation had greater dependence upon the total number of treatments, which likely can be extrapolated to NB-UVB phototherapy.1,31

The Vitiligo Working Group recently released guidelines on the use of NB-UVB that advise the maximal acceptable delivered NB-UVB dose in a given treatment as 1500 mJ/cm2 and 3000 mJ/cm2 for the face and body, respectively.26 In patients with skin phototypes IV-VI, the Vitiligo Working Group advises against defining an upper limit of NB-UVB dosing. In patients with skin phototypes I-III, a NB-UVB dosing upper limit is not suggested, as limited long-term studies are available to investigate the association between cumulative NB-UVB exposure and the potential for cutaneous malignancy, which remains a concern.26 Skin phototype and photosensitivity may also be used to guide upper limits of NB-UVB dosing.1

NB-UVB has become the preferred route of phototherapy as it has been demonstrated to be more efficacious, lacks a photosensitizer, requires a lower cumulative dose, and has fewer adverse effects compared to PUVA.32 NB-UVB is also safe in children and pregnant or lactating women.1 PUVA may still be an option in darker skin phototypes and treatment refractory vitiligo.1 Though concern exists, studies demonstrating increased risk of cutaneous malignancy with PUVA or NB-UVB are lacking. Recent literature suggests vitiligo may be protective against nonmelanoma and melanoma skin cancer.33

Surgical Management

Surgical therapies may be considered in vitiligo that is local or generalized, stable, or untreated for over a year since onset; it is also appropriate in patients who have failed a 6-month course of topical therapy with or without phototherapy.1 In generalized vitiligo, outcomes are less promising, which is attributable to the unstable disease course.

Disease stability is an important variable in surgical candidate selection. Published studies define stability as the lack of new or expanding depigmented patches for 6 months to 2 years. Other cutaneous markers of instability include the presence of koebnerization, confetti-like macules of depigmentation, trichrome pattern, or inflammatory borders.1 Patient report, serial photography, and validated scoring systems such as the Vitiligo Area Severity Index, Vitiligo European Task Force assessment, and Vitiligo Disease Activity Score can be used to confirm stability.1 In uncertain cases, a test punch graft in a stable, depigmented lesion may be performed.1

Recipient site (RS) locations on the face and neck have the most favorable repigmentation outcomes, followed by the extremities (excluding digits), and then the trunk.34 Acrofacial vitiligo (including distal fingertips and periungual and perioral areas) typically exhibits poor responses to repigmentation.35 Skin overlying joints also has poor treatment responses due to susceptibility to trauma.35 History of keloid formation, coagulopathy, and blood-borne infections should be considered, among other contraindications to surgery.1 Surgical therapy can be divided into tissue- and cellular-based grafting techniques.

Tissue Grafting Techniques

Tissue grafting involves transfer of intact tissue from an area of normal, unaffected skin (donor site, DS) to an area of depigmented skin (RS). Many tissue grafting techniques are available, but suction blister epidermal grafting and minipunch grafting are the most widely utilized.

In suction blister epidermal grafting, blisters are raised, harvested, and transferred from a DS to RS. Suction blister epidermal grafting is useful for difficult to treat areas such as the eyelids.36 Complications such as peripheral ‘halo’ depigmentation, milia, hypertrophy, and hyperpigmentation (especially in darker skin phototypes) may occur, including infection rarely.37

Using minipunch grafting, grafts are transferred from DS into RS chambers approximately 5 to 10 mm apart from each other, with slightly larger DS punches taken to account for graft contracture. Complications such as cobblestoning, color mismatch, hypertrophic scarring, keloid formation, and graft rejection can occur at the RS, and depigmentation and scarring at the DS. Minipunch grafting is considered the easiest, fastest, and most cost-effective surgical treatment and, with the exception of the angle of the mouth, can be used anywhere.38

Follicular unit transplant (FUT) capitalizes on the concept that pigmentation can be restored to affected vitiligo patches by targeting reservoirs of undifferentiated stem cells associated with hair follicles.39 Epidermal removal (or ultraviolet radiation) can induce inactive melanocytes to convert to active melanocytes that can then migrate upwards to the epidermis from the outer root sheath to induce perifollicular repigmentation.40 Donor grafts are typically harvested from the posterior-auricular or occipital scalp using the ‘strip method’ (also known as the FUT method), then dissected into follicular units and inserted with jeweler’s forceps into slits made at the RS using either a hair transplantation machine, curved cutting needle, or an 18-guage needle.41 FUT can be advantageous for hair-bearing sites, including difficult to treat areas such as the eyelashes.42

Follicular unit extraction accomplishes hair follicle isolation via 1-mm punch biopsies that are subsequently transferred to RS chambers created via 1-mm punch biopsies, spaced approximately 3 to 10 mm apart.41 In contrast to FUT, follicular unit extraction is considered an easier procedure and is preferred when limited DS area is available and also favored as a spot-treatment for achromic areas that have not repigmented following FUT.42

Cellular Grafting Techniques

Cellular grafting involves transferring melanocytes and keratinocytes from a DS to the RS as a suspension with or without the use of cell culture. Noncultured epidermal suspensions (also referred to as a melanocyte keratinocyte transplant procedure; NCES) has gained worldwide acceptance as a standard for vitiligo grafting, as it can be performed in a single office visit and does not require use of a laboratory.1

The main advantage of NCES is the small DS area required to cover a large RS area, in a 1:10 ratio, respectively. An ultra-thin skin graft is harvested from the DS and following cell processing, a cellular suspension is formed and applied to a RS denuded to the dermal-epidermal junction by either dermabrasion or ablative carbon dioxide laser.

Hair follicle outer root sheath cell suspensions were somewhat recently introduced in 2009 by Vanscheidt and Hunziker.43 This method involves the harvesting of hair follicles using the follicular unit extraction method, induction of cell separation using trypsin, incubation, centrifugation, and eventually application of collected cells to the RS. A notable drawback to hair follicle outer root sheath cell suspension is the low cell yield.44

Treatment-Refractory Options

A lack of response, delineated by lack of stability or repigmentation following 3 and 6 months of combination therapy, respectively, should warrant consideration of other treatment modalities to improve dyschromia. Disease extent and impact on quality of life can guide treatment selection.

Camouflaging Agents

In vitiligo, camouflaging agents are broadly classified as temporary or permanent. Temporary treatment options include foundation and sunless-tanners, whereas permanent methods include micropigmentation (tattooing).45 The ideal camouflaging agent is one that is waterproof, sweat resistant, opaque, and demonstrates good skin color match.45

Camouflaging makeup foundations contain 25% more pigment compared to traditional makeup and are generally waterproof, decreasing the need for reapplication.45 Dihydroxyacetone is a sunless tanning product that induces temporary staining of the skin by reacting with proteins in the stratum corneum to form brown chromophores termed melanoidins.46 Dihydroxyacetone provides longer-lasting coverage (approximately 5 to 7 days),47 though use may be limited by poor color match, allergic contact dermatitis,48 and the potential cytotoxic effect on keratinocytes as seen in a recent in vitro study.49

Micropigmentation (skin tattooing) is generally not recommended due to the risk of koebnerization and color variations over time, secondary to incorrect depth of pigment positioning, resulting in the need for re-application. Oxidation of tattoos containing metal oxides can also lead to a black discoloration, which can be difficult to remove.45 Summer tanning can also lead to undesirable skin color contrasts.50 Other reactions, including contact dermatitis, granulomatous reactions, and acquired transmission of herpes simplex virus, human immunodeficiency virus, hepatitis B and C, and secondary infections may also occur.45

Depigmentation Therapies

In patients with extensive, treatment-refractory vitiligo involving greater than 50% of the BSA, depigmentation therapies can be considered.1 Monobenzyl ether of hydroquinone (MBEH) is the only drug approved by the US Food and Drug Administration to induce depigmentation.1 In areas of residual pigmentation, 20% MBEH can be applied twice daily. Lack of response after 4 months of therapy is an indication to increase to 30% MBEH, and if no response is observed by 6 months, MBEH should be discontinued.1 Once complete depigmentation is achieved, applications can be reduced to a few times per week as maintenance. Complete depigmentation typically takes approximately 4 to 12 months, although darker skin phototypes may require longer treatment.1 Side effects include irritant contact dermatitis51 and rarely conjunctival melanosis.52 Mequinol is a phenol derivative that may be used to achieve depigmentation, though onset of depigmentation is typically slower.1

Laser-mediated depigmentation may be used to target remaining melanosomes in melanocytes through photothermolysis and photoacoustic effects.53,54 The Q-switched ruby (694 nm), Q-switched alexandrite (755 nm), and Q-switched Nd:YAG lasers (532 nm), are most commonly used. This modality is usually reserved for treatment resistant areas on the hands and face. The potential for koebnerization associated with laser therapy can also be an asset to enhance depigmentation.55

New Treatments in Vitiligo

Recent studies reveal the IFN-y-CXCL10 axis may be an effective target to treat vitiligo, which has given rise to a new class of targeted immunotherapies, the Janus kinase inhibitors.56 Significant repigmentation has been reported following treatment with 2 oral Janus kinase inhibitors, tofacitinib57 and ruxolitinib.58 Topical ruxolitinib has also shown efficacy, especially with respect to facial repigmentation.59 Combination with natural sunlight or NB-UVB may lead to improvements in their efficacy, as observed using oral tofacitinib.60 Although these therapies appear promising, studies involving larger cohorts are needed to validate their efficacy. A multi-center phase II clinical trial ( Identifier: NCT03099304) involving the use of topical ruxolitinib in vitiligo is currently underway.

Afamelanotide, a synthetic alpha melanocyte stimulating hormone, requires the presence of melanocortin 1 receptor and supplementation with NB-UVB to stimulate melanoblast differentiation, and may be an effective new vitiligo therapy.61


Frequent disease response monitoring is important to ensure appropriate management and allow for recognition of treatment failure early on, allowing for transition to alternative, potentially more effective therapies as needed. Generally, it is recommended that patients be reevaluated every 3 to 6 months until an effective, stable treatment regimen is established.1 Due to the significant psychosocial burden experienced by patients with vitiligo, providers should be mindful of the importance of incorporating conversations addressing mental health into patient visits.


Vitiligo is a psychosocially debilitating disease requiring a multidisciplinary approach to treatment. Patients should be made aware of all of the options available geared at repigmentation and depigmentation prior to formulating a treatment plan. Frequent follow-up for disease monitoring and incorporation of discussions centered on quality of life impact can provide treatment guidance and allow for individualized care.


  1. Rodrigues M, Ezzedine K, Hamzavi I, et al. Vitiligo Working Group. Current and emerging treatments for vitiligo. J Am Acad Dermatol. 2017 Jul;77(1):17-29.

  2. American Cancer Society. Key statistics for basal and squamous cell skin cancers. Last medical review: April 1, 2016; Last revised: January 8, 2019. Available at: detailedguide/skin-cancer-basal-and-squamous-cell-key-statistics. Accessed March 31, 2019.

  3. Lepe V, Moncada B, Castanedo-Cazares JP, et al. A double-blind randomized trial of 0.1% tacrolimus vs 0.05% clobetasol for the treatment of childhood vitiligo. Arch Dermatol. 2003 May;139(5):581-5.

  4. Taieb A, Alomar A, Bohm M, et al. Guidelines for the management of vitiligo: the European Dermatology Forum consensus. Br J Dermatol. 2013 Jan;168(1):5-19.

  5. Mehrabi D, Pandya AG. A randomized, placebo-controlled, double-blind trial comparing narrowband UV-B Plus 0.1% tacrolimus ointment with narrowband UV-B plus placebo in the treatment of generalized vitiligo. Arch Dermatol. 2006 Jul;142(7):927-9.

  6. Ostovari N, Passeron T, Lacour JP, et al. Lack of efficacy of tacrolimus in the treatment of vitiligo in the absence of UV-B exposure. Arch Dermatol. 2006 Feb;142(2):252-3.

  7. Goktas EO, Aydin F, Senturk N, et al. Combination of narrow band UVB and topical calcipotriol for the treatment of vitiligo. J Eur Acad Dermatol Venereol. 2006 May;20(5):553-7.

  8. Mohammad T, Sommariva E, Parks-Miller A, et al. Improvement of vitiligo after concurrent treatment of hypothyroidism: A case report. Pigmentary Disorders. 2015 Oct 20;2:220.

  9. Pasricha JS, Khaitan BK. Oral mini-pulse therapy with betamethasone in vitiligo patients having extensive or fast-spreading disease. Int J Dermatol. 1993 Oct;32(10):753-7.

  10. Radakovic-Fijan S, Furnsinn-Friedl AM, Honigsmann H, et al. Oral dexamethasone pulse treatment for vitiligo. J Am Acad Dermatol. 2001 May; 44(5):814-7.

  11. Kanwar AJ, Mahajan R, Parsad D. Low-dose oral mini-pulse dexamethasone therapy in progressive unstable vitiligo. J Cutan Med Surg. 2013 Jul-Aug; 17(4):259-68.

  12. Sosa JJ, Currimbhoy SD, Ukoha U, et al. Confetti-like depigmentation: a potential sign of rapidly progressing vitiligo. J Am Acad Dermatol. 2015 Aug;73(2):272-5.

  13. Zhu S, Stavrovskaya IG, Drozda M, et al. Minocycline inhibits cytochrome c release and delays progression of amyotrophic lateral sclerosis in mice. Nature. 2002 May 2;417(6884):74-8.

  14. Kraus RL, Pasieczny R, Lariosa-Willingham K, et al. Antioxidant properties of minocycline: neuroprotection in an oxidative stress assay and direct radicalscavenging activity. J Neurochem. 2005 Aug;94(3):819-27.

  15. Parsad D, Kanwar A. Oral minocycline in the treatment of vitiligo–a preliminary study. Dermatol Ther. 2010 May-Jun;23(3):305-7.

  16. Singh A, Kanwar AJ, Parsad D, et al. Randomized controlled study to evaluate the effectiveness of dexamethasone oral minipulse therapy versus oral minocycline in patients with active vitiligo vulgaris. Indian J Dermatol Venereol Leprol. 2014 Jan-Feb;80(1):29-35.

  17. Siadat AH, Zeinali N, Iraji F, et al. Narrow-band ultraviolet B versus oral minocycline in treatment of unstable vitiligo: a prospective comparative trial. Dermatol Res Pract. 2014 2014:240856.

  18. Garza-Mayers AC, Kroshinsky D. Low-dose methotrexate for vitiligo. J Drugs Dermatol. 2017 Jul 1;16(7):705-6.

  19. Singh H, Kumaran MS, Bains A, et al. A randomized comparative study of oral corticosteroid minipulse and low-dose oral methotrexate in the treatment of unstable vitiligo. Dermatology. 2015 231(3):286-90.

  20. Speeckaert R, Dugardin J, Lambert J, et al. Critical appraisal of the oxidative stress pathway in vitiligo: a systematic review and meta-analysis. J Eur Acad Dermatol Venereol. 2018 Jul;32(7):1089-98.

  21. Middelkamp-Hup MA, Bos JD, Rius-Diaz F, et al. Treatment of vitiligo vulgaris with narrow-band UVB and oral Polypodium leucotomos extract: a randomized double-blind placebo-controlled study. J Eur Acad Dermatol Venereol. 2007 Aug;21(7):942-50.

  22. Reyes E, Jaen P, de las Heras E, et al. Systemic immunomodulatory effects of Polypodium leucotomos as an adjuvant to PUVA therapy in generalized vitiligo: A pilot study. J Dermatol Sci. 2006 Mar;41(3):213-6.

  23. Parsad D, Pandhi R, Juneja A. Effectiveness of oral Ginkgo biloba in treating limited, slowly spreading vitiligo. Clin Exp Dermatol. 2003 May;28(3):285-7.

  24. Szczurko O, Shear N, Taddio A, et al. Ginkgo biloba for the treatment of vitiligo vulgaris: an open label pilot clinical trial. BMC Complement Altern Med. 2011 Mar 15;11:21.

  25. De Francesco V, Stinco G, Laspina S, et al. Immunohistochemical study before and after narrow band (311 nm) UVB treatment in vitiligo. Eur J Dermatol. 2008 May-Jun;18(3):292-6.

  26. Mohammad TF, Al-Jamal M, Hamzavi IH, et al. The Vitiligo Working Group recommendations for narrowband ultraviolet B light phototherapy treatment of vitiligo. J Am Acad Dermatol. 2017 May;76(5):879-88.

  27. Caron-Schreinemachers AL, Kingswijk MM, Bos JD, et al. UVB 311 nm tolerance of vitiligo skin increases with skin photo type. Acta Derm Venereol. 2005 85(1):24-6.

  28. Ezzedine K, Eleftheriadou V, Whitton M, et al. Vitiligo. Lancet. 2015 Jul 4; 386(9988):74-84.

  29. Do JE, Shin JY, Kim DY, et al. The effect of 308nm excimer laser on segmental vitiligo: a retrospective study of 80 patients with segmental vitiligo. Photodermatol Photoimmunol Photomed. 2011 Jun;27(3):147-51.

  30. Shen Z, Gao TW, Chen L, et al. Optimal frequency of treatment with the 308-nm excimer laser for vitiligo on the face and neck. Photomed Laser Surg. 2007 Oct;25(5):418-27.

  31. Hofer A, Hassan AS, Legat FJ, et al. Optimal weekly frequency of 308-nm excimer laser treatment in vitiligo patients. Br J Dermatol. 2005 May;152(5):981-5.

  32. Whitton ME, Pinart M, Batchelor J, et al. Interventions for vitiligo. Cochrane Database Syst Rev. 2015 Feb 24;(2):CD003263.

  33.  Jin Y, Birlea SA, Fain PR, et al. Variant of TYR and autoimmunity susceptibility loci in generalized vitiligo. N Engl J Med. 2010 May 6;362(18):1686-97.

  34. Mulekar SV, Isedeh P. Surgical interventions for vitiligo: an evidence-based review. Br J Dermatol. 2013 Oct;169 Suppl 3:57-66.

  35. Ghia D, Mulekar SV, Hamzavi IH. Surgical management of vitiligo. In: Hamzavi IH, Mahmoud BH, Isedeh PN, editors. Handbook of vitiligo: basic science and clinical management. London: JP Medical Publishers; p133 (2016).

  36. Gou D, Currimbhoy S, Pandya AG. Suction blister grafting for vitiligo: efficacy and clinical predictive factors. Dermatol Surg. 2015 May;41(5):633-9.

  37. Khunger N, Kathuria SD, Ramesh V. Tissue grafts in vitiligo surgery – past, present, and future. Indian J Dermatol. 2009 54(2):150-8.

  38. Lahiri K. Evolution and evaluation of autologous mini punch grafting in vitiligo. Indian J Dermatol. 2009 54(2):159-67.

  39. Cui J, Shen LY, Wang GC. Role of hair follicles in the repigmentation of vitiligo. J Invest Dermatol. 1991 Sep;97(3):410-6.

  40. Staricco RG. Amelanotic melanocytes in the outer sheath of the human hair follicle. J Invest Dermatol. 1959 Dec;33:295-7.

  41. Thakur P, Sacchidanand S, Nataraj HV, et al. A study of hair follicular transplantation as a treatment option for vitiligo. J Cutan Aesthet Surg. 2015 Oct-Dec;8(4):211-7.

  42. Malakar S, Dhar S. Repigmentation of vitiligo patches by transplantation of hair follicles. Int J Dermatol. 1999 Mar;38(3):237-8.

  43. Vanscheidt W, Hunziker T. Repigmentation by outer-root-sheath-derived melanocytes: proof of concept in vitiligo and leucoderma. Dermatology. 2009 218(4):342-3.

  44. Kumar A, Mohanty S, Sahni K, et al. Extracted hair follicle outer root sheath cell suspension for pigment cell restoration in vitiligo. J Cutan Aesthet Surg. 2013 Apr;6(2):121-5.

  45. Kaliyadan F, Kumar A. Camouflage for patients with vitiligo. Indian J Dermatol Venereol Leprol. 2012 Jan-Feb;78(1):8-15.

  46. Draelos ZD. Self-tanning lotions: are they a healthy way to achieve a tan? Am J Clin Dermatol. 2002 3(5):317-8.

  47. Rajatanavin N, Suwanachote S, Kulkollakarn S. Dihydroxyacetone: a safe camouflaging option in vitiligo. Int J Dermatol. 2008 Apr;47(4):402-6.

  48. Zokaie S, Singh S, Wakelin SH. Allergic contact dermatitis caused by dihydroxyacetone – optimal concentration and vehicle for patch testing. Contact Dermatitis. 2011 May;64(5):291-2.

  49. Smith KR, Granberry M, Tan MCB, et al. Dihydroxyacetone induces G2/M arrest and apoptotic cell death in A375P melanoma cells. Environ Toxicol. 2018 Mar;33(3):333-42.

  50. Khunger N, Molpariya A, Khunger A. Complications of tattoos and tattoo removal: stop and think before you ink. J Cutan Aesthet Surg. 2015 Jan-Mar; 8(1):30-6.

  51. Nordlund JJ, Forget B, Kirkwood J, et al. Dermatitis produced by applications of monobenzone in patients with active vitiligo. Arch Dermatol. 1985 Sep;121(9):1141-4.

  52. Hedges TR, 3rd, Kenyon KR, Hanninen LA, et al. Corneal and conjunctival effects of monobenzone in patients with vitiligo. Arch Ophthalmol. 1983 Jan;101(1):64-8.

  53. Rao J, Fitzpatrick RE. Use of the Q-switched 755-nm alexandrite laser to treat recalcitrant pigment after depigmentation therapy for vitiligo. Dermatol Surg. 2004 Jul;30(7):1043-5.

  54. Nelson JS, Applebaum J. Treatment of superficial cutaneous pigmented lesions by melanin-specific selective photothermolysis using the Q-switched ruby laser. Ann Plast Surg. 1992 Sep;29(3):231-7.

  55. Majid I, Imran S. Depigmentation therapy with Q-switched Nd: YAG laser in universal vitiligo. J Cutan Aesthet Surg. 2013 Apr;6(2):93-6.

  56. Frisoli ML, Harris JE. Vitiligo: Mechanistic insights lead to novel treatments. J Allergy Clin Immunol. 2017 Sep;140(3):654-62.

  57. Craiglow BG, King BA. Tofacitinib citrate for the treatment of vitiligo: a pathogenesis-directed therapy. JAMA Dermatol. 2015 Oct;151(10):1110-2.

  58. Harris JE, Rashighi M, Nguyen N, et al. Rapid skin repigmentation on oral ruxolitinib in a patient with coexistent vitiligo and alopecia areata (AA). J Am Acad Dermatol. 2016 Feb;74(2):370-1.

  59. Rothstein B, Joshipura D, Saraiya A, et al. Treatment of vitiligo with the topical Janus kinase inhibitor ruxolitinib. J Am Acad Dermatol. 2017 Jun;76(6):1054-60 e1.

  60. Liu LY, Strassner JP, Refat MA, et al. Repigmentation in vitiligo using the Janus kinase inhibitor tofacitinib may require concomitant light exposure. J Am Acad Dermatol. 2017 Oct;77(4):675-82 e1.

  61. Lim HW, Grimes PE, Lebwohl M. Indications and limitations of afamelanotide for treating vitiligo-reply. JAMA Dermatol. 2015 Mar;151(3):350.

Purchase Article PDF for $1.99