What makes UpToDate so powerful?

  • over 10000 topics
  • 22 specialties
  • 5,700 physician authors
  • evidence-based recommendations
See more sample topics
Find Print
0 Find synonyms

Find synonyms Find exact match

Vitiligo: Management and prognosis
UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2016 UpToDate®
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2016 UpToDate, Inc.
Vitiligo: Management and prognosis
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2016. | This topic last updated: Aug 24, 2016.

INTRODUCTION — Vitiligo is a relatively common acquired chronic disorder of pigmentation characterized by the development of white macules on the skin due to loss of epidermal melanocytes [1,2]. The depigmented areas are often symmetrical and usually increase in size with time. Given the contrast between the white patches and areas of normal skin, the disease is most disfiguring in darker skin types and has a profound impact on the quality of life of children and adults [3,4]. Patients with vitiligo often experience stigmatization, isolation, and low self-esteem [5-8].

Although there is no cure for the disease, the available treatments may halt the progression of the disease and induce varying degrees of repigmentation with acceptable cosmetic results in many cases. This topic review will discuss the management of vitiligo. The pathogenesis, clinical features, and diagnosis of vitiligo are discussed separately. Other pigmentation disorders are also discussed separately.

(See "Vitiligo: Pathogenesis, clinical features, and diagnosis".)

(See "Acquired hypopigmentation disorders other than vitiligo".)

(See "Approach to the patient with hyperpigmentation disorders".)

(See "Melasma".)

(See "Postinflammatory hyperpigmentation".)

PATIENT EVALUATION

Assessment of severity — The evaluation of the patient with vitiligo involves a detailed history and a complete skin examination to assess disease severity and individual prognostic factors. Factors that may influence the approach to treatment include:

Age at onset of lesions

Type of vitiligo (segmental, nonsegmental)

Mucosal involvement, Koebner phenomenon

Rate of progression or spread of lesions

Previous episodes of repigmentation

Type and response to previous treatments

Family history of vitiligo and/or autoimmune diseases

Presence of concomitant diseases

Current medications and supplements

Occupation, exposure to chemicals

Effects of disease on the quality of life

A full-body skin examination should be performed to assess the extent of the disease, with particular attention to sites of vitiligo predilection, such as the lips and perioral area, periocular areas, dorsal surface of the hands, fingers, flexor surface of the wrists, elbows, axillae, nipples, umbilicus, sacrum, groin, inguinal/anogenital regions, and knees [9]. The percentage of the body area involved can be estimated by the so-called 1 percent rule or "palm method." In both children and adults, the palm of the hand, including the fingers, is approximately 1 percent of the total body surface area (TBSA), while the palm excluding the fingers is approximately 0.5 percent of the TBSA. An alternative method is the "rule of nines":

Each leg represents 18 percent of the TBSA.

Each arm represents 9 percent of the TBSA.

The anterior and posterior trunk each represent 18 percent of the TBSA.

The head represents 9 percent of the TBSA.

Goals of treatment — The goals of treatment for vitiligo should be set with the individual patient or parents in the case of children, based upon the patient's age and skin type, the extent, location, and degree of disease activity, and the impact of the disease on the patient’s quality of life. An open discussion with the patient about the limitations of treatment may be helpful to create realistic expectations.

Nonsegmental vitiligo has an unpredictable course, and treatment is often challenging. However, multiple therapies, including topical agents, light therapies, and autologous grafting procedures, have demonstrated efficacy for repigmentation of vitiligo [10]. The response to treatments is generally slow and may be highly variable among patients and among different body areas in the same patient. The best outcomes are often achieved in darker skin types (Fitzpatrick IV to VI), although satisfactory results are often seen also in lighter skin types (Fitzpatrick II, III). Facial and truncal lesions respond well to treatment, while acral areas are extremely difficult to treat.

Psychosocial aspects — The patient’s psychological profile and ability to cope with a lifelong disease should be carefully evaluated at the time of treatment planning. Psychologic support should be offered to patients if needed. (See 'Psychologic interventions' below.)

APPROACH — Our approach to the management of patients with vitiligo is generally consistent with published guidelines [11,12]. Topical, systemic, and light-based therapies are available for the stabilization and repigmentation of vitiligo (table 1) [13-17]. Treatment modalities are chosen in the individual patient on the basis of the disease severity, patient preference (including cost and accessibility), and response evaluation. Despite treatment, however, vitiligo has a highly unpredictable course, and the long-term persistence of repigmentation cannot be predicted.

Stabilization of rapidly progressive disease — For patients who experience rapid progression of vitiligo, with depigmented macules spreading over a few weeks or months, we suggest low-dose oral corticosteroids as first-line therapy for the stabilization (cessation of spread) of the disease (table 1). Oral prednisone is given at the dose of 5 to 10 mg per day in children and 10 to 20 mg per day in adults for a maximum of two weeks. If needed, treatment can be repeated in four to six weeks.

In adult patients, alternatives to oral prednisone include oral mini-pulse therapy with dexamethasone 2.5 mg on two consecutive days weekly for an average of three months or intramuscular triamcinolone 40 mg in a single administration. Treatment with triamcinolone can be repeated in four to six weeks for a maximum of three injections. (See 'Systemic corticosteroids' below.)

Stabilization therapy can be given with or without concomitant narrowband ultraviolet B (NB-UVB) phototherapy. However, for patients with active disseminated disease affecting multiple anatomic sites, we suggest that systemic corticosteroids and NB-UVB phototherapy be initiated concomitantly. The disease is expected to stabilize in one to three months.

In both adults and children in whom systemic corticosteroids are contraindicated, NB-UVB phototherapy alone may be used to stabilize active vitiligo. NB-UVB is administered two to three times weekly. (See 'Narrowband ultraviolet B phototherapy' below.)

Vitiligo involving <10 percent of the TBSA

Localized disease — In patients with nonsegmental stable vitiligo (no increase in size of existing lesions and absence of new lesions in the previous three to six months) that involves <10 percent of the total body surface area (TBSA) and is limited to the face, neck (picture 1), trunk, or extremities, mid- to high-potency topical corticosteroids (groups two to four (table 2)) are the first-line therapy [12,18]. High-potency and mid-potency topical corticosteroids are applied to the involved skin once and twice daily, respectively. Agents with negligible systemic or local side effects, such as mometasone furoate, are preferred [12]. (See 'Topical corticosteroids' below.)

There are no studies evaluating the optimal duration of treatment with topical corticosteroids. In the author’s experience, topical corticosteroids can be used safely for two to three months, interrupted for one month, and then resumed for an additional two or three months. Others suggest a discontinuous scheme (eg, once-daily application for 15 days per month for six months) [11,12,19].

Patients must be monitored closely for adverse effects of topical corticosteroids, which include skin atrophy, telangiectasias, hypertrichosis, and acneiform eruptions. Limited quantities should be prescribed.

Topical calcineurin inhibitors (tacrolimus and pimecrolimus) are the preferred first-line therapy in patients with limited disease involving the face or areas at high risk for skin atrophy. Topical calcineurin inhibitors are generally applied twice daily. They can also be used in combination with a topical corticosteroid for the first month or two, applying each one once daily. (See 'Topical calcineurin inhibitors' below.)

For patients with limited disease who do not respond to topical corticosteroids or topical calcineurin inhibitors, targeted phototherapy administered twice weekly is an option (picture 2). (See 'Targeted phototherapy' below.)

Disseminated disease — For patients with disseminated areas of depigmentation affecting multiple anatomic sites but overall involvement of less than 10 percent of the TBSA, we suggest NB-UVB phototherapy as first-line therapy. NB-UVB phototherapy is administered two to three times weekly. In the author’s experience, less than 50 treatments are usually sufficient to achieve optimal outcomes. (See 'Narrowband ultraviolet B phototherapy' below.)

Segmental vitiligo — Topical corticosteroids, calcineurin inhibitors, or targeted phototherapy are the first-line therapy for segmental vitiligo. (See 'Topical corticosteroids' below and 'Topical calcineurin inhibitors' below and 'Targeted phototherapy' below.)

NB-UVB phototherapy can be used for more extensive disease affecting multiple dermatomes. For patients who do not respond to topical or light therapies, autologous grafting is a second-line option [20]. Given the stable nature of segmental vitiligo, long-term repigmentation can be achieved with autologous melanocyte transplantation [21]. (See 'Narrowband ultraviolet B phototherapy' below and 'Surgical therapies' below.)

Localized recalcitrant vitiligo — Surgical procedures are a therapeutic option for patients with localized stable vitiligo that does not respond to topical agents or NB-UVB phototherapy. Autologous grafting techniques include 1-mm punch grafts, suction blister grafts, or cellular suspensions. While all these techniques have proven success, most are technically challenging and expensive. One-millimeter punch grafts, however, can be performed with ease and without the need of special devices or equipment. (See 'Surgical therapies' below.)

Vitiligo involving 10 to 40 percent of the TBSA — For adults and children with stable nonsegmental vitiligo involving 10 to 40 percent of the TBSA, we suggest NB-UVB as first-line therapy (picture 3). (See 'Narrowband ultraviolet B phototherapy' below.)

NB-UVB is administered two to three times per week for an average of 9 to 12 months. Follicular areas of repigmentation usually begin to appear after 15 to 20 NB-UVB treatments (picture 4). If patients are responding well with continued repigmentation, treatment can be maintained beyond 9 to 12 months and up to 24 months or 200 sessions and then tapered off. Mid-potency topical corticosteroids or topical calcineurin inhibitors are often intermittently used in combination with phototherapy.

Home NB-UVB phototherapy is an option for patients unable to travel to the clinician’s office for weekly treatments [22]. Whole-body or portable, handheld units are available on the market (sample brand names include Daavlin, National Biological Solarc Systems). Patients should be provided with detailed instructions on the use of the home phototherapy units and return for in-office clinician follow-up on a regular basis.

Vitiligo involving >40 percent of the TBSA — NB-UVB is the first-line therapy for patients with extensive vitiligo involving greater than 40 percent of the TBSA. The suggested regimen and duration of treatment are similar to that discussed above for patients with more limited disease. (See 'Vitiligo involving 10 to 40 percent of the TBSA' above.)

However, for patients with extensive recalcitrant vitiligo that does not respond to repigmentation regimens and for patients with extensive vitiligo who do not desire undergoing repigmentation treatments, depigmentation of residual normally pigmented areas utilizing topical monobenzyl ether of hydroquinone (monobenzone) may be an option. Depigmentation therapy is usually initiated with monobenzone 10% cream for one month and then continued with monobenzone 20% cream. Monobenzone is applied on the areas of residual pigmentation once or twice daily; we typically treat exposed areas first. These sites include the face, neck, upper extremities, chest, and lower legs. Depigmentation usually begins at distant sites (where the drug has not been applied) after three to six months of continued use. Depigmentation therapy may require one to three years to achieve optimal outcomes. (See 'Depigmentation' below.)

Side effects of monobenzone are dose-dependent and include irritant contact dermatitis and severe xerosis. Monobenzone should never be used as a lightening agent in cases other than vitiligo. It will induce vitiligo in normal individuals.

Response assessment — Initial response to treatment is in most cases indicated by the appearance of perifollicular areas of repigmentation in the vitiliginous patch, which usually begins 8 to 12 weeks after the initiation of treatment or after 15 to 20 NB-UVB sessions (picture 4). Some patients may show a diffuse repigmentation pattern or a combination of diffuse and perifollicular [23,24]. Photographs should be taken before starting treatment and at each follow-up visit to evaluate the degree of repigmentation.

In patients who respond well to treatment and achieve optimal repigmentation, therapies can be gradually tapered and then discontinued. However, some patients may require maintenance treatment. Intermittent use of topical corticosteroids or topical calcineurin inhibitors (eg, twice weekly) and phototherapy every other week may be used as long-term maintenance treatments. For patients who relapse after stopping treatment or during the maintenance phase, another cycle of phototherapy can be administered.

TREATMENT MODALITIES

Topical therapies

Topical corticosteroids — Mid- to super-high-potency topical corticosteroids are commonly used as a first-line therapy for the treatment of limited vitiligo. Their efficacy is attributed to modulation of the immune response.

The efficacy of topical corticosteroids as monotherapy for the treatment of vitiligo is supported by a few small randomized trials [16]. A systematic review of 17 randomized trials examined the effect of topical corticosteroids in combination with other therapies (eg, narrowband ultraviolet B [NB-UVB], psoralen plus ultraviolet A with sunlight [PUVAsol], excimer laser) [25]. The combination of potent or super-potent topical corticosteroids (eg, betamethasone dipropionate, mometasone furoate, clobetasol propionate) with light therapies is more effective than light therapies alone in inducing repigmentation [26-28]. However, the quality of studies was generally poor, and the study results could not be pooled because of considerable heterogeneity in study design and outcome measure.

Adverse effects related to a prolonged use of topical corticosteroids, including folliculitis, mild atrophy, telangiectasia, and hypertrichosis, have been reported, generally in a small number of patients, in nearly all studies. Systemic absorption resulting in adrenal suppression is a concern when large areas of skin and areas with thin skin are treated for a prolonged time with potent steroids, especially in children [18].

Topical calcineurin inhibitors — Tacrolimus and pimecrolimus are topical immunomodulatory agents that affect the T-cell and mast-cell function and inhibit the synthesis and release of multiple proinflammatory cytokines, including interferon-gamma, tumor necrosis factor-alpha, interleukin (IL)-4, IL-5, and IL-10 [29-31]. In contrast with topical corticosteroids, topical calcineurin inhibitors do not induce skin atrophy, striae, or telangiectasias and are increasingly used for the treatment of facial vitiligo.

The efficacy of tacrolimus and pimecrolimus alone or in combination with other therapies for the treatment of nonsegmental vitiligo has been evaluated in several randomized trials including either adults or children with vitiligo [25].

In a randomized trial, 100 children (55 children with facial vitiligo; 45 with nonfacial vitiligo) were treated with topical corticosteroid (clobetasol propionate 0.05%), tacrolimus 0.1%, or placebo for six months [32]. Among children with facial vitiligo, the success rate (defined as repigmentation >50 percent) was the same in the topical corticosteroid and tacrolimus groups (58 percent); however, among children with nonfacial vitiligo, the success rate was higher in the topical corticosteroid group compared with the tacrolimus groups (39 versus 23 percent). The success rate in the placebo group was 7 percent.

Another randomized trial including 44 adult patients with stable vitiligo compared 0.1% tacrolimus ointment twice daily, 1% pimecrolimus cream twice daily, and NB-UVB phototherapy three times a week for 24 weeks [33]. At the end of the study, there was no significant difference among treatments in the repigmentation for any anatomical site.

In a 12-week open, randomized study, 53 patients with vitiligo were treated with 308 nm monochromatic excimer light (MEL) twice weekly plus 0.1% tacrolimus and oral vitamin E daily, 308 nm MEL twice weekly plus daily oral vitamin E, or daily oral vitamin E alone [34]. At the end of the study, good to excellent repigmentation was achieved in 70 percent of patients in the MEL plus tacrolimus and vitamin E group, 55 percent of those in the MEL plus vitamin E group, and in none of the patients in the vitamin E group.

In an open trial, 40 children with nonsegmental, focal, or segmental vitiligo were treated with 0.1% mometasone furoate cream once daily or 1% pimecrolimus cream twice daily for three months [35]. Moderate or marked responses were seen in 11 patients (55 percent) in the mometasone furoate group and in 7 (35 percent) in the pimecrolimus group, but the difference was not statistically significant.

Although the increased risk of skin cancer among transplant patients treated with systemic calcineurin inhibitors is well recognized, the use of topical calcineurin inhibitors does not seem to be associated with an increased risk for skin or systemic malignancies [36-38]. However, based upon animal studies documenting an increased risk of lymphoma and skin cancers associated with topical or systemic exposure to calcineurin inhibitors and to reports of cancer cases in children who used topical pimecrolimus or tacrolimus for atopic dermatitis, in 2006 the US Food and Drug Administration placed a boxed warning on the prescribing information for these medications. Labeling also recommends that these agents should not be used in combination with ultraviolet (UV) light therapy.

Unproven topical therapies — The benefit of topical vitamin D3 analogues in the treatment of vitiligo is controversial. A few small randomized trials evaluated the role of calcipotriol and tacalcitol in combination with psoralen plus ultraviolet A (PUVA), narrowband ultraviolet (NB-UV), or natural sunlight for the treatment of nonsegmental vitiligo with conflicting results [39-41].

In a prospective right-left 24-week comparative study including 24 patients with vitiligo, there were no statistically significant differences between the sides treated with NB-UVB monotherapy and the sides treated with NB-UVB plus calcipotriol [40].

In another right-left comparative study, 35 patients with generalized vitiligo applied calcipotriol 0.05 mg/g cream or placebo to the reference lesions one hour before PUVA treatment twice weekly [39]. Lesions on the side treated with calcipotriol plus PUVA had a fourfold increase in the likelihood of achieving greater than 75 percent repigmentation sooner than the side treated with placebo plus PUVA (mean number of PUVA sessions 9 and 12, respectively).

Phototherapy

Narrowband ultraviolet B phototherapy — NB-UVB involves the use of UV lamps with a peak emission of approximately 311 nm [42]. These shorter wavelengths provide higher-energy fluences and induce less cutaneous erythema. NB-UVB induces local immunosuppression and apoptosis; stimulates the production of melanocyte-stimulating hormones, basic fibroblasts, growth factor, and endothelin I; and increases melanocyte proliferation and melanogenesis [42-44]. (See "UVB therapy (broadband and narrowband)".)

Due to its lack of systemic toxicity and its good safety profile in both children and adults, NB-UVB phototherapy has emerged as the initial treatment of choice for patients with vitiligo involving >10 percent of the body surface area (BSA). NB-UVB can be used for both stabilization and repigmentation of vitiligo (picture 3).

A meta-analysis of three randomized trials comparing oral PUVA with NB-UVB found a 60 percent higher proportion of participants achieving >75 percent repigmentation in the NB-UVB group compared with the oral PUVA group [25]. The additive effect of tacrolimus ointment (0.1%) applied once daily combined with NB-UVB in the treatment of vitiligo has been evaluated in one randomized trial [45]. In this study, 40 patients with stable, symmetrical vitiligo were treated with tacrolimus ointment 0.1% on one side of their body and a placebo ointment on the other side plus whole-body NB-UVB two or three times weekly for at least three months. In 27 of 40 patients, a greater reduction in the target lesion area was seen in the side treated with tacrolimus compared with the side treated with NB-UVB alone (42 versus 29 percent). However, a possible increase in the risk of skin cancer with this combination therapy cannot be excluded.

Only a few small observational studies have evaluated the duration of repigmentation in patients with vitiligo treated with phototherapy. In a small observational study of 11 patients followed up for two years after treatment with NB-UVB phototherapy, five maintained areas of repigmentation and six experienced complete or partial relapse of vitiligo at previously repigmented sites [46]. In another study including 15 children treated with NB-UVB phototherapy and followed up for a mean of 12 months after completing treatment, six showed stable repigmentation, four further improvement, and three complete or partial regression of the pigmentation achieved with treatment [47].

PUVA photochemotherapy — Historically, photochemotherapy with topical or systemic PUVA radiation was the "gold standard" treatment for the repigmentation of vitiligo but has been largely replaced by NB-UVB phototherapy. PUVA is associated with substantial adverse effects, including phototoxicity and gastrointestinal discomfort, and requires patients to use ocular protection for 12 to 24 hours following treatment. In addition, the long-term risk of skin cancer is well established for PUVA [48]. (See "Psoralen plus ultraviolet A (PUVA) photochemotherapy".)

Targeted phototherapy — Targeted phototherapy using 308 nm monochromatic excimer lamps or lasers has demonstrated efficacy for the treatment of localized vitiligo (picture 2) [49]. These devices deliver high-intensity light only to the affected areas while avoiding exposure of the healthy skin and lowering the cumulative ultraviolet B (UVB) dose. (See "Targeted phototherapy".)

A systematic review of six randomized trials (411 patients with 764 lesions) found that excimer lamps and excimer lasers were equally effective in inducing ≥50 percent and ≥75 percent repigmentation [50]. Although the repigmentation may occur more rapidly with more frequent weekly treatments, the final result appears to be related to the overall number of treatment sessions rather than their frequency [51].

As with NB-UVB, targeted phototherapy can work synergistically with topical therapies, including tacrolimus ointment and topical corticosteroids [12,52].

In a study of eight patients with vitiligo, 24 symmetric vitiliginous areas were treated with the excimer laser three times per week for a total of 24 treatments [53]. Topical tacrolimus ointment or placebo was applied to randomized affected areas twice daily throughout the length of the trial. Fifty percent of the areas treated with the combination excimer laser and topical tacrolimus achieved ≥75 percent repigmentation compared with 20 percent of the areas treated with placebo.

In a 12-week open randomized study, 53 patients with vitiligo were treated with 308 nm MEL twice weekly plus 0.1% tacrolimus and oral vitamin E daily, 308 nm MEL twice weekly plus daily oral vitamin E, or daily oral vitamin E alone [34]. At the end of the study, good to excellent repigmentation was achieved in 70 percent of patients in the MEL plus tacrolimus and vitamin E group, 55 percent of those in the MEL plus vitamin E group, and in none of the patients in the vitamin E group.

Systemic therapies

Systemic corticosteroids — Low-dose oral corticosteroids are generally utilized for the stabilization of rapidly progressive vitiligo, often in combination with NB-UVB phototherapy. Evidence for their efficacy in halting the spread of vitiligo is limited to a few uncontrolled studies [54-56].

In one study, 81 patients were treated with prednisolone 0.3 mg/kg per day for two months, and then the dose was progressively reduced in the subsequent three months [54]. Control of disease progression was achieved in approximately 90 percent of patients and repigmentation in 74 percent.

In another study, 40 patients with extensive or rapidly spreading vitiligo were treated with oral mini-pulses of betamethasone or dexamethasone (5 mg in single dose) on two consecutive days per week for several months. After one to three months, vitiligo progression was arrested in 32 of 36 patients with active disease [55].

Oral corticosteroids are not effective as a repigmenting therapy for stable vitiligo. In a small open-label trial, 86 patients with progressive nonsegmental vitiligo were treated with oral mini-pulses of betamethasone (0.1 mg/kg twice weekly on two consecutive days for three months followed by 1 mg every month for the following three months) alone or in combination with PUVA, NB-UVB, or broadband UVB [57]. At six months, marked or moderate improvement was achieved in 15 percent of patients treated with corticosteroids alone versus 85 percent of patients treated with corticosteroids plus PUVA, 81 percent of those treated with corticosteroids plus NB-UVB, and 33 percent of those treated with corticosteroids plus broadband-UVB.

Complementary and alternative therapies — Oral supplementation with antioxidants and vitamins is often used as an adjunctive treatment for vitiligo, usually in combination with phototherapy. However, there is limited evidence from high-quality studies to support their use.

Vitamins – A few small uncontrolled studies have reported stabilization and repigmentation in vitiligo patients treated with UVB phototherapy and high-dose vitamin supplementation, vitamin C, vitamin B12, and folic acid [58,59].

Alpha-lipoic acid – Alpha-lipoic acid is an organosulfur compound derived from octanoic acid. It is widely available as an over-the-counter nutritional supplement and has been marketed as an antioxidant. The efficacy of alpha-lipoic acid in vitiligo was demonstrated in one randomized trial including 35 patients with nonsegmental vitiligo [60]. In this study, twice-daily oral supplementation with alpha-lipoic acid, vitamin E, polyunsaturated fatty acids, and cysteine monohydrate combined with NB-UVB twice weekly for six months resulted in significantly more patients (47 versus 18 percent) achieving >75 percent repigmentation compared with phototherapy alone. In addition, repigmentation occurred earlier with lower cumulative UVB dose. Biochemical evaluations at two and six months showed increased catalase activity, decreased intracellular reactive oxygen species production, and reduced membrane peroxidation in the combination-treatment group. Despite these promising results, further studies are needed to confirm the benefit of alpha-lipoic acid supplementation in the management of vitiligo.

Ginkgo biloba – Extracts from the Ginkgo biloba leaf have long been used in traditional Chinese medicine to treat various conditions, including cutaneous, neurologic, and vascular disorders. The two main groups of active constituents responsible for G. biloba's medicinal effects are terpene lactones (ginkgolides and bilobalides) and ginkgo flavone glycosides, which are present in varying concentrations in the leaf of the ginkgo tree. (See "Clinical use of ginkgo biloba".)

Only a few investigations have evaluated ginkgo's use in the management of vitiligo.

A small randomized trial reported that the spread of vitiligo was arrested in 20 of 25 subjects receiving 40 mg of G. biloba extract three times daily for six months but in none of 22 subjects in the placebo group [61]. In addition, 10 patients in the active treatment group but only two in the placebo group showed >75 percent repigmentation.

Another pilot study found significant improvements in total Vitiligo Area Scoring Index and Vitiligo European Task Force assessment in 12 participants following 12 weeks of supplementation with twice-daily G. biloba extract [62]. In addition to repigmentation, active depigmentation ceased in all patients with acrofacial vitiligo.

Polypodium leucotomos – In one randomized trial, NB-UVB in combination with oral extracts of Polypodium leucotomos, a tropical fern with antioxidant and immunomodulator properties, was more effective than NB-UVB alone in inducing repigmentation of vitiligo in the head and neck area (50 versus 19 percent) after 25 weeks [63]. No difference was noted in other body areas.

Surgical therapies — Surgical therapies have been used for vitiligo for the past 25 years and remain viable options for patients with localized depigmented areas that have been unresponsive to medical intervention [64-67]. They include:

Autologous suction blister grafts [68,69]

Minigrafts or punch grafts [70-72]

Split-thickness grafts [73,74]

Autologous melanocyte cultures

Cultured epidermal suspensions [75,76]

Autologous noncultured epidermal cell suspension [77]

Hair follicle transplantation [78-80]

The scope of transplantation procedures is the transfer of a reservoir of healthy melanocytes to vitiliginous skin for proliferation and migration into areas of depigmentation. Transplantation procedures are contraindicated for patients with a history of hypertrophic scars or keloids.

A systematic review of randomized trials and observational studies of autologous transplantation methods for vitiligo concluded that maximal repigmentation occurred in patients treated with split-thickness grafting and epidermal blister grafting [64]. Both treatment groups achieved success rates of 90 percent repigmentation.

Other studies have reported the benefits of transplantation of autologous melanocyte cultures and epidermal suspensions containing both melanocytes and keratinocytes [65,75,77]. In one randomized trial comparing autologous noncultured epidermal cell suspension with suction blister grafts in 41 patients, a repigmentation ≥75 percent was achieved in over 85 percent of lesions in both treatment groups [77]. However, more lesions in the noncultured epidermal cell suspension group achieved a 90 to 100 percent repigmentation compared with those in the suction blister group (70 versus 27 percent).

Adverse effects of surgical therapies include cobblestoning, scarring, graft depigmentation, and graft displacement. Suction blister grafts and split skin grafts may be associated with the Koebner phenomenon at the donor site, a complication of major clinical importance since it results in the development of new vitiligo lesions [25]. Other adverse effects include hypopigmentation, hyperpigmentation, scarring, and infection at both donor and recipient sites. Punch grafting or minigrafting adverse effects include lack of color blending and matching with the surrounding normal skin, cobblestoning, and "polka dot" appearance [81].

Factors influencing the outcome of transplantation techniques include age, site of lesion, and type of vitiligo. In a series of 117 patients, the best results were achieved for patients younger than age 20 and patients with segmental vitiligo, whereas the grafting site did not significantly affect the outcome [66].

Depigmentation — Since the 1950s, monobenzyl ether of hydroquinone (monobenzone) has been used as a depigmenting agent for patients with extensive vitiligo [82,83]. Monobenzone causes permanent destruction of melanocytes and induces depigmentation locally and remotely from the sites of application. Thus, the use of monobenzone for other disorders of pigmentation is contraindicated. The major side effects of monobenzone therapy are irritant contact dermatitis and pruritus, which usually respond to topical and systemic steroids. Other side effects include severe xerosis, alopecia, and premature graying.

Experimental therapies

Afamelanotide – Afamelanotide, a potent and longer-lasting synthetic analog of naturally occurring alpha-melanocyte-stimulating hormone (MSH), is a novel intervention for vitiligo [84,85]. Its use is based upon the demonstration of defects in the melanocortin system in patients with vitiligo, including decreased circulating and lesional skin levels of alpha-MSH [86]. Afamelanotide is delivered as a subcutaneous, bioresorbable implant that promotes melanocyte proliferation and melanogenesis.

The safety and efficacy of afamelanotide implants combined with NB-UVB were assessed in an observational study of four patients with generalized vitiligo [84]. Patients were treated three times weekly with NB-UVB for one month and then administered a series of four monthly implants containing 16 mg of afamelanotide. Follicular and confluent areas of repigmentation were evident within two days to four weeks after the initial implant. Afamelanotide induced fast and deep repigmentation as well as diffuse hyperpigmentation in all cases. In a subsequent randomized trial including 55 patients with skin type III to VI and vitiligo involving 15 to 50 percent of the BSA, patients in the NB-UVB plus afamelanotide group achieved a greater repigmentation than patients in the NB-UVB monotherapy group at five months (49 versus 33 percent) [85].

Prostaglandin E2 – Prostaglandin E2 (PGE2) is a potentially beneficial treatment for localized stable vitiligo. PGE2 controls the proliferation of melanocytes by means of stimulant and immunomodulatory effects. In a consecutive series of patients with stable vitiligo, repigmentation occurred in 40 of 56 patients treated with PGE2 0.25 mg/g gel twice daily for six months [87]. The response was excellent in 22 of 40 patients, with complete repigmentation observed in eight patients.

Bimatoprost – Bimatoprost, a synthetic analog of prostaglandin F2-alpha approved for the topical treatment of glaucoma and hypotrichosis of the eyelashes, is associated with hyperpigmentation of periocular skin caused by increased melanogenesis [88]. The efficacy of bimatoprost in the treatment of vitiligo was initially evaluated in a preliminary study of 10 patients with localized vitiligo treated with bimatoprost 0.03% ophthalmic solution twice daily for four months [89]. Of the 10 patients, three had 100 percent repigmentation, three had 75 to 99 percent repigmentation, and one patient had 50 to 75 percent repigmentation. The best responses were observed on the face.

A subsequent proof-of-concept randomized trial compared the efficacy of bimatoprost 0.03% ophthalmic solution alone and in combination with a topical steroid (mometasone) with mometasone alone in 32 patients with nonsegmental, nonfacial stable vitiligo involving <5 percent of the body surface area [90]. At 20 weeks, none of the patients achieved the prespecified end point of 50 to 75 percent repigmentation. However, in a post-hoc analysis using a less stringent definition of response (25 to 50 percent repigmentation), patients treated with bimatoprost, either alone or with mometasone, achieved a greater repigmentation in the neck and trunk than patients treated with mometasone alone.

PSYCHOLOGIC INTERVENTIONS — There is a scarcity of high-quality studies evaluating the efficacy of psychologic interventions in the management of patients with vitiligo. One small randomized trial found that cognitive-behavioral therapy in addition to conventional therapies was effective in improving the quality of life, self-esteem, and perceived body image in adult patients with vitiligo and even influenced the course of the disease itself [91].

CAMOUFLAGE — Cosmetic camouflage can be beneficial for patients with vitiligo affecting exposed areas such as the face, neck, and hands. Camouflage products include foundation-based cosmetics and self-tanning products containing dihydroxyacetone (DHA). DHA-based products are most popular because they provide lasting color for up to several days and are not immediately rubbed off onto clothing. Tattooing or micropigmentation should be avoided, given the risk of koebnerization and oxidation of tattoo pigment causing further dyschromia. (See "Vitiligo: Pathogenesis, clinical features, and diagnosis", section on 'Koebner phenomenon'.)

PROGNOSIS — Vitiligo is a chronic disease with a highly unpredictable course. Early-onset vitiligo appears to be associated with involvement of a greater body surface area involvement and increased rate of disease progression [92]. Despite treatment, most patients experience alternating periods of pigment loss and disease stability for their entire life. Occasionally, patients may experience spontaneous repigmentation.

Patients who have organ-specific autoantibodies have an increased risk of developing subclinical or overt autoimmune disease [93]. (See "Vitiligo: Pathogenesis, clinical features, and diagnosis", section on 'Associated disorders'.)

SUMMARY AND RECOMMENDATIONS

Vitiligo is a chronic, relapsing disease. The goals of treatment include the stabilization of active disease and the repigmentation of depigmented patches. However, the response to treatments is slow and may be highly variable among patients and among different body areas in the same patient. (See 'Patient evaluation' above and 'Assessment of severity' above and 'Goals of treatment' above.)

In patients with rapidly progressive vitiligo (ie, depigmented macules spreading over a few weeks or months), we suggest systemic corticosteroids as adjunct therapy to narrowband ultraviolet B (NB-UVB) phototherapy for stabilization (Grade 2C). (See 'Stabilization of rapidly progressive disease' above.)

For patients with vitiligo involving <10 percent of the total body surface area (TBSA), we suggest topical corticosteroids as initial therapy (Grade 2C). Topical corticosteroids are applied once daily for two to three months and then interrupted for one month. Topical calcineurin inhibitors are preferred to topical corticosteroids for body areas at increased risk of atrophy. Targeted phototherapy is an option for patients with limited vitiligo who do not respond to topical therapies. (See 'Vitiligo involving <10 percent of the TBSA' above.)

For patients with vitiligo involving 10 to 40 percent of the TBSA, we suggest phototherapy with NB-UVB (Grade 2B). Phototherapy is administered two to three times per week for 9 to 12 months or up to 200 treatments. Topical corticosteroids or topical calcineurin inhibitors may be intermittently used in combination with NB-UVB phototherapy. (See 'Vitiligo involving 10 to 40 percent of the TBSA' above.)

Surgical therapies involving the autologous transplantation of healthy melanocytes in depigmented areas are an option for patients with localized, recalcitrant vitiligo and for patients with segmental vitiligo. (See 'Localized recalcitrant vitiligo' above and 'Segmental vitiligo' above.)

Depigmentation of residual pigmented areas with monobenzyl ether of hydroquinone (monobenzone) can be considered for patients with extensive recalcitrant vitiligo that does not respond to repigmentation regimens and for those with extensive vitiligo who do not desire undergoing repigmentation treatments. (See 'Vitiligo involving >40 percent of the TBSA' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

  1. Ezzedine K, Eleftheriadou V, Whitton M, van Geel N. Vitiligo. Lancet 2015; 386:74.
  2. Mohammed GF, Gomaa AH, Al-Dhubaibi MS. Highlights in pathogenesis of vitiligo. World J Clin Cases 2015; 3:221.
  3. Krüger C, Schallreuter KU. Stigmatisation, Avoidance Behaviour and Difficulties in Coping are Common Among Adult Patients with Vitiligo. Acta Derm Venereol 2015; 95:553.
  4. Silverberg JI, Silverberg NB. Quality of life impairment in children and adolescents with vitiligo. Pediatr Dermatol 2014; 31:309.
  5. Robins A. Biological Perspectives on Human Pigmentation, Cambridge University Press, Cambridge, UK 2005. Vol 7.
  6. Grimes PE. Disorders of pigmentation. In: ACP Medicine, Dale DC, Federman DD (Eds), WebMD Scientific American Medicine, New York 2012. p.526.
  7. Porter J. The psychological effects of vitiligo: Response to impaired appearance. In: Vitiligo, Hann SK, Nordlund JJ (Eds), Blackwell Science, Oxford, UK 2000. p.97.
  8. Daniel BS, Wittal R. Vitiligo treatment update. Australas J Dermatol 2015; 56:85.
  9. Alikhan A, Felsten LM, Daly M, Petronic-Rosic V. Vitiligo: a comprehensive overview Part I. Introduction, epidemiology, quality of life, diagnosis, differential diagnosis, associations, histopathology, etiology, and work-up. J Am Acad Dermatol 2011; 65:473.
  10. Whitton M, Pinart M, Batchelor JM, et al. Evidence-based management of vitiligo: summary of a Cochrane systematic review. Br J Dermatol 2016; 174:962.
  11. Oiso N, Suzuki T, Wataya-Kaneda M, et al. Guidelines for the diagnosis and treatment of vitiligo in Japan. J Dermatol 2013; 40:344.
  12. Taieb A, Alomar A, Böhm M, et al. Guidelines for the management of vitiligo: the European Dermatology Forum consensus. Br J Dermatol 2013; 168:5.
  13. Yaghoobi R, Omidian M, Bagherani N. Vitiligo: a review of the published work. J Dermatol 2011; 38:419.
  14. Faria AR, Tarlé RG, Dellatorre G, et al. Vitiligo--Part 2--classification, histopathology and treatment. An Bras Dermatol 2014; 89:784.
  15. Falabella R, Barona MI. Update on skin repigmentation therapies in vitiligo. Pigment Cell Melanoma Res 2009; 22:42.
  16. Njoo MD, Spuls PI, Bos JD, et al. Nonsurgical repigmentation therapies in vitiligo. Meta-analysis of the literature. Arch Dermatol 1998; 134:1532.
  17. Grimes PE. Vitiligo. An overview of therapeutic approaches. Dermatol Clin 1993; 11:325.
  18. Kwinter J, Pelletier J, Khambalia A, Pope E. High-potency steroid use in children with vitiligo: a retrospective study. J Am Acad Dermatol 2007; 56:236.
  19. Meredith F, Abbott R. Vitiligo: an evidence-based update. Report of the 13th Evidence Based Update Meeting, 23 May 2013, Loughborough, U.K. Br J Dermatol 2014; 170:565.
  20. Mulekar SV, Al Eisa A, Delvi MB, et al. Childhood vitiligo: a long-term study of localized vitiligo treated by noncultured cellular grafting. Pediatr Dermatol 2010; 27:132.
  21. Mulekar SV. Long-term follow-up study of segmental and focal vitiligo treated by autologous, noncultured melanocyte-keratinocyte cell transplantation. Arch Dermatol 2004; 140:1211.
  22. Eleftheriadou V, Thomas K, Ravenscroft J, et al. Feasibility, double-blind, randomised, placebo-controlled, multi-centre trial of hand-held NB-UVB phototherapy for the treatment of vitiligo at home (HI-Light trial: Home Intervention of Light therapy). Trials 2014; 15:51.
  23. Parsad D, Pandhi R, Dogra S, Kumar B. Clinical study of repigmentation patterns with different treatment modalities and their correlation with speed and stability of repigmentation in 352 vitiliginous patches. J Am Acad Dermatol 2004; 50:63.
  24. Gan EY, Gahat T, Cario-André M, et al. Clinical repigmentation patterns in paediatric vitiligo. Br J Dermatol 2016; 175:555.
  25. Whitton ME, Pinart M, Batchelor J, et al. Interventions for vitiligo. Cochrane Database Syst Rev 2015; :CD003263.
  26. Sassi F, Cazzaniga S, Tessari G, et al. Randomized controlled trial comparing the effectiveness of 308-nm excimer laser alone or in combination with topical hydrocortisone 17-butyrate cream in the treatment of vitiligo of the face and neck. Br J Dermatol 2008; 159:1186.
  27. Akdeniz N, Yavuz IH, Gunes Bilgili S, et al. Comparison of efficacy of narrow band UVB therapies with UVB alone, in combination with calcipotriol, and with betamethasone and calcipotriol in vitiligo. J Dermatolog Treat 2014; 25:196.
  28. Khalid M, Mujtaba G, Haroon TS. Comparison of 0.05% clobetasol propionate cream and topical Puvasol in childhood vitiligo. Int J Dermatol 1995; 34:203.
  29. Tharp MD. Calcineurin inhibitors. Dermatol Ther 2002; 15:325.
  30. Kang S, Lucky AW, Pariser D, et al. Long-term safety and efficacy of tacrolimus ointment for the treatment of atopic dermatitis in children. J Am Acad Dermatol 2001; 44:S58.
  31. Grimes PE, Soriano T, Dytoc MT. Topical tacrolimus for repigmentation of vitiligo. J Am Acad Dermatol 2002; 47:789.
  32. Ho N, Pope E, Weinstein M, et al. A double-blind, randomized, placebo-controlled trial of topical tacrolimus 0·1% vs. clobetasol propionate 0·05% in childhood vitiligo. Br J Dermatol 2011; 165:626.
  33. Stinco G, Piccirillo F, Forcione M, et al. An open randomized study to compare narrow band UVB, topical pimecrolimus and topical tacrolimus in the treatment of vitiligo. Eur J Dermatol 2009; 19:588.
  34. Nisticò S, Chiricozzi A, Saraceno R, et al. Vitiligo treatment with monochromatic excimer light and tacrolimus: results of an open randomized controlled study. Photomed Laser Surg 2012; 30:26.
  35. Köse O, Arca E, Kurumlu Z. Mometasone cream versus pimecrolimus cream for the treatment of childhood localized vitiligo. J Dermatolog Treat 2010; 21:133.
  36. Margolis DJ, Abuabara K, Hoffstad OJ, et al. Association Between Malignancy and Topical Use of Pimecrolimus. JAMA Dermatol 2015; 151:594.
  37. Thaçi D, Salgo R. The topical calcineurin inhibitor pimecrolimus in atopic dermatitis: a safety update. Acta Dermatovenerol Alp Pannonica Adriat 2007; 16:58, 60.
  38. Ormerod AD. Topical tacrolimus and pimecrolimus and the risk of cancer: how much cause for concern? Br J Dermatol 2005; 153:701.
  39. Ermis O, Alpsoy E, Cetin L, Yilmaz E. Is the efficacy of psoralen plus ultraviolet A therapy for vitiligo enhanced by concurrent topical calcipotriol? A placebo-controlled double-blind study. Br J Dermatol 2001; 145:472.
  40. Khullar G, Kanwar AJ, Singh S, Parsad D. Comparison of efficacy and safety profile of topical calcipotriol ointment in combination with NB-UVB vs. NB-UVB alone in the treatment of vitiligo: a 24-week prospective right-left comparative clinical trial. J Eur Acad Dermatol Venereol 2015; 29:925.
  41. Rodríguez-Martín M, García Bustínduy M, Sáez Rodríguez M, Noda Cabrera A. Randomized, double-blind clinical trial to evaluate the efficacy of topical tacalcitol and sunlight exposure in the treatment of adult nonsegmental vitiligo. Br J Dermatol 2009; 160:409.
  42. Njoo MD, Bos JD, Westerhof W. Treatment of generalized vitiligo in children with narrow-band (TL-01) UVB radiation therapy. J Am Acad Dermatol 2000; 42:245.
  43. Yones SS, Palmer RA, Garibaldinos TM, Hawk JL. Randomized double-blind trial of treatment of vitiligo: efficacy of psoralen-UV-A therapy vs Narrowband-UV-B therapy. Arch Dermatol 2007; 143:578.
  44. Natta R, Somsak T, Wisuttida T, Laor L. Narrowband ultraviolet B radiation therapy for recalcitrant vitiligo in Asians. J Am Acad Dermatol 2003; 49:473.
  45. Nordal EJ, Guleng GE, Rönnevig JR. Treatment of vitiligo with narrowband-UVB (TL01) combined with tacrolimus ointment (0.1%) vs. placebo ointment, a randomized right/left double-blind comparative study. J Eur Acad Dermatol Venereol 2011; 25:1440.
  46. Sitek JC, Loeb M, Ronnevig JR. Narrowband UVB therapy for vitiligo: does the repigmentation last? J Eur Acad Dermatol Venereol 2007; 21:891.
  47. Percivalle S, Piccinno R, Caccialanza M, Forti S. Narrowband ultraviolet B phototherapy in childhood vitiligo: evaluation of results in 28 patients. Pediatr Dermatol 2012; 29:160.
  48. Stern RS, PUVA Follow-Up Study. The risk of squamous cell and basal cell cancer associated with psoralen and ultraviolet A therapy: a 30-year prospective study. J Am Acad Dermatol 2012; 66:553.
  49. Grimes PE. Advances in the treatment of vitiligo: targeted phototherapy. Cosmet Dermatol 2003; 16:18.
  50. Lopes C, Trevisani VF, Melnik T. Efficacy and Safety of 308-nm Monochromatic Excimer Lamp Versus Other Phototherapy Devices for Vitiligo: A Systematic Review with Meta-Analysis. Am J Clin Dermatol 2016; 17:23.
  51. Hofer A, Hassan AS, Legat FJ, et al. Optimal weekly frequency of 308-nm excimer laser treatment in vitiligo patients. Br J Dermatol 2005; 152:981.
  52. Asawanonda P, Amornpinyokeit N, Nimnuan C. Topical 8-methoxypsoralen enhances the therapeutic results of targeted narrowband ultraviolet B phototherapy for plaque-type psoriasis. J Eur Acad Dermatol Venereol 2008; 22:50.
  53. Kawalek AZ, Spencer JM, Phelps RG. Combined excimer laser and topical tacrolimus for the treatment of vitiligo: a pilot study. Dermatol Surg 2004; 30:130.
  54. Kim SM, Lee HS, Hann SK. The efficacy of low-dose oral corticosteroids in the treatment of vitiligo patients. Int J Dermatol 1999; 38:546.
  55. Pasricha JS, Khaitan BK. Oral mini-pulse therapy with betamethasone in vitiligo patients having extensive or fast-spreading disease. Int J Dermatol 1993; 32:753.
  56. Radakovic-Fijan S, Fürnsinn-Friedl AM, Hönigsmann H, Tanew A. Oral dexamethasone pulse treatment for vitiligo. J Am Acad Dermatol 2001; 44:814.
  57. Rath N, Kar HK, Sabhnani S. An open labeled, comparative clinical study on efficacy and tolerability of oral minipulse of steroid (OMP) alone, OMP with PUVA and broad / narrow band UVB phototherapy in progressive vitiligo. Indian J Dermatol Venereol Leprol 2008; 74:357.
  58. Don P, Iuga A, Dacko A, Hardick K. Treatment of vitiligo with broadband ultraviolet B and vitamins. Int J Dermatol 2006; 45:63.
  59. Elgoweini M, Nour El Din N. Response of vitiligo to narrowband ultraviolet B and oral antioxidants. J Clin Pharmacol 2009; 49:852.
  60. Dell'Anna ML, Mastrofrancesco A, Sala R, et al. Antioxidants and narrow band-UVB in the treatment of vitiligo: a double-blind placebo controlled trial. Clin Exp Dermatol 2007; 32:631.
  61. Parsad D, Pandhi R, Juneja A. Effectiveness of oral Ginkgo biloba in treating limited, slowly spreading vitiligo. Clin Exp Dermatol 2003; 28:285.
  62. Szczurko O, Shear N, Taddio A, Boon H. Ginkgo biloba for the treatment of vitilgo vulgaris: an open label pilot clinical trial. BMC Complement Altern Med 2011; 11:21.
  63. 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; 21:942.
  64. Njoo MD, Westerhof W, Bos JD, Bossuyt PM. A systematic review of autologous transplantation methods in vitiligo. Arch Dermatol 1998; 134:1543.
  65. van Geel N, Ongenae K, De Mil M, et al. Double-blind placebo-controlled study of autologous transplanted epidermal cell suspensions for repigmenting vitiligo. Arch Dermatol 2004; 140:1203.
  66. Gupta S, Kumar B. Epidermal grafting in vitiligo: influence of age, site of lesion, and type of disease on outcome. J Am Acad Dermatol 2003; 49:99.
  67. Falabella R. Surgical approaches for stable vitiligo. Dermatol Surg 2005; 31:1277.
  68. Ashique KT, Kaliyadan F. Long-Term Follow-up and Donor Site Changes Evaluation in Suction Blister Epidermal Grafting Done for Stable Vitiligo: A Retrospective Study. Indian J Dermatol 2015; 60:369.
  69. Gou D, Currimbhoy S, Pandya AG. Suction blister grafting for vitiligo: efficacy and clinical predictive factors. Dermatol Surg 2015; 41:633.
  70. Malakar S, Dhar S. Treatment of stable and recalcitrant vitiligo by autologous miniature punch grafting: a prospective study of 1,000 patients. Dermatology 1999; 198:133.
  71. Singh SK. Punch grafting in vitiligo : Refinements and case selection. Indian J Dermatol Venereol Leprol 1997; 63:296.
  72. Kato H, Furuhashi T, Ito E, et al. Efficacy of 1-mm minigrafts in treating vitiligo depends on patient age, disease site and vitiligo subtype. J Dermatol 2011; 38:1140.
  73. Al-Mutairi N, Manchanda Y, Al-Doukhi A, Al-Haddad A. Long-term results of split-skin grafting in combination with excimer laser for stable vitiligo. Dermatol Surg 2010; 36:499.
  74. Khandpur S, Sharma VK, Manchanda Y. Comparison of minipunch grafting versus split-skin grafting in chronic stable vitiligo. Dermatol Surg 2005; 31:436.
  75. Chen YF, Yang PY, Hu DN, et al. Treatment of vitiligo by transplantation of cultured pure melanocyte suspension: analysis of 120 cases. J Am Acad Dermatol 2004; 51:68.
  76. Guerra L, Primavera G, Raskovic D, et al. Erbium:YAG laser and cultured epidermis in the surgical therapy of stable vitiligo. Arch Dermatol 2003; 139:1303.
  77. Budania A, Parsad D, Kanwar AJ, Dogra S. Comparison between autologous noncultured epidermal cell suspension and suction blister epidermal grafting in stable vitiligo: a randomized study. Br J Dermatol 2012; 167:1295.
  78. Thakur P, Sacchidanand S, Nataraj HV, Savitha AS. A Study of Hair Follicular Transplantation as a Treatment Option for Vitiligo. J Cutan Aesthet Surg 2015; 8:211.
  79. Vinay K, Dogra S, Parsad D, et al. Clinical and treatment characteristics determining therapeutic outcome in patients undergoing autologous non-cultured outer root sheath hair follicle cell suspension for treatment of stable vitiligo. J Eur Acad Dermatol Venereol 2015; 29:31.
  80. Mapar MA, Safarpour M, Mapar M, Haghighizadeh MH. A comparative study of the mini-punch grafting and hair follicle transplantation in the treatment of refractory and stable vitiligo. J Am Acad Dermatol 2014; 70:743.
  81. Mulekar SV, Isedeh P. Surgical interventions for vitiligo: an evidence-based review. Br J Dermatol 2013; 169 Suppl 3:57.
  82. Gupta D, Kumari R, Thappa DM. Depigmentation therapies in vitiligo. Indian J Dermatol Venereol Leprol 2012; 78:49.
  83. Tan ES, Sarkany R. Topical monobenzyl ether of hydroquinone is an effective and safe treatment for depigmentation of extensive vitiligo in the medium term: a retrospective cohort study of 53 cases. Br J Dermatol 2015; 172:1662.
  84. Grimes PE, Hamzavi I, Lebwohl M, et al. The efficacy of afamelanotide and narrowband UV-B phototherapy for repigmentation of vitiligo. JAMA Dermatol 2013; 149:68.
  85. Lim HW, Grimes PE, Agbai O, et al. Afamelanotide and narrowband UV-B phototherapy for the treatment of vitiligo: a randomized multicenter trial. JAMA Dermatol 2015; 151:42.
  86. Graham A, Westerhof W, Thody AJ. The expression of alpha-MSH by melanocytes is reduced in vitiligo. Ann N Y Acad Sci 1999; 885:470.
  87. Kapoor R, Phiske MM, Jerajani HR. Evaluation of safety and efficacy of topical prostaglandin E2 in treatment of vitiligo. Br J Dermatol 2009; 160:861.
  88. Kapur R, Osmanovic S, Toyran S, Edward DP. Bimatoprost-induced periocular skin hyperpigmentation: histopathological study. Arch Ophthalmol 2005; 123:1541.
  89. Narang G. Efficacy and Safety of Topical Bimatoprost Solution 0.03% in Stable Vitiligo: A Prelliminary Study. World Congress of Dermatology Seoul, Korea, June 2011.
  90. Grimes PE. Bimatoprost 0.03% Solution for the Treatment of Nonfacial Vitiligo. J Drugs Dermatol 2016; 15:703.
  91. Papadopoulos L, Bor R, Legg C. Coping with the disfiguring effects of vitiligo: a preliminary investigation into the effects of cognitive-behavioural therapy. Br J Med Psychol 1999; 72 ( Pt 3):385.
  92. Mu EW, Cohen BE, Orlow SJ. Early-onset childhood vitiligo is associated with a more extensive and progressive course. J Am Acad Dermatol 2015; 73:467.
  93. Betterle C, Caretto A, De Zio A, et al. Incidence and significance of organ-specific autoimmune disorders (clinical, latent or only autoantibodies) in patients with vitiligo. Dermatologica 1985; 171:419.
Topic 106619 Version 4.0

All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.