FEATURE ARTICLE

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Vitiligo
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A Comprehensive Overview
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Julia Stiegler and Sylvana Brickley

ABSTRACT: Vitiligo is a common condition. This article pro- as key mediators interferon-γ and interleukin-22 (Gregg
vides a comprehensive overview of vitiligo including the et al., 2010; Klarquist et al., 2010; Lili et al., 2012;
clinical presentation, associated comorbid conditions, Rätsep et al., 2008). It is hypothesized that cytotoxic
treatment, emerging therapies, and psychosocial and CD8+ T cells are the predominant cell type that attack me-
cultural considerations. lanocytes in vitiligo, leading to loss of function (Benzekri &
Key word: Vitiligo Gauthier, 2017; Harris & Rashighi, 2018). Repigmentation
of vitiligo is dependent on a viable melanocyte reservoir.
BACKGROUND Unaffected melanocytes, found deep in the hair follicle
units of depigmented epidermis and at the periphery of
Vitiligo is an acquired chronic disease of depigmented white
vitiligo lesions, serve to repigment affected skin (Falabella &
macules and patches that result from destruction of mela-
Barona, 2009). In many patients, repigmentation is possible
nocytes in the affected skin. Vitiligo is common and affects
if these melanocytes are stimulated with the appropriate
approximately 1% of the world population (Whitton
topical or oral medications, often in combination with
et al., 2016). The disease has no prominent sex predilection.
ultraviolet (UV) light (Falabella & Barona, 2009).
Onset may occur from shortly after birth until late adult-
Genes play a significant role in the pathogenesis of
hood, although over half of individuals are affected before
vitiligo; however, these influences are complex and inter-
the age of 20 years (Taïeb & Picardo, 2009; Porter et al.,
act with nongenetic factors. A twin study of vitiligo in
1979). Flat white lesions of vitiligo can appear on any area
European-derived Whites found a 23% concordance of
of skin. The disease favors symmetric involvement of the
vitiligo in monozygotic twins, underscoring the impor-
face (particularly periorificial), hands, ankles, groin, and
tance of nongenetic factors (Alkhateeb et al., 2003). More
skin folds, with a predilection for sites of friction. Al-
recently, genome-wide association studies have identified
though the lesions of vitiligo are typically asymptomatic,
48 distinct genetic loci and a few specific genes that ac-
the psychosocial impact and physical disfigurement of the
count for 22.5% of vitiligo heritability in European-derived
condition are devastating to many patients and represent
Whites (Spritz & Andersen, 2017). Nearly all of the identified
a significant healthcare burden. Treatments may restore
genes encode proteins involved in apoptosis, melanocyte func-
pigment, but there is no cure.
tion, and immunoregulation. These genetic findings under-
Pathogenesis score the autoimmune basis of vitiligo, which has been
associated with other autoimmune diseases such as perni-
Although the complex pathogenesis of vitiligo is incom- cious anemia, thyroid disease, Addison disease, systemic
pletely understood, this multifactorial disease results in lupus erythematosus, rheumatoid arthritis, adult-onset Type
an absence of epidermal melanocytes in affected skin. 1 diabetes, and even psoriasis (Spritz & Andersen, 2017).
The host immune system plays a clear role in disease path-
ogenesis with Th1, Th17, cytotoxic T cells, regulatory T
cells, and dendritic cells found in affected tissues, as well
CLINICAL PRESENTATION
Sylvana Brickley, MSN, FNP-BC, DCNP, University of Rochester The most common presentation of vitiligo is depigmented
Medical Center, Rochester, NY. or hypopigmented macules or patches that may vary in
Julia Stiegler, MD, University of Rochester Medical Center, Rochester, NY. size from a few millimeters to several centimeters and are
The authors declare no conflict of interest. surrounded by normal skin. Well-developed lesions of vit-
Correspondence concerning this article should be addressed to Sylvana iligo are completely depigmented with well-demarcated
Brickley, MSN, FNP-BC, DCNP, University of Rochester Medical
Center, Rochester, NY. E-mail: [email protected] borders and may vary in shape from oval or round to lin-
Copyright © 2020 by the Dermatology Nurses’ Association. ear or irregular. If hair-bearing areas are involved, the hair
DOI: 10.1097/JDN.0000000000000589 may turn white.

18 Journal of the Dermatology Nurses’ Association

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 Physical Examination
TABLE 1. Classification and Consensus
During the physical examination of suspected vitiligo, the Nomenclature of Vitiligo According to the
astute clinician must differentiate hypopigmented from VETF, 2011
depigmented skin. A Wood's lamp is a type of UV lamp
that may be used for this purpose. Hypopigmented skin Category of Vitiligo Subtype
has decreased pigmentation because of a reduction in me- Nonsegmental vitiligo Acrofacial
lanocytes or melanin. Depigmented skin represents the ab- Mucosal (more than one
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mucosal site)
sence of functional melanocytes (Benzekri et al., 2012). Generalized
Under a Wood's lamp, depigmented skin fluoresces a bril- Universal
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liant bright white whereas hypopigmented skin does not Mixed

(Benzekri et al., 2012). As vitiligo is a depigmenting condi- Segmental vitiligo Unisegmental, bisegmental, or
tion, the clinician can expect to observe bright white fluo- plurisegmental
rescence of depigmented areas. Notable exceptions to this Undetermined/ Focal
rule include areas of early vitiligo and the trichrome viti- unclassified vitiligo Mucosal (one mucosal site in
isolation)
ligo variant, which may exhibit hypopigmented macules
or patches next to depigmented lesions. Active lesions of
nonsegmental vitiligo (NSV) may have a depigmented ap-
pearance with poorly or well-defined borders (Benzekri & “common.” Many authors have attempted to classify vit-
Gauthier, 2017). An increased number of depigmented iligo; however, for the purposes of this review, one classi-
patches over sites of trauma, such as elbows, hands, and fication was chosen for clarity.
knees, represent the Koebner phenomenon (KP), a common Vitiligo is classified based on clinical presentation into
finding in vitiligo (van Geel et al., 2019). Confetti-like depig- two major forms, segmental vitiligo (SV) and NSV (Ezzedine,
mentation, trichromic and hypochromic lesions with poorly Diallo et al., 2012). Rare clinical variants of vitiligo such
defined borders, inflammatory borders, itch, and as focal, inflammatory, confetti-like or “punctate,” and
leukotrichia are also associated with disease activity; how- trichrome have been reported but are difficult to defini-
ever, more data are needed to establish their utility as po- tively classify because they may fit into the general clinical
tential markers (van Geel et al., 2019). spectrum of disease (Ezzedine, Diallo et al., 2012). Trichrome,
inflammatory borders, and confetti-like lesions are considered
Koebner Phenomenon potential markers of active lesions (Goh & Pandya, 2017;
van Geel et al., 2019).
A characteristic trait of vitiligo is the KP also known as NSV has been used as umbrella term for different clin-
“isomorphic response.” KP is defined as the development ical subtypes of vitiligo that are clearly distinct from SV,
of lesions at the site of traumatized, previously uninvolved including acrofacial, generalized, mucosal, and universal
skin (Goh & Pandya, 2017) and is common in dermato- (Ezzedine, Diallo et al., 2012). NSV is characterized by
logic diseases such as psoriasis and lichen planus. The KP depigmented macules that vary in size from a few to sev-
is named after a German dermatologist, Heinrich Koebner eral centimeters in diameter, located on both sides of the
(1838–1904), who observed that his patients with psoriasis body with a tendency towards symmetrical distribution.
developed new lesions at sites of trauma (Kobner, 1877). Acrofacial vitiligo affects the distal extremities and face.
KP is estimated to occur in 21%–62% of patients with vit- Generalized vitiligo implies more widespread distribution
iligo (van Geel et al., 2011). KP helps to explain why viti- and more areas of involvement (Ezzedine, Diallo et al.,
ligo often presents in areas of friction and skin movement, 2012; Hann & Nordlund, 2000). Universal vitiligo involves
such as the nasolabial folds, lateral canthi, eyelids, penis, shins, complete or nearly complete depigmentation of skin;
elbows, and the perioral region (van Geel et al., 2019). sometimes, body hair, oral mucosa, and/or genital muco-
Patients may report KP by history, and careful examina- sae are involved. Mixed vitiligo is when features of SV
tion may reveal linear macules of depigmentation at sites and NSV are present, often first presenting as SV and then
of friction or abrasions (Goh & Pandya, 2017). progressing to NSV (Goh & Pandya, 2017).
SV is categorized into unisegmental, bisegmental, and
Classifications of Vitiligo plurisegmental subtypes. SV is typically associated with
In 2011, the Vitiligo European Taskforce convened at the rapid onset and leukotrichia (Ezzedine, Diallo et al., 2012).
Vitiligo Global Issues Consensus Conference and revised Other authors have defined SVas a unilateral patch of depig-
the classification of vitiligo. Table 1 below summarizes mentation that does not cross the midline (Goh & Pandya,
the classification of vitiligo according to the taskforce's 2017). The face is most commonly affected in SV, followed
consensus statement (Ezzedine, Diallo et al., 2012). The by the trunk, neck, extremities, and scalp (Goh & Pandya,
Vitiligo European Taskforce also recommended that the 2017).
term vitiligo “vulgaris” not be used as it conveys a nega- Undetermined or unclassified types of vitiligo that are
tive connotation, although “vulgaris” is synonymous with in the clinical spectrum of disease but excluded from other

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 categories include focal vitiligo and mucosal vitiligo skin. Wood's lamp examination is a widely accepted and
(Ezzedine, Diallo et al., 2012). Focal vitiligo describes a cost-effective tool to differentiate the depigmented lesions
long-standing, depigmented lesion that does not progress of vitiligo from hypopigmented lesions.
to NSV or SV after 2 years (Ezzedine, Diallo et al., 2012; Depending on patient history and a thorough review of
Goh & Pandya, 2017). The diagnosis of focal vitiligo systems, thyroid-stimulating hormone, antithyroid perox-
should be considered after ruling out all other causes of fo- idase antibody, free T4, antinuclear antibody, complete
cal hypopigmentation, such as nevus depigmentosus or blood count with differential, and/or fasting blood glu-
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trauma-induced leukoderma (Ezzedine, Lim et al., 2012; cose may be indicated to assess for comorbidities. Most
Goh & Pandya, 2017). Isolated mucosal vitiligo is rare patients do not have an accompanying autoimmune dis-
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but has been reported. Rare cases of lichen sclerosus si- ease, and routine laboratory monitoring in asymptomatic
multaneously occurring with vitiligo and a vitiligoid vari- patients is not recommended (Kroon et al., 2012).
ant of lichen sclerosus have been reported as well (Cooper
et al., 2008; Dennin et al., 2018; Weisberg et al., 2008). PROGNOSIS
Therefore, a biopsy may be warranted to confirm the di- Vitiligo typically shows an insidious onset, and the natural
agnosis of vitiligo in patients presenting with depigmented progression of the disease is unpredictable. It may show
macules isolated to the mucosa. slow spread with periods of stabilization or rapid evolution.
Punctate, inflammatory, and trichrome vitiligo are other Vitiligo may stabilize for years only to progress without clear
rare clinical variants that may fall into the clinical spectrum cause (Rodrigues et al., 2017). SV typically reaches the full
of disease. Punctate vitiligo is characterized by depigmented extent of involvement within 1–2 years and rarely spreads
confetti-like macules affecting any area of the body and further. Spontaneous remission is rare with the exception
should be differentiated from idiopathic guttate hypomelanosis of SV. However, the presence of halo nevi and leukotrichia
(Falabella et al., 1988). These confetti-like macules have in SV portends a higher likelihood of progression to mixed
been reported as a marker of rapidly progressing disease vitiligo (Ezzedine, Diallo et al., 2012).
(Goh & Pandya, 2017). When coinciding with NSV, Disease progression is clinically characterized by the
punctate vitiligo should be classified as NSV; however, if appearance of new hypopigmented or depigmented mac-
observed in isolation, it should be referred to as punctate ules, centrifugal enlargement of existing lesions, or both
vitiligo (Ezzedine, Lim et al., 2012). Inflammatory vitiligo (Bolognia et al., 2018). Inflammatory vitiligo, trichrome
describes erythema sometimes seen at the borders of le- vitiligo, peripheral hypopigmentation, and lesions with
sions and is thought to be a marker of disease activity poorly defined borders are considered markers of high
(Benzekri et al., 2012; Goh & Pandya, 2017). Trichrome disease activity, and aggressive treatment should be con-
vitiligo is characterized by a combination of intermixed sidered (Benzekri et al., 2012; Goh & Pandya, 2017).
hypopigmented, normal, and depigmented skin. Trichrome
vitiligo has been reported as a marker of rapid progression ASSOCIATED CONDITIONS
(Goh & Pandya, 2017; van Geel et al., 2011).
Association With Other Autoimmune Diseases
DIFFERENTIAL DIAGNOSIS AND DIAGNOSTIC Patients with vitiligo have been found to have a higher in-
EVALUATION cidence of autoimmune diseases such as thyroiditis, Type
1 diabetes, lupus, Addison disease, pernicious anemia,
Differential Diagnosis and alopecia areata (Spritz & Andersen, 2017). Many
The differential diagnosis for depigmented macules, as seen vitiligo susceptibility genes that encode proteins with im-
in vitiligo, includes discoid lupus erythematosus, sclero- munoregulatory and apoptotic functions have been asso-
derma, albinism, piebaldism, lichen sclerosus, medication- ciated with other autoimmune diseases that vitiligo is
or chemical-induced leukoderma, and onchocerciasis epidemiologically associated with (Spritz & Andersen, 2017).
(Bolognia et al., 2018). Mucosal vitiligo with isolated gen- Thyroid dysfunction was found in one large study to pre-
ital involvement should be evaluated with biopsy to rule cede the onset of vitiligo (Kroon et al., 2012). A focused
out lichen sclerosus (Ezzedine, Diallo et al., 2012). The review of systems, medical history, and physical examina-
differential diagnosis for hypopigmented macules, as seen tion should be used to guide laboratory evaluation for au-
in the trichrome variant and early lesions of vitiligo, in- toimmune diseases.
cludes tinea versicolor, pityriasis alba, postinflammatory
hypopigmentation, nevus depigmentosus, nevus anemicus, Association With Melanoma
idiopathic guttate hypomelanosis, morphea, and mycosis Vitiligo-like depigmentation may be seen in the setting of
fungoides (Bolognia et al., 2018). melanoma, and case reports have associated this with
metastatic disease (Cho et al., 2009; Duhra & Ilchyshyn,
Diagnostic Evaluation 1991; Kiecker et al., 2006; Ortonne et al., 1978). It is pre-
A skin biopsy is rarely necessary to make the diagnosis of sumed that the vitiligo-like depigmentation is secondary
vitiligo but would show a lack of melanocytes in the affected to an immune response against melanoma. The association

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 and (b) halo nevi are an early sign of vitiligo (Barona et al.,
1995). However, some cases of vitiligo clearly spare
melanocytic nevi, so the precise relationship between the
two remains to be fully elucidated (Jouary & Taieb, 2010).

TREATMENT
Early and aggressive treatment of vitiligo is associated
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with better outcomes, yet overall, treatment is only mod-

erately effective (Harris & Rashighi, 2018). Some patients
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will choose to forego treatment based on personal prefer-

ence; nevertheless, treatment should be offered to all pa-
tients (Rodrigues et al., 2017). Currently, there are no
treatments with the indication of inducing repigmentation
in vitiligo that are approved by the U.S. Food and Drug
Administration (FDA). Most treatments used today target
inflammation in a nonspecific manner and are used off-label
to induce repigmentation of affected skin (Rodrigues et al.,
2017). The only FDA-approved treatment for vitiligo is
monobenzyl ether of hydroquinone cream, a depigmenting
agent used to permanently lighten unaffected skin in rare
cases of severe recalcitrant vitiligo.
Optimal treatment of vitiligo depends on the subtype
of disease, percentage of body surface area (BSA) involved,
effect on quality of life, and the patient's perception of the
risk-to-benefit ratio (Rodrigues et al., 2017). Disease

FIGURE 1. Scattered depigmented macules of vitiligo. Photos

Courtesy of A. Borger. Used with patient permission.

is notable enough that, when an older adult presents with

new-onset vitiligo, providers should complete a full skin
examination to assess for suspicious pigmented lesions.
Vitiligo can be triggered by melanoma immunotherapy in-
cluding PD-1 and BRAF inhibitors and is considered a
good prognostic sign (Hua et al., 2016).
Surprisingly, patients with vitiligo have a threefold lower
probability of developing skin cancer, both melanoma and
nonmelanoma types, compared with matched peers, de-
spite exposure to higher levels of UV radiation (Paradisi
et al., 2014; Spritz & Andersen, 2017; Teulings et al.,
2013). At least six confirmed vitiligo loci encode melano-
cyte components or regulators of melanocyte function
(Spritz & Andersen, 2017). These vitiligo loci have been
implicated in both normal pigmentary variation and risk
of melanoma, and all have shown a remarkable inverse re-
lationship between the risk of vitiligo and melanoma (Jin
et al., 2016; Spritz & Andersen, 2017). Further studies
to elucidate the precise relationship between vitiligo and
a lower melanoma risk are needed.

Association With Halo Nevi

Halo nevi are common through adolescence and have a
striking clinical association with vitiligo. Two main theories FIGURE 2. Scattered depigmented macules of vitiligo on the
regarding the association between halo nevi and vitiligo dorsal hand. Evidence of Koebner phenomenon be appreci-
exist: (a) Halo nevi are a risk factor for developing vitiligo, ated at the fingertips where there is depigmentation.

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 are appropriate for treating the nonintertriginous torso
and extremities of adults; less potent TCSs are less effica-
cious in this setting (Rodrigues et al., 2017). Children with
vitiligo should be treated with midpotency TCSs or TCIs,
depending on body location (Rodrigues et al., 2017). TCIs
are recommended as a first-line treatment for the face,
neck, and intertriginous areas of adults and children
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FIGURE 3. Depigmented patches on the upper and lower

eyelids. This periocular location is very common in vitiligo.
Photos Courtesy of A. Borger. Used with patient permission.

location and activity warrant consideration when deter-

mining an appropriate treatment plan. The aim of treat-
ment is to prevent further destruction of melanocytes
and enable stimulation of the growth and proliferation of
existing melanocytes, leading to repigmentation (Bishnoi
& Parsad, 2018).
A recent Cochrane review examined a wide range of in-
terventions including topical treatments, surgical methods,
and psychological therapies (Whitton et al., 2015). The
quality of the examined studies was poor to moderate at
best, most studies had fewer than 50 participants, and very
few studies specifically included children (Whitton et al.,
2016). The best evidence from individual trials showed
short-term benefits from topical corticosteroids (TCSs)
and various forms of UV radiation combined with topical
preparations (Whitton et al., 2016). Further studies are
needed to assess psychological interventions.

Topical Therapies
Initial therapy for vitiligo with minimal BSA involvement
(<5%) includes TCSs and/or topical calcineurin inhibitors
(TCIs). The site of the lesion and age of the patient should
be considered when selecting a topical agent (Rodrigues FIGURE 4. A and B, Depigmented macules and patches of
et al., 2017). Potent or ultrapotent (Class I or II) TCSs the bilateral axillae.

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 because of the potential for TCS-induced cutaneous atro- other ongoing treatments. The presence of unstable viti-
phy, telangiectasia, and striae formation (Dillon et al., ligo lesions is a contraindication for surgical treatment
2017; Rodrigues et al., 2017; Taieb et al., 2013). Regi- (Benzekri et al., 2012).
mens that include daily or twice-daily application of TCSs
Oral Treatment
with “days off” in a cyclical fashion are commonly em-
ployed to avoid adverse effects of TCSs, although formal For rapidly progressing NSV, oral pulse steroids with or
evidence to support this practice is lacking (Rodrigues without phototherapy may be warranted to slow or halt
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et al., 2017). progression of the disease (Kanwar et al., 2013; Lee et al.,
2016; Pasricha & Khaitan, 1993; Whitton et al., 2015).
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Phototherapy EMERGING THERAPIES

When vitiligo is extensive, rapidly spreading, or unrespon- A number of emerging therapies exist for vitiligo. Janus
sive to topical treatments, phototherapy alone or in com- kinase (JAK) inhibitors, afamelanotide, and topical pros-
bination with topical treatment is the mainstay of therapy. taglandins are potentially promising future therapies at
Whole-body phototherapy with narrowband UV-B (NB-UVB) the time of this writing.
or psoralen plus UV-A (PUVA) is indicated for extensive disease Tofacitinib and ruxolitinib are JAK inhibitors that have
(>5%–10% BSA) and rapidly spreading diseases (Rodrigues shown promising regimentation in adult patients with vit-
et al., 2017). NB-UVB is the preferred method of phototherapy iligo (Craiglow & King, 2015; Joshipura et al., 2018;
as it is at least as effective as PUVA with lower risks of Rothstein et al., 2017). JAK inhibitors are a class of med-
burning and skin cancer (Bae et al., 2017; Rodrigues ications that act on the JAK-signal transducer and activa-
et al., 2017). NB-UVB phototherapy is also more widely tor of transcription pathway to block downstream
available than PUVA and does not require pretreatment cytokine-mediated signaling, which plays an important
with ingestion of psoralen, which causes nausea at thera- role in normal cell growth and immunoregulation (Cinats
peutic doses and posttreatment sun sensitivity of the eyes et al., 2018). A complete discussion of the JAK-signal trans-
and skin. The recent Cochrane review deemed PUVA ducer and activator of transcription pathway and the var-
to be inferior to NB-UVB in achieving >75% repigmentation ious processes through which it is implicated in autoimmune
in vitiligo, reinforcing the preference for NB-UVB (Whitton and malignant processes is outside the scope of this article
et al., 2015). and has been extensively reviewed prior (Borie et al., 2003;
Phototherapy combined with topical treatment is pre- Darnell & Levy, 2002; Hirahara et al., 2016; Villarino
ferred when >5%–10% BSA is affected or when focal et al., 2017).
areas are nonresponsive to topical treatment alone
(Rodrigues et al., 2017). For localized diseases such as fo- Afamelanotide
cal or acrofacial vitiligo, small NB-UVB phototherapy units Afamelanotide is a synthetic analog of alpha-melanocyte-
or excimer laser may be preferred (Rodrigues et al., 2017). stimulating hormone and melanocortin-1 receptor agonist
The greatest response to phototherapy should be antici- that stimulates melanogenesis and is administered via sub-
pated on the face and neck (Bae et al., 2017). cutaneous implant (Lim et al., 2015). Afamelanotide is
Phototherapy sessions are needed for two to three ses- currently only FDA approved to treat erythropoietic
sions per week for at least 12 weeks to determine efficacy protoporphyria. In 2015, a randomized multicenter trial
and then should be continued for at least several months reported that treatment of NSV with a combination of
in responders. Long-term phototherapy should be encour- subcutaneous afamelanotide implant with NB-UVB ther-
aged in responders to enhance treatment response (Bae apy (n = 28) resulted in clinically apparent, statistically
et al., 2017). Patients should be counseled to not apply significant repigmentation compared with NB-UVB
any topical products or sunscreens before phototherapy monotherapy alone (n = 27; Lim et al., 2015). Notable ad-
and should be vigilant about sun protection (Rodrigues verse events included erythema in both groups and minor
et al., 2017). In-office phototherapy can be expensive infections and nausea in the combination therapy group.
and time consuming, so a home phototherapy unit may Other, less common cutaneous events included hyperpig-
be considered for patients who wish to continue photo- mentation of unaffected skin, which was subjectively re-
therapy long-term. ported by all patients in the combination therapy group.
No hyperpigmentation of unaffected skin was reported
Surgical Treatment in the NB-UVB monotherapy group, suggesting that
Referral to a plastic surgeon or board-certified dermatolo- afamelanotide caused the hyperpigmentation of unaf-
gist for surgical treatment may be indicated for focal, sta- fected skin (Lim et al., 2015).
ble vitiligo lesions that are recalcitrant to other therapies
and cause the patient significant emotional distress. Surgi- JAK Inhibitors
cal techniques include punch grafting, epidermal blister Ruxolitinib is a selective JAK1/JAK2 inhibitor available in
grafting, or cellular grafts that are used in concert with oral and topical formulations (Cinats et al., 2018). Oral

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 ruxolitinib is FDA approved for use in myelofibrosis and Prostaglandin E2
polycythemia vera (Cinats et al., 2018). Research on more Prostaglandin E2 (PGE2) is synthesized in skin and regu-
selective JAK isoforms that inhibit a narrower range of cy- lates melanocyte proliferation, in addition to affecting
tokines is ongoing (Cinats et al., 2018). keratinocytes and Langerhans cells. PGE2 causes melano-
Tofacitinib, a JAK1/JAK3 inhibitor, is also available in cyte proliferation and is commercially available as a gel.
both oral and topical formulations. The oral formulation Preliminary studies have suggested that topical PGE2 may
is FDA approved for the treatment of rheumatoid arthritis be effective in the treatment of vitiligo (Kapoor et al.,
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but has also been used off-label in various immune regu- 2009; Parsad et al., 2002). Although interesting, further
lated disorders including alopecia areata. Recent case studies are needed to confirm these results.
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series and case reports have found that tofacitinib im-

proved vitiligo disease severity when used topically or CONTROVERSIAL THERAPIES
orally (Cinats et al., 2018; Craiglow & King, 2015; Kim
Systemic antioxidants and pseudocatalase with NB-UVB
et al., 2018).
have been examined for their utility in treating vitiligo;
Topical and oral JAK inhibitors are not currently FDA
however, further studies are needed to determine their utility.
approved for the treatment of vitiligo. The most common
adverse event of oral tofacitinib is infection. Unfortu- Pseudocatalase
nately, oral tofacitinib has also been associated with an in-
creased risk of malignancy (Cinats et al., 2018; McKesey Pseudocatalase cream has been proposed to work as a
& Pandya, 2019). Although oral JAK inhibitors have topical oxygen radical scavenger in the skin. Studies from
been shown to be effective in treating vitiligo in case series, Schallreuter and colleagues found that topical application
the side effect profiles, including reported increased rates of pseudocatalase enhanced repigmentation when combined
of infection and malignancy associated with oral tofacitinib with NB-UVB (Schallreuter et al., 2002, 1999, 1995).
and blood dyscrasias associated with oral ruxolitinib, po- However, subsequent studies by different investigators were
tentially limit their use in a nonfatal condition such as vit- unable to reproduce these findings (Bakis-Petsoglou et al.,
iligo (Kim et al., 2018; Liu et al., 2017). 2009; Naini et al., 2012; Patel et al., 2002). Further research
Topical formulations of JAK inhibitors are promising is needed to establish the utility of pseudocatalase as a po-
as they presumably will have fewer systemic side effects tential treatment for vitiligo.
than oral formulations. Recent case series have shown
Systemic Antioxidants
promising results regarding topical formulations of JAK
inhibitors for the treatment of vitiligo. In a recent study, Some providers may recommend use of systemic antioxi-
11 patients with facial vitiligo were treated for 2–4 months dants on the hypothesis that vitiligo results from a defi-
with tofacitinib 2% cream twice daily in conjunction with ciency of natural antioxidant mechanisms (Dell'Anna
NB-UVB 3 times weekly. The investigators reported a et al., 2007). Selenium, methionine, tocopherols, ascor-
mean improvement of 70%; however, they did not utilize bic acid, B12, folic acid, L-phenylalanine, Vitamin E, zinc
a control group (McKesey & Pandya, 2019). In a case se- sulphate, and ubiquinone are sometimes used (Dell'Anna
ries of 10 patients treated for generalized vitiligo with oral et al., 2007; Falabella & Barona, 2009; Whitton et al.,
tofacitinib, suction blister sampling revealed that the auto- 2015). To date, no controlled clinical trials have been per-
immune response was inhibited during treatment in both formed to validate the use of systemic antioxidants alone
responding and nonresponding lesions. This finding sug- for the treatment of vitiligo. One randomized, double-
gests that light was required for melanocyte regeneration blind, placebo-controlled, multicenter trial (n = 35) com-
in combination with oral tofacitinib (Liu et al., 2017). It pared supplementation with an antioxidant pool that
is hypothesized that photoactivation is required to stimu- contained α-lipoic acid, Vitamins C and E, and polyunsat-
late melanocytes to leave their stem cell niche and migrate urated fatty acids combined with NB-UVB phototherapy
to the epidermis while tofacitinib suppresses the autoim- with NB-UVB alone (Dell'Anna et al., 2007). No statisti-
mune response (Kim et al., 2018). When used in conjunc- cally significant difference in treatment response was found
tion with JAK inhibitors, the dose of NB-UVB phototherapy between the two groups (p = .226; Dell'Anna et al., 2007;
needed to stimulate repigmentation has been observed to be Whitton et al., 2015).
much lower than the dose required to achieve a similar effect
with NB-UVB alone (Kim et al., 2018). PSYCHOSOCIAL AND CULTURAL CONSIDERATIONS
Phase 3 clinical trials investigating the use of topical The unpredictable disease course and physical disfigure-
ruxolitinib 1.5% cream in the treatment of vitiligo are on- ment associated with vitiligo are challenging for patients
going (National Institutes of Health, 2020). Phase 2 clini- and may lead to psychological devastation and social stig-
cal trials for topical ruxolitinib showed promising results, matization (Nguyen et al., 2016; Rzepecki et al., 2018).
with 58% of subjects achieving at least 50% improvement Although vitiligo is not life threatening, the social and psy-
of their vitiligo and 52% of subjects achieving at least 75% chological ramifications of the condition can be profound.
improvement after 1 year (Rosmarin et al., 2020). Vitiligo may cause significant psychological morbidity,

24 Journal of the Dermatology Nurses’ Association

Copyright © 2021 Dermatology Nurses' Association. Unauthorized reproduction of this article is prohibited.
 and patients have reported associated feelings of embar- Benzekri, L., & Gauthier, Y. (2017). Clinical markers of vitiligo activity. Jour-
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sures needed to cover up their disease with clothing and/or and histological findings are potential indicators of activity in lesions of
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live in constant fear that their vitiligo will progress (Rzepecki treatments. International Journal of Molecular Sciences, 19(5), 1509. 10.3390/
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