Vitiligo

Vitiligo is a pigmentary disorder of the skin, which is characterized by circumscribed depigmented macules and patches. Vitiligo is a progressive disorder in which some or all of the melanocytes in the affected skin are selectively destroyed. Vitiligo affects 0.5-2% of the world population, and the average age of onset is 20 years. While vitiligo may be more obvious in patients with darker skin, this disorder does not have a racial or ethnic predilection.[8]

Vitiligo is a multifactorial polygenic disorder with a complex pathogenesis. It is related to both genetic and nongenetic factors. Although several theories have been proposed about the pathogenesis of vitiligo, the precise cause remains unknown. Generally agreed upon principles are an absence of functional melanocytes in vitiligo skin and a loss of histochemically recognized melanocytes, owing to their destruction. However, the destruction is most likely a slow process resulting in a progressive decrease of melanocytes. Theories regarding destruction of melanocytes include autoimmune mechanisms, cytotoxic mechanisms, intrinsic melanocyte defects, oxidant-antioxidant mechanisms, and neural mechanisms, as follows:

• Autoimmune and cytotoxic hypotheses: Aberration of immune surveillance results in melanocyte dysfunction or destruction. The autoimmune theory proposes alteration in humoral and cellular immunity in the destruction of melanocytes of vitiligo. ^{[9, 10, 11]} This theory is of particular relevance given the fact that nonsegmental vitiligo is more frequently associated with autoimmune conditions than is segmental vitiligo. ^[12] Hence, making a diagnosis of nonsegmental vitiligo in a person with a family history of autoimmune disease may warrant a more thorough workup. For these reasons, certain disorders have been linked to vitiligo, such as: Hashimoto thyroiditis, Graves disease, Addison disease and diabetes mellitus, alopecia areata, pernicious anemia, inflammatory bowel disease, psoriasis, and autoimmune polyglandular syndrome. The most convincing evidence of an autoimmune pathogenesis is the presence of circulating antibodies against melanocyte proteins in patients with vitiligo. ^[13] In addition to humoral immune mechanisms, strong evidence indicates involvement of cellular immunity. Destruction of melanocytes may be directly mediated by autoreactive CD8 ⁺ T cells. Activated CD8 ⁺ T cells have been demonstrated in perilesional vitiligo skin. ^{[10, 11]}
• Neural hypothesis: A neurochemical mediator destroys melanocytes or inhibits melanin production.
• Oxidant-antioxidant mechanisms: An intermediate or metabolic product of melanin synthesis causes melanocyte destruction.
• Intrinsic defect of melanocytes: Melanocytes have an inherent abnormality that impedes their growth and differentiation in conditions that support normal melanocytes.

Because none of these theories alone is entirely satisfactory, some have suggested a composite hypothesis.

Genetics of vitiligo

Vitiligo is characterized by incomplete penetrance, multiple susceptibility loci, and genetic heterogeneity.[14] Family and twin studies have shown that inheritance is complex and likely involves both genetic and environmental factors.[15] Additionally, it is believed that genetic factors may influence the age of onset of vitiligo.[16] The inheritance of vitiligo may include genes associated with the biosynthesis of melanin, a response to oxidative stress, and regulation of autoimmunity.[17]

Current research has not identified any associations with a certain human leukocyte antigen (HLA) type in a consistent manner. There is reason to believe that segmental vitiligo and nonsegmental vitiligo may have distinct genetic mechanisms, which could account for their different responses to treatment.

In the United States, the relative rate of vitiligo is 1%. Vitiligo is relatively common globally, with a rate of 1-2%. Approximately 30% of vitiligo cases occur with a familial clustering of cases.

A female preponderance has been reported for vitiligo, but it is not statistically significant and the discrepancy has been attributed to an increase in reporting of cosmetic concerns by female patients.

Although vitiligo may appear at any time from birth to senescence, onset is most commonly observed in persons aged 10-30 years. The average age of onset for vitiligo is approximately 20 years. The age of onset is unlikely to vary between the sexes.

Vitiligo presents as asymptomatic, milky white colored lesions. The lesions may be localized in focal or segmental vitiligo and generalized in non-segmental vitiligo. Universal vitiligo shows generalized depigmentation. Hairs in the affected region may be white, and this is known as leukotrichia. Patients with generalized vitiligo may present with sunburn due to inadvertent sun exposure or actinic keratosis in long-standing vitiligo. Lesions may appear at the site of trauma (koebnerization).

Vitiligo is almost always diagnosed clinically upon physical examination. Vitiligo manifests as acquired depigmented macules or patches surrounded by normal skin. The macules are chalk or milk-white in color and are well demarcated. Lesions can be round, oval, or linear in shape. The borders may be convex.[1] Lesions enlarge centrifugally over time at an unpredictable rate. Lesions range from millimeters to centimeters in size. A Wood lamp may be necessary to see lesions on patients with lighter skin. Dermoscopy may also help in the diagnosis of vitiligo. It shows diffuse white glow in established lesion;  reverse pigmentary pattern in evolving vitiligo; micro-koebnerization, comet-tail like appearance in unstable vitiligo and reticular pigment network and peri-follicular pigment in stable and repigmenting vitiligo.[18]

The most common sites of vitiligo involvement are the face, neck, forearms, feet, dorsal hand, fingers, and scalp. When found on the face, lesions may favor a periocular or perioral distribution. In the setting of widespread or generalized vitiligo, lesions may also occur around the genital region, areola, and nipple. Additionally, lesions may occur in regions frequently subjected to trauma, such as bony prominences, elbows, and knees. Koebner phenomenon is defined as the development of vitiligo in sites of trauma, such as a cut, burn, or abrasion. Koebnerization may occur in as many as 20-60% of vitiligo patients.[19]

Body hair in vitiliginous macules may be depigmented. This is known as leukotrichia, and it may indicate a poor prognosis with regard to repigmentation therapy.[20] Spontaneous repigmentation of depigmented hair is unlikely to occur.

Trichrome vitiligo is a clinical variant characterized by an intermediate zone of hypopigmentation located between the depigmented center and the peripheral unaffected skin. The natural evolution of the hypopigmented areas is progression to full depigmentation. This results in 3 shades of color in the same patient, as in the image below. The presentation and shades of trichrome vitiligo vary depending on the natural skin color of the patient.

Trichrome vitiligo.

Marginal inflammatory vitiligo is a very rare variant in which a red, raised border is present at onset or may appear several months or years after initial onset. Mild pruritus may be present. See image below.

Marginal inflammatory vitiligo.

Quadrichrome vitiligo is another variant of vitiligo, which reflects the presence of a fourth color (dark brown) at sites of perifollicular repigmentation. 

Blue vitiligo is a variant of vitiligo in which a bluish tinge is seen in the depigmented macule. This bluish hue is due to the presence of dermal melanophages. [21]

Vitiligo may be divided into 2 groups: segmental and nonsegmental. It is important to note that other classification systems exist that choose to break down types of vitiligo based on having a localized or generalized distribution, with localized implying the lesion is restricted to a specific area and generalized implying more than one area is involved. However, the distinction between segmental and nonsegmental may be the most useful to the clinician, as it has an impact on progression, prognosis, and treatment.

Segmental vitiligo

This type manifests as 1 or more macules that may follow the lines of Blaschko. It is unilateral and does not cross the midline. Segmental vitiligo usually has an early onset and rapidly spreads in the affected area. The course of segmental vitiligo can arrest, and depigmented patches can persist unchanged for the life of the patient. This type of vitiligo is not associated with thyroid or other autoimmune disorders. See the image below.

Segmental vitiligo.

Nonsegmental vitiligo

Nonsegmental vitiligo has served as an umbrella term to include all types of vitiligo that cannot be classified as segmental vitiligo.[22] Of note, nonsegmental vitiligo is more strongly linked than segmental vitiligo to markers of autoimmunity or inflammation such as halo nevi and thyroid antibodies.[23]

Examples of nonsegmental vitiligo include the following (see the image below):

• Focal vitiligo: This is characterized by one or more macules in a limited area that do not follow a segmental distribution.

• Generalized vitiligo: This follows a nonsegmental distribution and is more widespread than localized or focal vitiligo.

Subtypes of generalized vitiligo include the following:

• Acrofacial vitiligo: Depigmentation occurs on the distal fingers and periorificial areas.

• Vulgaris vitiligo: This is characterized by scattered patches that are widely distributed.

• Universal vitiligo: Complete or nearly complete depigmentation of the body occurs.

• Mucosal vitiligo

Nonsegmental vitiligo.

The visual nature of the disease results in severe psychosocial and psychological consequences, especially in individuals with darker skin. It can result in social stigma and depression. 

Inadvertent sun-exposure results in acute sunburn, and chronic sun damage can result in non-melanoma skin cancers 

Although the diagnosis of vitiligo generally is made on the basis of clinical findings, biopsy is occasionally helpful for differentiating vitiligo from other hypopigmentary disorders.

Because of the association with other autoimmune diseases and endocrinopathies, further testing may be necessary in patients with suggestive signs or symptoms to rule out an underlying condition. Vitiligo may be associated with thyroid disease, diabetes mellitus, pernicious anemia, Addison disease, and alopecia areata. Appropriate tests should be performed only in the presence of signs or symptoms of associated disease.[4, 31]

Laboratory work for vitiligo may include the following:

• Thyroid panel consisting of thyroid-stimulating hormone (TSH), free triiodothyronine (T3), and free thyroxine (T4) levels
• Antinuclear antibody
• Antithyroid peroxidase antibody
• CBC count with differential

Microscopic examination of involved skin shows a complete absence of melanocytes in association with a total loss of epidermal pigmentation. Superficial perivascular and perifollicular lymphocytic infiltrates may be observed at the margin of vitiliginous lesions, consistent with a cell-mediated process destroying melanocytes. Degenerative changes have been documented in keratinocytes and melanocytes in both the border lesions and adjacent skin. Other documented changes include increased numbers of Langerhans cells, epidermal vacuolization, and thickening of the basement membrane. Loss of pigment and melanocytes in the epidermis is highlighted by Fontana-Masson staining and immunohistochemistry testing.[2, 3]

Various types of medications, phototherapy, laser therapy, and surgical therapy exist. However, it is important to note that in patients with lighter skin, no intervention may be needed. Instead, diligent sun protection may be the best strategy in order to avoid the surrounding normal skin from becoming more tan and making the lesions more obvious. When therapy is necessary, topical steroids, topical calcineurin inhibitors, and narrow-band ultraviolet (UV)–B phototherapy are widely used and are now considered the mainstays of treatment. However, treatment must be individualized and patients should be made aware of the risks associated with therapy. No single therapy for vitiligo produces predictably good results in all patients, and the response to therapy is highly variable.[32, 33, 34, 35, 36]

Some types of vitiligo or lesions in certain locations may be more or less responsive to treatment. Segmental vitiligo and age of onset younger than 14 years have been associated with more refractory disease.[37]  Segmental vitiligo is more responsive to surgical therapy. 

During therapy, pigment cells arise and proliferate from the pilosebaceous unit, spare epidermal melanocytes,[38] and the border of lesions, and migrate up to 2-4 mm from the edge.

Phototherapy

Phototherapy induces satisfactory repigmentation in a majority of patients with early or localized disease.[4] Prolonged phototherapy courses should be encouraged, as a treatment period of at least 6 months may be necessary to accurately assess the responsiveness to the phototherapy.[39] It should be noted that phototherapy causes the normal skin surrounding the lesions to tan, thereby making the lesion more noticeable. This may be cosmetically unacceptable in some patients; therefore, careful counseling surrounding patient expectations and results is necessary before beginning treatment.

Narrowband UV-B (NB-UVB) is widely used and has become the first choice of phototherapy for adults and children with generalized vitiligo. Wavelengths of 311-312 nm typically are used. Treatment frequency is 2-3 times weekly. This treatment can be safely used in children, pregnant women, and lactating women. However, phototherapy may be difficult in pediatric patients who may be unable to cooperate. Short-term adverse effects of NB-UVB include burning, pruritus, and xerosis.

Psoralen photochemotherapy involves the use of psoralens combined with UV-A radiation and is also known as PUVA. Psoralens can be applied either topically or taken orally, followed by exposure to artificial UV-A radiation or natural sunlight. Adverse effects include phototoxic effects, nausea, and risk of skin cancer.

PUVA has largely been replaced by NB-UVB, which is highly effective and has fewer adverse effects. Literature reviews from 2017 have shown that NB-UVB therapy has an overall better response than therapy with PUVA.[39] Additional advantages of NB-UVB over PUVA include shorter treatment times, no drug costs, no nausea, and no need for subsequent photoprotection.

Laser therapy

The excimer laser produces monochromatic rays at 308 nm to treat limited, stable patches of vitiligo. This new treatment is an efficacious, safe, and well-tolerated treatment for vitiligo. However, therapy is expensive. Localized lesions of vitiligo are treated twice weekly for an average of 24-48 sessions.

Excimer laser has been combined with both topical tacrolimus and short-term systemic corticosteroids in the setting of segmental vitiligo, which is a type known to be more resistant to repigmentation in some patients.[40] Studies suggest that segmental vitiligo has a better repigmentation response with excimer laser treatment used at earlier stages of the disease.[41]

Additionally, the use of khellin 4% ointment in combination with monochromatic excimer light (MEL) at 308 nm has been investigated and may be a valid therapeutic option worthy of consideration in the treatment of vitiligo.[42]

Topical therapies

Steroids

A topical corticosteroid preparation is often chosen as a first-line treatment for localized vitiligo because it is easy and convenient for patients.. The results of therapy have been reported as moderately successful, particularly in patients with localized vitiligo and/or an inflammatory component to their vitiligo. Depending on the area being treated, a moderately potent topical steroid can be applied daily for a period of months and then tapered depending on response. Patients should be monitored closely for the possibility of steroid atrophy. 

Topical Janus kinase (JAK) inhibitors 

Topical JAK inhibitor therapy are an emerging option.[55] Ruxolitinib topical cream gained approval from the FDA in July 2022 for treatment of adults and adolescents aged 12 years and older with nonsegmental vitiligo. Approval was based on data from two Phase 3 trials (TRuE-V1 and TRuE-V2), that evaluated the safety and efficacy of ruxolitinib cream compared with vehicle in more than 600 people.

Topical ruxolitinib resulted in significant improvements in vitiligo area scoring index (VASI), which represent improvements in facial and total body repigmentation at Week 24 (primary analysis) compared with vehicle and in an open-label extension at Week 52. Results at Week 24, which were consistent across both studies, showed approximately 30% of patients treated with topical ruxolitinib achieved at least 75% improvement from baseline in the facial (VASI75), the primary endpoint, compared with approximately 8% and 13% of patients treated with vehicle in TRuE-V1 and TRuE-V2, respectively. At Week 52, approximately 50% of ruxolitinib-treated patients achieved F-VASI75.[56]  

Additionally, at Week 24, more than 15% of patients treated with topical ruxolitinib achieved at least 90% improvement from baseline in F-VASI (F-VASI90), compared with approximately 2% of patients treated with vehicle. At Week 52, the percentage of ruxolitinib-treated patients who achieved F-VASI90 doubled to approximately 30%.[56]  

Calcineurin inhibitors

Topical tacrolimus ointment (0.03% or 0.1%) and pimecrolimus cream are effective therapies for vitiligo, particularly when the disease involves the head and neck. These may be used in combination with topical steroids. Studies have suggested that augmenting topical calcineurin inhibitors with laser therapy or NB-UVB may yield better treatment results.[43, 44]

Vitamin D analogs

Vitamin D analogs, particularly calcipotriol and tacalcitol, have been used as topical therapeutic agents in vitiligo. They target the local immune response and act on specific T-cell activation. They do this by inhibition of the transition of T cells (early to late G1 phase) and inhibition of the expression of various proinflammatory cytokines that encode tumor necrosis factor-alpha and interferon-gamma. These vitamin D3 compounds influence melanocyte maturation and differentiation, in addition to up-regulating melanogenesis through pathways that are activated by specific ligand receptors (eg, endothelin receptor and c-kit).[45] More research is needed to examine the effectiveness of calcipotriol as a treatment for vitiligo, as it remains controversial.[46, 47, 48] Some studies have found that the addition of calcipotriol to combination treatments involving NB-UVB, PUVA, or topical steroids improved repigmentation,[46, 47] while others have found no significant differences.[47, 48] While the role of calcipotriol in vitiligo therapy is still not completely clear, it is more likely that it could act as a supplemental therapy rather than a monotherapy. 

Systemic Therapies

Afamelanotide

Afamelanotide is an emerging treatment for vitiligo that is a long-lasting synthetic analog of alpha-melanocyte–stimulating hormone (α-MSH).[49, 50] Afamelanotide binds to the melanocortin-1 receptor and stimulates melanocyte proliferation and melanogenesis. The premise of the treatment the knowledge that patients with vitiligo exhibit defects in the melanocortin system, which manifest as decreased levels of α-MSH in both systemic circulation and skin lesions.[51] Afamelanotide is delivered as a subcutaneous implant. A 55-patient phase I/II study showed that when used in conjunction with NB-UVB, a 7- to 10-day release implant of 16 mg afamelantotide produced faster repigmentation of facial and upper extremity lesions than NB-UVB alone. Adverse reactions included hyperpigmentation of normal skin, nausea, and abdominal pain.[50, 52]  

Janus kinase (JAK) inhibitor therapy

Oral tofacitinib and other JAK inhibitors have revolutionized the treatment of vitiligo. They are often combined with the other treatment modalities mentioned. Other forms of targeted immunotherapy are also emerging as treatment options.[53, 54]  

Systemic corticosteroid therapy

Systemic steroids (prednisone) have been used, although this treatment method is not recommended owing to its toxicity. Systemic corticosteroids can also be used as twice-weekly pulse therapy. 

Depigmentation therapy

If vitiligo is widespread and attempts at repigmentation do not produce satisfactory results, depigmentation may be attempted in very carefully selected patients.

The long-term social and emotional consequences of depigmentation must be considered. Depigmentation should not be attempted unless the patient fully understands that the treatment results in permanent depigmentation. Some authorities have recommended consultation with a mental health professional to discuss potential social consequences of depigmentation.[60]

A 20% cream of monobenzylether of hydroquinone is applied twice daily for 3-12 months. Burning or itching may occur. Allergic contact dermatitis may be seen.[61] The toxicity of monobenzylether of hydroquinone has been deemed mild; however, no research has been performed on the safety of using the drug over large surface areas of skin to induce widespread pigmentation.[62] Accordingly, it is suggested that depigmentation therapy be limited to the lesions that are most bothersome to the patient, such as ones on the face and hands.

Surgical alternatives exist for the treatment of vitiligo; however, because of the time-consuming nature of surgical therapies, these treatment regimens are limited to segmental vitiligo or localized vitiligo that is limited to a small region.

Characteristics of vitiligo patients that may be a surgical candidate include the following:

• Segmental vitiligo

• Vitiligo localized to a small area

• Vitiligo in areas that tend not to repigment well (eg, dorsal fingers, ankles, forehead, hairline)

Additionally, to be considered for surgery a lesion must be stable, which is to say that the vitiligo is not actively progressing. The most important factors indicating stability are as follows:

• No progression or growth of lesions for at least 2 years

• Spontaneous repigmentation (suggests that melanocytes are not being actively destroyed and indicates relative inactivity)

• A positive minigrafting test disclosing repigmentation at 4-5 minigrafts, which, to date, is the most accurate evidence of vitiligo stability

• Absence of new koebnerization, including the donor site for the minigrafting test

The surgical treatment of vitiligo can be classified according to the type of graft as tissue grafting and cellular grafting technique[63] . The tissue grafting technique includes suction blister grafting, mini-punch grafting and split-thickness graft. The cellular grafting techniques involve non-culture epidermal suspension (NCES), non-cultured outer root sheath follicular suspension and cultured melanocyte grafting. 

• Noncultured epidermal suspensions: After the achromic epidermis is removed, an epidermal suspension with melanocytes and keratinocytes previously prepared by trypsinization of normally pigmented donor skin is spread onto the denuded area and immediately covered with nonadherent dressings. Using noncultured epidermal cellular grafts, 71% of patients in one study achieved more than 75% repigmentation, especially in segmental vitiligo, piebaldism, and halo nevi.[64] Color mismatches may be problematic, and generalized vitiligo did not repigment as well.[65]

• Thin dermoepidermal grafts: The depigmented epidermis is removed by superficial dermabrasion, including the papillary dermis, and very thin dermoepidermal sheets harvested with a dermatome are grafted onto the denuded skin.

• Suction blister grafting: Epidermal grafts can be obtained by vacuum suction, usually with 150 mm Hg. The recipient site can be prepared by dermabrasion of the sites before grafting. The epidermal donor graft is placed on the vitiliginous areas. This technique is best suited for lip vitiligo[66]

• Punch minigrafting: Small donor grafts are inserted into the incision of recipient sites and held in place by a pressure dressing.  The size of punch used is 1 mm for the face and 1.5 mm for the rest of the body.  The graft heals readily and begins to show repigmentation within 4-6 weeks. Some pebbling persists but is minimal, and the cosmetic result is excellent.[67]

• Cultured epidermis with melanocytes or cultured melanocyte suspensions: Depigmented skin is removed using liquid nitrogen, superficial dermabrasion, thermosurgery, or carbon dioxide lasers; very thin sheets of cultured epidermis are grafted or suspensions are spread onto the denuded surface.[68]

Micropigmentation[69] is another option. Tattooing can be used to repigment depigmented skin in dark-skinned individuals. Color matching is difficult, the color tends to fade, and the treatment can possibly provoke the appearance of new lesions. Alternatively, skin can be dyed with dihydroxyacetone preparations, although the color match is often poor.

In cases where the patient’s vitiligo may be tied to an autoimmune disease or another underlying condition, referral to the respective specialist may be necessary. Consultation with an ophthalmologist may be warranted in cases with suspected ocular involvement or ocular symptoms. Additionally, psychological needs must be addressed on a continual basis with appropriate referrals to mental health specialists.[70]

Because vitiligo affects a person’s physical appearance, there are various associated psychological and social impacts. Higher levels of depression and social anxiety have been reported in patients with vitiligo.[71] Patients may also experience low self-esteem, social stigmatization, shame, avoidance of intimacy, adjustment disorder, fear, suicidal ideation, and other psychiatric morbidities.[72] Lower measures of quality of life have been reported.[73, 74, 75] Specifically, visible vitiligo lesions have been associated with more emotional distress and stigmatization than nonvisible lesions.[76, 77] With regard to the pediatric population, adolescents are more likely to report lower quality-of-life measures and greater psychological and emotional distress than young children.[72, 78]

British Association of Dermatologists

Clinical guidelines on the management of vitiligo released in 2021 by the British Association of Dermatologists include, but are not limited to, the following[79] :

• To identify people with vitiligo (including children) who have a greater likelihood of developing autoimmune thyroid disease, screen for antithyroid antibodies and thyroid function
• The quality of life and psychological distress level related to living with vitiligo should be assessed and monitored; tools for such assessment include the Patient Health Questionnaire-4 (PHQ-4), the Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder 7 (GAD7) and the Dermatology Life Quality Index (DLQI), and the Vitiligo Impact Patient scale (VIPs) or the vitiligo-specific quality-of-life instrument (VitiQoL)
• As first-line primary or secondary care treatment, people with vitiligo should be offered a potent or very potent topical corticosteroid once daily, to minimize potential side effects, with avoidance of the periocular area
• As an alternative to potent or very potent topical corticosteroids in people with facial vitiligo, topical tacrolimus 0.1% ointment twice daily should be considered
• When extensive vitiligo on visible sites is having a negative psychological effect, depigmentation therapies should be considered. However, adequate psychological assessment and/or intervention should first be performed
• To arrest the activity of rapidly progressive vitiligo, the use of oral betamethasone should be considered (after the risks and benefits have been carefully weighed), with the drug administered at 0.1 mg/kg twice weekly on 2 consecutive days for 3 months; the dose should then be tapered by 1 mg per month for an additional 3 months; treatment should be carried out in combination with narrowband ultraviolet B (NB-UVB) therapy
• Owing to the malignancy risk, people with vitiligo should not receive azathioprine in combination with psoralen–ultraviolet A (PUVA) or NB-UVB
• In people with vitiligo in whom the response to topical therapy has been inadequate and/or in whom extensive or progressive disease exists, whole-body or localized NB-UVB should be offered as first-line phototherapy; the risk-benefit ratio should be discussed, especially for children, since patients generally require a prolonged course; for localized disease sites, the treatment may be used in combination with a topical calcineurin inhibitor (the evidence being greater for tacrolimus) or a potent topical corticosteroid; patients should be counselled that upon treatment cessation, there is a significant risk of response loss
• When stable, segmental or nonsegmental vitiligo does not respond to other treatments, leaving the patient distressed, cellular grafting, such as blister grafting or cell suspension, should be considered
• For people with vitiligo who are suffering from moderate to severe psychological distress, referral should be offered to psychological services for group and/or individual cognitive behavioural therapy

The topical Janus kinase (JAK) inhibitor, ruxolitinib, is the first drug approved for vitiligo repigmentation. Other drugs (eg, topical corticosteroids, topical calcineurin inhibitors, psoralens, immunomodulators, and vitamin D analogs) have been used for treating vitiligo. 

Class Summary

Mechanism of action may involve disruption of interferon-gamma signaling and Janus kinase pathways involved in vitiligo.

Ruxolitinib topical (Opzelura)

Indicated for topical treatment of nonsegmental vitiligo in adults and adolescents aged 12 years and older.