US Pharm. 2012;37(4):46-48.
Vitiligo is a pigment disorder that involves the skin, the hair, and occasionally the mucous membranes.1,2 All skin types are affected, and in rare cases the iris of the eye can become discolored.3 Vitiligo is progressive and chronic, but some patients spontaneously repigment, although this is uncommon.1 The disorder affects approximately 1% of the U.S. population and 0.1% to 8% of the global population.1 Vitiligo can occur at any age, but the average age of onset is 20 years.1 There is no difference in prevalence between men and women, but women present more often because of cosmetic concerns.
Vitiligo is a complex disorder, and its exact causation is unknown.
It generally manifests as hypopigmented patches in areas that normally
are hyperpigmented, such as the face, hands, and elbows.1 The
disorder can be classified as localized, generalized, or universal.
Localized vitiligo is restricted to one general area, whereas
generalized vitiligo involves more than one area that is symmetrical and
usually includes mucous membranes.3,4 Universal vitiligo is the loss of pigment in more than 80% of the skin.1,3
Although the exact mechanism is unknown, the hypopigmentation that
characterizes vitiligo has been shown to be due to the absence of
functional melanocytes (melanin-producing cells).1,2 Genetic
and nongenetic factors are thought to contribute to the pathophysiology
of this condition, with 18% to 20% of all cases having a familial trait.1,5
Nongenetic factors theorized to be potentially associated with
melanocyte damage include autoimmune defect, melanocyte defect,
oxidative-antioxidant system stress, and nerve injury.1,6
Peripheral blood samples from vitiligo patients have been discovered to
contain melanocyte-specific autoantibodies and cytotoxic T cells,
suggesting an autoimmune disorder. Other research has found that there
is an intrinsic abnormality in melanocytes that makes them more
susceptible to trauma and environmental changes. (Trauma is believed to
precede the onset of vitiligo, causing melanocytic defects as well as
nerve injury.) Finally, the epidermis of vitiligo patients has been
shown to retain high levels of hydrogen peroxide. This accumulation
leads to oxidative stress in the epidermis, resulting in damage to the
melanocytes.6 While these are all separate hypotheses, they
are all a part of the big picture, and additional research is needed to
determine the definitive cause of vitiligo.
Vitiligo, which can be disfiguring, generally presents as round or oval macules with convex margins surrounded by normal skin.1,3
The disorder is most often diagnosed clinically, but the use of a
Wood’s lamp may be beneficial for its identification in fair-skinned
individuals.1,6 Biopsy also may be useful to verify the absence of melanocytes in the affected area.6
Although vitiligo is generally considered a cosmetic issue, it is
associated with the development of autoimmune disorders such as thyroid
disease, insulin-dependent diabetes mellitus, Addison’s disease, and
Quality of life in individuals with vitiligo is often overlooked and underestimated.1,7
The cosmetic nature of the disorder can have a negative impact on a
person’s self-esteem, body image, and intimate relationships, as well as
cause unnecessary stress.1,3,6 Often, these issues lead
people to seek treatment. The treatment of vitiligo can be difficult,
and because the exact mechanism is poorly understood, a multifaceted
approach is necessary.6,7
TREATMENT OPTIONS FOR VITILIGO
Currently there is no cure for vitiligo, but many options are available for treating vitiliginous lesions.7 Response to treatment is variable, and no single option works for all patients.8
There are three general approaches to treatment: camouflaging
depigmented skin, restoring pigmentation, and destroying the remaining
Camouflaging Depigmented Skin
Camouflage therapy is a nonpharmacologic treatment option for
vitiligo. It is performed to disguise vitiliginous lesions and to help
ease the psychological component of the disease for the patient.9 Products include self-tanners, stains, foundations, and powders.9
Most available foundation and powder products require daily application
and easily wear off with sweat and friction, whereas self-tanning
products offer a semipermanent option.10 Dihydroxyacetone, the active ingredient in most self-tanners, gives the skin a brown color that lasts up to 10 days.10
Self-tanners should be applied only to the vitiliginous lesions in
order to minimize color contrast and should be used sparingly on the
elbows, knees, and hands.9 Exfoliation of the skin prior to using the product aids in achieving an even application.9 Sun protection is important, as many self-tanning products do not contain sunscreen.
Vitiliginous lesions lack melanin, the body’s natural sunscreen. For
this reason, depigmented lesions have a higher risk of sun damage,
photoaging, and skin cancer.11 Sunscreen helps prevent
short-term and long-term damage and can minimize the contrast between
normal skin and depigmented skin. Patients should use a waterproof
sunscreen that protects against both ultraviolet A (UVA) and ultraviolet
B (UVB) rays and provides a sun protection factor of at least 15.11 Sunscreen should be reapplied every 90 minutes, and after swimming or sweating.11
Phototherapy and Photochemotherapy: One of the oldest vitiligo treatments is UV light, and its use in various forms remains the most common treatment option.7
Phototherapy consists of UVA and narrowband UVB (NB-UVB).
Photochemotherapy is the combination of a photoactive chemical (e.g.,
psoralen, khellin) plus UVA (psoralen plus UVA [PUVA]).7 PUVA
requires the patient to take an oral dose of psoralen or to apply it
topically via a lotion, cream, or bathing solution prior to UVA
exposure. In a single randomized trial comparing oral PUVA with NB-UVB,
NB-UVB was more effective, although both agents produced results.12
Side effects of phototherapy include blistering, hyperpigmentation of
the surrounding unaffected skin, and skin malignancies (rare).7
Topical Medications: Generally, the first-line
pharmacologic treatment for vitiligo is topical corticosteroids (CSs),
which can be applied to most skin lesions.10 The efficacy of
CSs is attributed to the drugs’ modulation of immune response.
Vitiliginous lesions on the neck and face respond better to CSs than
lesions in other areas; however, the use of CSs on the face is limited
because of the thinness of the skin and subsequent increased absorption.10 Potent and highly potent products (TABLE 1) are recommended over less potent agents.13,14
Potent CSs such as betamethasone valerate should be tried first, and
only if the patient does not respond should high-potency CSs such as
clobetasol propionate be used.5 Of note, high-potency CSs
should be used for only 1 to 2 months, after which time they should be
slowly tapered to a lesser strength.3 In one study, 10% of
patients prescribed clobetasol propionate 0.05% achieved near-complete
repigmentation, as opposed to 25% of those treated with betamethasone
valerate 0.1%.15,16 High-potency CSs should be applied in a
thin layer once daily to the depigmented area only, as this will help
reduce the risk of side effects such skin atrophy, striae, steroid
folliculitis, hypertrichosis, and acne.3,5,10 Systemic
absorption is also a concern, especially in patients with thin skin,
those with large areas of depigmentation, those with head or neck
vitiligo, and children. Potential systemic side effects include
insomnia, agitation, weight gain, and adrenal insufficiency.10
Calcineurin inhibitors (CIs)—pimecrolimus 1% and tacrolimus 0.03% or 0.01%—are another effective topical choice.5,10,17
CIs provide immunomodulatory effects without the side effects of CSs,
but with similar efficacy. As with CSs, lesions of the head and neck
respond best to CIs.5,10,17 The application of hydrocolloid
dressings in conjunction with the use of CIs has been shown to enhance
repigmentation of resistant arm and leg lesions.18 Common
side effects associated with CIs include erythema, pruritus, burning,
and irritation. CIs are typically dosed twice daily and are approved for
short-term use (2-4 weeks) or intermittent long-term use.10,17
CIs are considered alternatives to topical steroids because of similar
efficacy and a better tolerated side-effect profile. Also, CIs may be
used in patients with lesions on the face or neck, areas where steroid
therapy is less desirable.5,10,17
A third topical immunomodulatory agent is calcipotriene, a vitamin D
analogue that enhances the development of melanocytes in vitiligo.10,17,19
Although calcipotriene has been shown to be inferior to topical CSs for
monotherapy, it may be an effective adjunctive treatment.20
When calcipotriene is combined with CSs, the rate of repigmentation
increases, the delay to repigmentation onset shortens, and there is
greater stability of repigmentation compared with either agent alone.20,21 Erythema, dryness, stinging, and burning have been reported as the most common side effects of calcipotriene use.
Complementary Therapy: Patients often look to natural
products to prevent or minimize symptoms of various afflictions. Several
studies have examined complementary therapies for vitiligo. Ginkgo biloba,
an herb used in traditional Chinese medicine, has been studied as a
potential therapy because of its antioxidant and immunomodulatory
properties.22 In a small double-blind, placebo-controlled study, patients who took G biloba 40 mg three times daily experienced a statistically significant delay in disease progression.23 Also, patients who took G biloba were more likely to have an increase in repigmentation. G biloba has been noted to be well tolerated in most individuals, although some patients report headache, nausea, and bleeding.24 Although G biloba shows some promise in vitiligo treatment, further studies need to be conducted before it can be recommended to patients.
Surgery: Patients who respond poorly to medical
treatment may consider undergoing surgery to transplant functional
melanocytes to depigmented skin.5 Various surgical techniques
are used, but they can be broken down into two main categories:
grafting melanocyte-rich tissue and grafting melanocyte cell
suspensions.10 It is recommended that surgery be done only on
sites that have had no new lesions and no extension of lesions within
the past 12 months.3 Also, patients have better outcomes if
their vitiligo is more localized, rather than on the extremities. Risks
include scarring, graft failure, new lesions at the site of surgery, and
Destroying the Remaining Pigmentation
Depigmentation: Depigmentation is an option for
patients who have vitiligo on more than 50% of their body and who have
failed other treatment modalities.5,10 Monobenzone and
hydroquinone are topical agents used to induce the death of the
remaining melanocytes. These agents may produce results in as little as 1
month, but more often take up to 10 months to achieve desired results.3 Side effects of these medications include erythema, burning, and possible repigmentation.10
Complete depigmentation results in extreme sensitivity to sunlight, so
it is important to stress the importance of daily sunscreen use in
patients who opt for this treatment.
Although vitiligo is not one of the most common dermatologic
disorders, it can result in significant cosmetic and psychosocial
challenges for individuals who are afflicted with it. Patients suspected
to have vitiligo should be referred to a physician for diagnosis and
treatment. The pharmacist’s role is to provide information about the
application of topical prescription and nonprescription products and
cosmetic agents. Pharmacists also have the responsibility to review
medication profiles and to provide counseling on the appropriate use of
products and the management of potential side effects.
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