The general goals of medical management of vitiligo are to repigment vitiliginous areas of skin and to stabilize the progression of depigmentation. However, for some patients with vitiligo affecting extensive body surface areas who are unresponsive to repigmentation therapies, depigmentation of the remaining normal skin may be a better choice. Candidates for depigmentation therapy should be carefully screened and patient education is essential. Permanent topical therapies used for depigmentation include monobenzyl ether of hydroquinone, 4-methoxyphenol, and 88% phenol. Physical modalities, such as cryotherapy and lasers, are also being used successfully.
Key points
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The general goals of medical management of vitiligo are to repigment affected areas of skin and to stabilize the progression of depigmentation.
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However, for some patients with vitiligo affecting extensive body surface areas who are unresponsive to repigmentation therapies, depigmentation of the remaining normal skin may be a better choice.
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Candidates for depigmentation therapy should be carefully screened and patient education is essential.
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Permanent topical therapies used for depigmentation include monobenzyl ether of hydroquinone, 4-methoxyphenol, and 88% phenol. Physical modalities, such as cryotherapy and lasers, are also being used successfully.
Introduction
Vitiligo is a common acquired disorder of the epidermis and hair follicles that manifests clinically as progressive depigmentation due to loss of functioning melanocytes. It affects 1% to 2% of the global population. Studies suggest an equal incidence in all racial-ethnic groups. However, because of the highly visible contrast between the constitutive skin color and the white patches, vitiligo can be particularly disfiguring in darker-complexioned skin types. Given the disfiguring aspect of the disease, vitiligo can profoundly impact the quality of life in children and adults.
Multiple theories have been proffered for the pathogenesis of vitiligo, including autoimmune, biochemical, oxidative stress, neural, melanocytorrhagy and viral mechanisms. However, multiple recent studies document the expanding role of immune mechanisms in the pathogenesis of vitiligo.
In general, therapies for vitiligo address stabilization of the disease and repigmentation of affected sites. Stabilization agents include systemic corticosteroids, oral mini-pulse corticosteroid therapy, minocycline, and methotrexate. First-line therapies for repigmentation are calcineurin inhibitors, topical corticosteroids, and narrow band (NB)-UVB phototherapy. Although many patients achieve successful repigmentation outcomes, others develop progressive disease affecting extensive body surface areas and fail to respond to repigmentation protocols. The goal for such patients with extensive disease would be to create a uniform skin tone by depigmenting the remaining pigmented skin sites.
Introduction
Vitiligo is a common acquired disorder of the epidermis and hair follicles that manifests clinically as progressive depigmentation due to loss of functioning melanocytes. It affects 1% to 2% of the global population. Studies suggest an equal incidence in all racial-ethnic groups. However, because of the highly visible contrast between the constitutive skin color and the white patches, vitiligo can be particularly disfiguring in darker-complexioned skin types. Given the disfiguring aspect of the disease, vitiligo can profoundly impact the quality of life in children and adults.
Multiple theories have been proffered for the pathogenesis of vitiligo, including autoimmune, biochemical, oxidative stress, neural, melanocytorrhagy and viral mechanisms. However, multiple recent studies document the expanding role of immune mechanisms in the pathogenesis of vitiligo.
In general, therapies for vitiligo address stabilization of the disease and repigmentation of affected sites. Stabilization agents include systemic corticosteroids, oral mini-pulse corticosteroid therapy, minocycline, and methotrexate. First-line therapies for repigmentation are calcineurin inhibitors, topical corticosteroids, and narrow band (NB)-UVB phototherapy. Although many patients achieve successful repigmentation outcomes, others develop progressive disease affecting extensive body surface areas and fail to respond to repigmentation protocols. The goal for such patients with extensive disease would be to create a uniform skin tone by depigmenting the remaining pigmented skin sites.
Candidates for depigmentation therapy
Depigmentation therapy can be a viable therapeutic alternative in patients with extensive disease affecting greater than 30% to 40% of body surface areas.
Most patients who choose depigmentation have failed to achieve optimal repigmentation. Depigmentation therapy can be used in all skin types devastated by the contrasting areas of normal and vitiliginous skin. Patient selection is of paramount importance, given the permanency of depigmentation therapy ( Box 1 ). Prospective patients should be carefully screened. A detailed medical history should be obtained including any history of psychiatric illness portending unrealistic therapeutic outcomes. An extended consultation should be conducted with patients and their families when possible. Issues that should be discussed in depth are included in Box 2 . It is imperative that potential patients thoroughly understand the permanent nature of the process. It is important with younger patients and their families to explain that if medical advances provide new therapies for repigmentation, they may not be candidates for such therapies if they have undergone depigmentation. All patients treated at the Vitiligo & Pigmentation Institute of Southern California sign an informed consent before initiating depigmentation therapy. A sample template of the authors’ informed consent is included in Box 3 .
Patients with severe disease affecting greater than 30% or 40% body surface areas who have failed repigmentation therapies
Patients with severe disease affecting greater than 30% or 40% depigmentation who are unable to undergo the time and rigors of repigmentation therapies
Emotionally stable patients
Patients willing to adhere to photoprotection
A willingness to accept the inability to tan
Permanency of the treatment
Realistic expectations
Color match with areas of depigmentation
Treatment time and cost
Mechanism of action of the drug, including depigmentation at sites distal to areas of use
Drug-related side effects
The potential for patchy repigmentation
Consort depigmentation with inappropriate use
I have been informed by ______________________ of the benefits, risks, possible alternative methods of treatment, and possible consequences involved in depigmentation therapy with monobenzyl ether of hydroquinone (MBEH, monobenzone) for the relief of vitiligo.
Depigmentation therapy for vitiligo has been explained to me in detail. The benefits include evening out of my skin tone by removing the remaining pigmentation with MBEH cream 20%. Higher concentrations can also be used (30%, 40%).
MBEH cream is a depigmenting agent whose mechanism of action is not fully understood. MBEH may cause destruction of melanocytes (skin cells that produce pigment) and permanent depigmentation. It may take 1 to 4 months before lightening begins to appear. When applied to my skin, this drug induces progressive and diffuse depigmentation of the normal pigmented skin. After several months, depigmentation also commonly develops on areas of normal skin where the drug has never been applied. Exposure to sunlight reduces the depigmenting (fading) effect of the drug. The appearance of the skin when examined under a microscope after depigmentation with topical monobenzone is the same as that seen in vitiligo; the skin is normal except for the absence of identifiable melanocytes.
Potential side effects include recurrence of pigmentation after depigmentation, severe allergic reactions of the skin, alopecia, dermatitis, dry skin, redness of the skin, itching, premature graying, and vitiligolike pigment loss in a spouse or other individuals if intimate contact occurs. My skin must be protected from sun exposure at all times. Sun exposure can cause depigmented areas to repigment. My treated skin will not tan.
In a small minority of patients, intense hyperpigmentation (darken of the skin) can occur after use of MBEH.
Understanding that stated above, I hereby authorize the above doctor, or whomever he or she may designate, to administer such treatment to me. If I had any questions regarding this treatment, I have asked the doctor and have received all needed answers.
_______________________________________________________________________________________________
Name of patient
_______________________________________________________________________________________________
Signature of patient
_______________________________________________________________________________________________
Signature of witness
The decision to undergo depigmentation of areas of normal skin is especially complex. For example, the decision may be more complicated for African Americans and Asians by the continued presence of secondary racial characteristics, such as facial features and hair texture. Thus, the potential sociocultural issues should be thoroughly explored with patients before initiating therapy.
Topical depigmentation therapies
The most readily available depigmenting agents include monobenzyl ether of hydroquinone (MBEH), 4-methoxyphenol (4MP, mequinol or p-hydroxyanisole) and phenol ( Table 1 ). In addition, physical therapies, such as lasers and cryotherapy, both as monotherapy and as adjuncts to topical treatments, are also used for depigmentation.
| First-Line Therapies | Emerging Therapies |
|---|---|
| MBEH/monobenzone | Imatinib |
| Monomethyl ether of hydroquinone/4-methoxyphenol | Imiquimod |
| 88% Phenol | Diphencyprone |
| Cryotherapy | |
| Lasers | |
| Q-switched ruby | |
| Q-switched alexandrite | |
Depigmentation is a gradual process characterized by gradual progressive fading of patients’ unaffected normal pigmentation. Complete depigmentation may require 1 to 3 years of treatment. In the authors’ experience, most patients are satisfied with the therapeutic outcomes.
Monobenzyl Ether of Hydroquinone
MBEH (p-benzyloxy-phenol, monobenzone) is the only topical depigmenting agent that is currently approved for vitiligo by the Food and Drug Administration. Moreover, the only indication for use of the drug is in patients with vitiligo ( Figs. 1 and 2 ). It is a hydroquinone (HQ) derivative. MBEH was ushered into the realm of dermatology in the late 1930s following seminal observations by McNally and Oliver and colleagues. They reported that workers exposed to MBEH, which was used as an antioxidant in the rubber tannery industry, developed depigmentation. Tannery workers developed white patches at the site of chemical contact from their rubber gloves that contained Agerite Alba (MBEH). Depigmentation also developed at sites distal to exposure to the chemical.
Related posts:
The Medical Treatment of Vitiligo
Quality of Life, Burden of Disease, Co-morbidities, and Systemic Effects in Vitiligo Patients
Skin Cancer Risk (Nonmelanoma Skin Cancers/Melanoma) in Vitiligo Patients
Phototherapy and Combination Therapies for Vitiligo
Surgical Therapies for Vitiligo
Vitiligo Pathogenesis and Emerging Treatments
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