Doctor, my skin is turning white! What is Vitiligo (hypopigmentation) and how to treat it?15 November 2019
The skin is the largest organ of the human body and is comprised of the epidermis, dermis and subcutaneous fat. The epidermis consists of keratinocytes, melanocytes, Langerhans cells and Merkel cells. The melanocyte is the sole pigment producing cell of the skin. Melanocytes produce melanin within small cellular organelles called melanosomes. Melasonomes transfer their melanin to overlying keratinocytes, which migrate from the basal layer of the epidermis to the stratum corneum where they are desquamated into the environment. Differences in innate skin colour are determined by the size and number of melanosomes, not the number of melanocytes. In other words, the number of melanocytes in the epidermis is the same irrespective of an individual’s race.
Disorders of pigmentation can broadly be categorized into disorders of hyperpigmentation and hypopigmentation (the latter including disorders of depigmentation).
Hypopigmentation is the term used to describe the partial or complete loss of pigmentation, resulting in clinically apparent white areas of skin. It can be caused by the inhibition of synthesis and transfer of melanin, as in the case of pityriasis versicolor and pityriasis alba, resulting in mild to moderate hypopigmentation, or by a complete loss of melanocytes, resulting in depigmentation as is seen in vitiligo.
Here, we let’s review – Vitiligo, the most common disorder of hypopigmentation seen in everyday office practice.
Vitiligo is a common acquired pigment disorder characterized by a complete loss of functional epidermal melanocytes. It presents with areas of progressive depigmentation involving the skin, hair or mucosa.
Vitiligo is the most prevalent pigmentary disorder in the world, with an incidence between 0.1% and 2%. It is believed that this incidence is higher among those with pigmented skin.
- Vitiligo usually begins before the age of 30 and is less common in the elderly, but can occur at any age. Both sexes are equally affected. Approximately 20% of patients with vitiligo have a positive family history.
- Vitiligo is neither symptomatic, life-threatening nor contagious but causes an enormous amount of psychosocial distress to those affected. Patients often identify it as the “Michael Jackson disease.”
- The etiopathogenesis of vitiligo is complex and unknown but thought to be related to the interaction of genetic, immunological and neurological factors. Clinical experience highlights that stress, illness and physical trauma can trigger vitiligo patches; however, genetic susceptibility and other neural factors are also involved.
- Vitiligo can be associated with a variety of other autoimmune disorders such as thyroid disease, pernicious anemia, lupus, diabetes, psoriasis and alopecia areata.
- It typically presents as symmetrical, well-demarcated depigmented macules and patches of varying sizes that can occur on any skin or mucosal surface.
- Periorificial lesions (eyes, nose, mouth, anus, vulva) are common, as are lesion at sites of trauma (elbows knees, hands). Concomitant whitening of the hairs associated with vitiligo patches is not uncommon.
Vitiligo can be classified into two major clinical subtypes: Segmental and Non-segmental
- Segmental vitiligo is the less common, more stable subtype characterized by localized patches confined to a particular segment of the skin typically in a dermatomal distribution.
- Non-segmental or generalized vitiligo is more common, involves diffuse areas of skin, and tends to be associated with autoimmune disease. The course of vitiligo is unpredictable. The patches may remain static or expand exposure.
Be informed about these treatment options:
The diagnosis of vitiligo is mostly clinical, however a Wood’s lamp examination can accentuate affected skin and help confirm the diagnosis. The differential diagnosis includes pityriasis versciolor, pityriasis alba, piebaldism and idiopathic guttate hypomelanosis. The treatment of vitiligo generally falls into the categories of non-medicinal (sun protection and camouflage agents) and medicinal (repigmentation and depigmentation therapies). Although vitiligo is resistant to all forms of skin cancer, it is still subject to sunburn from excess sun.
- Sunburns can also result in Koebnerization of normal skin.
As such, counselling patients about the importance of sun safety, including the liberal use of broad-spectrum sunscreens, sun protective clothing and general sun avoidance, is an important component of vitiligo management.
- Camouflage agents and selftanners containing dihydroxyacetone are useful for evening out contrasting skin patches of vitiligo and masquerading the disease. They lessen the stigma and psychosocial impact of the disease but offer no therapeutic benefit.
- Tattooing over vitiligo skin should be avoided as it can also trigger Koebnerization. The medical treatment of vitiligo is challenging and imperfect, and the response to therapy is highly variable. The head and neck area tend to respond well to treatment while the hands and feet are resistant.
Treatment options for Vitiligo:
For localized vitiligo, potent topical steroids are the most commonly used first-line treatment, with reported repigmentation rates of 45% over three to six months of treatment. Topical calcineurin inhibitors are steroid-sparing immunomodulators that are also commonly used for the treatment of localized disease, especially on the face and neck.
Phototherapy & Photochemotherapy for Vitiligo
Phototherapy options for vitiligo include narrowband ultraviolet B therapy and the 308-nm excimer laser (a focused ultraviolet B device). Photochemotherapy refers to the use of a topical or oral photosensitizing agent (such as psoralen) with ultraviolet A therapy.
Phototherapy and photochemotherapy are used for patients with extensive disease but are not readily available in all locales and require a time commitment of two to three visits per week over several weeks.
Surgical grafting is not performed in routine practice.
Depigmentation Topical Therapy
For patients with extensive, recalcitrant disease, depigmentation topical therapy with 20% monobenzyl ether of hydroquinone twice daily over several months can be used to create diffuse depigmentation that may be more cosmetically acceptable for patients centrifugally. Spontaneous repigmentation has been reported to occur in 10% to 20% of patients. The lack of melanocytes precludes the development of melanoma skin cancer within vitiligo patches. And despite the lack of protective melanin, patches of vitiligo are remarkably resistant to the development of non-melanoma skin cancers— which are not derived from melanocytes—such as basal cell carcinoma and squamous cell carcinoma.