Vitiligo is a chronic disorder of depigmentation resulting from the loss of melanin-producing melanocytes in the skin. It affects about 0.5% of the world population without preference toward race or gender.¹ Although vitiligo can occur at any age, the incidence peaks in young adults. Vitiligo is one of the most psychologically devastating skin diseases, particularly in skin of color due to the enhanced contrast between normal and diseased skin, thus making it more apparent to the eye.

The course of vitiligo is unpredictable. Areas of hypopigmentation may remain stable or slowly progressive for years. Occasionally, widespread depigmentation can rapidly occur. Vitiligo tends to develop in areas exposed to friction or pressure such as the face (especially around the eyes and mouth), hands, feet, genitals, mucous membranes, and extensor surfaces of the arms and legs. The most common pattern of vitiligo is known as non-segmental or generalized, which refers to extensive and usually symmetric patches of depigmentation. Segmental vitiligo refers to a more localized and unilateral disease. Further differences exist between these two types, but they are beyond the scope of this review.

The diagnosis is based on clinical examination and usually does not require a biopsy. Clinicians may also recommend screening for thyroid disease and other autoimmune disorders given their high association with vitiligo. Some other dermatologic conditions that may resemble vitiligo include post-inflammatory hypopigmentation, tinea versicolor, pityriasis alba, and occupational exposure to certain chemicals.

The cause of vitiligo remains unclear but likely involves autoimmune, genetic, oxidative stress, and neural mechanisms. A genetic component appears to exist given that 20% of patients have at least one first-degree relative also affected by the disease.² Immunologic factors may also play role based on the presence of comorbid autoimmune diseases and abnormal antibodies to melanocytes in some patients with vitiligo.Oxidative stress has received particular attention based on new research suggesting an impaired antioxidant defense system in the body may lead to free radical-induced damage to melanocytes.³ Although many theories exist, current thought favors a multifactorial etiology based on a complex set of interactions of the aforementioned mechanisms.

Unfortunately, there is no silver bullet when it comes to treating vitiligo.Several options are available, each with advantages and disadvantages, and varying degrees of efficacy.

Narrowband UV-B phototherapy has emerged as a first line therapy for patients with moderate to severe involvement.⁴ Other options include topical medications (calcineurin inhibitors and corticosteroids) and surgery.Cosmetic camouflage is a safe and relatively cheap alternative that can be customized to match a particular skin tone.In some instances, patients with extensive vitiligo may choose to depigment the rest of their normal skin in order to achieve a more cosmetically appealing uniform skin color.


References
1. Taieb A , Picardo M. Clinical practice. Vitiligo. N Engl J Med 2009; 360:160-9.
2. Nath SK, Majumder PP , Nordlund JJ. Genetic epidemiology of vitiligo: multilocus recessivity cross-validated. Am J Hum Genet 1994; 55:981-90.
3. Sravani PV, Babu NK, Gopal KV, Rao GR, Rao AR, Moorthy B et al. Determination of oxidative stress in vitiligo by measuring superoxide dismutase and catalase levels in vitiliginous and non-vitiliginous skin. Indian J Dermatol Venereol Leprol 2009; 75:268-71.
4. Grimes PE. New insights and new therapies in vitiligo. JAMA 2005; 293:730-5.

About the Author
Aanand N. Geria, M.D. is currently a transitional resident at Lehigh Valley Health Network in Allentown, PA.He graduated from UMDNJ – New Jersey Medical School with a passion for diseases of the skin.He plans to complete his training in dermatology at Howard University Hospital in Washington DC.Dr. Geria is an active member of the American College of Physicians and Alpha Omega Alpha, honor medical society.