Response to Narrow-band UVB – Vitiligo-melasma versus Vitiligo

A Comparative Study

Parikshit Sharma; Harsha S. Pai; Ganesh S. Pai; Maria Kuruvila; Reshma Kolar


Am J Clin Dermatol. 2011;12(2):127-132. 

In This Article

Abstract and Introduction


Background: Vitiligo is the most common depigmentary disorder of the skin and hair, resulting from selective destruction of melanocytes. Melasma, a hyperpigmentary disorder, presents as irregular, brown, macular hypermelanosis. A small subset of vitiligo patients paradoxically also have melasma.
Objective: To evaluate and compare the response to narrow-band UVB in a group of patients with vitiligo, and another group of patients with vitiligo and coexisting melasma (vitiligo-melasma).
Methods: Patients in both groups were treated with narrow-band UVB and a comparison of the zonal repigmentation was made at 4, 8, and 12 weeks after the initiation of therapy.
Results: At the end of 12 weeks, 86% of patients in the vitiligo-melasma group attained ≥75% pigmentation on the face, whereas this was achieved in only 12.5% of patients in the vitiligo group. Over the limbs, 73% of patients in the vitiligo-melasma group attained 75% or more pigmentation at the end of 12 weeks compared with only 9% in the vitiligo group. On the trunk, only 20% of vitiligo-melasma patients showed ≥75% pigmentation at 12 weeks compared with 63% of patients in the vitiligo group.
Conclusion: Patients having both vitiligo and melasma have a significantly better prognosis for repigmentation on the face and limbs with narrow-band UVB compared with patients with vitiligo alone; the vitiligo-melasma patients achieve repigmentation much earlier and also attain a greater level of repigmentation. Unexpectedly, for truncal lesions, patients with vitiligo alone responded better than those with both conditions. Although the vitiligo-melasma group with truncal lesions started repigmenting earlier, the final pigmentation was more extensive in the vitiligo group.


Vitiligo is the most common depigmentary disorder of the skin and hair, resulting from selective destruction of melanocytes. It affects all age groups with no predilection for either sex. Though worldwide in distribution, it is more common in India, Egypt, and other tropical countries.[1] It affects approximately 1–4% of the world population.[2] Patterns of distribution include generalized, acral or acrofacial, localized, and segmental.[2,3] Several theories have been proposed concerning the pathogenesis of vitiligo including the autoimmune, autocytotoxic, and neural theories.[2]

Antibodies exist against melanocyte surface antigens and the extent of depigmentation is correlated with the incidence and level of these antibodies. The surface antigens include tyrosinase and tyrosinase-related proteins 1 and 2.[2]

The findings of an increased frequency of antithyroid microsomal, antiparietal cell, and antiadrenal antibodies in vitiligo patients support the autoimmune hypothesis.[4,5]

The autocytotoxic theory stems from the belief that cytotoxic precursors in melanin synthesis accumulate and this results in cell death. All intermediates in the biosynthesis of melanin are phenols and related compounds. The excessive accumulation or production of phenolic radicals would injure or kill the cell.[6]

The neural hypothesis proposes that norepinephrine or some other neural agent released by nerve endings may be deleterious to melanocytes.[7] The neural theory would explain the loss of melanocytes in a segmental pattern and the abnormal sweating patterns in the involved skin.[8,9]

The convergence theory states that stress, accumulation of toxic compounds, infection, autoimmunity, mutations, altered cellular environment, and impaired melanocyte migration and/or proliferation can all contribute to vitiligo etiopathogenesis in varying proportions.[10]

Melasma, on the contrary, is a common, hyperpigmentary skin disorder that appears as an irregular, brown or light-to-gray brown, macular hypermelanosis.[11] There are three distinct patterns of melasma: centrofacial, malar, and mandibular.[12,13] Although the precise cause of melasma is unknown, multiple factors have been implicated in the etiopathogenesis of this condition.[12] These include genetic influences, exposure to UV radiation, pregnancy, oral contraceptives, estrogen-progester-one therapies, thyroid dysfunction, cosmetics, and phototoxic and antiseizure drugs. Of the aforementioned factors, Pathak et al.[13] suggest that genetic influences and exposure to UV radiation are the most important.

We observed that a small subset of vitiligo patients paradoxically also had melasma. The purpose of our study was to examine how coexistent melasma changes the therapeutic outcome of vitiligo in patients receiving narrow-band (NB) UVB.

NB-UVB is the treatment of choice for vitiligo. It is highly effective and better tolerated than psoralen plus UVA therapy.[14,15] In order to evaluate how patients who have both vitiligo and melasma respond to NB-UVB, we conducted a study of 39 patients with vitiligo, 18 of whom had melasma, and compared the response in the two groups.


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.