Translate this page into:
Vitiligo
Correspondence Address:
D M Thappa
Department of Dermatology and STD, JIPMER, Pondicherry
India
How to cite this article: Thappa D M. Vitiligo. Indian J Dermatol Venereol Leprol 2002;68:227-228 |
Vitiligo is a common dermatological disorder accounting for nearly 1-2% of our OPD attendance and often poses a therapeutic challenge to the practising dermatologist owing to its prolonged course and varied outcome. The treatment of vitiligo needs to be individualized and thus a tentative plan of management should be decided at the very outset and a realistic goal should be set.
The management of vitiligo begins with a through clinical assessment, which becomes very important in the context of inconclusive investigational parameters. Salient points to be noted in the history include-age, occupation, duration of the disease, history of progression (defined as increase in size of existing lesions or onset of new lesions), treatment history, family history of vitiligo and history of any other associated illness. On examination one should note the sites involved, the extent of involvement, mucosal disease, presence of leucotrichia and Koebnerisation. The patients can be classified depending on the type of vitiligo as:
- Localized - Focal, segmental, mucosal
After the initial clinical assessment, the patients can be broadly compartmentalized into certain clinical groups to decide on the general line of treatment to be pursued. Thus, most patients would fall into one of the following categories
- Recent onset disease with rapid progression.
- Generalized, indolently progressive disease.
- Localized vitiligo
- Disease warranting surgical management.
The first two groups that is those with actively progressing disease and those with widespread lesions are candidates for systemic medical therapy and we prefer to use systemic steroids in the form of betamethasone oral mini pulse therapy (OMP). After baseline investigations, essential prior to giving oral steroids, oral betamethasone is given in a dose of 5 mg (2.5 mg for children) on two consecutive days each week. The patient is assessed every two weeks initially and monthly thereafter to look for any side effects of steroids and to note any improvement in the lesions. One can wait for upto three months for repigmentation to appear which is usually perifollicular and perilesional. Betamethasone is continued till complete or maximal repigmentation is achieved and therapy should not be discontinued abruptly as the repigmentation may be reversed. Systemic steroids have a dual role in that they suppress the autoimmune damage and halt progression of the disease and thereafter induce pigmentation. In our experience, OMP with betamethasone is not associated with any significant side effects and the only adverse effect that we have encountered is weight gain, though without cushingoid features. Other modality of treatment in these patients would be PuvA therapy though it is advisable to wait till the disease is stabilized and then administer PuvA. Our experience with systemic PUVA is minimal, largely because it requires frequent visits and as most of our patients are manual labourers requiring to work outdoors. However, once the disease is stable, repigmentation of cosmetically important sites can be enhanced with topical PUVA. We use psoralen in 1:10 dilution to be applied thrice weekly on alternate days and weekends off. It should be applied with an applicator or cotton swab to the lesion and the borders should be protected with petrolatum and a sunscreen. After about 30 minutes the lesion is exposed to sunlight beginning with duration of 30 seconds and gradually increasing till erythema appears (usually to a maximum of 5 minutes). The patient is clearly instructed to wash the treated area thereafter with soap and water, apply sunscreen and if feasible wear clothing to cover that site. Repigmentation may take 20-30 exposures to begin with and maximal improvement may take upto 150-300 exposures.
The next group of patients includes those who have localized vitiligo. Focal vitiligo has a good prognosis in that it is more amenable to topical therapy and we have found good results with high potent topical steroids which should be applied once daily with a steroid holiday for at least one week each month to prevent tachyphylaxis. Newer topical steroids like mometasone furoate and fluticasone propionate offer a high safety: efficacy ratio and can be used for longer duration. One can wait for upto three months for repigmentation to appear and thereafter treatment may be continued till maximal repigmentation. The other modality of treatment for focal vitiligo includes topical PUVA which can be used singly or in combination with topical steroids. We have also used topical placental extract, usually in combination with topical steroids and the results have been variable, more often on the lower side of efficacy. The other form of localized vitiligo is segmental vitiligo, which is known to have a better prognosis in that it does not progress inexorably like non-segmental vitiligo. However, response to topical medical therapy in segmental vitiligo is mostly unsatisfactory as would be expected owing to its non-autoimmune etiology and these patients in our experience do best with surgical procedures. Mucosal vitiligo is another form of localized vitiligo with poor response to medical therapy, obviously due to lack of hair follicles acting as pigment reservoirs at these sites. After an initial trial of topical therapy, especially aimed at stabilizing the disease, these patients may also be recruited for surgery.
Patients are recruited for surgical procedures based on certain clinical criteria including
- Disease, which is stable for at least two years.
- Failure of appropriate and adequate medical therapy.
- Localized vitiligo.
Stability of the disease is the most important factor, which must be ensured before undertaking surgical procedures, and it is preferable to put a graft before proceeding with the full procedure. In our center good results have been achieved with punch grafting, blister grafting (especially for mucosal lesions) and tattooing (for smaller areas). Grafting can be followed with application of topical PUVA-SOL once the acute edema of the procedure has subsided to enhance spread of the transplanted pigment.
Vitiligo in children is essentially managed along the same lines as an adult with a few differences. Firstly, it must be remembered that children tend to have a better prognosis and so depending on the extent and activity of the disease, the appropriate treatment should be decided. Most children were found to do fairly well with topical steroids especially those with a high safety index like mometasone furoate and fluticasone propionate. In those children who had widespread disease, we have used oMP with betamethasone at a dose of 2.5mg on two consecutive days each week. Results with this therapy have been largely very satisfactory and contrary to the usual belief, side effects have been noted very rarely.
Another important aspect in the management of vitiligo is to identify the prognostic factors in each patient as this would be essential to decide on the end point of any modality of therapy. In our experience, poor prognostic factors includes history of progression, family history of vitiligo, widespread disease, non-segmental vitiligo, acrofacial vitiligo, mucosal involvement and leukotrichia.
We would also advise that all patients of vitiligo should be given sunscreens antioxidants and options regarding cosmetic camouflage. Finally, the management of vitiligo would not be complete without good counseling, motivation and psychological support to the patient.