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Original Article
2003:69:2;135-137
PMID: 17642858

The efficacy of low-dose oral corticosteroids in the treatment of vitiligo patient

K Banerjee, JN Barbhuiya, AP Ghosh, SK Dey, PR Karmakar
 Dept. of Dermatology, STD, Community Medicine, Nilratan Sarkar Medical College, Kolkata, India

Correspondence Address:
J N Barbhuiya
81, Banerjeepara Road, Kolkata - 41
India
How to cite this article:
Banerjee K, Barbhuiya J N, Ghosh A P, Dey S K, Karmakar P R. The efficacy of low-dose oral corticosteroids in the treatment of vitiligo patient. Indian J Dermatol Venereol Leprol 2003;69:135-137
Copyright: (C)2003 Indian Journal of Dermatology, Venereology, and Leprology

Abstract

Autoimmunity is one of the most probable pathogenesis of vitiligo. Systemic corticosteroids may arrest the progression of vitiligo and lead to repigmentation by suppressing immunity. The clinical efficacy of low-dose oral corticosteroids was assessed to minimize the side-effects in actively spreading vitiligo patients. One hundred (100) patients with vitiligo were evaluated. The patients took daily doses of oral prednisolone (0.3mg/kg body weight) initially as a single oral dose after breakfast for the first 2 months. The dosage was then reduced to half the initial dose during the 3rd month and was halved again for the 4th and final month. After 4 months of treatment, 76% showed repigmentation while the arrest of progression (both repigmentation and stationary) was noted in 90% of patients. Male sex, and patients under 15 years of age showed pronounced repigmentation with statistical significance. According to this study low-dose oral prednisolone is an effective method in preventing progression and inducing repigmentation of fast-spreading vitiligo without the associated serious side-effects.
Keywords: Vitiligo, Corticosteroids

Introduction

Vitiligo is a common idiopathic pigmentary skin disorder which affects 0.5-4% of the world′s population′ and approximately 3% of the Indian population.[1] The aim for the treatment of vitiligo is to achieve repigmentation in the lesions and to steady the depigmenting process. Repigmentation leads to an improvement of the cosmetic appearance and of the skin tolerance for sunburn.[3] There are many therapeutic modalities for vitiligo, buttheir effects have been limited. Psoralen plus ultraviolet A (PUVA) is the main treatment but only approximately one-third of patients achieve excellent results from PUVA therapy.

On the presumption of a role for autoimmunity in the aetiology of vitiligo, systemic corticosteroids may arrest the progression of vitiligo and lead to repigmentation by suppressing immunity. The serum of actively spreading vitiligo patients who received oral corticosteroids treatment with clinical improvement showed a decrease in complement-mediated cytotoxicity by autoantibodies to melanocytes and a reduced antibody titre to surface antigen of melanocytes.[1] Systemic corticosteroids therapy for the treatment of vitiligo has been well established .[4] Side-effects are a major problem especially when steroids are given in moderate to high dosed for prolonged periods. In vitiligo patients with extensive or fast-spreading disease to minimize the side-effects, oral mini-pulse therapy with betamethasone has been tried.[5],[6]

In this study, a low daily dose of oral prednisolone (0.3mg/kg body weight) was used in fast spreading vitiligo patients to minimize the side-effects.

Materials and Methods

The study population included one hundred (100) patients with actively spreading vitiligo involving limited and generalized areas during a period of 2 years. The duration of the disease in these patients were less than 2 years. The patients had received no treatment within the last 3 months. Pregnant and lactating patients and those with systemic diseases such as diabetes mellitus, hypertension, thyroid and other autoimmune disease and peptic ulcer disease were excluded. Patients were divided into two groups according to their age. Those less than 15 years were taken in group I and those above 15 yearsin group II. All patients had routine investigations done such as complete blood count, urinalysis, blood biochemistry and chest X ray. The treatment schedule consisted of daily doses of prednisolone, 0.3mg/kg body weight as a single oral dose after breakfast initially for the first 2 months. The dosage was then reduced to half the initial dose during the 3′d month and was halved again for the 4th and final month. During the study, all other modalities of treatment for vitiligo were withheld. The improvement was graded as follows: 1. repigmentation, when there was 25%-75% of pigmentation, 2. stationary, when there was no sign of pigmentation and 3. spreading when there was appearance of new lesions and increasing size of the existing lesions. Side-effects were examined at each visit.

Result

One hundred patients (40 men, 60 women) with actively spreading vitiligo were evaluated. The youngest and oldest patients were 5 years and 65 years old respectively. The extent of cutaneous involvement ranged from 1 % to 70%.

After 4 months of treatment, 76 of the 100 patients (76%) showed repigmentation while the arrest of progression of vitiligo (both repigmentation and stationary) was noted in 90 of 100 patients (90%). Men showed repigmentation in 35 of 40 patients (87.5) and women showed repigmen-tation in 41 of 60 cases (68.3), so men showed greater repigmentation than that in the women (statistically significant) [Table - 1]

According to age, the effects of therapy were more pronounced in the younger age group (statistically significant) [Table - 2]. Forty six of 47 patients (97.8%) below 15 years age group showed repigmentation while 40 of 53 patients (75.4%) above 15 years age group showed repigmentation.

The treatment result for generalized and localized type of vitiligo were different, repigmentation noted in 55 of 63 patients (87.3%) with the localized type. In the generalized type, repigmentation occurred in the 21 of 37 patients (56.7%) but the spread of vitiligo also developed in 10 of 37 patients. [Table - 3]. In relation to the site of vitiligo repigmentation of facial lesions proved to be the most effective (59 of 82 patients, (71.9%) [Table - 4].

Side-effects with this treatment as monitored monthly were minimal and reversible and were not serious, and so did not affect the treatment schedule. Very few patients did complain of slight epigastric discomfort and weight gain.

Discussion

The two most frequently used modalities in the treatment of vitiligo are PUVA and topical corticosteroids.[1] In actively spreading vitiligo, PUVA therapy is not an ideal treatment. Class 3 corticosteroids and narrow-band UVB seems to be the most effective and safest therapies for localized and for generalized vitiligo respectively,[3] but it may cause unwanted side-effects, such as skin atrophy, telangiectasia and striae distensae, acne and local hypertrichosis. There have been a few reports on the use of systemic steroids in vitiligo therapy. Indian dermatologist, Desai and other,[7] have long believed that systemic prednisolone is a helpful adjunct to therapy. Gokhale and Gokhales also reported success with adrenocorticotropic hormone in patients who were unresponsive to PUVA therapy.

Comprehensive evaluation of oral corticosteroids for the treatment of vitiligo has been lacking until now. Systemic corticosteroids therapy for a prolonged period may cause unacceptable side-effects. In extensive or fast-spreading vitiligo patients, oral mini-pulse therapy with betamethasone was reported by Pasricha and Khaitan[5] to minimize its side-effects. Beta methasone/dexamethasone 5 mg was used as a single oral dose after breakfast on two consecutive days per week, repigmentation was reported in 80% and arrested progression of vitiligo in 89% of 40 vitiligo patients without serious side-effects. Another oral mini-pulse therapy was studied by Kanwar et al[6] in 37 patients with rapidly spreading vitiligo. In this study adult patients received dexamethasone, 5 mg on two consecutive days a week in the morning. For children (Less than 16 years of age), the dose was halved. A total of 5-25 doses were tried. Only 43.8% showed arrest of progression of vitiligo and also mild to moderate repigmentation. Four children out of nine had mild to moderate repigmentation. No side-effects were reported.

In our study, we observed the arrested progression of vitiligo in 90% and repigmentation in 76% of 100 patients with actively spreading vitiligo using a low dose of oral corticosteroids. Male patients and patients under 15 years of age showed pronounced repigmentation with statistically significant result. With regard to the site of vitiligo, facial lesions showed the best results. The effects of low-dose oral prednisolone were more pronounced in the localized type than in the generalized type. These may be due to the location of the lesions (localized lesions in our study mainly located on the face) influenced the effect of treatment. We were unable to perform a control study by giving placebo to some patients. We used a daily dosage of oral prednisolone of 0.3mg/kg body weight. With this dosage long term treatment was possible and side-effects were kept to minimum. The treatment schedule was not affected in most patients, because the side-effects reported were not serious. These subsided on stopping prednisolone treatment. According to this study low-dose oral prednisolone is an effective method in preventing progression and inducing repigmentation of fast-spreading vitiligo without the associated serious side-effects, which is otherwise difficult to treat with topical corticosteroids of PUVA.

References
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