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 Table of Contents  
ORIGINAL ARTICLE
Year : 2019  |  Volume : 39  |  Issue : 2  |  Page : 78-82

Topical calcipotriol mixed with topical steroid versus topical steroid alone in treatment of alopecia areata


Department of Dermatology, Zagazig University, Zagazig, Egypt

Date of Submission10-Jun-2018
Date of Acceptance17-Mar-2019
Date of Web Publication03-Jul-2019

Correspondence Address:
Mohamed I El-Ghareeb
Department of Dermatology, Zagazig University, Zagazig, 44511
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejdv.ejdv_24_18

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  Abstract 


Background Alopecia areata (AA) is an autoimmune T-cell mediated disease characterized by a localized patchy hair loss from scalp and other hairy body parts. Topical steroid is one of the traditional therapeutic options for AA. It is considered as a recommended tool in the treatment of mild-to-moderate AA, especially when used early in the course of the disease. Calcipotriol is a vitamin D analog and acts as a potent immunomodulatory agent and can be used in the treatment of AA.
Rationale Recently, vitamin D deficiency was observed in patients with autoimmune diseases including patients with AA. Calcipotriol is emerging as a novel agent in the treatment of AA in many published studies. The therapeutic effect of the mixture of topical calcipotriol and topical steroid in the treatment of AA was not mentioned in previous studies.
Aim The aim of this study is to evaluate the efficacy and safety of topical calcipotriol mixed with topical steroid in the treatment of AA in comparison with topical steroid alone.
Patients and methods A total of 40 patients with mild-to-moderate AA were involved in this study throughout a 12-week trial. Institutional review board (IRB) approval was obtained with informed consents from all patients. The patients were divided into two groups: 20 patients in group A and another 20 patients in group B. Group A patients had been treated with topical steroid (betamethasone valerate 0.1%) twice daily throughout the 12 weeks. Group B patients had been treated with a topical gel preparation containing calcipotriol 0.005% mixed with betamethasone dipropionate 0.05%. This gel preparation was applied to the affected area twice daily throughout the 12 weeks. Severity of Alopecia Tool (SALT) score was calculated at baseline and at 3, 6, 9, and 12 weeks.
Results There was a statistically highly significant decrease in SALT scores after the 3-month treatment in group A, and there was a statistically significant decrease in SALT scores after the 3-month treatment in group B.
Conclusion Topical calcipotriol mixed with topical steroid in a gel formulation is a novel therapeutic tool of AA with efficacy nearly the same as of topical steroid alone and with less adverse effects.

Keywords: alopecia areata, calcipotriol, steroid


How to cite this article:
El-Ghareeb MI. Topical calcipotriol mixed with topical steroid versus topical steroid alone in treatment of alopecia areata. Egypt J Dermatol Venerol 2019;39:78-82

How to cite this URL:
El-Ghareeb MI. Topical calcipotriol mixed with topical steroid versus topical steroid alone in treatment of alopecia areata. Egypt J Dermatol Venerol [serial online] 2019 [cited 2019 Jul 23];39:78-82. Available from: http://www.ejdv.eg.net/text.asp?2019/39/2/78/262035




  Introduction Top


Alopecia areata (AA) is an autoimmune inflammatory hair loss. This disease is chronic and relapsing, and no effective cure or preventive treatment has been established [1].

For many reasons, it is difficult to assess treatment options for AA. There is a high rate of spontaneous remission in patchy AA. There are also deficient randomized controlled trials investigating treatment efficacy. Another important drawback in these studies is the great variation in evaluation of treatment outcome from one investigator to another one. To overcome these obstacles, the Severity of Alopecia Tool (SALT) score seems to be an ideal objective method of follow-up and good evaluation of any therapeutic option [2],[3] ([Figure 1]).
Figure 1 Severity of Alopecia Tool-I score for determining scalp surface area.

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Treatment of AA depends on the age of patient as well as the extent and duration of the disease. Treatments include steroids, topical immunotherapy, topical minoxidil, anthralin, and immunosuppressants. Each case must be dealt with on a customized individual basis [4].

Intralesional corticosteroids (preferably triamcinolone acetonide) are injected in the deep dermal/upper subcutaneous plane using a half inch long 30 G needle: 0.1 ml is injected at 0.5–1 cm intervals every 4–6 weeks. Various concentrations (2.5–10 mg/ml) are used. Treatment should be stopped if there is no improvement after 6 months. Adverse effects include transient atrophy and telangiectasia [2].

Midpotent and potent topical corticosteroids are widely used in the treatment of AA. Adverse effects include folliculitis (more with ointment), rarely skin atrophy, and telangiectasia [5].

Topical immunotherapy is used in the treatment of AA. The mechanism of action of topical sensitizers (e.g. diphenylcyclopropenone) is poorly understood. Many theories have been suggested, including antigenic competition, perifollicular lymphocytes apoptosis, changes in the peribular CD4/CD8 lymphocyte ratio, and interleukin (IL)-10 secretion [4].

Vitamin D analog is recently introduced as a novel option in the treatment of AA. The mechanism by which the topical calcipotriol induces hair regrowth in AA lesions is by regulating the differentiation of B cells, T cells, dendritic cells, and the expression of Toll-like receptors [6].

The effect of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] on the acquired antigen-specific immune response is T-lymphocyte proliferation inhibition, particularly of the Th1 arm [7]. Moreover, 1,25(OH)2D3 leads to decreased secretion of IL-2 and interferon-γ by CD4 T cells and promotes IL-5 and IL-10 production, which further tilts the T-cell response toward Th2 dominance [8]. Vitamin D has also been shown to inhibit antibody secretion and autoantibody production in B cells [9].

In vitro, 1,25(OH)2D3 inhibits the differentiation of monocytes into dendritic cells and interferes with T-cell-induced stimulatory activity [10]. It has been shown that 1,25(OH)2D3 is one of the most powerful blockers of dendritic cell differentiation and of IL-12 secretion. IL-12 inhibition is achieved through the direct interaction of 1,25(OH)2D3 bound to the vitamin D receptors, which interferes with nuclear factor κB-induced transcription of IL-12 [11].


  Patients and methods Top


Forty patients with mild-to-moderate untreated AA were involved in this interventional study throughout 12 weeks. Institutional review board (IRB) approval was obtained with informed consents from all patients. The patients were divided into two groups: 20 patients in group A and another 20 patients in group B. Group A patients had been treated with topical steroid twice daily throughout the 12 weeks. This topical steroid was betamethasone valerate 0.1% lotion (1 mg/g) Betnovate lotion; GSK, 980 Great Wast Rd, Brentford, London, United Kingdom). Group B patients were treated with a topical gel preparation containing calcipotriol 0.005% 50 µg/g) mixed with betamethasone dipropionate 0.05% (500 µg/g) (Xamiol gel; LEO Pharma, Industriparken 55, DK-2750, Ballerup, Denmark). This gel preparation was applied to the affected area twice daily throughout the 12 weeks. SALT score was calculated at baseline and at 3, 6, 9, and 12 weeks. After the end of the 12 weeks, all patients were followed up for 1 month.


  Results Top


There were no significant differences regarding age between the two groups. The age range of group A was 10–50 years and that of group B was 10–54 years. They were age matched.

On comparing the results of SALT-I scores of patients with AA in group A before and after treatment with Betnovate lotion, there were a statistically highly significant decrease after the 3 months using this treatment.

There was a statistically significant decrease in SALT-I scores of patients of group B after the 3 months of treatment with Xamiol gel.

On comparison between SALT-I score changes after using the two treatment options in patients of the two groups, there were no significant differences. This may suggest that the efficacy of both treatment options is nearly the same ([Table 1], [Figure 2] and [Figure 3]).
Table 1 Comparison between groups A and B regarding Severity of Alopecia Tool-I score changes before and after treatment

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Figure 2 (a) A patient from group B before treatment. (b) The same patient from group B after treatment, with good improvement.

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Figure 3 (a) A patient from group A before treatment. (b) The same patient from group A after treatment, with good improvement.

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  Discussion Top


Many therapeutic options for AA exist, but none are curative or preventive. One of these traditional options is the topical application of steroid, but it has many adverse effects such as skin atrophy, folliculitis, and telangiectasia, as it is used daily for a relatively long period.

A novel therapeutic option with the use of topical vitamin D analog (calcipotriol) in treatment of AA is emerging. The effectiveness of calcipotriol in the treatment of AA is controversial, but its limited adverse effects need to be considered.

In this study, we studied two groups of patients with AA. One group was treated with topical steroid alone and the other group was treated with a gel containing both calcipotriol and topical steroid. Both groups were treated for 3 months and evaluation of the therapeutic results was done using SALT-I score before and after treatment period.

Regarding the group treated with topical steroid lotion alone, there was a statistically highly significant decrease of SALT-I scores after the 3 months of therapy. This goes with the results of Tosti et al. [5], which stated the efficacy of topical steroid as a considerable therapeutic option of AA. We noted that folliculitis was a predominant adverse effect in this group.

There was a statistically significant decrease in SALT-I scores in the patient group treated with a gel containing calcipotriol and topical steroid after the 3-month period of therapy. This may give a promising therapeutic option in the treatment of AA. The gel preparation was tolerated by the patients, and minimal adverse effects were reported in this group.

On comparing the SALT-I score changes after using the two treatment options in patients of the two groups, there were no significant differences. This may suggest that the efficacy of both treatment options is nearly the same.


  Conclusion Top


Topical calcipotriol mixed with topical steroid in a gel formulation is a novel therapeutic tool of AA with efficacy nearly the same as of topical steroid alone and with less adverse effects.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Kim DH, Lee JW, Kim IS, Choi SY, Lim YY, Kim HM et al. Successful treatment of alopecia areata with topical calcipotriol. Ann Dermatol 2012; 24:341–344.  Back to cited text no. 1
    
2.
Alkhalifah A, Alsantali A, Wang E, McElwee KJ, Shapiro J. Alopecia areata update: part II. Treatment. J Am Acad Dermatol 2010; 62:177.  Back to cited text no. 2
    
3.
Elise A, Olsen MD, Douglas Canfield BS. SALT II: a new take on the Severity of Alopecia Tool (SALT) for determining percentage scalp hair loss. J Am Acad Dermatol 2016; 75:1268–1270.  Back to cited text no. 3
    
4.
Shapiro J. Current treatment of alopecia areata. J Investig Dermatol Symp Proc 2013; 16:S42–S44.  Back to cited text no. 4
    
5.
Tosti A, Piraccini BM, Pazzaglia M, Vincenzi C. Clobetasol propionate 0.05% under occlusion in the treatment of alopecia totalis/universalis. J Am Acad Dermatol 2003; 49:96–98.  Back to cited text no. 5
    
6.
Nancy AL, Yehuda S. Prediction and prevention of autoimmune skin disorders. Arch Dermatol Res 2009; 301:57–64.  Back to cited text no. 6
    
7.
Arnson Y, Amital H, Shoenfeld Y. Vitamin D and autoimmunity: new aetiological and therapeutic considerations. Ann Rheum Dis 2007; 66:1137–1142.  Back to cited text no. 7
    
8.
Van Etten E, Mathieu C. Immunoregulation by 1, 25-dihydroxyvitamin D3: basic concepts. J Steroid Biochem Mol Biol 2005; 97:93–101.  Back to cited text no. 8
    
9.
Linker-Israeli M, Elstner E, Klinenberg JR, Wallace DJ, Koeffler HP. Vitamin D(3) and its synthetic analogs inhibit the spontaneous in vitro immunoglobulin production by SLE-derived PBMC. Clin Immunol 2001; 99:82–93.  Back to cited text no. 9
    
10.
Griffin MD, Lutz W, Phan VA, Bachman LA, McKean DJ, Kumar R. Dendritic cell modulation by 1alpha,25 dihydroxyvitamin D3 and its analogs: a vitamin D receptor-dependent pathway that promotes a persistent state of immaturity in vitro and in vivo. Proc Natl Acad Sci USA 2001; 98:6800–6805.  Back to cited text no. 10
    
11.
D’Ambrosio D, Cippitelli M, Cocciolo MG, Mazzeo D, Di Lucia P, Lang R et al. Inhibition of IL-12 production by 1, 25-dihydroxyvitamin D3. Involvement of NF-kappaB downregulation in transcriptional repression of the p40 gene. J Clin Invest 1998; 101:252–262.  Back to cited text no. 11
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1]



 

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