Topical Medications in Vitiligo

Koushik Lahiri and Anupam Das

Introduction

Vitiligo is a fairly common dermatosis resulting into significant deterioration in the quality of life [1]. With recent advances in the field of medical sciences, numerous treatment options have emerged for the management of the distressing condition. The basic objectives are to minimize disease progression, attain repigmentation, and achieve cosmetically pleasing results [1]. It is crucial to understand each and every therapeutic modality with respect to the mechanism of action, indications, and contraindications. In this chapter, the topical medications available to treat vitiligo are discussed (Table 26.1).

Topical Corticosteroids (TCS)

Topical steroids are the first-line drugs for the management of vitiligo. They are responsible for reduction of macrophages and T lymphocytes in vitiliginous patches

[9] , they likewise reduce the complement-mediated destruction of melanocytes

[10] . In children and adults with limited, extrafacial involvement, once-daily application of potent steroids is advisable for not more than 3 months [11]. The response

K. Lahiri (*)

WIZDERM and Department of Dermatology, Apollo Gleneagles Hospitals, Greenwood Nook, Coral Isle, 14 RB, 369/2 Purbachal, Kalikapur, E M Bypass, Kolkata 700078, India e-mail: This email address is being protected from spam bots, you need Javascript enabled to view it

A. Das

Department of Dermatology, KPC Medical College and Hospital, Kolkata, India e-mail: This email address is being protected from spam bots, you need Javascript enabled to view it

© Springer India 2017

E.B. Handog, M.J. Enriquez-Macarayo (eds.), Melasma and Vitiligo in Brown Skin, DOI 10.1007/978-81-322-3664-1_26

Table 26.1 Summary of various topical agents used in the treatment of vitiligo

Drug

Mechanism of action

Level of evidence

Corticosteroids

Modulate the immune response by reducing the macrophages and T cells Reduce autoantibodies Inhibit complement-mediated melanocyte destruction

IA

Calcineurin inhibitors

Reduce the tissue counts of IFN-y, IL-1, IL-2, IL-3, IL-4, IL-5, GM-CSF, TNF-a

Enhance melanocyte and melanoblast proliferation

IA (children) IIA (adults)

Vitamin D3 analogs

Target the local immune response in vitiligo, by acting on specific T-cell activation

Inhibit the transition of T cells from early to late G1 phase Inhibit the expression of TNF-a IFN-y

Modulate melanocyte maturation and differentiation

Upregulates melanogenesis through pathways activated by vitamin D ligand receptors (endothelin receptor and c-kit) [2]

IIA (monotherapy), IB if combined with topical steroids

Photochemotherapy

Psoralens stimulate melanogenesis; photoconjugation of psoralens in melanocyte DNA leads to mitosis, replication and proliferation of melanocytes, increased number of melanosomes, and subsequent apocopation

PUVA stimulates the activity of cAMP; leads to increased synthesis of tyrosine, the precursor of melanin; induces a suppressor T-cell response which releases IL-10 suppressing the autoimmune stimulus responsible for the destruction of melanocytes PUVA induces basic fibroblast growth factor (bFGF) and hepatocyte growth factor, leading to re-growth and migration of follicular melanocytes to stratum basale [3-5]

PUVA: IV Khellin: III

L-Phenylalanine

Stimulates melanogenesis in vitiliginous patches

IIB

(continued)

Table 26.1 (continued)

Drug

Mechanism of action

Level of evidence

Monobenzyl ether of hydroquinone (MBEH)

Reacts with tyrosinase to form a reactive quinone product that binds to cysteine residues in tyrosinase proteins to form hapten-carrier complexes causing destruction of melanocytes

Induces lysosomal degradation of melanosomes by autophagy A contact sensitizer inducing a delayed-type hypersensitivity response [6]

IV

Antioxidants

Increase catalase activity leading to a decrease in reactive oxygen species Inhibit ROS-mediated destruction of melanocytes

IB

5-Fluorouracil

Direct stimulation of melanocyte proliferation

Inhibits agents or cytotoxic cells which destroy melanocytes Immunomodulator stabilizing the vitiligo disease [7]

IV

Pipeline

Stimulates the proliferation of melanocytes [8]

IV

Prostaglandin E2

Increases melanocyte proliferation and density

IB

Capsaicin and curcumin

Inhibit apoptosis of melanocytes Reduce the generation of ROS and lipid peroxidation Improve mitochondrial activity Enhance survival of melanocytes

IB

to this therapy is better in children as compared to adults. Moreover, lesions over the head and neck region respond well [12].

There are multiple studies supporting the efficacy of topical corticosteroids. Kwinter et al. reported response rates of 64 % in a study conducted on children who were treated with TCS alone [13]. Complete repigmentation rates are approximately

49.3 % [14].

The efficacy has been compared with other agents. When compared with topical calcineurin inhibitors, the response is equivocal to high [14, 15]. Repigmentation rates are however the same when compared with ultraviolet A (UVA) light phototherapy [16].

Even though TCS are very effective in the treatment of vitiligo, local side effects and topical steroid abuse limit the ultimate use of these agents. Skin atrophy, telangiectasia, hypertrichosis, acneiform eruptions, and striae caused by potent or very potent TCS are well known. Moreover, systemic absorption should be kept in mind while treating large areas of skin, thin skin and children with potent steroids. Lower potency TCS and newer class III TCS, like mometasone furoate and methylpred- nisolone aceponate, are devoid of these untoward side effects [11].

 
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