Introduction

Alopecia areata (AA) is an inflammatory autoimmune disease that presents as nonscarring hair
loss. Although the exact pathogenesis of AA is still unknown up to now, there is a widely
1,2
accepted hypothesis that AA is related with autoreactivity of cytotoxic T cells. Therefore,
intralesion corticosteroid is frequently used for AA to suppress immune attack 3. The other
hypothesis is associated with Vitamin D Receptor (VDR). The keratinocytes lining the outer
layer of the hair follicle possess Vitamin D Receptor (VDR). 4 This VDR plays important role in
hair cycle, especially anagen initiation.5 Loss of VDR function leads to loss of hair follicle
cycling and alopecia.4 Metabolite of vitamin D which interact with VDR is the biologically active
1, 25-dihydroxycholecalciferol [1, 25(OH)2D3].6 These explain why topical analog of vitamin D
can be used to treat AA. In this study, we report a 30-years-old man with AA in his scalp which is
fully recovered after application of calcipotriol.

Case Report

A 30-years-old healthy Indonesian man presented with a sudden hair loss in annular shape on his
scalp. Pain and itching was not complained. There was a similar symptom on his cousin. On
physical examination, we found a single 1 x 1,5 cm well-sircumscribed patch on occipitoparietal
dextra region without any signs of inflammation. Hair pull test was positive on edge of the
lesion. Patient was treated with 5-times triamcinolone acetonide injections, 5% minoxidil
solutions, and Pantogar. After three months therapy, the patchs size was become extensive, 4
x 5 cm. The patient decided to discontinue all treatments due to his frustration. In the fourth
month, the patient came back with complaint that the patch became extremely broader, 5 x 6 cm.
We prescribed only calcipotriol topical ( Daivonex, 50 mcg/g) to be given given twice daily.
Two weeks after, velus was found at the edge of the patch. Terminal hairs were found in entire
lesion after four months calcipotriol application. Hair pull test was no longer positive. No hair
loss relapse was observed over the next four months.
References

1. Alkhalifah A, Alsantali A, Wang E, McElwee KJ, Shapiro J. Alopecia areata update: part I.
Clinical picture, histopathology, and pathogenesis. J Am Acad Dermatol. 2010 Feb;62(2):177-88.
2. Taisuke I. Recent advances in the pathogenesis of autoimmune hair loss disease alopecia
areata. Hindawi Publishing Corporation Clinical and Developmental Immunology. Volume 2013,
Article ID 348546, 6 pages. ??
3. Kumaresan M. Intralesional steroids for alopecia areata. International journal of trichology. Int
J Trichology. 2010 Jan-Jun; 2(1) : 63-65.
4. Bikle DD. Vitamin D and the skin: Physiology and pathophysiology
5. Amor KT, Rashid RM, Mirmirani P. Does D matter? The role of vitamin D in hair disorders
and hair follicle cycling. Dermatology Online Journal 16 (2): 3
6. Sakai Y, Kishimoto J, Demay MB. Metabolic and cellular analysis of alopecia in vitamin D
receptor knockout mice. J Clin Invest 2001;107:961-966.

Discussion

Alopecia areata (AA) is a non-scarring, inflammatory hair loss that can affect any hair-bearing
area7. AA occurrs in 1% to 2% of the population and affecting both sexes equally. 8
It may
presents at any age, but the onset before the 4th decade was reported as much as 85.5% in the
2
Asian population. This disease can present as a single, well-demarcated patch of hair loss,
multiple patches, total loss of scalp hair (alopecia totalis) or loss of entire scalp and body hair
(alopecia universalis).7 Hair pull test may be positive at the edge of the patch. 8 The diagnosis is
usually made clinically and no further investigation is required.

In AA, hair follicles enter telogen and late catagen prematurely. On horizontal sections of
lesional scalp biopsies, a decreased anagen-to-telogen ratio of hair follicles is observed.
Pathodynamically, involved hair follicles in AA are thought to undergo arrest in early anagen
during which the inner root sheath of the hair follicle is conical and keratinized, and
differentiation of the underlying hair cortex has just begun. From this stage, arrested hair follicles
may return prematurely to telogen the resting phase and continue to undergo shortened
cycles. 9
References

7. Alsantali A. Alopecia areata : A new treatment plan. Clin Cosmet Investig Dermatol. 2011; 4:
107115.
8. Dombrowski NC and Bergefeld WF. Alopecia areata: What to expect
from current treatments. CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 72
NUMBER 9 SEPTEMBER 2005. page 758-68.

9. Alopecia areata: autoimmune basis of hair loss

European Journal of Dermatology. Volume 14, Number 6, 364-70, November-December 2004, Review article

Summary

Author(s) : Andrew F ALEXIS, Raghunandan DUDDA-

SUBRAMANYA, Animesh A SINHA , Ronald O. Perelman Department
of Dermatology, New York University School of Medicine, New York,
NY, Department of Dermatology, Joan and Sanford Weill Medical
College of Cornell University, New York, NY.

a b

c d
 e

a. Pertama kali datang

b. Setelah 5x injeksi KS

c. Setelah pemakaian daivonex

d. Daivonex 2 bulan

e. Akhir 4 bulan Daivonex

Case report

A case of corticosteroid-unresponsive, rapid-progressive alopecia areata

successfully treated with calcipotriol

Suswardana, MD1, Amalia-Umar F, MD2, and Andriani R, MD1

Department of Dermatology, Dr. Mintohardjo Navy Hospital, Jakarta, Indonesia

Correspondence:
Suswardana, MD
Department of Dermatology, Dr. Mintohardjo, Navy Hospital, Jakarta, Indonesia
Email: sus_wardana@yahoo.com

Conflicts of interest: None

Introduction
Alopecia areata (AA) is a non scarring inflammatory hair loss relatively encountered
by dermatologist. However, the etiopathogenesis is still unclear, but the most
widely accepted hypothesis is that it is a T cell mediated autoimmune condition in
genetically predisposed person.1
 1) Madjid I, Keen A. Management of alopecia areata: an update. BJMP2012; 5
(3): a530-35.

Ilustrasi Kasus

Seorang pria, usia 30 tahun datang dengan keluhan rambut rontok

membentuk sebuah lingkaran pada puncak bagian sebelah kiri kepala, pasien tidak
menyadari sejak kapan kerontokan mulai berlangsung. Keluhan gatal dan nyeri
disangkal. riwayat keluhan seperti ini sebelumnya disangkal. Riwayat penyakit
diabetes, tiroid disangkal. Riwayat atopi positif (riwayat alergi debu dan udang,
riwayat asma pada adik pasien). Riwayat keluhan yang sama pada saudara sepupu
pasien.

Pada pemeriksaan didapatkan pada occipitoparietal dextra didapatkan

alopesia ukuran 1x1,5 cm, tidak didapatkan skuama maupun eritem atau tanda
radang lainnya. Hair pull test positif pada rambut di tepi lesi.

Pasien diterapi dengan triamcinolone acetonide intralesi dengan interval (2

minggu-1 bulan), minoxidil 5% solution dua kali sehari, fluocinolone acetonide
cream dua kali sehari, dan suplemen Pantogar kapsul 3 kali sehari.

Pada kontrol 2 minggu kemudian, keluhan belum ada perbaikan, penyuntikan

triamcinolone acetonide diteruskan sampai 5 kali penyuntikan (interval 2 minggu-1
bulan) namun tidak dirasakan adanya perbaikan, melainkan keluhan kebotakan
dirasakan semakin besar. Saat ini pasien mengalami depresi mengingat
kemungkinan kebotakan rambut kepala yang semakin meluas, sehingga pasien
menolak untuk dilakukan penyuntikan kembali. Saat ini didapatkan lesi meluas
dengan ukuran 5x6cm.

Pasien diberikan terapi lain yaitu calcipotriol 50 mcg/g ointment dua kali
sehari (4 bulan setelah keluhan pertama). Kontrol 2 minggu kemudian, didapatkan
perbaikan ditandai dengan adanya pertumbuhan rambut halus (velus), pemberian
calcipotriol dilanjutkan sampai dengan 4 bulan kemudian, perbaikan sangat
signifikan, rambut terminal sudah didapatkan pada keseluruhan lesi. Tidak
didapatkan efek samping seperti iritasi maupun keluhan lain pada pemakaian
calcipotriol. Rasa kepercayaan diri pasien kembali terbentuk dan pasien sudah
percaya diri memangkas pendek rambutnya kembali seperti sediakala. Hair pull test
negative.