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the latest Bulletin Asian Society for Pigment Cell dermatitis


the latest Bulletin Asian Society for Pigment Cell dermatitis

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Asian Pigment Bulletin Vol 5., No.3
From the Editor
Asian Pigment Bulletin Vol.5,No.1, April 2010

Dear friends,

Another year dawns for the Asian Society for Pigment Cell Research and also Asian Pigment
Bulletin! We gear up for the Fourth ASPCR meeting at Guangzhou,China from 12-14 June 2010
which again promises to be a step forward in understanding the basics,pathogenesis and effective
management of pigmentary disorders.We would like to invite all the members to participate in this
rich scientific and academic event.

Several disorders of hyperpigmentation deserve more attention .In this issue,we have focused on
“Ashy dermatosis”.also known as the entity,”Lichen planus pigmentosus” in the Indian
subcontinent.This is seen frequently and the effective treatment remains challenging.I,once
again,request the readers to contribute articles for APB.Meanwhile,let us wish moreglory to the

With best wishes,

Dr Rashmi Sarkar


                                  Message From the President

Dear ASPCR members,

Along with the publication of ASPCR bulletin, I am very happy to announce that we are going to
have 4th ASPCR meeting to be held from 12-14 June 2010 at Guangzhou, China. We will provide
travel support to young scientists/dermatologists who wish to present their work.

I believe that it will be a fruitful year with a successful ASPCR in Guangzhou and hope we can
make more strides continuously.

Don’t forget to attend IPCC next year which will be held in Bordeaux in France.

With best wishes,

Prof Kyoung-Chan Park,


Asian Pigment Bulletin Vol 5., No.1

    Ashy Dermatosis
    Calendar of events
    Membership form for ASPCR
    ASPCR Secretariat


                                      ASHY DERMATOSIS

                    Dr Chitralekha Keisham MD, Dr Rashmi Sarkar MD,MNAMS,
                                  Dr Vijay Kumar Garg MD,MNAMS
                   Department of Dermatology, Maulana Azad Medical College
                              and Lok Nayak Hospital,New Delhi, India

Erythema dyschromican perstans was first described by Oswaldo Ramirez at the first Central
American Congress of Dermatology in El Salvador in 1957. Ramirez termed the condition
“dermatosis cenicienta,” meaning the ash-colored ones. This patients exclusively came from
Central and South America.1 The term “erythema dyschromicum perstans, was suggested by Dr.
Sulzberger. EDP occurs worldwide in all races, but appears to be more common in Latin America
and Asia. Of the cases reported so far in the English language literature, a total of 39 children have
been described.2 Unlike adult patients, who are most commonly of Hispanic origin, children with
EDP are usually Caucasian. In prepubertal children with EDP there is absence of consistent trigger
factors and an eventual improvement or resolution of the lesions in 50% cases. 2

The etiology of erythema dyschromicum perstans is unknown. However, a number of eitiological
factors have been implicated. These include ingestion of ammonium nitrite, nematodes infestation
(whipworm infection, control of which produced erythema dyschromicum perstans remission),
radiographic contrast media, aminopenicillins use, cobalt allergy and chlorothalonil exposure
among banana farm workers.3,4,5,6,7

The most frequent allele associated with EDP in Mexican was HLA-DR4 seen in 65% cases as
compared to 23% in controls. 8 Both sexes are affected, but women are affected more often than
men. Darker-skinned individuals are affected more often.


Erythema dyschromicum perstans has a slow onset and is unlikely to resolve spontaneously. but in
children, erythema dyschromicum perstans may be more likely to resolve within 2-3 years.7

The age of onset is usually between the first to third decades of life. Starts abruptly or slowly as a
ashy gray to blue asymtommatic disseminated symmetric macular lesion 0.5 cm -2 cm that starts
over the trunk and spreads centrifugally to face and extremities without preference for exposed or
nonexposed areas. Early lesion have elevated erythematous active border 1-2 mm. However, this
border is often not present, and eventually disappears after several months. Lesions are oval,
polycyclic, or irregularly shaped, gray-blue hyperpigmented macules on the trunk, the arms, the
face, and the neck. The palms, soles, scalp, nails and mucous membranes are typically spared.
Histology shows lichenoid dermatitis. 9 Direct immunofluoresence microscopy studies have
demonstrated colloid staining of IgM and C4, and presence of fibrinogen at the dermoepidermal
junction.10 A case with unilateral and asymmetric involvement affecting the left trunk and leg has
also been reported. 11

Bhutani et al described 40 Indian patients with similar symptoms to those reported by Ramirez,
except that about one-third had associated lichen planus clinically and histologically.12 This entity
was called lichen planus pigmentosus and it considered as a macular variant of lichen planus.
Vega et al reported in 1992 that LPP and ashy dermatosis are distinct entities and presented
clinical differences between the two.   13 Some   argue that it may be a variant of LP. This was based
on the clinical observation that EDP may accompany, precede or follow lesions of LP, and from the
similarities shared on histology and immunofluoresence. The presence of a lichenoid tissue
reaction in some cases of EDP favors a diagnosis of lichen planus, but such a reaction is not
specific to lichen planus. The two disorders may be histologically indistinguishable. 12,13 LP is
differentiated by the distribution of lesion in photoexposed and flexures, presence of lesions of LP
subsequently or simultaneously and the associated pruritis. The pattern of pigmentation in are
mostly diffuse (77.4%), followed by reticular (9.7%), blotchy (7.3%) and perifollicular (5.6%).   14   It is
chronic condition with relapses and remissions. On the other hand, EDP do not have any
predilection for photoexposed or nonexposed areas. It is chronic and insidious. The lesions are
distributed symmetrically. There can be an erythematosus and raised border. There can be
residual hypopigmented halo in cases of EDP. Cases of erythema dyschromicum perstans have


negative results laboratory study results, which include the following: Bacterial, viral, mycologic
cultures and erythrocyte sedimentation rate. 2-14

In 1978, further confusion was added when Degos et al. introduced “idiopathic eruptive macular
pigmentation” as a new entity. However the clinical picture of the condition was similar to that of
EDP in some patients described by Degos et al. In 1996, further confusion was added when
idiopathic eruptive macular pigmentation was defined and to made a specific entity by Sanz de
Galdeano et al., outlined basic criteria for the diagnosis of the condition. 15 The main criteria were:
(i) the absence of any preceding or associated inflammatory lesions; and (ii) the absence of
interfacial dermatitis. In their cases, spontaneous resolution of the lesions occurred within several
months to a few years. Though there are many reports of idiopathic macular hyperpigmentation
being different from EDP. However, the presence or absence of mild interfacial dermatitis should
not be a decisive factor in differentiation between the two conditions, as interfacial dermatitis may
disappear in the late phase of any lichenoid tissue reaction. Histopathologic examination was not
specific and consisted of hyperpigmentation of the basal cell layer, melanin pigment, and a mild
lymphohistiocytic perivascular infiltrate in the papillary dermis. Similarly colour can,t be a used as a
differentiating feature in these conditions as different shades have been seen in both condition.

There are many therapeutic options are available for erythema dyschromicum perstans (EDP), of
which clofazimine was found to be useful. 16 Other therapeutic modalities are ultraviolet exposure,
ultraviolet avoidance, chemical peels, antibiotics, corticosteroids, vitamins, tetracyclines,
antihistamines, griseofulvin, isoniazid, chloroquine, dapsone and psychotherapy.


1 Ramirez CO. Los cenicientos: problema clinica. In: proceedings of the frist Central American
congress of Dermatology. 1957:122-130.
2 Torrelo A et al. Erythema dyschromicum perstans in children: a report of 14 cases . J Eur Acad
Dermatol Venereol. 2005 Jul;19(4):422-6.
3. Jablonska S. Ingestion of ammonium nitrate as a possible cause of erythema dyschromicum
perstans (ashy dermatosis). Dermatologica. 1975;150(5):287-91.


4 Lambert WC, Schwartz RA, Hamilton GB. Erythema dyschromicum perstans. Cutis. 1986

5 Zenorola P, Bisceglia M, Lomuto M. Ashy dermatosis associated with cobalt allergy. Contact
Dermatitis. 1994 Jul;31(1):53-4.

6 Penagos H, Jimenez V, Fallas V, O'Malley M, Maibach HI. Chlorothalonil, a possible cause of
erythema dyschromicum perstans (ashy dermatitis). Contact Dermatitis. Oct 1996;35(4):214-8.
7 Silverberg NB, Herz J, Wagner A, Paller AS. Erythema dyschromicum perstans in prepubertal
children. Pediatric Dermatology. 2003;vol20(5):398-403.
8 Correa MC, Memije EV, Vargas-Alarcon G, et al. HLA-DR association with the genetic
susceptibility to develop ashy dermatosis in Mexican Mestizo patients. J Am Acad
Dermatol. Apr 2007;56(4):617-20.
9 S Zaynoun, N Rubeiz, A-G Kibbi. Ashy dermatoses – a critical review of the literature and
a proposed simplified clinical classification Inter l of Dermatol. 2008: 47, 542–544.
10 Tschen JA, Tschen EA, McGavran MH. Erythema dyschromicum perstans. J Am Acad
Dermatol. 1980 Apr;2(4):295-302.
11 Novick NL, Phelps R. Erythema dyschromicum perstans. Int J Dermatol. 1985 Dec;24(10):630-
12 Bhutani LK, Pandhi RK, Bedi TR. Lichen planus pigmentosus. Dermatologica 1974;149(1):43-
13 Vega ME et al. Ashy dermatosis and lichen planus pigmentosus: A clinicopathological study of
31 cases.1992 Feb;31(2):90-4.
14 JKanwar AJ, Dogra S, Handa S, Parsad D, Radotra BD. A study of 124 Indian patients with
lichen planus pigmentosus. Clin Exp Dermatol. 2003 Sep;28(5):481-5.
15 Sanz de Galdeano C, Lèautè-Labrèze C, Bioulac-Sage P, et al. Idiopathic eruptive macular
pigmentation: report of five patients. Pediatr Dermatol 1996; 13: 274–277.
16 Arbiser JL, Moschella SL. Clofazimine: a review of its medical uses and mechanisms of
action. J Am Acad Dermatol. Feb 1995;32(2 Pt 1):241-7.


                               MEMBERSHIP FORM OF ASPCR
Join ASPCR Please send a bank draft/cheque for US$ 50 or Indian Rs 2200/- in favour of ASPCR
payable at Chandigarh by mail at following address:
Dr Davinder Parsad
PO BOX 1510
Department of Dermatology
Postgraduate Institute of Medical Education & Research
Chandigarh - 160012, India.

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