ARTICLE
Auteur(s) : Selda Pelin
Kartal Durmazlar, Hatice Akpinar, Cemile Eren, Fatma Eskioglu,
Semih Tatlican
Department of Dermatology, Ministry of Health Ankara
Diskapi Yildirim Beyazit Education and Research Hospital,
Ankara, Turkey
accepté le 7 Avril 2009
Acrodermatitis continua of Hallopeau (ACH) is a rare, chronic
disease characterized by pustular eruptions predominantly involving
the distal phalanges of the hands and feet with marked involvement
of the nail bed [1]. Atrophic skin changes, onychodystophy and
osteolysis are frequently present, causing painful and disabling
lesions [2]. ACH is generally considered as a rare variant of
pustular psoriasis, though some authors classify it as a separate
entity [3]. Treatment of ACH is very difficult and often
disappointing. Phototherapy is one of the safest and most effective
treatments for psoriasis [4]. The use of narrowband ultraviolet B
(NB-UVB) phototherapy, with a peak emission wavelength at
311 nm, has been used for the treatment of psoriasis and other
inflammatory disorders for more than 20 years [5]. NB-UVB has
been reported to be more effective than broadband (BB) UVB [4] and
as effective as systemic psoralen plus UVA (PUVA) in psoriasis [5].
Topical 8-methoxypsoralen (8-MOP) has been reported to enhance the
therapeutic results of targeted NB-UVB [6]. Topical 8-MOP/NB-UVB
has been used successfully to treat psoriasis [7].
We describe a patient with ACH who responded to the treatment of
topical 8-MOP/NB-UVB successfully. To the best of our knowledge, we
report the first case of successful treatment of ACH with topical
8-MOP/NB-UVB.
Case report
A 24-year-old man presented with an 11-year history of recurrent
flares of painful pustular and scaly lesions on the distal portion
of fingers and toes, with persistent nail dystrophy. On
examination, pustular and erythematosquamous psoriasiform lesions
were observed on the dorsal and ventral aspects of several fingers
and dorsal aspect of several toes, with associated nail dystrophy
(figure 1).
There were no skin lesions elsewhere. Earlier treatment had
included topical antibiotics, antimycotics, potent corticosteroids,
calcipotriol as well as methotrexate (15 mg/week for one year
at age 21) without any success. The patient’s past medical history
was otherwise unremarkable and he had no personal or family history
of psoriasis. Clinical and microbiological examination gave no
evidence for bacterial or fungal infection. Histological features
of psoriasis were found in a biopsy specimen from lesional skin.
X-ray examination revealed no osteolytic changes of the bones or
joint deformities. Based on the clinical and histopathological
findings, ACH was diagnosed. Because of the disease progression,
which led to severe disability, the lack of response to previous
treatments, rejection of systemic medication by the patient and in
reference to a previous report on the successful use in psoriasis
[7], our patient was given twice weekly local NB-UVB phototherapy
with preceding 0.1% 8-MOP over the lesional areas.
The photoelectrical device used in the treatment (Daavlin,
Bryan, OH, USA, 4356) had a local system with a hand and foot unit
and contained 8 lamps; 4 emitting UVA (Voltarc F24T12/B4HO 16121)
and the other 4 emitting NB-UVB (Philips TL-01 20W/01RS). We used
the device only equipped with Philips TL-01 lamps and NB-UVB was
applied only in combination with topical 8-MOP. A proprietary
formulation containing 0.1% MOP in a hydrophilic water/oil emulsion
(Vitpso 0.1% gel, Orva pharmaceuticals, Izmir, Turkey) was applied
30 minutes prior to irradiations without occlusion. The
perilesional area was protected with pure vaseline. The patient did
not use any other medication between sessions except topical
emollients. The minimal erythema dose (MED) determined on gluteal
areas of the patient was 300 mJ/cm2. The initial
dose was 70% of the MED. If erythema did not occur, a dose
increment of 40% was applied. If there was erythema, a 20% dose
increment was administered. When more prominent erythema occurred,
the dose was not increased, instead it was reduced by a ratio of
1:2. After reaching 2,000 mJ/cm2 the dose remained
constant. Already after the fifth session, the lesions responded to
the treatment (figure
2). Ten weeks later, when the patient had received 20
sessions, almost all lesions had cleared (figure 2) and the
cumulative dose reached was 18,359 mJ/cm2.
Unfortunately, the patient was lost to follow-up as he moved to
another city.
Discussion
The treatment of ACH is known to be difficult. Lesions of ACH are
painful and disabling and associated with skin atrophy,
onycodystrophy and osteolysis. Histologically, the characteristic
feature of ACH is a subcorneal cavity filled with polymorphonuclear
neutrophils [8]. Because of the histopathological similarity of ACH
with pustular psoriasis, it is generally accepted as a variant of
localized pustular psoriasis [1, 9, 10]. As high numbers of T
lymphocytes and neutrophilic granulocytes infiltrating the skin
lesions play a major pathophysiological role in ACH, most treatment
regimens aim at downregulating the disease-related proinflammatory
cytokines [11]. Unfortunately, no therapeutic guidelines exist,
only anecdotal observations have been reported in the literature
and every successfully treatment of ACH contributes to the
therapeutic armamentarium [3, 9, 12]. For the treatment of ACH,
various topical and systemic agents, as well as combined schemes,
have been used. Topical treatments such as corticosteroids, tar,
dithranol, fluorouracil, calcipotriol and calcineurin inhibitors
have been used in combination with systemic drugs or alone [11].
Retinoids, cyclosporine, methotrexate, tetracycline, dapsone,
colchicine, anti-tumour necrosis factor-α (TNF-α) agents and PUVA
phototherapy have been reported as systemic therapies [1-3, 8-12].
Topical 8-MOP/NB-UVB therapy has never been used to treat ACH.
NB-UVB phototherapy is an effective treatment for psoriasis [13]
and has been reported to be more effective than BB-UVB [4] and as
effective as PUVA therapy in psoriasis [5]. Because of the
histopathological similarity of ACH with psoriasis, among various
treatment alternatives we decided to give topical 8-MOP/NB-UVB
phototherapy in reference to the previous report on its successful
use in psoriasis [7]. In this report, topical 8-MOP/NB-UVB
phototherapy was applied once a week and fluencies of UVB delivered
to each spot were four multiples of MED and remained constant
throughout the study [7]. We applied topical 8-MOP/NB-UVB
phototherapy two times a week, because the initial dose started was
70% of the MED and our patient could attend the irradiation program
two times a week.
It has been shown that UVB primarily affects the T cells in
lesional skin of psoriasis [14]. However, UVB therapy has also been
shown to suppress lymphocyte production by decreasing the
production of proinflammatory cytokines and by inducing the
production of anti-inflammatory cytokines within the lymph nodes
[13]. UVB therapy has been proposed to have immunosuppressive
effects in psoriasis through induction of apoptosis in T cells, and
NB-UVB has been reported to be directly cytotoxic to T cells in
vivo, resulting in a higher depletion of dermal and epidermal T
cells in psoriatic skin [15]. It has been shown that patients
treated with NB-UVB secreted interleukin-10 (IL-10), an
anti-inflammatory cytokine, and showed a markedly decreased
production of IL-1β, IL-2, IL-5 and IL-6 [13]. Treatment with
recombinant IL-10 has been reported to be effective in psoriasis
and UVB irradiation was shown to induce the production of IL-10
both in human and murine skin [13]. IL-10 has been demonstrated to
inhibit the production of IL-1α, IL-1β, IL-6, IL-8 and TNF-α by
human monocytes [16]. It was reported that the addition of topical
0.1% 8-MOP to local NB-UVB significantly enhanced the therapeutic
effects of the light treatment without increasing the adverse
effects [7].
We reported a case with resistant ACH which responded well to
treatment with topical 8-MOP/NB-UVB. The therapy was well tolerated
and might be assumed as an effective treatment option for ACH.
Acknowledgements
Financial support: none. Conflict of interest: none.
References
1 Kuijpers AL, van Dooren-Greebe RJ, van de
Kerkhof PC. Acrodermatitis continua of Hallopeau: response to
combined treatment with acitretin and calcipotriol ointment.
Dermatology 1996; 192: 357-9.
2 Mang R, Ruzicka T, Stege H. Successful
treatment of acrodermatitis continua of Hallopeau by the tumor
necrosis factor-α inhibitor infliximab (Remicade). Br J Dermatol
2004; 150: 379-80.
3 Sotiriadis D, Patsatsi A, Sotiriou E,
Papagaryfallou I, Chrysomallis F. Acrodermatitis continua
of Hallopeau on toes successfully treated with a two-compound
product containing calcipotriol and betamethasone dipropionate. J
Dermatol Treat 2007; 18: 315-8.
4 Kaur M, Oliver B, Hu J, Feldman S.
Nonlaser UVB-targeted phototherapy treatment of psoriasis. Cutis
2006; 78: 200-3.
5 Sezer E, Erbil AH, Kurumlu Z, Tastan HB,
Etikan I. Comparision of the efficacy of local narrowband
ultraviolet B (NB-UVB) phototherapy versus psoralen plus
ultraviolet A (PUVA) paint for palmoplantar psoriasis. J
Dermatol 2007; 34: 435-40.
6 Asawanonda P, Amornpinyokeit N, Nimnuan C.
Topical 8-methoxypsoralen enhances the therapeutic results of
targeted narrowband ultraviolet B phototherapy for plaque-type
psoriasis. J Eur Acad Dermatol Venereol 2008; 22: 50-5.
7 Amornpinyokeit N, Asawanonda P. 8-methoxypsoralen
cream plus targeted narrowband ultraviolet B for psoriasis.
Photodermatol Photoimmuol Photomed 2006; 22: 285-9.
8 Adısen E, Oztas M, Gurer MA. Lack of efficacy
of etanarcept in acrodermatitis continua of Hallopeau. Int J
Dermatol 2007; 46: 1205-7.
9 Brunasso AM, Lo Scocco G, Massone C.
Recalcitrant acrodermatitis continua of hallopeau treated with
calcitriol and tacrolimus 0.1% topical treatment. J Eur Acad
Dermatol Venereol 2008; 22: 1272-3.
10 Jo SJ, Park JY, Yoon HS, Youn JI. Case of
acrodermatitis continua accompanied by psoriatic arthritis. J
Dermatol 2006; 33: 787-91.
11 Wilsmann-Theis D, Hagemann T, Dederer H,
Wenzel J, Bieber T, Novak N. Successful treatment of
acrodermatitis continua suppurativa with topical tacrolimus 0.1%
ointment. Br J Dermatol 2004; 150: 1194-7.
12 Van Dooren-Greebe RJ, van de Kerkhof PC,
Chang A, Happle R. Acitretin monotherapy in
acrodermatitis continua Hallopeau. Acta Dermatol Venereol 1989; 69:
344-6.
13 Sigmundsdottir H, Johnston A, Gudjonsson JE,
Valdimarsson H. Narrowband-UVB irradiation decreases the
production of pro-inflammatory cytokines by stimulated T cells.
Arch Dermatol Res 2005; 297: 39-42.
14 Krueger JG, Wolfe JT, Nabeya RT, et al.
Successful ultraviolet B treatment of psoriasis is accompanied by a
reversal of keratinocyte pathology and by selective depletion of
intraepidermal T cells. J Exp Med 1995; 182: 2057-68.
15 Grundmann-Kollmann M, Ludwig R, Zollner TM,
et al. Narrowband UVB and cream psoralen-UVA combination
therapy for plaque-type psoriasis. J Am Acad Dermatol 2004; 50:
734-9.
16 De Waal Malefyt R, Abrams J, Bennett B,
Figdor CG, de Vries JE. Interleukin 10 (IL-10) inhibits
cytokine synthesis by human monocytes: an autoregulatory role of
IL-10 produced by monocytes. J Exp Med 1991; 174: 1209-20.
|
Printable version
Version PDF
