Eczema molluscatum in tacrolimus treated atopic dermatitis

ARTICLE

Auteur(s) : Stefanie WETZEL, Andreas WOLLENBERG

Department of Dermatology, Ludwig-Maximilians-University, Frauenlobstrasse 9-11, D-80337 Mnchen, Germany

Article accepted on 10/11/2003

Case report

A 26-year-old male locksmith had suffered from atopic dermatitis (AD), primarily involving the head and neck, for more than 10 years. There was no history of an underlying immunodeficiency syndrome or previous molluscum contagiosum infection. 0.1% tacrolimus ointment was applied twice daily in particular to his neck area. Following 3 months of continous monotherapy with tacrolimus, he developed about 30 erythematous, non-scaly, centrally umbilicated papules on the right side of his neck (Fig. 1). At this time, only a few areas of his AD were apparent. Our clinical diagnosis of eczema molluscatum (EM) was confirmed by electron microscopic examination revealing the typical brick-shaped virions of molluscum contagiosum virus (MCV) (Fig. 2). There was no clinical sign of superinfection with staphylococcus aureus.
We advised our patient to interrupt his treatment with tacrolimus. Since he had only mild remaining dermatitis, we discontinued all antiinflammatory therapy. After three weeks, EM had disappeared completely without scarring, but mild lesions had reappeared. Upon readministration of tacrolimus ointment, the underlying AD healed completely without a relapse of EM. For the past three years, the patient has not experienced a second episode of EM and his AD is well controlled with tacrolimus 0.1% ointment monotherapy.

Discussion

MCV is transmitted via close skin contact and appears exclusively in humans. Therapeutic options for MCV infection include curettage of the lesions, destruction with carbon dioxide laser, cryotherapy, topical cidofovir [1], topical podophyllotoxin cream and imiquimod cream. In most cases, the lesions show only little inflammatory reaction and are self-healing over several months. Atypical lesions are frequently seen in immunodeficient patients. Recently, a number of unique MCV genes such as the soluble interleukin-18 binding protein (IL-18BP) have been found that help the virus to avoid immune detection [2]. IL-18 is a proinflammatory cytokine that may enhance both innate and acquired immune responses and protects against microbial infection. Upon detection of MCV by the patients immune system, the MCV is cleared from the human body, but this process may be attenuated in immunocompromized patients.
The disturbed skin barrier and impaired cellular immunity of AD patients may put them at a higher risk to develop bacterial and viral skin infections, such as EM. Earlier studies suggested an excess noradrenaline-binding affinity as the cause of this susceptibility to diffuse viral infections in AD patients [3]. Newer investigations point to an impaired recruitment of plasmocytoid dendritic cells (PDC) in AD patients as a relevant risk factor for viral infections such as EM or eczema herpeticum (EH) [4]. In addition, the impaired production of antiviral peptides such as the cahelicidin LL37 may increase the risk for patients with AD of developing EM [5].
Various forms of therapy may also increase a patient's risk of developing skin infections. Whereas some older studies assumed a causative relation between corticosteroid use and viral skin infections such as EH [6] or EM [7], a newer study indicates that it is not corticosteroid use but large, untreated skin lesions which may put AD patients at risk of developing EH [8].
Topical immunomodulators (TIM) act by inhibiting gene transcription of several proinflammatory cytokines in T cells, among them interferon-γ [9]. As interferons play a key role in the host defence system, inhibition of this cytokine by TIMs may lead to an impaired defence mechanism against viral skin infections [10]. The clinical relevance of such an effect is not established.
In conclusion, AD patients have a higher risk of developing cutaneous viral infections such as EH or EM. EH may occur in TIM treated patients [11], but clinical data from 16,000 treated study patients is not indicative of an impaired cellular immunity or an increased risk of viral skin infections [12, 13]. While the spontaneous regression of EM during a 3 week treatment pause supports an active role for TIM treatment in this infection, the rarity of EM in the many patients treated with TIM, as well as the lack of recurrence over three years of continued TIM use, do not support this assumption. Acknowledgements. We thank Mrs. E. Januschke for the electron microscopic demonstration of MCV in our patient and Prof. Dr. W. Burgdorf for critical reading of the manuscript. n

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