ARTICLE
Auteur(s) : Francesco Cusano1, Silvia Saletta
Iannazzone1, Giacomo Riccio2, Fabio Piccirillo1
1Dermatology Unit, “Gaetano Rummo” General
Hospital
2Dermatology Unit, Terme di Telese, Via dell'Angelo 1,
82100 Benevento, Italy
Psoriasis is occasionally accompanied by bullous diseases and
the role of TNF-α in the pathogenesis of both is well known
[1].
A 49-year-old woman with a long history of psoriasis was treated
in another dermatological unit with topical therapies and UVB
phototherapy. In May 2006, the skin lesions worsened; cyclosporine
3 mg/kg/d did not give significant results, nor did
methotrexate 10 mg weekly and NB/UVB phototherapy. Moreover,
some bullae appeared on her chest and a skin biopsy showed results
consistent with bullous pemphigoid (BP). In October 2006,
prednisone 50 mg/d was started, with complete clinical
clearing of BP and improvement of the psoriasis; after
6 weeks, it was progressively tapered down to a minimum dose
of 5 mg twice a week and finally stopped in May 2008.
Unfortunately, after about 8 weeks, without any topical or
systemic medication both the BP and psoriasis rapidly relapsed, and
the patient was referred for the first time to our Unit.
Physical examination revealed plaque-type psoriasis with a PASI
of 17.2 and scattered bullous lesions on an erythematous
background (figure
1A). A new skin biopsy, histology and direct
immunofluorescence confirmed the diagnosis of BP. Due to previous
side effects (particularly, increased body weight), the patient
refused steroid treatment. Therefore, according to positive
preliminary experiences with combined therapies including TNF-α
antagonists in the treatment of coexisting BP and psoriasis [2, 3],
etanercept 100 mg weekly was started, with the eventual aim of
introducing steroids later. Surprisingly, while the psoriasis
slowly improved, the BP cured dramatically in just a few days.
After 12 weeks’ treatment, all the skin symptoms almost
completely disappeared (absence of bullae and PASI 1.3; figure 1B), and it was
reduced to 50 mg weekly. At a 16 week follow-up, the
patient was almost free of skin lesions but, 2 weeks later, a
severe outbreak of a new morphology of lesions was observed, with
erythematous plaques on her legs and soles, pustules (figure 1C), leg edema and
pain on the knees and ankles. A skin biopsy was performed and
the histological examination concluded that the intra-epidermal
sterile pustules were compatible with pustular psoriasis; therefore
acitretine 0.5 mg/kg/d was added and the rash progressively
improved in 8 weeks; the dosage was subsequently reduced and
finally stopped after a further 12 weeks. At a 6 week
follow-up after acitretine was withdrawn, the BP and psoriasis were
in remission and etanercept was stopped. After a further
12 weeks, the patient showed a slight recurrence of psoriasis
(PASI of 4.5), managed with topical drugs.
We describe a patient in whom remission of BP was obtained with
etanercept used as a single drug therapy. In the literature,
2 cases of BP [2, 3] treated with etanercept are described,
both coexisting with psoriasis; the first achieved remission using
etanercept when the steroid dose was lowered [2], the second
patient was given etanercept for psoriasis after being completely
cured of BP with rituximab [3].
Surprisingly, our patient's BP was better controlled than her
psoriasis. In fact, after 18 weeks of treatment with TNF-α
blockers, an erythemato-pustular rash was observed on the legs and
feet. The occurrence of palmoplantar pustulosis during TNF-blocking
therapy [4], or a relapse after steroid withdrawal, or a pustular
psoriasis following BP [5, 6], were hypothesized. In our case, the
rash did not require stopping the TNF blocking therapy.
In conclusion, the literature and our case show that TNF-α
antagonists might represent an effective alternative therapy for
co-existing BP and psoriasis, since corticosteroids may induce a
relapse of psoriasis and other well-known side effects, and
traditional systemic therapies are often associated with organ
toxicity. Further studies are needed to establish the efficacy of
anti-TNF in the treatment of other immunobullous disorders.
Acknowledgements
Financial support: none. Conflict of interest: none.
References
1 Rhodes LE, Hashim IA, McLaughlin PJ,
Friedmann PS. Blister fluid cytokines in cutaneous
inflammatory bullous disorders. Acta Derm Venereol 1999; 79:
288-90.
2 Yamauchi PS, Lowe NJ, Gindi V. Treatment of
coexisting bullous pemphigoid and psoriasis with the tumor necrosis
factor antagonist etanercept. J Am Acad Dermatol 2006; 54 (3 Suppl
2): S121-S122.
3 Saraceno R, Citarella L, Spallone G,
Chimenti S. A biological approach in a patient with psoriasis
and bullous pemphigoid associated with losartan therapy. Clin Exp
Dermatol 2008; 33: 154-5.
4 Ko JM, Gottlieb AB, Kerbleski JF. Induction and
exacerbation of psoriasis with TNF-blockade therapy: A review
and analysis of 127 cases. J Dermatolog Treat 2009; 20: 100-8.
5 Yasukawa S, Dainichi T, Kokuba H, et al.
Bullous pemphigoid followed by pustular psoriasis showing Th1, Th2,
Treg and Th17 immunological changes. Eur J Dermatol 2009; 19:
69-71.
6 Miyakura T, Yamamoto T, Tashiro A, et al.
Anti-p200 pemphigoid associated with annular pustular psoriasis.
Eur J Dermatol 2008; 18: 481-2.
|