Sorafenib-Associated Psoriasiform Eruption in a Patient With Hepatocellular Carcinoma
August 2014 | Volume 13 | Issue 8 | Editorials | 899 | Copyright © August 2014
Turna İlknur MD,a Sevgi Akarsu MD,a
Saim Çarşanbalı MD,a Banu Lebe MD,b
and Emel Fetil MDa
aDokuz Eylül University, Faculty of Medicine, Department of Dermatology, İzmir, Turkey
bDokuz Eylül University, Faculty of Medicine, Department of Pathology, İzmir, Turkey
To our knowledge, there have been only a few reported
cases of psoriasiform eruption associated with sorafenib
therapy.1-6 Although drug-induced psoriasiform eruptions are
indistinguishable from idiopathic psoriasis, they may be differentiated
histologically by the absence of tortuous capillaries
in the dermal papillae associated with suprapapillary thinning,
and presence of eosinophils around the blood vessels of the superficial
plexus.8 While the second biopsy taken from our case
was consistent with psoriasiform drug eruption, we cannot definitively
determine if the patient’s elbow lesions were due to a
sorefanib-induced psoriasis exacerbation or psoriasiform drug
eruption. However, he reported a direct correlation between
starting sorefanib and appearence of elbow lesions.
The pathogenesis of sorefanib induced psoriasis remains
obscure, but the presence of dysfunctional CD4+CD25+ immunosuppressive
regulatory T cells leading to an imbalance
between regulatory and effector T-cell functions in patients
with psoriasis has been hypothesized to play an important role.
It has been suspected that tyrosine kinase inhibitors including
sorafenib may block the signal transduction pathways in both
regulatory and effector T cells.4 It has been also suggested that
sorafenib might alter the keratinocyte proliferation and differentiation
by a yet unknown mechanism.3
Actually, the occurrence of psoriasiform eruptions in patients
associated with sorafenib seems paradoxical. In recent trials,
the spectrum of diseases in which kinase inhibitors are used has
increasingly expanded to include immune-mediated diseases.
It was proposed that blocking kinases may be an effective way
to inhibit immune cell activation and abnormal epidermal angiogenesis,
involved in the pathogenesis of psoriasis. To this
respect, a patient with metastatic hypernephroma and concomitant
recalcitrant psoriasis who responded well to sorafenib has
been reported.9 More recently, novel protein kinase inhibitors
are also under clinical investigation based on this hypothesis
for treatment of psoriasis.10
Consequently, the pathogenesis of sorafenib-induced psoriasiform
eruptions is difficult to explain. Further molecular
investigations exploring the connection between sorafenib and
psoriasis may increase our understanding of this issue.
None of the authors have declared any relevant conflicts.
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