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A.A. Sinha, To (anti‐)TNF or not (anti‐)TNF? That is the question in pemphigus, British Journal of Dermatology, Volume 172, Issue 3, 1 March 2015, Pages 564–565, https://doi.org/10.1111/bjd.13664
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ORIGINAL ARTICLE, p 760
Pemphigus vulgaris (PV) is a prototypical organ‐specific human autoimmune disease in which autoantibodies in the blood and skin target cell adhesion molecules expressed at the surface of keratinocytes leading to blister formation. Although the widespread use of systemic steroids has improved disease outcomes, mortality remains unacceptably high at 10–15%.1 No consensus guidelines exist for therapeutic management of the disease. An extensive Cochrane review, published first in 20092 and subsequently in 2011,3 could not find support for universally effective and safe treatments. A major issue remains: the limited number of randomized controlled trials and small sample sizes for most studies. Advancement in management strategies will rely on further advancements in our understanding of underlying disease mechanisms.
The strong human leucocyte antigen associations reported in PV support a model in which autoreactive T cells are involved in the induction and maintenance of autoantibody production. It thus follows that cytokines are likely to be key players in disease pathogenesis. While an integrated view of cytokine networks in PV is incomplete, qualitative and quantitative alterations in several mediators have been reported (reviewed in Giordano and Sinha4).
