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Psoriasis vulgaris flare during efalizumab therapy does not preclude future use: a case series

DOI: 10.1186/1471-5945-5-9

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Abstract:

We present two patients with severe chronic plaque psoriasis who received numerous systemic anti-psoriatic therapies with varied results. Both responded well to initial treatment with efalizumab (anti-CD11a), but then experienced a flare of their disease after missing a dose. However, after disease stablization, both patients responded well to re-introduction of efalizumab, one patient requiring concurrent treatment with infliximab (anti-TNF-α).These cases are presented to characterize this "flare" reaction, and to inform health care providers that efalizumab can still be administered after disease flare, and again may be a successful therapy.Psoriasis may be a long-lasting disease resulting in great morbidity in affected patients. Newer biological therapies may offer a real alternative to those with severe disease, and they are associated with a different toxicity profile than traditional systemic therapies [1]. The agents currently approved by the US FDA are alefacept (anti-CD2, Amevive, Biogen), efalizumab (anti-CD11a, Raptiva, Genentec Inc) and etanercept (anti-TNF receptor, Enbrel, Amgen). Infliximab (anti-TNF-α, Remicade, Centocor) has not yet been approved for psoriasis vulgaris, although it has recently been approved for psoriatic arthritis.Efalizumab is a humanized monoclonal antibody targeting the α chain of the T cell adhesion integrin lymphocyte function-associated antigen (LFA)-1. The LFA-1- intracellular adhesion molecule (ICAM)-1 interaction plays a crucial role in T cell adhesion at several key points in immune activation pathways. By binding to ICAM-1 on dendritic cell (DCs), endothelial cells and keratinocytes, T cells may be activated, migrate, and interact with keratinocytes respectively. The mechanism of action is not yet completely understood, however during therapy peripheral lymphocytosis is observed, which is most likely due to inhibition of T cell trafficking and blockade of memory T cells entering inflamed skin [2]. Efalizumab is associate

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