Alefacept (lymphocyte function-associated molecule 3/IgG fusion protein) treatment for atopic eczema
Department of Dermatology, Inselspital, University of Bern, Bern, Switzerland.The Journal of allergy and clinical immunology (Impact Factor: 11.48). 08/2008; 122(2):423-4. DOI: 10.1016/j.jaci.2008.06.010
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- "At the same time, a phase II study was performed in 10 patients with AD (Table 1). A significant clinical improvement was observed in all subjects and was maintained at least 10 weeks after treatment (NCT00376129). "
ABSTRACT: Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases that affect both children and adults with a prevalence of 30% and 10%, respectively. Even though most of patients respond satisfactory to topical anti-inflammatory drugs, about 10% require one or more systemic treatments to achieve good control of their illness. The progressive and increasingly detailed knowledge in the immunopathogenesis of AD has allowed research on new therapeutic targets with very promising results in the field of biological therapy. In this article, we will review the different biological treatments with a focus on novel drugs. Their mechanism of action, current status and results from clinical trials and observational studies will be specified.
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- "A number of case reports and pilot studies have been published recently, however representative, randomized, placebo controlled studies evaluating the efficacy and safety of biologicals in AD are still not available. Approaches resulting in reduced T cell activation using agents such as alefacept (fusion protein of lymphocyte function antigen (LFA)-3 (CD58) and immunoglobulin (Ig)G, rituximab (anti-CD20 antibody) and efalizumab (anti-CD11a antibody, no longer available) have been shown to be effective in selected patients with moderate to severe AD and were mentioned in guidelines [2,41-44]. "
ABSTRACT: Difficult to control atopic dermatitis (AD) presents a therapeutic challenge and often requires combinations of topical and systemic treatment. Anti-inflammatory treatment of severe AD most commonly includes topical glucocorticosteroids and topical calcineurin antagonists used for exacerbation management and more recently for proactive therapy in selected cases. Topical corticosteroids remain the mainstay of therapy, the topical calcineurin inhibitors tacrolimus and pimecrolimus are preferred in certain locations. Systemic anti-inflammatory treatment is an option for severe refractory cases. Microbial colonization and superinfection contribute to disease exacerbation and thus justify additional antimicrobial / antiseptic treatment. Systemic antihistamines (H1) may relieve pruritus but do not have sufficient effect on eczema. Adjuvant therapy includes UV irradiation preferably of UVA1 wavelength. “Eczema school” educational programs have been proven to be helpful.
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ABSTRACT: Recent insights into the relevance of the epidermal barrier function and its interaction with components of the innate and adaptive immune responses in patients with atopic dermatitis (AD) give rise to a number of novel potential treatment options. In particular, the identification of loss-of-function mutations in the barrier protein filaggrin and of a diminished expression of certain antimicrobial peptides in AD skin stimulates new concepts to think beyond the T(H)1/T(H)2 paradigm. This review will focus on these most recent discoveries and will discuss new and corresponding proof-of-concept trials in patients with AD. It will further speculate on novel ways to restore the homeostasis among the 3 major components in AD skin suspected to be clinically relevant.
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