Effective treatment with
etanercept results from a congregation of immunological signaling and modulating roles played by
tumor necrosis factor-alpha (
TNF-alpha), a pervasive member of the TNF super-family of
cytokines participating in numerous immunologic and metabolic functions. Macrophages, lymphocytes and other cells produce TNF as part of the deregulated immune response resulting in
psoriasis or other chronic inflammatory disorders.
Tumor necrosis factor is also produced by macrophages and lymphocytes responding to foreign
antigens as a primary response to potential
infection. Interference with
cytokine signaling by
etanercept yields therapeutic response. At the same time, interference with
cytokine signaling by
etanercept exposes patients to potential adverse events. While the efficacy of
etanercept for the treatment of
psoriasis is evident, the risks of treatment continue to be defined. Of the potential serious adverse events, response to
infection is the best characterized in terms of physiology, incidence, and management. Rare but serious events: activation of
latent tuberculosis,
multiple sclerosis,
lymphoma, and others, have been observed but have questionable or yet to be defined association with
therapeutic uses of
etanercept. The safe use of
etanercept for the treatment of
psoriasis requires an appreciation of potential adverse events as well as screening and monitoring strategies designed to manage patient risk.