Psoriasis biologic therapy

Weinberg JM et al Biologic therapy for psoriasis An update on the tumor necrosis factor inhibitors infliximab, etanercept, and adalimumab, and the T-cell-targeted therapies efalizumab and alefacept. J Drugs Dermatol 2005 4 544. [PMID 16167412]... 

IL)-8, which are believed to be important in the pathophysiology of psoriasis. All of these cytokines are important in the development of psoriasis and represent possible targets of biologic therapies. 

Once thought to be primarily a disorder of keratinocyte hyperproliferation, psoriasis now is known to be an autoimmune process mediated by T lymphocytes that can react with epidermal keratinocytes (Figure 62-2). The mechanism of biological therapies in psoriasis can be illustrated... 

Systemic therapies are seldom used for mild to moderate psoriasis, and are generally reserved for patients with moderate to severe psoriasis.17 29 Oral agents include sulfasalazine, acitretin, methotrexate, cyclosporine, mycophenolate mofetil, azathioprine, tacrolimus, and hydroxyurea. Parenteral agents include the biologic response modifiers alefacept, efalizumab, etanercept, infliximab, and many others, currently at various stages of research or approval for psoriasis. 

The type of lesion and whether the patient also has psoriatic arthritis are important issues in cleterinining therapy. Steroid topical creams, cyclosporine andmethotraxate are useful in treatment of psoriasis. Oral tazarotene, a non-biologic retinoid is pending FDA approval for moderate to severe psoriasis. As with most autoimmune disorder s, different patients respond differently and newer more targeted therapies are important goals. 

The conclusion of this review is that linear and angular psoralens [l-ll, 58, 59] exhibit very interesting biological effects on eukaryotic cells and should be considered as promising drugs in the therapy of several diseases, including psoriasis, mycosis fungoides, cancer. 

With the introduction of biologies for the treatment of rheumatoid arthritis and psoriasis, the annual cost of treatment has multiplied 10-fold to 25,000. Only about 10% of the eligible RA patients in the United States and Europe are currently on TNFa therapy. If all RA patients were to receive TNFa therapy, the total cost of therapy would reach 100 billion just for one disease only. The current or future health-care systems are not likely to fund such cost increases for anemia. 

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