Clinical response of psoriasis to both etanercept and adalim

Clinical response of psoriasis to both etanercept and adalimumab is less impressive in our series compared to previous reports. The lower PASI75 response in Taiwan reports may be due to the known difference between clinical trials and practical uses. In addition, it may be due to a higher percentage of high-need and recalcitrant patients because of the stringent reimbursement criteria in Taiwan. In addition, known differences between human leukocyte antigen found in Taiwan and those found in Western countries may also be important. A randomized controlled comparative study (CHAMPION) has shown that the response to adalimumab is rapid with a 57% improvement in mean PASI observed at Week 4.Another phase II/III randomized controlled study in Japan has also shown that adalimumab has a rapid onset of action (early at 4 weeks), and the percentages of patients achieving PASI75 continue to increase until Week 16 and are maintained through Week 24. However, our series show a trend of increased therapeutic improvement from Week 12 to Week 24. It is likely that longer time is required to achieve full therapeutic response in recalcitrant patients, as in case of our patients. Patients who showed inadequate primary response to etanercept also seemed to respond less favorably to subsequent adalimumab treatment. There may be several possible reasons. First, it is likely that other cytokines may be more important in these patients. In fact, recent studies suggest Th17 to be at least as important as TNF in the pathogenic pathway of psoriasis. Second, in one study, non-neutralizing antietanercept PD 0332991 were reported in up to 18% of patients taking etanercept for psoriasis over a period of 96 weeks. However, it is unknown if prior use of etanercept will trigger an increased production of antiadalimumab antibodies. Only one study has shown that patients of rheumatoid arthritis who previously formed antibodies against infliximab are more likely to develop antibodies against adalimumab and that it is more likely that some patients are more prone to develop an immune response, possibly related to the genetic background. In addition, 0.6–12% psoriatic patients would develop antiadalimumab antibodies. It has been found from studies on PsA that antiadalimumab antibodies develop in a minority of patients, and are associated with lower serum levels of adalimumab and diminished clinical response to treatment. Third, the efficacy of anti-TNF antagonists would diminish with time, and the drug survival of patients who previously failed one or more anti-TNF antagonists is more poor compared with the anti-TNF antagonists-naive patients. The scalp is one of the most common sites affected by psoriasis, and scalp psoriasis has a substantial impact on the patients\' quality of life. Previous studies have revealed that etanercept exerts impressive therapeutic effects on scalp lesions of psoriasis. Although adalimumab can be effective in patients who are poor responders to etanercept, compound is not more effective in those with scalp psoriasis in our case series. The exact reason is unknown, but it is possible that either etanercept has a slightly different mode of action or scalp is an easy target for both agents. For the nonresponders of both agents, a master cytokine other than TNF may be presented. There are no published randomized controlled trials that provide a head-to-head comparison of the effectiveness of the three TNF antagonists (adalimumab, etanercept, and infliximab) in treating patients with PsA. Some authors have reported that etanercept might have better effects in controlling PsA. However, in our series, subjective improvement in arthralgia with adalimumab was comparable to that with etanercept. No severe adverse events were recorded in our series, but one HCV carrier and one HBV carrier had elevated liver function tests. An increased risk for HBV carriers has been found in patients with psoriasis in Taiwan. Nevertheless, the use of anti-TNF-alpha therapy for HBV carriers with psoriasis or PsA is still controversial. Due to a lack of consensus in managing HBV carriers with psoriasis or PsA, antiviral prophylaxis is usually used in conjunction with anti-TNF therapy, based on the suggestions for HBV carriers receiving chemotherapeutic agents for their malignancies. However, these patients may develop resistance to antiviral agents, especially lamivudine, during long-term use and show subsequent elevation of aspartate aminotransferase/alanine aminotransferase (AST⁄ALT) levels. In addition, different anti-TNF antagonists may have different impacts on HBV reactivation. Infliximab is associated with more cases of HBV activation compared to etanercept or adalimumab. This may be due to more pronounced clearance of TNF-α, as the drug binds both soluble and membrane-bound TNF-α and is also cytotoxic for TNF-expressing cells. But there are no data comparing between the impact of etanercept and adalimumab on HBV. The increased HBV viral load after switching from etanercept to adalimumab in our patient might be due to either a time factor after prolonged antiviral treatment or a stronger immunosuppressive effect of adalimumab. However, it seems safe to use adalimumab for treating psoriatic patients who are HBV carriers under closer monitoring.