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Early detection of psoriatic arthritis (PsA) remains a challenge in clinical practice. Tools such as the German Psoriasis Arthritis Diagnostic (GEPARD) questionnaire have been developed for this purpose. The aim of this study was to determine the performance of the GEPARD questionnaire in the detection of PsA in psoriasis patients following rheumatology evaluation in daily clinical practice in Germany. This was a multicenter study involving 59 dermatology units (university/general hospital/office based), and the GEPARD questionnaire was distributed to psoriasis patients. Patients who had a sum score of ≥4 positive answers were referred to a rheumatologist for evaluation of PsA. We recruited 1,512 patients, of whom approximately 50% were referred. One third of the referred patients were classified as having PsA after rheumatological assessment. Rates of PsA in university/general hospital settings were higher than those observed in a doctor's office-based setting (43.7 vs. 25.8%). The GEPARD questionnaire demonstrated easy screening of psoriasis patients for PsA.

Background: The association between skin and joint manifestations in patients with psoriatic arthritis (PsA) requires further characterization. Objective: We evaluated the association between severity of skin disease and joint involvement and the effectiveness and safety of adalimumab in PsA patients by baseline psoriasis severity. Methods: Descriptive statistics and regression analyses were used to evaluate data from 1,918 PsA patients starting adalimumab treatment. Subgroup analyses were conducted on patients empirically grouped by baseline target lesion score as a marker of psoriasis severity. Results: Psoriasis severity was not associated with joint manifestations at baseline or after 12 months of treatment. All subgroups showed improvements in skin and joints during therapy, and adalimumab was safe and well tolerated in all subgroups. Conclusion: The severity of skin manifestations does not correlate with the severity of joint disease in PsA patients; even patients with mild skin disease may have extensive musculoskeletal involvement.

Centocor Inc is developing CNTO-1275 (ustekinumab), a subcantaneous mAb against the p40 subunit of IL-12 and IL-23, for the potential treatment of inflammatory diseases such as psoriasis, psoriatic arthritis, multiple sclerosis (MS) and Crohn's disease (CD). In July 2004, a phase II trial for MS had commenced, and by July 2006 this study was no longer recruiting patients. By May 2005, CNTO-1275 was in phase II studies for CD, and by January 2006 the antibody was in phase III studies for psoriasis. In December 2005, a phase II trial in patients with psoriatic arthritis had commenced and had finished recruiting by January 2007.

Crohn’s disease (CD) is characterized by intestinal infiltration of activated immune cells and distortion of the gut architecture. Here, we demonstrate that IL-22, a cytokine that is mainly produced by activated Th1 and Th17 cells, was present in high quantities in the blood of CD patients in contrast to IFN-[gamma] and IL-17. In a mouse colitis model, IL-22 mRNA expression was elevated predominantly in the inflamed intestine but also in the mesenteric lymph nodes. Simultaneously, IL-22BP showed strong a constitutive expression in the gut and lymph nodes and was decreased in the inflamed intestine. To investigate the possible role of systemic IL-22 in CD, we administered IL-22 to healthy mice and found an up-regulation of LPS binding protein blood levels reaching concentrations known to neutralize LPS. This systemic up-regulation was associated with increased hepatic but not renal or pulmonary LBP mRNA levels. IL-22 also enhanced the secretion of LBP in hepatocytes in vitro. This increase was mainly transcriptionally regulated and synergistic with that of other LBP inducers. Finally, elevated LBP levels were detected in CD patients and the mouse colitis model. These data suggest that systemic IL-22 may contribute to the prevention of systemic inflammation provoked by LPS present in the blood of CD patients through its induction of hepatic LBP.