Results showed that T helper 1 (Th1), Th2 and Th17 prevalence was higher, while regulatory T cell (Treg) prevalence was lower in early RA than healthy controls. After treatment, glucocorticoids alone decreased Th2 prevalence, while glucocorticoids + methotrexate decreased Th17 prevalence.[40] In addition, early RA patients exhibited increased levels of CRP and ESR, and had a high disease activity score as measured by the DAS-28. The Akt inhibitors in clinical trials patients also had higher serum levels of total cholesterol, plasma levels of small dense low-density lipoprotein cholesterol

(sdLDL-C) whereas their serum high-density lipoprotein cholesterol (HDL-C) levels were significantly lower compared with controls. After administration of methotrexate and prednisone, patients showed a significant increase in HDL-C levels.[41] Treatment BIBW2992 solubility dmso led to a significant decrease in the inflammatory markers CRP and ESR, as well as in the reduction of DAS-28.[41] Similarly, PET/CT images showed intense articular uptake in hands and wrists

before anti-TNF therapy (infliximab). After 2 months treatment, reduced FDG articular uptake in hands and wrists were found in RA patients.[42] Furthermore, active RA patients underwent whole-body FDG PET and clinical assessment before and after treatment with infliximab for 3 months.[43] Results indicated that the PET-based total joint score was similarly high before onset as was the clinical total joint score. The decrease of FDG joint uptake in the follow-up PET scans was significantly related to the clinical assessment.[43] In addition, 6 months after the anti-TNF therapies (infliximab, etanercept), the average values of DAS-28, Protein kinase N1 DAS-28 (CRP), ESR and matrix metalloproteinase-3 (MMP-3) were markedly decreased compared with baseline.[14, 44] The SUV of the right ankle, right hip, right elbow, left shoulder, bilateral wrists and bilateral knees were decreased in comparison with the SUV at baseline in each patient.[45] These data imply

that usage of FDG PET/CT is available and effective in monitoring treatment response (DMARDs and anti-TNFs).[31] Collagen-induced arthritis (CIA) is an animal model of RA that has been used to discuss the pathogenesis of the disease and to validate therapeutic targets. The dominant pathological features of CIA involved proliferative synovitis, erosion of bone, cartilage degradation, pannus formation, with infiltration of polymorphonuclear and mononuclear cells. In CIA mice, 18F-FDG PET depicted swollen joints, and 18F-FDG accumulation increased with the progression of arthritis.[46, 47] Histologically, a higher level of 18F-FDG accumulation was related to the pannus rather than the infiltration of inflammatory cells around the joints.[46] Similarly, the mean SUVmax of 18F-FDG for knees and ankles was significantly higher for CIA mice than for control mice, respectively.