g., heart

muscle and eyes) or organs of the excretory system (e.g., kidneys and bladder) before arthritis onset (day 2).[20] Epigenetics Compound Library cell line However, additional 18F-FDG signaling can be detected in the joints of fore and hind paws in acute experimental arthritis at day 13, suggesting a specific 18F-FDG uptake in inflamed joints. PET/CT imaging showed hot spots of inflammatory metabolic activity in wrist and ankle joints. After treatment of human sTNFR (etanercept) or saline with G6PI-induced mice, PET/CT found a marked 4.9-fold decrease of total 18F-FDG uptake in sTNFR (etanercept)-treated arthritic mice. Comparable results were obtained using histopathological assessment of therapeutic intervention.[20] Thus, PET/CT is a convenient technique

for monitoring disease activity or efficacy of treatment in experimental arthritis. It is noteworthy that FDG PET/CT may help predict therapeutic response to novel treatments. In a group of active RA patients, before infliximab treatment, all patients indicated enhanced 18F-FDG uptake in at least one metacarpophalangeal region or wrist.[49] After 14 and 22 weeks, selleck chemical DAS decreased to 4.3 ± 1.5 and 3.9 ± 1.3, respectively. The change in mean SUV after 2 weeks of infliximab treatment correlated markedly with DAS at 14 and 22 weeks, respectively.[49] The study found a strong correlation between early changes in 18F-FDG for uptake in hand joints and clinical disease activity after 14 and 22 weeks of treatment. At a group level, the findings suggest that 18F-FDG

PET may therefore be a valuable technique for predicting the efficacy of infliximab therapy as early as 2 weeks after initiation of treatment. Rituximab, a chimeric monoclonal antibody against the CD20 antigen, has been approved for the treatment of RA patients.[50] Tran et al.[51] radiolabeled rituximab with 124Iodine (124I) for PET imaging. Results showed that patients who did not receive pre-treatment with unlabeled rituximab indicated localization of nearly all radioconjugate in the spleen and to a lesser extent bone marrow, examined by PET/CT imaging 10 min after administration of 124I-rituximab.[51] Findings after 24 h indicated that the uptake in the spleen was largely diminished while the radioactivity accumulated in the thyroid.[51] In contrast, 124I-rituximab has favorable pharmacokinetics for targeting pathological B cells after pre-treatment with unlabeled rituximab, where patients predosed with unlabeled rituximab indicated persistent tracer availability in the central circulation for multiple days, with almost no splenic uptake.[51] Furthermore, PET imaging of patients received 124I-rituximab at 24 h and later exhibited accumulation of the tracer in joints (e.g.