Papers of the Week

Complex Regional Pain Syndrome (CRPS) develops after fracture. The acute CRPS phenotype resembles exaggerated inflammation which is explained by local and systemic activation of a pro-inflammatory network including peptides and cytokines. Epidemiologic data suggest that inactivation of the peptidase angiotensin converting enzyme (ACE) in patients treated for hypertension increases the odds to develop CRPS. This hint lead us to investigate the serum protease network activity in CRPS patients vs. respective controls. For this purpose, we developed a dabsyl-bradykinin (DBK)-based assay and used it to investigate CRPS patients, as well as healthy (HC) and pain (painful diabetic neuropathy; dPNP) controls. The major result is that the degradation of DBK to fragments 1-8 and 1-5 in HC and dPNP is shifted to higher values for DBK1-8 and lower values for DBK 1-5 at one hour of incubation in CRPS patients. Using this novel reporter peptide assay, we have been able to show that the resolving protease network for mediators like BK might be different in CRPS patients; having a look at the the clinical signs, which resemble inflammation, this resolving protease network is probably less effective in CRPS.