• Simone König, Malte Bayer, Violeta Dimova, Myriam Herrnberger, Fabiola Escolano-Lozano, Josef Bednarik, Eva Vlckova, Heike Rittner, Tanja Schlereth, and Frank Birklein.
• Core Unit Proteomics, Interdisciplinary Center for Clinical Research, Medical Faculty, University of Münster, Münster, Germany.
• Pain. 2019 Jun 1; 160 (6): 1402-1409.

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

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