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The serum protease network-one key to understand complex regional pain syndrome pathophysiology

S. König, M. Bayer, V. Dimova, M. Herrnberger, F. Escolano-Lozano, J. Bednarik, E. Vlckova, H. Rittner, T. Schlereth, F. Birklein,

. 2019 ; 160 (6) : 1402-1409. [pub] -

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc20023922

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 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.

Citace poskytuje Crossref.org

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$a Complex regional pain syndrome (CRPS) develops after fracture. The acute CRPS phenotype resembles exaggerated inflammation, which is explained by local and systemic activation of a proinflammatory network including peptides and cytokines. Epidemiologic data suggest that inactivation of the peptidase angiotensin-converting enzyme in patients treated for hypertension increases the odds to develop CRPS. This hint leads us to investigate the serum protease network activity in patients with CRPS vs respective controls. For this purpose, we developed a dabsyl-bradykinin (DBK)-based assay and used it to investigate patients with CRPS, as well as healthy and pain (painful diabetic neuropathy [dPNP]) controls. The major result is that the degradation of DBK to fragments 1-8 and 1-5 in healthy control and dPNP is shifted to higher values for DBK1-8 and lower values for DBK1-5 at 1 hour of incubation in patients with CRPS. Using this novel reporter peptide assay, we have been able to show that the resolving protease network for mediators such as BK might be different in patients with CRPS; having a look at the clinical signs, which resemble inflammation, this resolving protease network is probably less effective in CRPS.
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$a Bednarik, Josef $u Central European Instutite of Technology and Medical Faculty, Masaryk University, Brno, Czech Republic. Department of Neurology, University Hospital Brno, Czech Republic.
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$a Vlckova, Eva $u Central European Instutite of Technology and Medical Faculty, Masaryk University, Brno, Czech Republic. Department of Neurology, University Hospital Brno, Czech Republic.
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$a Schlereth, Tanja $u Department of Neurology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany. Deutsche Klinik für Diagnostik, DKD Helios Klinik Wiesbaden, Wiesbaden, Germany.
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