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

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Publikace nespadá pod Filozofickou fakultu, ale pod Lékařskou fakultu. Oficiální stránka publikace je na webu muni.cz.
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KONIG Simone BAYER Malte DIMOVA Violeta HERRNBERGER Myriam ESCOLANO-LOZANO Fabiola BEDNAŘÍK Josef VLČKOVÁ Eva RITTNER Heike SCHLERETH Tanja BIRKLEIN Frank

Rok publikování 2019
Druh Článek v odborném periodiku
Časopis / Zdroj Pain : the journal of the international association for the study of pain.
Fakulta / Pracoviště MU

Lékařská fakulta

Citace
www http://dx.doi.org/10.1097/j.pain.0000000000001503
Doi http://dx.doi.org/10.1097/j.pain.0000000000001503
Klíčová slova Complex regional pain syndrome; Chronic pain; Bradykinin; Serum peptidase
Popis 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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