Effects of shock wave therapy in the skin of patients with progressive systemic sclerosis: a pilot study.
Vasculopathy, immunological abnormalities, and excessive tissue fibrosis are key elements in the pathogenesis of progressive systemic sclerosis (SSc). Extracorporeal shock waves (ESW) have anti-inflammatory and regenerative effects on different tissues. We hypothesized that ESW can reduce endothelial cell damage and skin fibrosis in patients with SSc. We enrolled 30 patients affected by SSc, 29 females and 1 male. Rodnan Skin Score (RSS) and Visuo-Analogical Scale (VAS) for skin wellness were performed before and immediately after ESW therapy (ESWT) and at 7, 30, 60, and 90 days after the treatment. Sonographic examination of the patients' arms was performed before and 7, 30, 60, 90 days after treatment. Blood samples were obtained before and 30 and 60 days after treatment to measure serological levels of von Willebrand factor, vascular endothelial growth factor, intracellular adhesion molecule-1, monocyte chemotactic protein-1. The number of endothelial progenitor cells (EPCs) and circulating endothelial cells (CECs) were determined at the same time points. After ESWT we observed a rapid and persistent reduction of RSS and decrease of VAS. There was no difference in skin thickness before and after ESWT; however, we observed a more regular skin structure and an improvement in skin vascularization 90 days after treatment. EPCs and CECs increased 60 and 90 days after treatment, while serological biomarkers showed no variation before and after therapy. In conclusion, ESWT resulted in an improvement of VAS, RSS, and of skin vascular score, and in an increase of CECs and EPCs.
Tinazzi
Elisa
E
Department of Clinical and Experimental Medicine, University of Verona, Verona, Italy.
Amelio
Ernesto
E
Marangoni
Elettra
E
Guerra
Claudio
C
Puccetti
Antonio
A
Codella
Orazio Michele
OM
Simeoni
Sara
S
Cavalieri
Elisabetta
E
Montagnana
Martina
M
Adani
Roberto
R
Corrocher
Roberto
R
Lunardi
Claudio
C
D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D005260:Female; D005355:Fibrosis; D019220:High-Energy Shock Waves / Q000627:therapeutic use*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007558:Italy; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000097:blood; D010865:Pilot Projects; D045743:Scleroderma, Diffuse / Q000097:blood / Q000473:pathology / Q000628:therapy*; D012867:Skin / Q000098:blood supply / Q000000981:diagnostic imaging / Q000473:pathology*; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D016896:Treatment Outcome; D014464:Ultrasonic Therapy / Q000379:methods*; D018615:Ultrasonography, Doppler, Color; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D014841:von Willebrand Factor; D018799:Intercellular Adhesion Molecule-1; D009569:Nitric Oxide