Turkish Journal of Medical Sciences
DOI
10.3906/sag-0904-48
Abstract
It is known that renin-angiotensin system, inflammation, signaling pathways, and genetic predisposition play a major role in the pathogenesis of heart valve disease. Scarring and collagen deposition in the valves and destruction of myocytes may result from the combined effects of rheumatic and degenerative process in heart valve diseases. Prolidase plays an important role in collagen metabolism, matrix remodeling and cell growth. The aim of the study was to comparatively assess the serum prolidase activity in rheumatic and degenerative heart valve diseases. Materials and methods: The study included 26 patients who had undergone valve replacement due to rheumatic etiology (Group I), 24 patients who had undergone valve replacement due to degenerative etiology (Group II) and 20 healthy volunteers (Group III). Prolidase activity was determined in all subjects. High sensitive C-reactive protein and white blood cell count were studied in only valve patients. Results: Prolidase activity was significantly greater in control group than in patients group (51.23.± 5.9 U/L vs. 39.40 ± 4.6 U/L, respectively; P < 0.001). There was no statistically significant difference between Group I and Group II (P = 0.721). No correlation was detected between serum prolidase activity and severity of valve disease (P > 0.05). Conclusion: These results suggested that rheumatic and degenerative heart valve diseases seem to be associated with decreased serum prolidase activity.
Keywords
Prolidase activity, rheumatic valve disease, degenerative valve disease
First Page
687
Last Page
692
Recommended Citation
RABUŞ, MURAT BÜLENT; DEMİRBAĞ, RECEP; SEZEN, YUSUF; TAŞAR, MEHMET; TAŞKIN, ABDULLAH; AKSOY, NURTEN; KIRALİ, KAAN; and YAKUT, CEVAT
(2010)
"Serum prolidase activity in patients with degenerative and rheumatic heart valve diseases,"
Turkish Journal of Medical Sciences: Vol. 40:
No.
5, Article 3.
https://doi.org/10.3906/sag-0904-48
Available at:
https://journals.tubitak.gov.tr/medical/vol40/iss5/3