Background Recent researches demonstrated presence of local RAS in myocardium, ovary and brain. Angiotensin converting enzyme (ACE) was shown to be produced by synovial membrane macrophages. Angiotensin II is a potent vasoconstrictor, and also can stimulate angiogenesis, fibroblast proliferation and growth factor expression. Hypertrophy and hyperplasia of synovium and angiogenesis are well documented in persistant rheumatoid synovitis.
Objectives In this cross-sectional study we aimed to detect ACE and renin levels in serum and synovial fluid (SF) of patients with RA and osteoarthritis OA.
Methods Sixteen patients with RA (13F, 3M), 13 patients with OA (8F, 5M) and 11 healthy controls (HC) (5F, 6M) were enrolled in the study. The commercially available Angiotensin-Converting Enzyme kit and ACE calibrator were used. Renin assay was carried out with a two-site immunoreactive assay.
Results Median serum ACE levels were 48 U/l, 45 U/l, and 33 U/l in RA patients, OA patients, and HC, respectively. Median serum renin levels were 12.9 pg/ml, 11.8 pg/ml, and 17.9 pg/ml in RA patients and OA patients, respectively. Neither of these results were statistically significant (p > 0.05). SF levels of ACE and renin were found to be increased in RA patients (44 U/l and 3.5 pg/ml) compared to OA patients (24 U/l and 1.2 pg/ml) (Table 1). Synovial fluid renin levels in patients with RA was negatively correlated with disease duration.
Conclusion In this study we demonstrated that ACE and renin levels were elevated in SF of RA patients while serum ACE and renin levels were comparable to those in OA patients and healthy controls. These observations suggest presence of local RAS in RA synovium. Since angiotensin have stimulatory roles in angiogenesis and fibroblast proliferation, local RAS may participate in pannus formation and joint destruction in patients with RA. Negative correlation of synovial renin with disease duration may be compatible with previous observations that joint erosion is most prominent during the first months of the disease. Further studies, including mRNA of ACE and angiotensin II are needed to clarify exact roles of RAS in the pathogenesis of RA.
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