Background Life expectancy in rheumatoid arthritis (RA) patients is reduced by 3-10 years mainly due to cardiovascular diseases. Cystatin C is a basic microprotein, widely distributed in human tissues and body fluids. Cystatin C has been shown to be elevated in the synovial fluid of patients with RA, compared to patients with other joint diseases. The renal function is an important determinant of coronary atherosclerosis, and serum cystatin C is a novel, accurate measure of the glomerular filtration rate and a predictor of cardiovascular events and mortality, as stated by Maahs et al. Cystatin C has been reported not to be dependent on age, gender or muscle mass. Cystatin C has been demonstrated to be better predictor of atherosclerotic cardiovascular events than serum creatinine.
Methods The study group comprised of 68 premenopausal non-diabetic female RA patients. Forty healthy subjects, matched by age and sex, were selected as a control group. RA was diagnosed according to the 1987 revised criteria of the American College of Rheumatology. Ultrasound examination of carotid arteries was performed. Results of intima media thickness (IMT) and plaques were statistically studied and correlated with cystatin C and some other risk factors for atherosclerosis as well as with CRP and disease activity score-28 (DAS-28).
Results The IMT in patients was 0.63±0.10 mm and in controls 0.51±0.09 mm (p=0.000). Patients had statistically significant more plaques than controls - 17 versus 2 (p=0,006). The mean value for cystatin C in patients with RA was 0.69 ± 0.14 g/L, and in the control group the mean value was 0.67 ± 0.08 g/L. We did not find a statistically significant difference between the groups (p>0.05). We correlated cystatin C and IMT. The Spearman’s correlation coefficient calculated was low (r=0.153) and not statistically significant (p>0.05). We calculated Pearson’s correlation coefficient between cystatin C and plaques. The correlation coefficient was low (r=0.161) and not statistically significant (p=0.165).
Conclusions We did not find any differences between the study group and the control group in cystatin C levels, nor did we find any correlation with the atherosclerotic changes in RA patients. Therefore, we cannot conclude that cystatin C would be a predictor of accelerated atherosclerosis in RA patients as is in patients with chronic renal disease and in patients with diabetes. Considering the statistically significant difference in IMT and number of plaques in RA patients’ group and control group we could conclude that the atherosclerosis is accelerated even in premenopausal non-diabetic RA patients. However, the pathogenesis could be connected with inflammation more than with classical risk factors for atherosclerosis as is cystatin C.
Hansen T, Petrow PK, Gaumann A, Keyszer GM, Eysel P, Eckardt A, Bräuer R, Kriegsmann J. Cathepsin B and its endogenous inhibitor cystatin C in rheumatoid arthritis synovium. J Rheumatol. 2000 Apr;27(4):859-65.
Maahs DM, Ogden LG, Kretowski A, Snell-Bergeon JK, Kinney GL, Berl T, Rewers M. Serum cystatin C predicts progression of subclinical coronary atherosclerosis in individuals with type 1 diabetes. Diabetes. 2007 Nov;56(11):2774-9.
Disclosure of Interest None Declared
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