Iman H Bassyouni1, Tamer A Gheita, Roba M Talaat. 1. Department of Rheumatology and Rehabilitation, Faculty of Medicine, Cairo University, Cairo 12613, Menoufya, Egypt. imanbassyouni@yahoo.com
Abstract
OBJECTIVE: To evaluate the clinical significance of anti-angiogenic receptor cluster of differentiation 36 (CD36) in serum of patients with SSc. METHODS: We studied 47 SSc patients (28 with lcSSC and 19 with dcSSC) and 38 age- and gender-matched healthy controls. Demographic, clinical, autoantibodies and serological data were prospectively assessed. Peripheral vascular affection was classified into mild, moderate, severe or end-stage based on a vascular severity scale. Soluble CD36 (sCD36) serum levels were measured using ELISA. RESULTS: Serum sCD36 levels were significantly higher in patients with SSc compared with healthy controls (P = 0.045). When the patients were divided into clinical subsets, sCD36 was higher in lcSSc than in healthy controls (P = 0.03). Levels of sCD36 were found to be positively correlated with pulmonary artery systolic pressure (PASP) and negatively correlated with percentage diffusing lung capacity for carbon monoxide (DL(CO)). In the multivariate analysis, 50% of the variation of sCD36 levels could be explained by elevated PASP (0.000), telangiectasias (0.026) and increasing vascular severity (P = 0.003). CONCLUSION: Serum sCD36 levels were higher in SSc patients (particularly the limited subset) than in healthy controls and were found to be correlated with PASP and vascular severity. We conclude that sCD36 may be a marker for elevated PASP and vascular involvement in SSc. To confirm our results we propose that larger scale, multicentre studies with longer evaluation periods are needed.
OBJECTIVE: To evaluate the clinical significance of anti-angiogenic receptor cluster of differentiation 36 (CD36) in serum of patients with SSc. METHODS: We studied 47 SSc patients (28 with lcSSC and 19 with dcSSC) and 38 age- and gender-matched healthy controls. Demographic, clinical, autoantibodies and serological data were prospectively assessed. Peripheral vascular affection was classified into mild, moderate, severe or end-stage based on a vascular severity scale. Soluble CD36 (sCD36) serum levels were measured using ELISA. RESULTS: Serum sCD36 levels were significantly higher in patients with SSc compared with healthy controls (P = 0.045). When the patients were divided into clinical subsets, sCD36 was higher in lcSSc than in healthy controls (P = 0.03). Levels of sCD36 were found to be positively correlated with pulmonary artery systolic pressure (PASP) and negatively correlated with percentage diffusing lung capacity for carbon monoxide (DL(CO)). In the multivariate analysis, 50% of the variation of sCD36 levels could be explained by elevated PASP (0.000), telangiectasias (0.026) and increasing vascular severity (P = 0.003). CONCLUSION: Serum sCD36 levels were higher in SSc patients (particularly the limited subset) than in healthy controls and were found to be correlated with PASP and vascular severity. We conclude that sCD36 may be a marker for elevated PASP and vascular involvement in SSc. To confirm our results we propose that larger scale, multicentre studies with longer evaluation periods are needed.