Type III procollagen N-terminal propeptide, soluble interleukin-2 receptor, and von Willebrand factor in systemic sclerosis
Y.J. Lee, K.C. Shin, S.W. Kang1, E.B. Lee, H.A. Kim, Y.W. Song
Department of Internal Medicine, Clinical Research Institute, College of Medicine, Seoul National University, and 1Chungnam National University, Korea
ABSTRACT
Objective
To evaluate the blood concentration of type III procollagen N-terminal propeptide (PIIINP), soluble interleukin-2 receptor (sIL-2R), and von Willebrand factor (vWF) in systemic sclerosis (SSc) patients.
Methods
PIIINP, sIL-2R, and vWF were measured in the sera and plasma of 29 SSc patients and 29 sex- and age-matched healthy controls. Serum PIIINP was determined by radioimmunoassay. Both serum sIL-2R and plasma vWF were measured by enzyme-linked immunosorbent assay (ELISA). Associations between concentrations and clinical and laboratory features were evaluated.
Results
Serum levels of PIIINP and sIL-2R were significantly higher in the SSc group than in the control group (p < 0.01 for both). No differences in serum PIIINP and sIL-2R levels were found between the limited and diffuse cutaneous subsets. However, PIIINP concentrations were significantly higher in anti-Scl-70 positive SSc patients compared with those of anti-Scl-70 negative patients (p = 0.01). Serum PIIINP levels were significantly higher in SSc patients with restrictive pulmonary function (FVC < 80%) than in patients with normal pulmonary function (p < 0.05). The correlation between PIIINP levels and FVC (p < 0.05) was negative, but the correlation between PIIINP levels and
modified Rodnan skin scores (p < 0.05) was positive. sIL-2R levels were not correlated with skin and pulmonary involvement of SSc. There was no difference in vWF levels between those of the SSc patients and those of the control groups.
Conclusion
These results suggest that serum PIIINP serves as a biologic marker for the extent of skin and
pulmonary involvement in systemic sclerosis. Increased serum levels of sIL-2R in SSc patients
support a role for T lymphocyte activation in the pathogenesis of systemic sclerosis.
Key words
PIIINP, sIL-2R, vWF, systemic sclerosis.
This study was supported by a grant from Seoul National University.
Please address correspondence and reprint requests to: Yeong Wook Song, MD, Department of Internal Medicine, Seoul National University Hospital,
Yongon-dong 28, Chongno-gu, Seoul, Korea 110-744.
E-mail: ysong@snu.ac.kr
Clin Exp Rheumatol 2001; 19: 69-74.
© Copyright Clinical and Experimental
Rheumatology 2001.