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Elevated Vascular Endothelial Growth Factor in Systemic Sclerosis

JIN-JUNG CHOI, DO-JUNE MIN, MI-LA CHO, SO-YOUN MIN, SEON-JOON KIM, SHIN-SEOK LEE, KYUNG-SU PARK, YOUNG-IL SEO, WAN-UK KIM, SUNG-HWAN PARK, and CHUL-SOO CHO

ABSTRACT.

Objective. To determine the serum levels of vascular endothelial growth factor (VEGF) in patients with systemic sclerosis (SSc) and to search for relationships between its serum levels and the clinical manifestations.

Methods. Serum levels of VEGF in patients with SSc and healthy controls were determined by ELISA. At the time of blood sampling, individual organ involvement was assessed, and a video microscope and PC based image processing were used to visualize nailfold capillaries and to quantify capillary density.

Results. Serum levels of VEGF in 48 patients with SSc were significantly higher than in 30 controls (432 ± 356 vs 91 ± 64 pg/ml; p < 0.001). Patients with diffuse cutaneous SSc (n = 21) had higher levels of serum VEGF than those with limited cutaneous SSc (n = 27) (432 ± 356 vs 135 ± 127 pg/ml; p < 0.001). Serum VEGF levels correlated well with the extent of skin sclerosis, as determined by modified Rodnan skin score (r = 0.656, p < 0.001) and serum TGF-ß levels (r = 0.530, p < 0.001). In particular, serum VEGF levels were inversely correlated with the capillary density of nailfold (r = –0.649, p < 0.001). However, no significant differences were found in the serum levels of VEGF between patients with systemic organ involvement and those without.

Conclusion. The extent of skin sclerosis may contribute to the elevation of serum VEGF and high VEGF levels may serve as a surrogate indicator of capillary damage in SSc. (J Rheumatol 2003;30:1529-33)

Key Indexing Terms:

SYSTEMIC SCLEROSIS
VASCULAR ENDOTHELIAL GROWTH FACTOR
RODNAN SKIN SCORE
CAPILLARY DENSITY
ANGIOGENESIS
NAILFOLD CAPILLARY MICROSCOPY


From the Department of Internal Medicine, Division of Rheumatology, St. Mary's Hospital, Research Institute of Immunobiology, Catholic Research Institutes of Medical Sciences, The Catholic University of Korea, Seoul; and Department of Internal Medicine, Chonnam National University Medical School, Kwangju, Korea.

Supported by grant R01-2000-00156 from the Basic Research Program of the Korea Science and Engineering Foundation.

J-J. Choi and D-J. Min are co-first authors. J-J. Choi, MD; D-J. Min, MD; M-L. Cho, PhD; S-Y. Min, PhD; S-J. Kim, BS, Division of Rheumatology, Catholic University of Korea; S-S. Lee, MD, Department of Internal Medicine, Chonnam National University Medical School; K-S. Park, MD; Y-I. Seo, MD; W-U. Kim, MD; S-H. Park, MD; C-S. Cho, MD, Division of Rheumatology, St. Mary's Hospital, Catholic University of Korea.

Address reprint requests to Dr. C-S. Cho, Department of Internal Medicine, Division of Rheumatology, St. Mary's Hospital, School of Medicine, Catholic University of Korea, 62 Youido-dong, Youngdeungpo-ku, Seoul, 150-713, Korea. E-mail: chocs@catholic.ac.kr

Submitted May 31, 2002; revision accepted December 28, 2002.




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