BACKGROUND: Our study evaluated the expression of vascular endothelial growth factor (VEGF), CD31 and D2-40 in involved and uninvolved skin of 18 patients with rosacea. METHODS: Immunostaining of facial skin specimens with VEGF, CD31 and D2-40 was compared between the lesional and the non-lesional skin of patients with erythemotelangiectatic and papulopustular rosacea. RESULTS: Significantly increased dermal expression of VEGF in lesional vs. non-lesional skin (88.9% and 55.6%) was observed. Dermal expression of CD31 and D2-40 was also increased in lesional vs. non-lesional skin. There was no statistically significant difference in cutaneous expression of VEGF, CD31 and D2-40 between patients with papulopustular and erythemotelangiectatic rosacea, and no correlation was found between disease duration and immunoreactivity of VEGF, CD31or D2-40. CONCLUSIONS: Our study showed marked immunostaining of lesional skin with VEGF, CD31 and D2-40 compared with non-lesional skin. Increased immunoreactivity of D2-40 in lesional skin is interesting, given that none of the patients had facial edema. There are no published data regarding the role of lymphangiogenesis in patients with non-phymatous rosacea; thus, our study represents a new understanding of its pathogenesis. Lack of correlation between D2-40 expression and disease duration suggests that lymphatics are involved early in the pathogenesis of rosacea and do not constitute a late event.
BACKGROUND: Our study evaluated the expression of vascular endothelial growth factor (VEGF), CD31 and D2-40 in involved and uninvolved skin of 18 patients with rosacea. METHODS: Immunostaining of facial skin specimens with VEGF, CD31 and D2-40 was compared between the lesional and the non-lesional skin of patients with erythemotelangiectatic and papulopustular rosacea. RESULTS: Significantly increased dermal expression of VEGF in lesional vs. non-lesional skin (88.9% and 55.6%) was observed. Dermal expression of CD31 and D2-40 was also increased in lesional vs. non-lesional skin. There was no statistically significant difference in cutaneous expression of VEGF, CD31 and D2-40 between patients with papulopustular and erythemotelangiectatic rosacea, and no correlation was found between disease duration and immunoreactivity of VEGF, CD31or D2-40. CONCLUSIONS: Our study showed marked immunostaining of lesional skin with VEGF, CD31 and D2-40 compared with non-lesional skin. Increased immunoreactivity of D2-40 in lesional skin is interesting, given that none of the patients had facial edema. There are no published data regarding the role of lymphangiogenesis in patients with non-phymatous rosacea; thus, our study represents a new understanding of its pathogenesis. Lack of correlation between D2-40 expression and disease duration suggests that lymphatics are involved early in the pathogenesis of rosacea and do not constitute a late event.