Background Angiogenesis plays an important role in the pathogenesis of psoriasis. TNFa is an essential mediator that induces the expression of VEGF, which activates the endothelial cells, promoting angiogenesis.
Objectives Our aims were: a) to quantify the angiogenesis and the VEGF expression in healthy skin and in plaque psoriasis before and 6 months after starting adalimumab (ADA), and b) to correlate these parameters with clinical assessment scales.
Methods Prospective study of a series of patients with moderate/severe psoriasis who completed 6 months of treatment with ADA.Two biopsies of healthy skin and of plaque psoriasis were performed, one before starting ADA and the other was performed at 6 months. In each sample, an immunohistochemical study to VEGF, TNFα and CD31 was performed. Quantification of angiogenesis (CD31) was analyzed using an Automated Cellular Imaging sistem (DAKO).
Results Twenty three patients (13 W/10 M;mean age of 37±12 years) with a mean evolution of psoriasis of 19,9±13.1 years were included. Six patients also had (26%) arthritis. Comparison of clinical and histological parameters at baseline and 6 months of treatment with ADA shown in TABLE. At the baseline visit the following values were significantly higher in skin biopsy with psoriasis than in healthy skin: a) levels of angiogenesis (endothelial area positive-CD31): 2274,2±833,1 vs 810,61±425,2 (p<0.001); b) positive expression of VEGF: 87% vs 8,7% (p<0.001) y c) positive expression of TNFα: 82,6 vs 4,3% (p<0.001). A significant clinical and histological improvement in the expression of TNF, VEGF and angiogenesis was observed after treatment with ADA. The clinical parameters of psoriasis and angiogenesis (VEGF, TNF and CD31) only showed a significant correlation between the improvement in PASI and basal CD31. Thus, patients with lower baseline PASI had a greater response to therapy (r=0,590; p<0,003).
Conclusions In this series, ADA reduces the levels of VEGF and angiogenesis in plaque psoriasis. This fact seems to suggest that a part of their effect is due to inhibition of angiogenesis.
Disclosure of Interest None declared