Clinical and Capillaroscopic Modifications of the Psoriatic Plaque during Therapy: Observations with Oral Acitretin

Psoriasis is considered to be an inflammatory autoimmune disease, where angiogenesis plays an undefined pathogenetic role. The well-known changes of the superficial microvasculature in the psoriatic plaque can be easily assessed in vivo by videocapillaroscopy. In the last years, several studies reported the clinical and capillaroscopic response of the psoriatic plaque during different topical and systemic treatments. In the present work we evaluated the effects of acitretin (0.8？mg/kg/day) on videocapillaroscopic alterations and the clinical response in 11 patients affected by plaque psoriasis at the baseline (T0) and after 4 (T1), 8 (T2), and 12 (T3) weeks. A clinical improvement during the treatment with a complete clinical healing of the plaque in 7 of the 11 patients was observed. The typical “basket-weave” capillaries of the psoriatic lesions showed a reduction of 65.4% in diameter at the end of the study; only 3 patients returned to a normal capillaroscopic pattern. As observed during previous our studies, we found a discrepancy between clinical and capillaroscopic results, with a far greater improvement in the first than in the second. This finding could be in agreement with a secondary role of blood vessels in the pathogenesis and persistence of psoriatic lesions. 1. Introduction Psoriasis is a chronic debilitating inflammatory dermatosis characterized by recurring well-demarcated reddish skin plaques covered with silvery scales. The histological hallmarks observed within psoriatic lesions include a thickened epidermis from rapid keratinocyte proliferation and aberrant differentiation, a reduced or absent granular layer, an increase of vascularity in the papillary dermis, and dense clusters of inflammatory cells composed of T cells and dendritic cells in the dermis and CD8+ T cells and neutrophils in the epidermis [1]. Among these changes, vascular alterations are thought to be the first to occur, thus supporting a fundamental role of angiogenesis and microangiopathy in the development of psoriasis through the promotion of an inflammatory response [1–3]. Several angiogenic mediators are involved in psoriasis including vascular endothelial growth factor (VEGF), hypoxia-inducible factors, angiopoietins, and proangiogenic cytokines, such as tumour necrosis factor (TNF), interleukin- (IL-) 8, and IL-17 [2]. Following the release of these molecules, the papillary dermal microvessels in psoriatic lesions show both functional changes (increased expression of inflammation-associated adhesion molecules such as E-selectin, intercellular adhesion