## 4 Discussion  
New systematic treatment approaches for psoriasis are numerous with the aim to improve patients' quality of life; however, there is still a need for new therapeutic alternatives where these treatment modalities are not suitable. If the finding of this study could be confirmed by a wide clinical study, a new hypothesis could be made about the involvement of the platelets in the onset of this pathology, and the CGF could be a useful in vitro tool to evaluate the kinetic release of growth factors over time; moreover, it could simulate the psoriasis microenvironment in 2D and 3D human skin models. Nevertheless, this study presents some limitations that must be considered in the comprehensive evaluation of the obtained results during the case study. The first limitation is the evaluation of only one psoriasis subject, which is a case report. Thus, the researchers want to address a new hypothesis on the onset of this pathology considering the data of this study, which should be validated in the future. The second limitation is the presence of leucocytes in CGF, which can secrete TNF-\(\alpha\), VEGF, TGF-\(\beta\)1, and PDGF-AB. Thus, the data obtained cannot be associated with only one cell type even if, in this study, based on our previous morphological research, the contribution of platelets in the growth factor production was expected to be important [14; 19]. The quantitative count of the different cell types was hindered by the solid nature of CGF; the cells are entrapped in the fibrin network formed during the centrifugation without the aid of additives. Nevertheless, a study by [PERSON] et al. [16] evidenced a specific trend of VEGF release and an alteration of the fibrin  
Figure 2: Schematic diagram of the potential influence of growth factors from blood cells on keratinocytes in psoriasis. Growth factors released from CGF are altered in the presence of skin pathology. Generally, it greatly increased with psoriasis and decreased with vitltigo compared with the control. We could suppose that these cells may have inherent aberrations that make them particularly vulnerable to extracellular insult; thus, an alteration in the supply of trophic factors concurs with the onset of the pathology. network in the presence of leukocytes. Two different platelet-rich plasma preparations have been considered: leucocyte free and leucocyte rich. The release of different growth factors was evaluated in vitro over 8 days, and the availability of VEGF greatly decreased after 3 days and was almost absent on the 7 th day using the leucocyte-rich preparation. On the contrary, the VEGF kinetic release observed in our experiments on CGF was similar to the leucocyte-free preparation. Moreover, the fibrin network in the leukocyte-rich preparation resulted in a more heterogeneous and loose mesh, which was less evident in CGF during our previous studies [14]. The results obtained from V2 are valuable and important because they are usually difficult to obtain; they permit the description of the growth factor status in patients some days before symptoms onset. Our data showed a general increase in growth factors released that could sustain some hypotheses described in the scientific literature. Evidence for an in vivo platelet activation, which could contribute to the development of thrombotic events, has been established in psoriasis patients [4]. Recently, [PERSON] et al. [20] demonstrated a higher presence in the blood of psoriasis patients of microparticles derived from platelets, endothelial cells, and monocytes/macrophages compared with controls. Some markers of platelet activation, such as mean platelet volume (MPV), spontaneous platelet hyperaggregability, platelet factor 4, and plasma levels of \(\beta\)-thromboglobulin, were significantly higher in psoriasis patients. In contrast, platelet count and circulating platelet aggregates were normal.