## 4 Discussion
The obtained results may indicate that circulating P-selectin in CD patients is mostly cleaved from the surface of platelets, while in UC, the main source of P-selectin could be the endothelial cells. Regarding the lack of significant difference in PLT count between patients with CD and UC, this hypothesis should be further analyzed. The performed analysis of the ROC curve in our study indicated that the P-selectin profile allowed [PERSON]'s disease to be differentiated from ulcerative colitis with a moderate value, indicating a potential use of this parameter in differential diagnosis. Moreover, another advantage of this biomarker is that the serum P-selectin level can reflect the risk of thrombotic events among patients with both CD and UC, as its level is related to the activation of platelets, often occurring during the course of IBD. The serum P-selectin level in healthy individuals usually equals 100 ng/mL, while in the CD group, the median level was 838.1 ng/mL, and 275.4 ng/mL in the UC group, indicating the increased activation of platelets in both CD and UC [12]. Another adhesive molecule that increased in the group of CD patients compared to UC patients is E-selectin, being expressed on the surface of endothelial cells. The observed increase in E-selectin in the serum of CD patients, together with the good ability of this biomarker of differentiating the CD from UC, demonstrates a potential use of this parameter in diagnosis of the diseases. The observed changes in E-selectin level between CD and UC patients may be explained by the study conducted by [PERSON] et al. 's [10], in which, upon exposure of the intestinal tissue collected from CD and UC patients to a proinflammatory medium, the expression of E-selectin increased 5.5 times in CD patients and 2 times in UC patients. These results indicate valid differences in the excess of E-selectin upregulation between CD and UC patients in response to the inflammatory microenvironment. One of the factors enhancing the expression of E-selectin is a well-known proinflammatory cytokine--IL-18--whose activation and release were enhanced in CD compared to UC in [PERSON] et al. 's study [20]. These results suggest that the activation and release of IL-18 are enhanced in CD compared to UC; therefore, the observed enhanced expression of E-selectin can be related to the upregulation of IL-18. Regarding the valid increase in E-selectin level upon exposition to the proinflammatory environment on the tissue level, as well as in the serum of CD patients compared to UC, this parameter might be used for the differential diagnosis of these two diseases. This suggestion can be further confirmed by the ROC curve analysis, which showed that E-selectin presented a moderate value of sensitivity and specificity in differentiating [PERSON]'s disease from ulcerative colitis. In the group of patients with CD, we also noted a significant increase in serum IL-1\(\alpha\) compared to the UC group. IL-1\(\alpha\) is expressed constantly in the epithelial cells; however, it can also be upregulated in response to different triggers such as oxidative stress, agonists of Toll-like receptors, and inflammatory cytokines including IL-18 [21]. Regarding the increased release of IL-18 from circulating mononuclear cells noted in the CD group compared to UC in [PERSON] et al. 's study [20], the elevation of IL-1\(\alpha\) during [PERSON]'s disease may also be triggered by the upregulation of IL-18. Another explanation for the increased IL-1\(\alpha\) in the serum of CD patients may be the interactions of P-selectin with leukocytes. The binding of P-selectin to its ligand on the surface of leukocytes may induce the generation of oxidative free radicals in neutrophils, which could serve as a potential source of oxidative stress triggering the release of IL-1\(\alpha\). Considering that IL-1\(\alpha\) is typically located inside cells, its extracellular location can indicate cell damage and trigger the inflammatory response.