Acne vulgaris involves complex biochemical and immunologic mechanisms that extend beyond the traditional concepts of follicular obstruction and increased sebum production. Emerging evidence highlights the contribution of systemic lipid mediators-particularly sphingolipids-in influencing keratinocyte behavior, sebaceous gland activity, and inflammatory signaling pathways. Disturbances in circulating ceramides and their downstream metabolites may reflect dysregulated lipid homeostasis that parallels the clinical manifestations of acne.
In this study, specific attention is given to three sphingolipid biomarkers that have been increasingly linked to cutaneous biology: Ceramide C16, Ceramide C24, and Sphingosine-1-phosphate (S1P). These molecules participate in cell differentiation, apoptosis, and immune responses, and their altered levels may provide insight into acne-related metabolic shifts. By quantitatively assessing their serum concentrations in affected individuals and comparing them with healthy subjects, the study aims to characterize potential biochemical patterns associated with disease presence and activity.
All biological samples will be processed using a validated LC-MS/MS analytical platform to ensure precise measurement of each sphingolipid species. The findings may help to clarify whether systemic sphingolipid disturbances contribute to acne pathophysiology and could support the development of lipid-based biomarkers or therapeutic strategies in future dermatologic research.