Vitiligo is a common depigmenting skin disorder classified as an autoimmune ailment. It is linked to immune mechanisms, oxidative stress, and disturbances in the cellular environment. Among the factors contributing to histological changes, proteolytic enzymes such as collagenase stand out, due to their role in degrading components of the extracellular matrix. Prolidase is a key enzyme in collagen metabolism, involved in the breakdown of proline-rich peptides. Objective: This study aims to investigate the mechanism of collagen decline in Iraqi vitiligo patients, prolidase activity and basic homeostasis to understand their roles in disease progression. This study was conducted as a cross-sectional comparative study, and 150 participants were included in the present study, divided equally into three groups as follows: patients treated with Narrowband Ultraviolet B (NB-UVB) (PUV), a newly diagnosed group (PN) and an apparently healthy control group (C). The sample size was determined based on statistical power analysis (0.80), ensuring adequate comparison between groups using G Power. The collagenase level was measured using the ELISA immunological method, and prolidase activity was measured using the modified Chinchard’s method. Several biochemical parameters, including manganese (Mn2+), zinc (Zn2+), and calcium (Ca2+), were measured using colourimetric analysis. The results showed significant increases in collagenase level and prolidase activity of PUV as well as PN compared with the control (p < 0.001). The results indicated no significant difference in Mn2+ and Zn2+ levels between PUN,PN and control. However, a significant reduction in Ca2+ levels was observed in PUV compared to the control. According to the results, high collagenase levels and prolidase activity in the serum contribute to the development of vitiligo by weakening the skin structure in affected areas.
