Abstract
BACKGROUND: Endometriosis involves the presence of endometrial-like tissue outside the uterus, driven by inflammatory pathways including elevated interleukin-32 and vascular endothelial growth factor. One potential anti-inflammatory agent is active vitamin D (1,25(OH)(2)D(3)). OBJECTIVES: This research investigates the correlation among 1,25(OH)(2)D(3) levels, interleukin-32, and vascular endothelial growth factor in confirmed endometriosis cases. METHODS: This observational analytic correlational study aimed to explore the relationship between these inflammatory factors and vitamin D levels in endometriosis. The study involved 46 participants, with histopathologically confirmed endometriosis cyst tissue collected from patients undergoing laparotomy or laparoscopy at three hospitals: Dr. Hasan Sadikin Hospital Bandung, Cibabat General Hospital Cimahi, and Limijati Maternity and Children's Hospital. The levels of interleukin-32, vascular endothelial growth factor, and 1,25(OH)(2)D(3) were measured using the enzyme-linked immunosorbent assay method at the Clinical Pathology Laboratory of Dr. Hasan Sadikin Hospital Bandung. RESULTS: The study revealed significant negative correlations between 1,25(OH)(2)D(3) and both interleukin-32 (r = -0.346; p = 0.019) and vascular endothelial growth factor levels (r = -0.316; p = 0.032). Conversely, there was a significant positive correlation between vascular endothelial growth factor and interleukin-32 (r = 0.490; p = 0.001). CONCLUSIONS: These findings underscore the role of active vitamin D in mitigating inflammation associated with endometriosis by reducing interleukin-32 and vascular endothelial growth factor, critical factors in inflammatory responses and blood vessel formation. Moreover, the positive association between vascular endothelial growth factor and interleukin-32 highlights their collaborative role in the inflammatory processes underlying endometriosis. This study contributes to understanding how vitamin D may modulate key inflammatory pathways implicated in the pathogenesis of this condition.