ENDOPAIN4D assesment and platelet mediators in adenomyosis insights from thromboxane A2 and platelet activating factor

Abstract Adenomyosis is a common benign uterine disorder in women of reproductive age, often associated with pelvic pain, abnormal uterine bleeding, and infertility. Platelet-derived mediators such as thromboxane A2 (TXA 2 ) and platelet-activating factor (PAF) have been implicated in disease pathophysiology. However, their relationship with pain perception in adenomyosis remains incompletely understood. The cross-sectional nature of the available evidence limits conclusions regarding temporal or causal relationships between platelet-derived mediators and pain. This study aims to compare TXA 2 and PAF levels in adenomyosis and non adenomyosis uterine tissue. This cross-sectional study included 64 women aged 20–49 years, divided into an adenomyosis (n = 32) and non-adenomyosis uterine tissue (n = 32) groups. The comparison group consisted of women undergoing gynecological surgery whose uterine tissue showed no histopathological evidence of adenomyosis. Pain perception was assessed using the ENDOPAIN-4D questionnaire. Tissue levels of TXA 2 and PAF were measured using ELISA. Statistical analyses included t-tests or Mann–Whitney tests for group comparisons. TXA2 levels were significantly higher in adenomyosis tissue (287.26 ± 29.57 ng/L) compared to non-adenomyosis uterine tissue (177.33 ± 15.75 ng/L; p = 0.0001). PAF levels were also significantly higher in adenomyosis tissue (200.97 ± 22.83 ng/mL) compared to non-adenomyosis uterine tissue (128.52 ± 24.68 ng/mL; p = 0.0001). The observed differences indicate an association between adenomyosis and higher tissue levels of TXA2 and PAF but do not establish causality. TXA2 and PAF levels are elevated in adenomyosis tissue compared with non-adenomyosis uterine tissue. These findings suggest that TXA2 and PAF may be involved in the pathophysiology of adenomyosis; however, further studies are needed to clarify their mechanistic roles.