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Multicenter cross-sectional study investigates urinary excretion correlates of bone metabolism in adults, indicating significant relationships.
Background: Prostaglandin E2 (PGE2) is a key lipid mediator involved in inflammation and bone homeostasis. Its systemic production is reliably reflected by 24 h urinary excretion of PGE2 (U-PGE2) and its major metabolite (U-PGEM). However, the physiological association between systemic PGE2 production, calcium-phosphorus homeostasis and bone turnover markers remains unclear. This study aims to elucidate these relationships in a general Chinese adult population. Methods: In this multicenter, cross-sectional study, 737 Chinese adults underwent standardized 24 h urine collection. Multivariable linear regression was used to assess independent associations with bone metabolism markers. Restricted cubic spline models were further employed to examine nonlinear relationships. Results: The median 24 h U-PGE2 and U-PGEM excretion levels were 133.87 and 246.76 pg/mmol creatinine, respectively, with no significant sex differences (both p > 0.05). Multivariable regression analyses revealed that both 24 h U-PGE2 and U-PGEM were independently and positively associated with advancing age. Notably, both 24 h U-PGE2 and U-PGEM maintained a significant inverse association with serum calcium (Overall p < 0.05). Restricted cubic spline analyses further demonstrated a significant non-linear association between both 24 h U-PGE2 and U-PGEM and total procollagen type 1 N-propeptide (P1NP; both Overall p < 0.05). This relationship was characterized by a steep decline in U-PGE2 and U-PGEM excretion at lower P1NP concentrations, which subsequently plateaued at higher concentrations (Overall p < 0.05). Additionally, U-PGEM exhibited a significant inverse linear association with intact parathyroid hormone (PTH; Overall p < 0.05). Conclusions: This study provided valuable insights into the clinical determinants of 24 h U-PGE2 and U-PGEM in Chinese adults and their independent associations with calcium-phosphorus homeostasis and bone turnover markers.
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Lu et al. (2026) studied this question.
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