Published online Oct 19, 2026. doi: 10.5498/wjp.121314
Revised: May 29, 2026
Accepted: July 1, 2026
Published online: October 19, 2026
Processing time: 203 Days and 6.9 Hours
Dysglycemia and hypercoagulability frequently coexist in psychiatric inpatients, elevating venous thromboembolism risks. However, the specific biological cascades connecting varied glycemic indicators to coagulation remain uncharacterized. We hypothesize that fasting plasma glucose (FPG), fructosamine (FA), and glycated hemoglobin (HbA1c) distinctly influence D-dimer-defined hypercoagulability through specific upstream multisystem pathways, primarily mediated by systemic inflammation.
To delineate the mechanisms linking multi-time-scale glycemic indicators to hypercoagulability via multisystem pathways using structural equation modeling (SEM).
In a retrospective cross-sectional study at Hangzhou Seventh People’s Hospital, we extracted electronic medical records of 4976 psychiatric inpatients. FPG, FA, and HbA1c were parallel exposures. We constructed a serial SEM to evaluate pathways connecting glycemia, multisystem nodes (lipids, blood pressure, inflammation, nutrition), coagulation substrates, and D-dimer hypercoagulability, ad
Among 4976 psychiatric inpatients (D-dimer positivity: 14.4%), the SEM demonstrated excellent fit, explaining 18.4% of D-dimer variance. FPG exerted a positive total effect on D-dimer positivity [standardized beta coefficient (Std.β) = 0.112], whereas FA showed a robust negative effect (Std.β = -0.196); Effects related to HbA1c were weak and largely failed to reach statistical significance. Mechanistically, glycemic indicators drove hypercoagulability predominantly via multisystem pathways. The inflammatory pathway most strongly influenced the coagulation substrate node (Std.β = 0.42), which inversely correlated with D-dimer (Std.β = -0.09). These mechanistic patterns remained highly consistent across schizophrenia, bipolar disorder, and major depressive disorder subgroups, alongside multiple sensitivity analyses. Finally, multi-indicator joint modeling outperformed single-indicator models, confirming robust study conclusions.
Glycemic indicators in psychiatric inpatients influence hypercoagulability via multisystem pathways. FPG increases risk, FA decreases it; HbA1c effects are limited. Inflammation is central to clinical risk assessment.
Core Tip: This study innovatively applies structural equation modeling to reveal how glycemic indicators across different time scales influence hypercoagulability, marked by D-dimer, in psychiatric inpatients. Fasting plasma glucose actively promotes hypercoagulability via inflammatory pathways. Conversely, fructosamine robustly protects against it, acting as a surrogate for nutritional and anticoagulant reserves rather than mere glycemic control. Glycated hemoglobin showed negligible direct acute effects. These findings shift the paradigm of psychiatric coagulopathy from a simplistic metabolic complication to a multi-system cascade, highlighting the necessity of integrated metabolic, inflammatory, and nutritional clinical assessments.