A Distinct Circulating Biomarker Signature of Acute Thrombophlebitis: Associations Among Heparin, Midkine, Pleiotrophin, Dermcidin, and Ghrelin.

Background

Acute superficial venous thrombosis (SVT) presenting with clinical features of thrombophlebitis is increasingly recognized as a thromboinflammatory disorder in which innate immunity and coagulation are closely interconnected. Nonetheless, the role of endogenous antimicrobial peptides and heparin-binding growth factors in its pathogenesis is still inadequately comprehended. We investigated circulating dermcidin (DCD), ghrelin (GHR), heparin (HP), midkine (MK), and pleiotrophin (PTN) to explore their potential involvement in the thromboinflammatory network underlying SVT.

Methods

In this prospective case-control study, 30 individuals with SVT and 28 healthy controls matched for age and sex were recruited. DCD, GHR, HP, MK, and PTN concentrations were quantified using enzyme-linked immunosorbent assays.

Results

Patients with SVT exhibited significantly higher circulating DCD, GHR, MK, and PTN concentrations and significantly lower the measured HP concentration than healthy controls (all p < 0.05). Following LMWH treatment, the measured HP concentration increased significantly (p < 0.05), whereas DCD, GHR, MK, and PTN showed downward trends.

Conclusions

Acute superficial venous thrombosis is associated with coordinated alterations in circulating the measured heparin, dermcidin, ghrelin, midkine, and pleiotrophin, reflecting a systemic thromboinflammatory biomarker profile. These findings suggest potential interactions among heparin biology, heparin-binding growth factors, and innate immune mediators but do not establish direct molecular interactions, heparin sequestration, functional depletion, or causality. This biomarker profile establishes a foundation for creating hypotheses for forthcoming investigations that include direct biochemical validation, standardized longitudinal sampling, and independent cohorts.