Effects of low molecular weight heparin on inflammatory, coagulation, and immune markers in hyperlipidemic acute pancreatitis.

BACKGROUND

This study investigates the biochemical impact of low molecular weight heparin (LMWH) on key immunological, coagulation, and inflammatory markers in patients with hyperlipidemic acute pancreatitis (HLAP). The objective is to elucidate the role of LMWH in modulating serum immunoglobulins (IgA, IgG, IgM), coagulation parameters (PT, TT, FIB, APTT), proinflammatory cytokines (TNF-a, IL-6, IL-8), and digestive enzyme activity (amylase), thereby providing insight into its therapeutic mechanism.

METHODS

A total of 100 HLAP patients treated between January 2022 and December 2024 were assigned to a control group (CG) receiving standard medical treatment, and an experimental group (EG) receiving standard treatment plus LMWH. Biomolecular markers were analysed to assess changes in coagulation dynamics, inflammatory signalling, immunoglobulin response, and lipid metabolism. Comparative analysis between groups was conducted to evaluate the biochemical effects of LMWH.

RESULTS

Compared to the control group, the LMWH-treated group demonstrated significant reductions in inflammatory mediators: TNF-a decreased by 38.2%, IL-6 by 34.5%, and IL-8 by 36.7% (all P<0.01). Serum amylase and urinary amylase levels declined by 41.3% and 39.6%, respectively (P<0.01). Coagulation profiles improved with PT prolonged by 13.8%, TT by 15.2%, FIB reduced by 12.4%, and APTT normalised by a 17.1% increase (P<0.01). Immune markers IgA, IgG, and IgM increased by 22.5%, 26.3%, and 24.8%, respectively (P<0.01). Additionally, the LMWH group showed better lipid regulation (TG reduced by 45.7%) and a lower complication rate (6% vs. 22%, P=0.02).

CONCLUSIONS

LMWH exhibits a multifaceted biochemical effect in HLAP patients, encompassing anti-inflammatory action, immunomodulation, and correction of coagulation abnormalities. These findings support LMWH as a potential adjunctive therapeutic agent in the biochemical management of HLAP warranting further molecular studies to explore its mechanistic pathways.