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Coagulopathy and the prognostic potential of D-dimer in hyperlipidemia-induced acute pancreatitis
Ning Yang1, Dong-Lei Zhang, Jian-Yu Hao
1Department of Gastroenterology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China. haojianyucyyy@sina.com.
Insights
Hyperlipidemia-induced acute pancreatitis (AP) shows altered coagulation. D-dimer is a sensitive marker for AP severity, particularly in hyperlipidemia patients, indicating potential thrombosis risks.
Area of Science:
- Gastroenterology
- Hematology
- Metabolic Disorders
Background:
- Coagulopathy in acute pancreatitis (AP) and its link to hyperlipidemia (HL) remain unclear.
- Understanding coagulation homeostasis in AP is crucial for disease management.
Purpose of the Study:
- To evaluate the relationship between coagulation homeostasis and AP severity.
- To compare coagulation parameters in hyperlipidemia-induced AP (HLP) versus non-hyperlipidemia-induced AP (NHLP).
Main Methods:
- 106 AP patients were stratified by severity (mild vs. moderately severe) and etiology (HLP vs. NHLP).
- Coagulation parameters (D-dimer, protein C) and lipid metabolism were assessed.
- Correlations between disease severity, D-dimer, and protein C were analyzed.
Main Results:
- Moderately severe AP patients exhibited higher D-dimer and lower protein C levels than mild AP patients.
- HLP patients had higher protein C levels than NHLP patients.
- D-dimer and protein C levels correlated significantly with AP severity, independent of etiology. D-dimer also correlated with LDL cholesterol.
Conclusions:
- Coagulation homeostasis differs between HLP and NHLP, suggesting HL contributes to thrombosis/fibrinolysis in HLP.
- D-dimer serves as a robust marker for AP disease severity, especially in hyperlipidemia patients.
Background:
Coagulopathy and its association with disease severity in hyperlipidemia (HL)- and non-hyperlipidemia (NHL)-induced acute pancreatitis (AP) are not clear. The present study was to evaluate the relationship between coagulation homeostasis and AP.
Methods:
This study included 106 AP patients admitted to our hospital between October 2011 and January 2013. Stratified by disease severity, the patients were divided into two groups: a mild AP (MAP) group (n=69); and a moderately severe AP (MSAP) group (n=37). Based on disease etiology, there were 31 HL-induced AP (HLP) cases and 75 NHL-induced AP (NHLP) cases. The HLP and NHLP groups were compared for parameters of coagulation homeostasis, lipid metabolism, and disease severity. Correlations between disease severity and levels of D-dimer and protein C were investigated, and the prognostic potential of D-dimer was evaluated.
Results:
Compared with MAP patients, MSAP patients showed higher levels of D-dimer and lower levels of protein C. HLP patients had higher protein C levels than NHLP patients. Both D-dimer and protein C levels were significantly associated with the disease severity, not the disease etiology. D-dimer levels correlated positively with low density lipoprotein cholesterol levels and performed well as a sensitive and specific predictor of disease severity in AP patients, especially in HLP patients.
Conclusions:
The coagulation homeostasis is different between HLP and NHLP patients, and HL may be a contributing factor for thrombosis and fibrinolysis in HLP. D-dimer may be a robust marker of disease severity in HLP.
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