d-Dimer change in human acute pancreatitis as determined by serumal triglyceride.

OBJECTIVES: The aim of this present study was to investigate the d-dimer in acute pancreatitis and its associations with triglyceride (TG). METHODS: The d-dimer was measured in 45 patients with mild acute pancreatitis, 43 patients with severe acute pancreatitis, and 45 healthy controls. Eighty-eight patients were divided into high and low TG groups based on their TG levels. Twenty outpatients with serumal TG levels higher than 5.65 mM were chosen as hypertriglyceridemia controls. We investigated whether there were any correlations between the d-dimer levels and serumal TG in acute pancreatitis. RESULTS: In 45 patients with mild acute pancreatitis, the d-dimer increased to approximately 2 times over the reference value, whereas in 43 patients with severe acute pancreatitis, the d-dimer level increased to 6 times above the limit; the difference was significant. Both TG and acute pancreatitis could cause an elevation of the d-dimer level, in which TG takes a more important role. The increase in the d-dimer was also directly related to the severity of acute pancreatitis. CONCLUSIONS: Plasma concentrations of the d-dimer increase in acute pancreatitis. The increase in TG is probably the main cause of the d-dimer elevation in patients with acute pancreatitis.

[Serum D-dimer changes and prognostic implication in acute pancreatitis].

OBJECTIVE: To investigate the role of D-dimer in human acute pancreatitis (AP) and its relation to the severity of the disease. METHODS: Plasma concentration of D-dimer was measured in 31 patients with mild AP (MAP), 30 patients with severe AP (SAP) and 30 normal people as a control group. The results of routine laboratory tests, 48-hour Ranson and 24-hour APACHE II scores were all recorded. We attempted to find a relationship between D-dimer level and the results of routine laboratory tests, 48-hour Ranson scores and 24-hour APACHE II scores. RESULTS: (1) As compared with the control group, the plasma concentration of D-dimer was much higher in MAP (0.21 +/- 0.21) mg/L (P = 0.029) and SAP patients (0.69 +/- 0.32) mg/L (P = 0.000). The D-dimer level in the SAP group was higher than that in the MAP group (P = 0.000). (2) The rise in the D-dimer level was directly related to 48-hour Ranson (P = 0.000) and 24-hour APACHE II scores (P = 0.000). (3) The rise in the D-dimer level was directly related to leukocyte count, blood glucose, creatinine, prothrombin time and partial thromboplastin time (P < 0.05) and inversely related to hematocrit, albumin and calcium (P < 0.05). CONCLUSIONS: Plasma concentration of the D-dimer rises in AP patients; D-dimer level is related to the disease severity.