Abstract
Organ failure is the most important determinant of the severity of acute pancreatitis (AP). Soluble fms-like tyrosine kinase 1 (sFlt-1) is positively associated with organ failure in sepsis. Our aim was to evaluate the diagnostic utility of automated sFlt-1 measurements for early prediction of AP severity. Adult patients (66) with AP were recruited, including 46 with mild (MAP), 15 with moderately-severe (MSAP) and 5 with severe AP (SAP). Serum and urine samples were collected twice. Serum sFlt-1 was measured with automated electrochemiluminescence immunoassay. Serum concentrations of sFlt-1 were significantly higher in patients with MSAP and SAP as compared to MAP. SAP patients had the highest concentrations. At 24 and 48 h, sFlt-1 positively correlated with inflammatory markers (leukocyte count, C-reactive protein), kidney function (creatinine, urea, cystatin C, serum and urine neutrophil gelatinase-associated lipocalin, urine albumin/creatinine ratio), D-dimer and angiopoietin-2. sFlt-1 positively correlated with the bedside index of severity in AP (BISAP) score and the duration of hospital stay. Serum sFlt-1 above 139 pg/mL predicted more severe AP (MSAP + SAP). In the early phase of AP, sFlt-1 is positively associated with the severity of AP and predicts organ failure, in particular kidney failure. Serum sFlt-1 may be a practical way to improve early assessment of AP severity.
Highlights
Acute pancreatitis (AP) is the leading cause of hospital admissions due to gastrointestinal diseases in developed countries [1,2]
We have verified that the addition of severe acute pancreatitis (AP) (SAP) patients did not significantly change the moderately-severe AP (MSAP) group
All clinical characteristics related to the severity of the disease were significantly worse in MSAP + SAP group, resulting in more intensive treatment and a longer hospital stay (Table 1)
Summary
Acute pancreatitis (AP) is the leading cause of hospital admissions due to gastrointestinal diseases in developed countries [1,2]. The disease is mild; up to 20% develop the severe form, associated with persistent organ failure and high mortality [3]. Systemic inflammatory response syndrome (SIRS), diffuse endothelial activation and dysfunction and microcirculatory disorders are involved in the pathogenesis of organ failure in acute conditions, including AP [4,5,6]. Angiopoietin-2 (Ang-2), associated with endothelial dysfunction and vascular leakage in acute states [7], has been recently proposed as a marker of severity in AP [8,9,10]. Other markers of endothelial activation and dysfunction were shown to be increased in severe AP, including soluble E-selectin, tissue factor or von Willebrand factor and endothelial-specific microRNAs [5,11,12,13]
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