Elevated Serum Creatinine as a Marker of Pancreatic Necrosis in Acute Pancreatitis

Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, UPMC Presbyterian Hospital, University of Pittsburgh School of Medicine, 200 Lothrop Street, Pittsburgh, PA 15213, USA.
The American Journal of Gastroenterology (Impact Factor: 10.76). 01/2009; 104(1):164-70. DOI: 10.1038/ajg.2008.66
Source: PubMed


Pancreatic necrosis is a serious complication of acute pancreatitis. The identification of simple laboratory tests to detect subjects at risk of pancreatic necrosis may direct management and improve outcome. This study focuses on the association between routine laboratory tests and the development of pancreatic necrosis in patients with acute pancreatitis.
In a cohort of 185 patients with acute pancreatitis prospectively enrolled in the Severity of Acute Pancreatitis Study, patients with contrast-enhanced computerized tomography performed were selected (n=129). Serum hematocrit, creatinine, and urea nitrogen on admission and peak values within 48 h of admission were analyzed. The volume of intravenous fluid resuscitation was calculated for each patient.
Of 129 patients, 35 (27%) had evidence of pancreatic necrosis. Receiver operating characteristic curves for pancreatic necrosis revealed an area under the curve of 0.79 for admission hematocrit, 0.77 for peak creatinine, and 0.72 for peak urea nitrogen. Binary logistic regression yielded that all three tests were significantly associated with pancreatic necrosis (P<0.0001), with the highest odds ratio, 34.5, for peak creatinine. The volume of intravenous fluid resuscitation was similar in patients with and without necrosis. Low admission hematocrit (< or =44.8%) yielded a negative predictive value of 89%; elevated peak creatinine (>1.8 mg/dl) within 48 h yielded a positive predictive value of 93%.
We confirm that a low admission hematocrit indicates a low risk of pancreatic necrosis (PNec) in patients with acute pancreatitis. In contrast, an increase in creatinine within the first 48 h is strongly associated with the development of PNec. This finding may have important clinical implications and warrants further investigation.

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    • "Some of them are: a) the Acute Physiology, Age and Chronic Health Evaluation (Apache II) [4] [7] [9] [14]; b) Structured Interview of Reported Symptoms (SIRS) [4] [9]; c) the Ranson score [4] [7] [9]; d) Bedside index for severity in AP (BISAP) (blood urea nitrogen >25mg/dl, impaired mental status, Systemic inflammatory response syndrome, age >60 years and pleural effusions) [2] [3] [15]; e) The Harmless Acute Pancreatitis Score (HAPS) (no rebound tenderness and/ or guarding, normal hematocrit and normal serum creatinine level) allows rapid identification of patients who present mild AP in 98% of cases; f) CT severity index (CTSI) based on local complications and percentage of pancreatic necrosis seen on a CT scan [2] [4] [5] [17] [18]. Various laboratory tests and biomarkers for predicting AP outcome have been described: a) elevated C-reactive protein (CRP) [1] [4] [13] [14] [19] [20]; b) elevated hematocrit (Ht) [5] [7] [14] [21] [22]; and c) high serum creatinine, as a doubtful predictor of pancreatic necrosis [23] [24]. Some of the recently described individual markers of severity include procalcitonin [25] [26] [27], urinary trypsinogen activation peptide, intra-abdominal hypertension (>15mmHg) [7], angiogenic factors [28] and interleukins (IL-6 and IL-8) [29]. "
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    ABSTRACT: Abstract None of the definitions of severity used in acute pancreatitis (AP) is ideal. Many of the scoring systems used to predict and measure its severity are complex, cumbersome and inaccurate. Aim to evaluate the usefulness of the most commonly used early markers for predicting severity, necrosis and mortality in patients with AP, and the need for surgery or Intensive Care Unit (ICU) admission. Material&methods Prospective study was performed from March 2009 to August 2010 based on patients diagnosed with AP seen consecutively at a secondary hospital. The early prognostic markers used were Apache II score ≥8 and Ranson’s score ≥3, RCP>120mg/l and Ht>44% in the first 24 hours. Results 131 patients were prospectively enrolled. Median age was 63 years, 60% were men. The most frequent etiology of AP was biliary (68%). Fifteen patients were admitted to the ICU (11.6%) and five (3.9%) required surgery. Twelve patients (9.2%) had necrosis on CT. Four patients (3%) died, all of them in the Severe AP group. Only hematocrit>44 was predictor of mortality in univariate analysis. Conclusion hematocrit ≥ 44% was a significant predictor of mortality. The other indicators present limitations for predicting severity, necrosis and mortality, especially in the first 24 hours.
    Full-text · Article · Aug 2014 · Central European Journal of Medicine
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    • "Some investigators report that the stressful condition with acute pancreatitis causes the diminished blood supply or hypoperfusion in the gastric mucosa, and the counter-diffusion of gastric hydrogen ion (H+) is an important factor for AGML as well [3], [4]. Other investigations discovered that the serum and ascitic fluid from AP patients and experimental animals contained a large amount of toxic substances, such as pancreatic enzymes, endotoxins, inflammatory mediators [5], [6], which may contribute to the multiple organ dysfunctions in acute pancreatitis [7], [8]. "
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    ABSTRACT: Acute pancreatitis (AP), especially severe acute pancreatitis often causes extra-pancreatic complications, such as acute gastrointestinal mucosal lesion (AGML) which is accompanied by a considerably high mortality, yet the pathogenesis of AP-induced AGML is still not fully understood. In this report, we investigated the alterations of serum components and gastric endocrine and exocrine functions in rats with experimental acute pancreatitis, and studied the possible contributions of these alterations in the pathogenesis of AGML. In addition, we explored the intervention effects of cannabinoid receptor agonist HU210 and antagonist AM251 on isolated and serum-perfused rat stomach. Our results showed that the AGML occurred after 5 h of AP replication, and the body homeostasis was disturbed in AP rat, with increased levels of pancreatic enzymes, lipopolysaccharide (LPS), proinflammtory cytokines and chemokines in the blood, and an imbalance of the gastric secretion function. Perfusing the isolated rat stomach with the AP rat serum caused morphological changes in the stomach, accompanied with a significant increment of pepsin and [H(+)] release, and increased gastrin and decreased somatostatin secretion. HU210 reversed the AP-serum-induced rat pathological alterations, including the reversal of transformation of the gastric morphology to certain degree. The results from this study prove that the inflammatory responses and the imbalance of the gastric secretion during the development of AP are responsible for the pathogenesis of AGML, and suggest the therapeutic potential of HU210 for AGML associated with acute pancreatitis.
    Preview · Article · Dec 2012 · PLoS ONE
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    ABSTRACT: Acute pancreatitis (AP) is a common and potentially lethal acute inflammatory process. Approximately 10-20% of patients develop a severe course and suffer systemic inflammatory response and/or pancreatic necrosis (PNec). To date, there is no single biomarker proven to perform better than clinical judgment in predicting severe AP. The available prognostic clinical scoring systems are used primarily for research purposes. Management of AP is limited to supportive care and treatment of complications when they develop. Patients with mild AP require regular ward admission, fluid administration, bowel rest and pain management. Patients with signs of severe AP should be identified early and admitted promptly to an intensive-care unit. Nutrition support via nasojejunal feedings should be initiated. Sterile PNec is managed conservatively. Infected PNec requires minimally invasive debridement via endoscopic or surgical approaches. The lack of scientific advancements in the management of AP reflects the limited understanding of the early pathogenetic mechanisms and our moderate-to-poor ability to predict severe course at the time of admission.
    No preview · Article · Sep 2009 · Expert review of gastroenterology & hepatology
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