scholarly journals Role of Biomarkers in Diagnosis and Prognostic Evaluation of Acute Pancreatitis

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Susanta Meher ◽  
Tushar Subhadarshan Mishra ◽  
Prakash Kumar Sasmal ◽  
Satyajit Rath ◽  
Rakesh Sharma ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Biochemical Markers ◽  
Necrotizing Pancreatitis ◽  
Pancreatic Tissue ◽  
Pancreatic Acinar Cell ◽  
Early Assessment ◽  
Prognostic Evaluation ◽  
Reactive Protein ◽  
Life Threatening

Acute pancreatitis is a potentially life threatening disease. The spectrum of severity of the illness ranges from mild self-limiting disease to a highly fatal severe necrotizing pancreatitis. Despite intensive research and improved patient care, overall mortality still remains high, reaching up to 30–40% in cases with infected pancreatic necrosis. Although little is known about the exact pathogenesis, it has been widely accepted that premature activation of digestive enzymes within the pancreatic acinar cell is the trigger that leads to autodigestion of pancreatic tissue which is followed by infiltration and activation of leukocytes. Extensive research has been done over the past few decades regarding their role in diagnosis and prognostic evaluation of severe acute pancreatitis. Although many standalone biochemical markers have been studied for early assessment of severity, C-reactive protein still remains the most frequently used along with Interleukin-6. In this review we have discussed briefly the pathogenesis and the role of different biochemical markers in the diagnosis and severity evaluation in acute pancreatitis.

scholarly journals Role of C-reactive protein in predicting the outcome of acute pancreatitis

2021 ◽  
Vol 9 (1) ◽  
pp. 165
Author(s):  
Venkatesh S. ◽  
Neetha V. ◽  
Manish S. ◽  
Krishnan P. B.
Keyword(s):  
Acute Pancreatitis ◽  
Clinical Practice ◽  
Scoring Systems ◽  
C Reactive Protein ◽  
Early Assessment ◽  
Serum Lipase ◽  
Protein Levels ◽  
Reactive Protein ◽  
Delayed Recovery

Background: Acute pancreatitis is one of the most commonly encountered clinical entities in surgical practice and controversy still exists regarding the clinical features of acute pancreatitis. An early diagnosis, however, is regarded as mandatory for successful treatment. Over the years many Authors have proposed different scoring systems for the early assessment of the clinical evolution of acute pancreatitis. The most widely used scoring systems are often cumbersome and difficult to use in clinical practice because of their multi factorial nature. Thus, a number of unifactorial prognostic indices have been employed in routine hospital practice, such as C-reactive protein (CRP), serum amylase and serum lipase. These serum enzymes are easy to obtain in normal clinical practice and many authors consider them as reliable as multi factorial scoring systems.Methods: A hospital based observational prospective study was done with 30 patients to measure C reactive protein levels in patients of acute pancreatitis and evaluate if CRP levels predict the severity of pancreatitis.Results: In cases where CRP was raised >100 mg/dl on day 7 and beyond showed either a complication or increased duration of stay and delayed recovery. This correspondence of CRP with the clinical outcome co related well with other parameters like blood counts, serum lipase and amylase levels too.Conclusions: Hence, CRP can be a very useful uni factorial tool in assessing and thereby predicting the outcome in a case of pancreatitis.

scholarly journals Assessment of BISAP Scoring System and C-Reactive Protein Analysis in Predicting Severity of Acute Pancreatitis

2021 ◽  
Vol 10 (35) ◽  
pp. 2985-2988
Author(s):  
Aditya Vasant Ghunage ◽  
Kiran Shrikant Kher
Keyword(s):  
Acute Pancreatitis ◽  
Sensitivity And Specificity ◽  
Necrotizing Pancreatitis ◽  
Scoring Systems ◽  
Cost Effective ◽  
Severity Index ◽  
C Reactive Protein ◽  
Key Words Acute Pancreatitis ◽  
Reactive Protein

BACKGROUND Acute pancreatitis (AP) is a dormant deadly illness. The range of seriousness of the ailment goes from mellow self-restricting disease to an exceptionally lethal severe necrotizing pancreatitis. The disease has such a variable course that it may manifest as a simple pain in the abdomen to severe haemorrhagic pancreatitis with septicaemic shock, multi-organ dysfunction syndrome and ultimately leading to death. A cost-effective better prognosticative index is needed for the assessment of the severity of AP. Here in this study, we wanted to assess the role of BISAP scoring systems and CRP for analysis and comparing their values to determine the severity of AP and the prognosis of the disease. METHODS A prospective observational study was done on 83 patients diagnosed with AP after fulfilment of inclusion criteria. Patients were subjected to severity index, bedside index for severity in acute pancreatitis (BISAP) score and CRP calculation and statistical analysis was done with SPSS software. RESULTS In our study, AP was more prevalent in males 87.95 % than females 12.05 %. AP was found to be more common in cases ≤ 40 years of age, however, the mean age of presentation was 38.14 ± 12.59 years. We calculated the sensitivity and specificity of the BISAP score and C-reactive protein (CRP) by co-relating it with CT severity index as gold standard according to which the sensitivity was found to be 64 % and specificity was found to be 85 % for BISAP. The sensitivity and specificity of CRP was 64 % and 85 % respectively. CONCLUSIONS BISAP is an easy way to anticipate the severity of AP within 24 hours. It also helps to prognosticate AP. CRP can also be used to aid BISAP in the assessment of severe acute pancreatitis (SAP). KEY WORDS Acute Pancreatitis, BISAP, CRP.

scholarly journals Impairment of PGC-1 Alpha Up-Regulation Enhances Nitrosative Stress in the Liver during Acute Pancreatitis in Obese Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 887
Author(s):  
Sergio Rius-Pérez ◽  
Isabel Torres-Cuevas ◽  
María Monsalve ◽  
Francisco J. Miranda ◽  
Salvador Pérez
Keyword(s):  
Acute Pancreatitis ◽  
Nitrosative Stress ◽  
Energy Charge ◽  
Pancreatic Tissue ◽  
Obese Mice ◽  
Antioxidant Genes ◽  
Regulated Expression ◽  
Distant Organ ◽  
Nos2 Expression

Acute pancreatitis is an inflammatory process of the pancreatic tissue that often leads to distant organ dysfunction. Although liver injury is uncommon in acute pancreatitis, obesity is a risk factor for the development of hepatic complications. The aim of this work was to evaluate the role of PGC-1α in inflammatory response regulation in the liver and its contribution to the detrimental effect of obesity on the liver during acute pancreatitis. For this purpose, we induced acute pancreatitis by cerulein in not only wild-type (WT) and PGC-1α knockout (KO) mice, but also in lean and obese mice. PGC-1α levels were up-regulated in the mice livers with pancreatitis. The increased PGC-1α levels were bound to p65 to restrain its transcriptional activity toward Nos2. Lack of PGC-1α favored the assembly of the p65/phospho-STAT3 complex, which promoted Nos2 expression during acute pancreatitis. The increased transcript Nos2 levels and the pro-oxidant liver status caused by the down-regulated expression of the PGC-1α-dependent antioxidant genes enhanced nitrosative stress and decreased energy charge in the livers of the PGC-1α KO mice with pancreatitis. It is noteworthy that the PGC-1α levels lowered in the obese mice livers, which increased the Nos2 mRNA expression and protein nitration levels and decreased energy charge during pancreatitis. In conclusion, obesity impairs PGC-1α up-regulation in the liver to cause nitrosative stress during acute pancreatitis.

Meta-analysis of the role of C-reactive protein in predicting severity of acute pancreatitis

Pancreatology ◽  
2013 ◽  
Vol 13 (2) ◽  
pp. e39-e40
Author(s):  
T. Jin ◽  
K. Altaf ◽  
J.J. Xiong ◽  
M.A. Javed ◽  
W. Huang ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Meta Analysis ◽  
C Reactive Protein ◽  
Reactive Protein

Platelet-Activating Factor Mediates Pancreatic Function Derangement in Caerulein-Induced Pancreatitis in Rats

1994 ◽  
Vol 87 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Ricardo Alonso ◽  
Angel Montero ◽  
Miguel Arévalo ◽  
Luis J. García ◽  
Concepción Sánchez-Vicente ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Platelet Activating Factor ◽  
Blood Platelet ◽  
Pancreatic Tissue ◽  
Portal Blood ◽  
Blood Levels ◽  
Inflammatory Infiltration ◽  
Subcutaneous Injections ◽  
Protein Output

1. We have assessed the role of platelet-activating factor in caerulein-induced acute pancreatitis (four subcutaneous injections of caerulein at a dose of 20 μg/kg) by measuring platelet-activating factor levels in portal blood, pancreatic tissue and peritoneal exudate in rats with and without pancreatitis. 2. We have also observed the effect of the platelet-activating factor antagonist, BN-52021, on the hyper-amylasaemia and exocrine pancreatic secretion impairment associated with pancreatitis. 3. In rats with pancreatitis the basal pancreatic flow rate was increased (1.63 ± 0.41 versus 0.25 ± 0.03 μl/min). Total protein output was similar in both untreated (5.98 ± 1.93 μg/min) and caerulein-injected (6.5 ± 2.0 μg/min) animals. Amylase output was lower in rats with pancreatitis (19.6 ± 4.8 μ-units/min) than in controls (39.4 ± 16.6 μ-units/min). 4. Caerulein-treated animals had significantly higher serum amylase levels than untreated animals. BN-52021 significantly reduced the caerulein-induced hyperamylasaemia. 5. Portal blood platelet-activating factor levels increased in rats with pancreatitis and in rats infused with cholecystokinin. Rats injected with caerulein and BN-52021 had portal blood levels of platelet-activating factor that were lower than those with pancreatitis. 6. Morphological derangements associated with pancreatitis (inflammatory infiltration and cell vacuolization) were also markedly reduced in BN-52021-treated animals. 7. The results of this study suggest that platelet-activating factor is involved in the development of caerulein-induced acute pancreatitis in rats.

Mechanisms of polyamine catabolism-induced acute pancreatitis

2007 ◽  
Vol 35 (2) ◽  
pp. 326-330 ◽  
Author(s):  
M.T. Hyvönen ◽  
M. Merentie ◽  
A. Uimari ◽  
T.A. Keinänen ◽  
J. Jänne ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Cathepsin B ◽  
Tissue Injury ◽  
Necrotizing Pancreatitis ◽  
Acinar Cells ◽  
Pancreatic Tissue ◽  
Early Event ◽  
Zymogen Activation ◽  
Polyamine Catabolism ◽  
Trypsinogen Activation

Acute pancreatitis is an autodigestive disease, in which the pancreatic tissue is damaged by the digestive enzymes produced by the acinar cells. Among the tissues in the mammalian body, pancreas has the highest concentration of the natural polyamine, spermidine. We have found that pancreas is very sensitive to acute decreases in the concentrations of the higher polyamines, spermidine and spermine. Activation of polyamine catabolism in transgenic rats overexpressing SSAT (spermidine/spermine-N1-acetyltransferase) in the pancreas leads to rapid depletion of these polyamines and to acute necrotizing pancreatitis. Replacement of the natural polyamines with methylated polyamine analogues before the induction of acute pancreatitis prevents the development of the disease. As premature trypsinogen activation is a common, early event leading to tissue injury in acute pancreatitis in human and in experimental animal models, we studied its role in polyamine catabolism-induced pancreatitis. Cathepsin B, a lysosomal hydrolase mediating trypsinogen activation, was activated just 2 h after induction of SSAT. Pre-treatment of the rats with bismethylspermine prevented pancreatic cathepsin B activation. Analysis of tissue ultrastructure by transmission electron microscopy revealed early dilatation of rough endoplasmic reticulum, probable disturbance of zymogen packaging, appearance of autophagosomes and later disruption of intracellular membranes and organelles. Based on these results, we suggest that rapid eradication of polyamines from cellular structures leads to premature zymogen activation and autodigestion of acinar cells.

Subcellular kinetics of early trypsinogen activation in acute rodent pancreatitis

1998 ◽  
Vol 274 (1) ◽  
pp. G71-G79 ◽  
Author(s):  
Kai Mithöfer ◽  
Carlos Fernández-Del Castillo ◽  
David Rattner ◽  
Andrew L. Warshaw
Keyword(s):  
Acute Pancreatitis ◽  
Cathepsin B ◽  
Necrotizing Pancreatitis ◽  
Subcellular Compartment ◽  
Trypsinogen Activation ◽  
Intracellular Compartments ◽  
Trypsinogen Activation Peptide ◽  
Kinetics Of ◽  
Pancreatic Edema

To investigate the debated role of intracellular trypsinogen activation and its relation to lysosomal enzyme redistribution in the pathogenesis of acute pancreatitis, rats were infused with the cholecystokinin analog caerulein at 5 μg ⋅ kg−1⋅ h−1for intervals up to 3 h, and the changes were contrasted with those in animals receiving saline or 0.25 μg ⋅ kg−1⋅ h−1caerulein. Saline or 0.25 μg ⋅ kg−1⋅ h−1caerulein did not induce significant changes. In contrast, 5 μg ⋅ kg−1⋅ h−1caerulein caused significant hyperamylasemia and pancreatic edema within 30 min. Pancreatic content of trypsinogen activation peptide (TAP) increased continuously (significant within 15 min). TAP generation was predominantly located in the zymogen fraction during the first hour but expanded to other intracellular compartments thereafter. Cathepsin B activity in the zymogen compartment increased continuously throughout the experiments and correlated significantly with TAP generation in the same compartment. Total trypsinogen content increased to 143% with marked interstitial trypsinogen accumulation after 3 h. Supramaximal caerulein stimulation causes trypsinogen activation by 15 min that originates in the zymogen compartment and is associated with increasing cathepsin B activity in this subcellular compartment. However, a much larger pool of trypsinogen survives and accumulates in the extracellular space and may become critical in the evolution of necrotizing pancreatitis.

Serum interleukin-6, interleukin-8, andβ 2-Microglobulin in early assessment of severity of acute pancreatitis comparison with serum C-reactive protein

1995 ◽  
Vol 40 (11) ◽  
pp. 2341-2348 ◽  
Author(s):  
Raffaele Pezzilli ◽  
Paola Billi ◽  
Rita Miniero ◽  
Manuela Fiocchi ◽  
Onda Cappelletti ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Interleukin 6 ◽  
Interleukin 8 ◽  
C Reactive Protein ◽  
Early Assessment ◽  
Reactive Protein

scholarly journals Aspirin Protects against Acinar Cells Necrosis in Severe Acute Pancreatitis in Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Guotao Lu ◽  
Zhihui Tong ◽  
Yanbing Ding ◽  
Jinjiao Liu ◽  
Yiyuan Pan ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Acinar Cell ◽  
Acinar Cells ◽  
Pancreatic Tissue ◽  
Pancreatic Acinar Cell ◽  
Cell Nuclei ◽  
Associated Proteins ◽  
Anti Inflammatory

Aspirin has a clear anti-inflammatory effect and is used as an anti-inflammatory agent for both acute and long-term inflammation. Previous study has indicated that aspirin alleviated acute pancreatitis induced by caerulein in rat. However, the role of aspirin on severe acute pancreatitis (SAP) and the necrosis of pancreatic acinar cell are not yet clear. The aim of this study was to determine the effects of aspirin treatment on a SAP model induced by caerulein combined with Lipopolysaccharide. We found that aspirin reduced serum amylase and lipase levels, decreased the MPO activity, and alleviated the histopathological manifestations of pancreas and pancreatitis-associated lung injury. Proinflammatory cytokines were decreased and the expression of NF-κB p65 in acinar cell nuclei was suppressed after aspirin treatment. Furthermore, aspirin induced the apoptosis of acinar cells by TUNEL assay, and the expression of Bax and caspase 3 was increased and the expression of Bcl-2 was decreased. Intriguingly, the downregulation of critical necrosis associated proteins RIP1, RIP3, and p-MLKL was observed; what is more, we additionally found that aspirin reduced the COX level of pancreatic tissue. In conclusion, our data showed that aspirin could protect pancreatic acinar cell against necrosis and reduce the severity of SAP. Clinically, aspirin may potentially be a therapeutic intervention for SAP.

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