Severe acute pancreatitis is related to increased early urinary levels of the activation peptide of pancreatic phospholipase A2

Mayer, Jens; Raraty, Michael; Slavin, John; Kemppainen, Esko; Fitzpatrick, John M.; Hietaranta, Antti J.; Puolakkainen, Pauli; Beger, H. G.; Neoptolemos, John P.

doi:10.1159/000066098

Cited by 12 publications

(8 citation statements)

References 50 publications

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“…This adds an interesting aspect to the assessment of this activation peptide in a way that urinary PLAP levels correlated with the systemic infl ammatory response as well [30] . A recent multicenter trial could show that urinary PLAP/PROP provides reasonable discrimination between mild and severe attacks achieving a sensitivity of 71% and a specifi city of 59% within 48 h of symptom onset [32] . However, urinary PLAP/PROP was of no value in predicting remote organ failure due to the rapid decline in the further course of the disease.…”

Section: Carboxypeptide Activation Peptidementioning

confidence: 99%

Laboratory Markers of Severe Acute Pancreatitis

Rau

Schilling

Beger

2004

Dig Dis

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Background: A large array of parameters has been proposed for the biochemical stratification of severity and prediction of complications in acute pancreatitis. However, the number of accurate and readily available variables for routine application is still limited. Methods: The literature was reviewed for laboratory markers of acute pancreatitis with special regard to their clinical usefulness and test performance for stratifying severity and monitoring disease progression. Results: Several parameters, such as trypsinogen and procarboxypeptidase B activation peptide, PMN-elastase, interleukin-6 (IL-6) and 8 (IL-8), serum amyloid A (SAA), and procalcitonin (PCT), can differentiate between mild and severe acute pancreatitis within 48 h of disease onset with favorable diagnostic accuracy. Because fully automated assays have become available, IL-6, IL-8, PCT, and SAA are the most interesting parameters in this respect. For monitoring disease progression beyond 48 h, acute-phase proteins, IL-6, IL-8, and PCT are valuable markers. PCT is the first biochemical variable for predicting severe pancreatic infections and overall prognosis throughout the course of acute pancreatitis with high sensitivity and specificity. Conclusions: Among all the biochemical variables available, C-reactive protein is still the standard for a fast, reliable, and cost-effective assessment of severity in acute pancreatitis. PCT substantially contributes to an improved stratification of patients at risk to develop major complications and deserves routine application.

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Section: Carboxypeptide Activation Peptidementioning

confidence: 99%

Laboratory Markers of Severe Acute Pancreatitis

Rau

Schilling

Beger

2004

Dig Dis

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“…It is generally recognized that the PLA2 content or activity rises when SAP occurs [25] . The abnormal release and activation of PLA2 can change lecithin into hemolytic lecithin, cause lysis and breakdown of pancreatic cell membrane, and lead to autodigestion of the pancreas [26][27][28] . The excessive free radicals generated in body during SAP may cause the accumulation of MDA, a lipid oxidative product.…”

Section: Discussionmentioning

confidence: 99%

Experimental study of therapeutic efficacy of Baicalin in rats with severe acute pancreatitis

Zhang

Zhang²,

He³

et al. 2007

WJG

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AIM:To observe the therapeutic efficacy of Baicalin in rats with severe acute pancreatitis (SAP) and explore its therapeutic mechanisms. METHODS:The SAP rat models were randomly divided into the model control group, Baicalin treatment group, octreotide treatment group and sham operation group. All groups were randomly subdivided into 3 h, 6 h and 12 h groups with 15 rats in each group. The survival, ascites volume and pathological changes of pancreas in all rats were observed at different time points after operation. The plasma amylase content and serum TNF-α, IL-6, malonaldehyde (MDA) and PLA2 contents were also determined. RESULTS:The survival was not obviously different between the treated groups, and was significantly higher in treated groups at 12 h compared to the model control group (P < 0.05, 15 vs 10). The ascites/body weight ratio at 3 h and 6 h was significantly lower in Baicalin treatment group compared to the model control group and octreotide treatment group (P < 0.05, 1.00 vs 2.02 and 1.43 and P < 0.001, 2.29 (1.21) vs 2.70 (0.80) and 2.08 (2.21), respectively). The contents of amylase, TNF-α, IL-6, MDA and PLA2 were significantly lower in the treated groups than in the model control group (P < 5.36 in IL-6, respectively). The pathological scores of pancreas in the treated groups were significantly lower than that in the model control group (P < 0.05, 9.00 vs 10.05, 6.00 vs 9.00, 8.00 vs 10.05), but no marked difference was found between the treated groups. CONCLUSION:The Baicalin injection has significant therapeutic effects on SAP rats, its effects are similar to those of octreotide. The Baicalin injection is also cheap and has a big application range, quite hopefully to be used in clinical treatment of SAP.

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“…During the initial phase, this organ dysfunction is caused by excessive mediator release rather than pancreatic infection [1••]. This response occurs very quickly after the onset of symptoms, as reflected in the high Acute Physiology and Chronic Health Evaluation (APACHE II) scores in these patients upon hospital admission [36][37][38][39].…”

Section: Natural Historymentioning

confidence: 99%

“…Several clinical, biochemical (inflammatory or pancreatic breakdown products), and radiologic prognostic scoring systems have been proposed to identify this group, but all have their limitations. The most useful is a combination of clinical assessment by an experienced physician and C-reactive protein greater than 150 mg/L at 48 hours, although urinary trypsinogen activation peptide or serum amyloid A may supersede this [38,39]. These clinical and biochemical parameters do not directly predict the extent of necrosis, which is best assessed by contrastenhanced computed tomography (CECT) [1••,37].…”

Section: Identification Of Those Who Have or Will Develop Severe Acutmentioning

confidence: 99%

Acute pancreatitis and organ failure: Pathophysiology, natural history, and management strategies

Raraty

Connor

Criddle

et al. 2004

Curr Gastroenterol Rep

Self Cite

105

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Acute pancreatitis is a common condition that carries a significant risk of morbidity and mortality. It is characterized by intra-acinar cell activation of digestive enzymes and a subsequent systemic inflammatory response governed by the release of proinflammatory cytokines. In 80% of patients the disease runs a self-limiting course, but in the rest, pancreatic necrosis and systemic organ failure carry a mortality rate of up to 40%. The key to management is early identification of the patients liable to have a severe attack and require treatment in a high-dependency or critical-care setting by a specialist team. In gallstone-induced pancreatitis, early removal of ductal calculi by endoscopic sphincterotomy is indicated. The use of prophylactic antibiotics to prevent the infection of pancreatic necrosis remains controversial, but once established, infected necrosis must be removed. Although a number of techniques to accomplish this end have been described, minimally invasive techniques are gaining in popularity.

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Severe acute pancreatitis is related to increased early urinary levels of the activation peptide of pancreatic phospholipase A2

Cited by 12 publications

References 50 publications

Laboratory Markers of Severe Acute Pancreatitis

Laboratory Markers of Severe Acute Pancreatitis

Experimental study of therapeutic efficacy of Baicalin in rats with severe acute pancreatitis

Acute pancreatitis and organ failure: Pathophysiology, natural history, and management strategies

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