Abstract Acute Pancreatitis Research Articles

Serum levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in predicting the severity of acute pancreatitis.

Acute pancreatitis (AP) is a severe disease associated with significant morbidity and mortality. The overall outcome has improved, but specific treatment(s) remains elusive. The challenge is the early identification and treatment of patients who will develop severe acute pancreatitis. Therefore, the aim of the present study is to investigate plasma levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in the initial phase of predicted severe acute pancreatitis. Between June 2014 and January 2016, 64 patients with acute pancreatitis and 36 healthy individuals were included to study. Four blood samples, for serum TWEAK measurement, were taken from each individual in each group. The first measurement was taken from the admission blood sample. The subsequent three samples were taken at 12, 24, and 48h after the hospital admission. Serum TWEAK levels were significantly higher in patients with acute pancreatitis when compared with healthy controls. TWEAK plasma concentrations in severe pancreatitis patients were significantly higher than in mild pancreatitis patients. Serum TWEAK levels increase progressively with the severity of acute pancreatitis and TWEAK might be a novel early marker of severity in acute pancreatitis.

Prognostic evaluation of severity of acute pancreatitis: not as black as it is painted

Acute pancreatitis (AP) is a systemic disease involving acute inflammation of the pancreatic gland due to premature activation of pancreatic proenzymes and different degree of damage to the adjacent tissues and sometimes more distant organs. An increasing trend is observed with the incidence of AP approximately 72 cases/100,000 inhabitants per year (1).

The use of epidural analgesia in the treatment of acute pancreatitis

Acute pancreatitis (AP) is one of the most frequent gastrointestinal diseases requiring hospital of microcirculation and ischemia of the pancreas are the main causes of pancreatic necrosis. There is currently no specific therapy of acute pancreatitis. Symptomatic therapy admissions worldwide. AP has an overall mortality of 1%, increasing to 30% in its severe form. Violation focuses on aggressive rehydration, early nutrition, acceptable analgesia, oxygenation, and use of antibiotics is the main treatment for OP. Increasing evidence shows benefits of TEA in animal AP: improved splanchnic and pancreatic perfusion, improved pancreatic microcirculation, reduced liver damage, and significantly reduced mortality. This article provides an overview of research on the use of thoracic epidural anesthesia in the treatment of acute pancreatitis.

Protective Effects of Hydrogen Gas on Experimental Acute Pancreatitis

Acute pancreatitis (AP) is an inflammatory disease mediated by damage to acinar cells and pancreatic inflammation. In patients with AP, subsequent systemic inflammatory responses and multiple organs dysfunction commonly occur. Interactions between cytokines and oxidative stress greatly contribute to the amplification of uncontrolled inflammatory responses. Molecular hydrogen (H2) is a potent free radical scavenger that not only ameliorates oxidative stress but also lowers cytokine levels. The aim of the present study was to investigate the protective effects of H2 gas on AP both in vitro and in vivo. For the in vitro assessment, AR42J cells were treated with cerulein and then incubated in H2-rich or normal medium for 24 h, and for the in vivo experiment, AP was induced through a retrograde infusion of 5% sodium taurocholate into the pancreatobiliary duct (0.1 mL/100 g body weight). Wistar rats were treated with inhaled air or 2% H2 gas and sacrificed 12 h following the induction of pancreatitis. Specimens were collected and processed to measure the amylase and lipase activity levels; the myeloperoxidase activity and production levels; the cytokine mRNA expression levels; the 8-hydroxydeoxyguanosine, malondialdehyde, and glutathione levels; and the cell survival rate. Histological examinations and immunohistochemical analyses were then conducted. The results revealed significant reductions in inflammation and oxidative stress both in vitro and in vivo. Furthermore, the beneficial effects of H2 gas were associated with reductions in AR42J cell and pancreatic tissue damage. In conclusion, our results suggest that H2 gas is capable of ameliorating damage to the pancreas and AR42J cells and that H2 exerts protective effects both in vitro and in vivo on subjects with AP. Thus, the results obtained indicate that this gas may represent a novel therapy agent in the management of AP.

Translational Insights Into Peroxisome Proliferator-Activated Receptors in Experimental Acute Pancreatitis.

Acute pancreatitis (AP) is an inflammatory disorder of the exocrine pancreas frequently associated with metabolic causes, contributing factors, or consequences, including hypertriglyceridemia, obesity, and disorders of intermediary metabolism, respectively. To date, there is no specific therapy for this disease. Future optimal therapy should correct both inflammatory and metabolic components of the disease. Peroxisome proliferator-activated receptors (PPARs) are lipid-sensing nuclear receptors that control inflammatory and metabolic pathways via ligand-dependent and ligand-independent mechanisms. There are 3 known subtypes, PPAR-α, PPAR-β/δ, and PPAR-γ, which are differentially expressed in various tissues. The PPARs interact closely with other transcription factors such as nuclear factor κB and signal tranducers and activators of transcription that have pivotal roles in the pathobiology of AP. In this comprehensive review, we summarize the role of PPARs in AP, highlighting important in vitro and in vivo experimental findings. Finally, we propose future research directions as well as potential translational use of PPAR agonists in the treatment of AP.

The Role of MRCP on Management of the Acute Biliary Pancreatitis

Acute pancreatitis (AP) an acute inflammation of the pancreas, is the most common cause of admission to hospital because of acute gastro-intestinal tract in the USA. In etiology, factors such as cholelithiasis, alcohol, drugs, hypertriglyceridemia, and sphincter of oddi dysfunction play a role. Acute biliary pancreatitis (ABP) constitutes %40 of all pancreatitis cases. The management of patients with ABP are vital for the cases in which choledocholithiazis exists. This review focuses on the management of such patients. The timing of ERCP and the use of MRCP was investigated in this review. For this review, various studies and reviews were critically evaluated.

Acute Pancreatitis

Acute pancreatitis (AP) is defined as the presence of two of the following findings: (1) upper abdominal pain; (2) serum amylase or lipase greater than three times the upper limit of normal; and/or (3) characteristic findings of AP on abdominal imaging (contrast-enhanced computed tomography, magnetic resonance imaging, or abdominal ultrasonography). This review addresses AP, detailing the subclassification, epidemiology, pathophysiology, etiology, diagnosis and differential diagnosis, treatment, complications, and prognosis. Figures include abdominal imaging of patients with AP, an algorithm depicting pancreatic collections, and an endoscopic image of the gastric portion of the cystogastrostomy. Tables list systemic inflammatory response syndrome; classification of the severity of AP; etiologies of AP, gallstones, biliary sludge, microlithiasis, and crystals; secondary causes of hypertriglyceridemia; common drugs and drug classes associated with AP; conditions mimicking AP; diagnostic criteria for infected necrosis; and prognostic scoring systems for AP. This review contains 3 highly rendered figures, 9 tables, and 182 references.

Early Cytokine Profile Changes In Interstitial And Necrotic Forms Of Acute Pancreatitis

ABSTRACT Acute pancreatitis (AP) is a common, potentially lethal, acute inflammatory process with a highly variable clinical course. The aim of this study was to analyse early changes in the serum concentrations of pro- and anti-inflammatory cytokines in the peripheral blood of patients with the interstitial form of acute pancreatitis (IAP) and necrotic acute pancreatitis (NAP), especially in those patients who had lethal outcomes. The prospective study enrolled 52 patients who were divided into IAP (65.38% of patients) and NAP (34.62% of patients) groups. The serum levels of interleukins (IL) 6, 8 and 10, together with tumour necrosis factor (TNF)-alpha were measured on the 1st and 3rd day of hospitalisation. Significantly higher values of IL-6, IL-8 and IL-10 were found on day 1 and 3 in NAP than in IAP. IL-6 was significantly higher on both days of measurement, whereas IL-10 on the first day and IL-8 on the third day were significantly higher in the group of patients who did not survive in comparison with patients who had the interstitial form of AP. In conclusion, the data from this study showed that immune suppression and excessive immune stimulation in the first three days after admission could indicate the development of NAP and a potentially lethal outcome.

The Effect of Atorvastatin on Acute Pancreatitis in Rat: Biochemical and Pathological study

Acute pancreatitis (AP) is a common clinical disease caused mainly by gallstone impacting the distal common bile-pancreatic duct and alcohol abuse, but other potential causes as Endoscopic retrograde cholangiopancreatography (ERCP), intra duct papillary mucinous tumor and hypercalcemia are claimed . The incidence of AP has been increasing in recent years . Accordingly, AP is a multifactorial disease associated with tissue edema, acinar necrosis, hemorrhage and the release of digestive enzymes to the pancreatic interstitium and to the systemic circulation with increased cytokine production and release, which can ultimately lead to deleterious local and systemic effects . Previous evidence suggests that the pathogenesis of both AP and chronic pancreatitis can be associated with oxidative stress, regardless of the etiology of pancreatitis and is considered as a major pathogenic factor in AP . In fact, reactive oxygen species (ROS) are the important mediators in the initiation and development of the disease which destroy the cellular membrane, releasing the digestive enzymes and cellular proteins into the pancreatic interstitium .

Acute Pancreatitis and Splenic Vein Thrombosis due to Hypertriglyceridemia.

Acute pancreatitis (AP) is a condition characterised by the activation of the normally inactive digestive enzymes due to an etiological factor and digestion of the pancreatic tissues, resulting in extensive inflammation and leading to local, regional, and systemic complications in the organism. It may vary from the mild edematous to the hemorrhagic and severely necrotising form. The most common causes are biliary stones and alcohol abuse. In this case study, we would like to present a patient with AP due to hypertriglyceridemia (HPTG), which is a rare cause of pancreatitis, and splenic vein thrombosis, which is a rare complication of pancreatitis.

Ischemia-reperfusion rat model of acute pancreatitis: protein carbonyl as a putative early biomarker of pancreatic injury.

Acute pancreatitis (AP) is an inflammatory disorder that can affect adjacent and/or remote organs. Some evidence indicates that the production of reactive oxygen species is able to induce AP. Protein carbonyl (PC) derivatives, which can also be generated through oxidative cleavage mechanisms, have been implicated in several diseases, but there is little or no information on this biomarker in AP. We investigated the association between some inflammatory mediators and PC, with the severity of ischemia-reperfusion AP. Wistar rats (n=56) were randomly assigned in the following groups : control; sham, 15- or 180-min clamping of splenic artery, with 24 or 72h of follow-up. The relationships between serum level of PC and thiobarbituric acid reactive species (TBARS) to myeloperoxidase (MPO) activity in tissue homogenates and to cytokines in culture supernatants of pancreatic samples were analyzed. MPO activity was related to the histology scores and increased in all clamping groups. Tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), and interleukin-6 were higher in the 180-min groups. Significant correlations were found between MPO activity and the concentrations of TNF-α and IL-1β. PC levels increased in the 15-min to 24-h group. TBARS levels were not altered substantially. MPO activity and TNF-α and IL-1β concentrations in pancreatic tissue are correlated with AP severity. Serum levels of PC appear to begin to rise early in the course of the ischemia-reperfusion AP and are no longer detected at later stages in the absence of severe pancreatitis. These data suggest that PC can be an efficient tool for the diagnosis of early stages of AP.

Analysis of the power of common diagnostic tools in the management of acute pancreatitis.

Acute pancreatitis (AP) is a serious medical condition usually associated with severe upper abdominal pain. The purpose of our study is to assess the therapeutic consequences of contrast-enhanced computed tomography (CE-CT) and the predictive value of CRP for severe pancreatitis. We included patients with a threefold increase of plasma lipase who had received a CE-CT or had a CRP of =150 mg/dl. A total of 74 out of 283 patients got a contrast-enhanced CT scan; in 11 cases the CT was followed by endoscopic or surgical interventions as therapeutic consequences compared with 19 out of 50 control cases. 69 out of 283 patients (24,3%) had CRP >150 mg/dl within 48 hours after admission. 32 of them had SAP. The CRP cutoff of 150 mg/L had a sensitivity of 80% and a specificity of 65%. The positive predictive value for SAP in patients beyond the cutoff is 46.4%. The negative predictive value for SAP in patients below the cutoff was 89.5%. Our results support the opinion that an early CE-CT is usually not indicated. CRP helps to assess the course of AP; levels below 150 mg/dl between the first 48 h indicate a mild course in most of the cases.

P55 Endogenous hydrogen sulfide ameliorates secretory phospholipase A2 (sPLA2)-induced acute pancreatitis model in the rat

Acute pancreatitis (AP), a painful and inflammatory disease of the pancreas, is one of the most common patient gastrointestinal diseases worldwide, but there is still no effective pharmacological treatment. It is usually associated with high serum concentrations of phospholipase A2 (PLA2). Recently, it has been suggested that the endogenous gasotransmitter hydrogen sulfide (H2S) acts as a mediator of acute pancreatitis. Endogenously, H2S is produced as a metabolite of homocysteine (Hcy) by cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST). This study aimed to investigate the effects of endogenous H2S in a model of AP in rats. AP was evoked by injection of secretory PLA2 from Crotallus durrisus terrificus (Cdt; 300 mg/kg) snake venom into the common bile duct of rats pretreated with an inhibitor of CSE, propargylglycine (Pgly; 50 mg/kg; i.p., −30 min) or vehicle (0.1 ml). Four hours later, rats were submitted to abdominal nociceptive behavioral test (von Frey) and euthanized. Blood and pancreas were collected and processed to measure plasma amylase, H2S generation and inflammatory parameters (oedema, myeloperoxidase activity) in pancreas. Treatment with PGly markedly reduced inflammation in the pancreas of rats with pancreatitis, but neither increased serum amylase nor abdominal hyperalgesia was affected by this treatment. The kinetics of H2S generation over 60 min in pancreas revealed that CSE and CBS are both expressed in naive pancreas tissue, and a significant difference is seen between control and inflamed pancreas. Inhibition of CSE and CBS reduces H2S generation in pancreas. We conclude that endogenous gaseous messenger molecule H2S plays a functional role in mediating microvascular and cellular changes (oedema and cell influx) in the pancreas, but not the related nociceptive mechanisms of PLA2-induced AP.

Clinics related to acute pancreatitis wonder whether IFN-γ can attenuate pancreatic injury or not

Acute pancreatitis (AP) is an inflammatory disease of the pancreatic tissue associated with little or no fibrosis of the gland. Continued clinical and experimental studies/trials are important for understanding AP pathogenesis and its current treatment approaches. Meng et al. [ 1 ] contribute to our knowledge on NF-κB and cytokines IL-18 and IL-27 in experimental AP at 6 h, 12 h, 24 h and 48 h after IFN-γ treatment. However, the messages are implicit both in presentation of results and in the paper itself are complicated by the fact that is likely to be data interferences in relation to AP treated with IFN-γ. For instance, the conclusion that “ the increase in NF-κB and 1L-18 may exert influence on pro-inflammatory cytokines to deteriorate inflammation in the pancreas. Thus, to control the IFN-γ might has promise to attenuate pancreatitis… IFN-γ treatment might be associated with JAK-STAT mediated transcription activation ” is based on a speculative opinion. There are just similar sentences taken from different articles excepting for cited references in introduction section, the amount of the application dose for IFN-γ is unknown and the authors are no interpretation their own findings on discussion section in this study. According to this study, serum amylase level, the edema, the NF-κB and TNF-a expression in the pancreas were significantly increased in the treatment of IFN-γ after AP. As a result of these findings, the application of IFN-γ can cause a deleterious effect within the pancreas in the course of AP. On the other hand, Hayashi et al. [ 2 ] reported that recombinant murine IFN-γ therapy markedly alleviated acute pancreatitis when administered 4 hours in mice, with reduced NF-κB activation and COX-2 expression. Thus, IFN-γ may possess anti-inflammatory effects on AP by repression of the proinflammatory consequences of NF-κB activation. In addition, Rau et al. [ 3 ] have indicated that immunostimulative treatment with recombinant rat IFN-γ attenuated the progression of intrapancreatic necrosis within the first 24 hours after AP induction along with a substantial reduction of subsequent neutrophil tissue infiltration and decreased TNF-a at the late stage of AP. Moreover, plasma IFN-γ concentration is known to increase at the early stage of disease in mild and severe AP patients compared with healthy controls. Therefore, immunostimulative regime could be more effective during the late stage of this disease when infectious complications and immunoparalysis might be a dominant cause of mortality in the course of AP. Actually, pharmacological therapies are limited in the treatment of AP, and none of the therapeutic agents used for therapy are effectively curative. Regardless of AP severity, hospitalization of the patients with suspected acute pancreatitis for observation and diagnostic study is generally mandatory. After the diagnosis, patients with moderate to severe disease should be transferred to the ICU for observation, and supportive treatments and interventions. Treatment may change depending on the etiology and severity of the disease. Antibiotic therapy, peritoneal lavage, sphincterotomy with ERCP and even surgical operations can be applied [ 4 , 5 ]. Novel effective therapeutic strategies in the treatment of AP may be evolved.

Cannabinoid HU210 Protects Isolated Rat Stomach against Impairment Caused by Serum of Rats with Experimental Acute Pancreatitis

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.

Laparoscopic Pancreatic Necrosectomy in a Child with Severe Acute Pancreatitis

Acute pancreatitis (AP) in children usually follows a mild course but occasionally may be severally problematic. We report the case of a 12-year-old boy with severe AP who was managed with repeated laparoscopic pancreatic necrosectomy. Three weeks later he represented with a pancreatic pseudocyst that was treated with endoscopic gastrocystotomy. His abdominal pain persisted and a subsequent magnetic resonance cholangiopancreatogram showed multiple gallbladder and common bile duct (CBD) stones that were missed on previous imaging investigations. He underwent laparoscopic cholecystectomy with transcystic exploration of the CBD. The patient is currently well, more than 2 years following the definitive corrective surgery. To the best of our knowledge, this is the first case of laparoscopic pancreatic necrosectomy in a child.

Honokiol attenuates the severity of acute pancreatitis-associated lung injury by acceleration of acinar cell apoptosis

Acute pancreatitis (AP) is a complicated immunological response that leads to multiple organ failure. Apoptosis is a beneficial form of cell death in AP. Acute lung injury is the most severe complication. Honokiol (HK) is a component of Asian herbal teas. It displays an anti-inflammatory and apoptotic induction effect. In the experiments, we investigated the therapeutic efficacy of HK in AP.

Acute pancreatitis in a pregnant female with peripartum cardiomyopathy

Abstract Acute pancreatitis (AP) and peripartum cardiomyopathy (PPC) are rare complications during pregnancy and can lead to high maternal mortality and fetal loss. We report a case of a 34-year-old multigravida at 36 weeks gestation diagnosed to have AP who delivered a cyanosed fetus. Subsequently, she developed PPC and recovered on conservative treatment.

Current management and novel insights in acute pancreatitis

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.

Monocyte and neutrophil direct counts correlate with C-reactive protein plasma concentration in patients with acute pancreatitis

Abstract Acute pancreatitis (AP) is associated with the intensive inflammatory response in white blood cells (WBC) and C-reactive protein (CRP). This paper presents the relationship between the CRP plasma concentration and the direct counts of peripheral WBC in AP during the initial five days. The study consisted of 56 patients with AP, 36 patients with mild form of AP and 20 patients with severe form of AP. ABX VegaRetic hematological analyzer was used to perform the count of blood cells, and the immunonephelometric method was performed to measure the CRP concentration levels. AP patients presented with WBC count values in the range of 3.2 − 22.4 × 103/µl and CRP concentration levels in the range 3.3 − 599.8 mg/l. The WBC count correlates with CRP levels during the entire observation period. The relationship of CRP and WBC is expressed in the following regression equation: WBC (103/µl) = 3.66 + 1.40 × logeCRP (mg/l). The highest median neutrophil count (8.15 × 103/µl) was observed on the first day. The count decreased to 5.27 × 103/µl on the fifth day. The most substantial finding in this study involved the values found for the monocytes and CRP (r= 0.53; p<0.001). Day two and day three were the highest (r=0.59, p<0.001). On day two, the regression equation for this relationship is: Monocytes (103/µl) = −0.34 + 0.21 × logeCRP(mg/l). The correlation between direct monocyte count and plasma CRP concentration in AP reflect a CRP-dependent stimulation of IL-6 release from activated blood monocytes.