Article

AGA Institute Technical Review on Acute Pancreatitis

Wake Forest University, Winston-Salem, North Carolina, United States
Revista de gastroenterologia de Mexico 05/2007; 72(3):257-85. DOI: 10.1053/j.gastro.2007.03.065
Source: PubMed
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    • "Acute pancreatitis (AP) is a common inflammatory disease, most of which presents with mild acute pancreatitis (MAP), a self-limited systemic inflammation, but 10-15% occur in patients with severe acute pancreatitis (SAP), multiple organ failure, pancreatic necrosis with infection , with a mortality rate up to 30-47%[1,2]. The current ideal drug for the treatment of SAP is still in need and standardized treatment of consensus is only confined to fluid therapy, nutritional support, treatment of necrosis and infection, endoscopic procedures of biliary stones[3,4]. "
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    ABSTRACT: Mesenchymal stem cells (MSCs) have shown an obvious protective effect on systemic inflammation. The purpose of this study is to assess the effect and possible mechanism of bone marrow MSCs (bmMSCs) on acute pancreatitis (AP). BmMSCs of SD rats were isolated and cultured in vitro. L-Arginine-induced acute pancreatitis was used as AP model in vivo. Pancreatic injury was assessed by serum amylase, lipase, cytokines and pancreatic histology. RT-PCR was applied to investigate mRNA expression of pancreas tissue. Western-blot and immunohistochemistry (IHC) were applied to test the role of NF-κB p65 signaling pathway. Tracking and Positioning of CM-Dil labeled bmMSCs in vivo was further studied. Treatment with bmMSCs attenuated acute pancreatic injury and AP-associated lung injury obviously, with decreased serum IL-1β, IL-6, TNF-α, down-regulated expressions of IL-1α, IL-6, TNFα in pancreas tissue and reduced nuclear translocation of NF-κB p65 in AP. Localization of bmMSCs in vivo was due to being passively trapped in related organs, but not actively homing to inflammatory sites of pancreas during the early phase of AP. Taken together, the results showed that bmMSCs played a protective role in AP in many aspects, which might protect against experimental pancreatitis partly by regulating release of inflammatory cytokines by an exocrine secretion.
    Full-text · Article · Jul 2015 · International journal of clinical and experimental pathology
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    • "Acute pancreatitis (AP) is an acute inflammatory process of the pancreas. Currently, it is the leading cause of gastrointestinalrelated admissions in the United States placing an extensive burden on the health care system [1] [2]. It is associated with acute onset of symptoms such as epigastric pain that radiates to the back, nausea, and vomiting. "
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    ABSTRACT: Endoscopic retrograde cholangiopancreatography (ERCP) is a widely used therapeutic endoscopic procedure with small risk of complications. The most common and dreadful complication is post-ERCP pancreatitis (PEP). Concerning the definition of PEP itself and classification of its severity, there is still some ambiguity. The most commonly used definition is the one proposed in the 1991 consensus, although there are indications that the current clinical definition and the two new severity classifications, namely the revised Atlanta (RAC) and the Determinant-Base Classification (DBC) are more accurate in diagnosing and classifying PEP respectively. Pathogenesis-wise, although the inflammatory cascade after trypsin activation is the same regardless of the etiology and has been studied intensively over the last few years, the data on the initial pancreatic insult in PEP is scarce. Several factors have been proposed as the first trigger to include mechanical trauma and/or thermal injury to the papilla, high hydrostatic pressure in the pancreatic duct (PD), contrast-induced injury, and/or contamination of the PD by intestinal flora. The authors impression is that the onset of PEP is likely multifactorial, a combination of the above mechanisms in an already susceptible subject carrying, yet to be identified, environmental and/or genetic risks. Trypsin is the main digestive, but also regulatory, enzyme that activates the rest of the zymogens. Intrapancreatic activation of trypsinogen results in pancreatic autodigestion and a subsequent burst of cytokine release that may progress to either a local or a systemic inflammatory response.
    Full-text · Article · Oct 2014 · Techniques in Gastrointestinal Endoscopy
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    • "The latter is associated with a 35% to 50% mortality rate [8,9]. Accurate prediction of persistent OD is needed because these patients will benefit from general supportive care, including early fluid resuscitation, in the ICU [10,11]. "
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    ABSTRACT: Introduction Severe acute pancreatitis (AP) is associated with high morbidity and mortality. Early prediction of severe AP is needed to improve patient outcomes. The aim of the present study was to find novel cytokines or combinations of cytokines that can be used for the early identification of patients with AP at risk for severe disease. Methods We performed a prospective study of 163 nonconsecutive patients with AP, of whom 25 had severe AP according to the revised Atlanta criteria. Admission serum levels of 48 cytokines and growth factors were determined using Bio-Plex Pro Human Cytokine Assay 21-plex and 27-plex magnetic bead suspension panels. Admission plasma levels of C-reactive protein (CRP), creatinine and calcium were measured for comparison. In subgroup analyses, we assessed the cytokine profiles of patients with severe AP (n = 14) who did not have organ dysfunction (OD) upon admission (modified Marshall score <2). Results Of 14 cytokines elevated in the severe AP group, interleukin 6 (IL-6) and hepatocyte growth factor (HGF) levels were independent prognostic markers of severe AP. IL-6, HGF and a combination of them predicted severe AP with sensitivities of 56.0%, 60.0% and 72.0%, respectively, and specificities of 90.6%, 92.8% and 89.9%, respectively. The corresponding positive likelihood ratio (LR+) values were 5.9, 8.3 and 7.1, respectively. The predictive values of CRP, creatinine and calcium were comparable to those of the cytokines. In subgroup analyses of patients with severe AP and without OD upon admission, we found that IL-8, HGF and granulocyte colony-stimulating factor (G-CSF) levels predicted the development of severe AP, with G-CSF being the most accurate cytokine at a sensitivity of 35.7%, a specificity of 96.1% and a LR+ of 9.1. Conclusions IL-6 and HGF levels upon admission have prognostic value for severe AP which is similar to levels of CRP, creatinine and calcium. Although IL-6 and HGF, as either single or combined markers, were not perfect in identifying patients at risk for severe AP, the possibility that combining them with novel prognostic markers other than cytokines might improve prognostic accuracy needs to be studied. The accuracy of IL-8, HGF and G-CSF levels in predicting severe AP in patients without clinical signs of OD upon admission warrants larger studies.
    Full-text · Article · May 2014 · Critical care (London, England)
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