Biliary Versus Alcohol-Related Infected Pancreatic Necrosis Similarities and Differences in the Follow-Up

Reszetow, Jacek; Hać, Stanisław; Dobrowolski, Sebastian; Stefaniak, Tomasz; Wajda, Z; Gruca, Z; Śledziński, Zbigniew; Studniarek, Michał

doi:10.1097/mpa.0b013e31805b8319

Cited by 20 publications

(23 citation statements)

References 25 publications

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“…There were two RCTs [ 30 , 55 ] for PERT versus placebo and one for the endoscopic versus surgical step-up approach [ 64 ]. Ten studies [ 36 , 44 , 46 , 47 , 49 , 51 , 53 , 54 , 57 , 64 ] had a consecutive cohort design, and the remainders were non-consecutive cohort studies. Three studies [ 55 , 56 , 64 ] were multicenter.…”

Section: Resultsmentioning

confidence: 99%

Exocrine Pancreatic Insufficiency Following Acute Pancreatitis: Systematic Review and Meta-Analysis

et al. 2019

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Background/Objectives The epidemiology of exocrine pancreatic insufficiency (EPI) after acute pancreatitis (AP) is uncertain. We sought to determine the prevalence, progression, etiology and pancreatic enzyme replacement therapy (PERT) requirements for EPI during follow-up of AP by systematic review and meta-analysis. Methods Scopus, Medline and Embase were searched for prospective observational studies or randomized clinical trials (RCTs) of PERT reporting EPI during the first admission (between the start of oral refeeding and before discharge) or follow-up (≥ 1 month of discharge) for AP in adults. EPI was diagnosed by direct and/or indirect laboratory exocrine pancreatic function tests. Results Quantitative data were analyzed from 370 patients studied during admission (10 studies) and 1795 patients during follow-up (39 studies). The pooled prevalence of EPI during admission was 62% (95% confidence interval: 39–82%), decreasing significantly during follow-up to 35% (27–43%; risk difference: − 0.34, − 0.53 to − 0.14). There was a two-fold increase in the prevalence of EPI with severe compared with mild AP, and it was higher in patients with pancreatic necrosis and those with an alcohol etiology. The prevalence decreased during recovery, but persisted in a third of patients. There was no statistically significant difference between EPI and new-onset pre-diabetes/diabetes (risk difference: 0.8, 0.7–1.1, P = 0.33) in studies reporting both. Sensitivity analysis showed fecal elastase-1 assay detected significantly fewer patients with EPI than other tests. Conclusions The prevalence of EPI during admission and follow-up is substantial in patients with a first attack of AP. Unanswered questions remain about the way this is managed, and further RCTs are indicated. Electronic supplementary material The online version of this article (10.1007/s10620-019-05568-9) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Exocrine Pancreatic Insufficiency Following Acute Pancreatitis: Systematic Review and Meta-Analysis

et al. 2019

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“…1 This is supported by clinical data that suggest that alcoholics are predisposed to acute pancreatitis, as well as to an earlier onset, more frequent episodes, and an increased risk of chronic pancreatitis. 2,3 Experimental models of alcoholic pancreatitis in rats have revealed that endotoxemia can initiate acute and chronic alcoholic pancreatitis and that the inflammatory response to injury is more pronounced in alcoholic pancreatitis than in nonalcoholic pancreatitis. 4,5 Increased gut permeability and subsequent bacterial translocation across the mucosal barrier have been described in alcoholics.…”

Section: Introductionmentioning

confidence: 99%

Impaired autophagosome-lysosome fusion in the pathogenesis of pancreatitis

Fortunato

Kroemer²

2009

Autophagy

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In contrast to apoptosis, necrosis is generally viewed as a pro-inflammatory cell death mechanism. Accumulation of autophagosomes and massive acinar cell necrosis is observed in human acute pancreatitis, a severe and potentially lethal inflammatory condition. We have investigated the incidence of apoptosis, autophagy and necrosis affecting acinar cells in a rat model of acute pancreatitis induced by chronic alcohol intake and acute endotoxemia. We have observed that the combination of alcohol exposure and endotoxemia results in substantial accumulation of autophagosomes without an increase in autolysosomes, coupled to the depletion of LAMP-2, a lysosomal protein required for the proper fusion of autophagosomes with lysosomes. Alcohol plus endotoxemia favors the switch from apoptotic to necrotic cell death, as indicated by histopathological examination, reduced ATP levels, suppressed caspase activation, as well as the nuclear release of the proinflammatory factor HMGB1. Importantly, patients with alcoholic pancreatitis also exhibit local LAMP-2 depletion, recapitulating the results obtained in the animal model. We suggest that acinar cell vacuolization in pancreatitis is mediated by an endotoxemia-induced depletion of LAMP-2, which in turn facilitates the accumulation of autophagosomes due to the deficient formation of autolysosomes. Hence, we postulate that the depletion of lysosomal proteins may play a critical role in the pathogenesis of acute pancreatitis.

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“… 22 , 24 Alcoholics seem more susceptible to AP, a condition associated with an earlier onset, more frequent episodes and an increased risk of CP. 25 , 26 , 27 , 28 Alcoholic patients also have elevated serum LPS concentrations, which have been correlated with the severity of alcoholic AP. 29 , 30 Interestingly, chronic sub-clinical endotoxemia has been linked to insulin resistance, obesity, and diabetes, as well as cardiovascular disease, indicating that LPS has important clinical relevance not only for alcoholics with pancreatitis, but also for other metabolic disorders.…”

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confidence: 99%

Necro-inflammatory response of pancreatic acinar cells in the pathogenesis of acute alcoholic pancreatitis

Gu¹,

Werner²,

Bergmann

et al. 2013

Cell Death Dis

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The role of pancreatic acinar cells in initiating necro-inflammatory responses during the early onset of alcoholic acute pancreatitis (AP) has not been fully evaluated. We investigated the ability of acinar cells to generate pro- and anti-inflammatory mediators, including inflammasome-associated IL-18/caspase-1, and evaluated acinar cell necrosis in an animal model of AP and human samples. Rats were fed either an ethanol-containing or control diet for 14 weeks and killed 3 or 24 h after a single lipopolysaccharide (LPS) injection. Inflammasome components and necro-inflammation were evaluated in acinar cells by immunofluorescence (IF), histology, and biochemical approaches. Alcohol exposure enhanced acinar cell-specific production of TNFα, IL-6, MCP-1 and IL-10, as early as 3 h after LPS, whereas IL-18 and caspase-1 were evident 24 h later. Alcohol enhanced LPS-induced TNFα expression, whereas blockade of LPS signaling diminished TNFα production in vitro, indicating that the response of pancreatic acinar cells to LPS is similar to that of immune cells. Similar results were observed from acinar cells in samples from patients with acute/recurrent pancreatitis. Although morphologic examination of sub-clinical AP showed no visible signs of necrosis, early loss of pancreatic HMGB1 and increased systemic levels of HMGB1 and LDH were observed, indicating that this strong systemic inflammatory response is associated with little pancreatic necrosis. These results suggest that TLR-4-positive acinar cells respond to LPS by activating the inflammasome and producing pro- and anti-inflammatory mediators during the development of mild, sub-clinical AP, and that these effects are exacerbated by alcohol injury.

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Biliary Versus Alcohol-Related Infected Pancreatic Necrosis Similarities and Differences in the Follow-Up

Abstract: Patients after alcohol-induced IPN had lower quality of life compared with biliary etiology. Biliary and alcohol-induced IPN patients after surgical treatment have nonsignificant differences of endocrine and exocrine pancreatic functions.

Cited by 20 publications

References 25 publications

Exocrine Pancreatic Insufficiency Following Acute Pancreatitis: Systematic Review and Meta-Analysis

Exocrine Pancreatic Insufficiency Following Acute Pancreatitis: Systematic Review and Meta-Analysis

Impaired autophagosome-lysosome fusion in the pathogenesis of pancreatitis

Necro-inflammatory response of pancreatic acinar cells in the pathogenesis of acute alcoholic pancreatitis

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