Pancreas
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Stasis of the pancreatic microcirculation initiates and aggravates acute pancreatitis. Bovine hemoglobin has been shown to improve microcirculation in acute pancreatitis if prophylactically infused 15 minutes after initiation of acute pancreatitis. The purpose of this study was to evaluate the therapeutic effectiveness of bovine hemoglobin on pancreatic microcirculation and tissue damage later in the course of experimental acute rodent pancreatitis. ⋯ Therapeutic intravenous infusion of bovine hemoglobin improves pancreatic microcirculation and reduces pancreatic tissue damage in severe acute rodent pancreatitis but is not as effective as early (prophylactic) administration.
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Early diagnosis of acute pancreatitis remains a challenge. A rapid dipstick screening test for acute pancreatitis has been developed. This prospective study was designed to evaluate the diagnostic value and time course of the rapid urinary trypsinogen-2 test strip in acute pancreatitis, with comparisons with serum amylase and serum lipase. ⋯ The rapid urinary trypsinogen-2 test is a reliable and simple method for the early diagnosis of acute pancreatitis. A positive test identifies patients in need of further diagnostic measures. The urinary trypsinogen-2 test can be performed in health care units where laboratory testing facilities are not immediately available.
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Calcitonin precursors: early markers of gut barrier dysfunction in patients with acute pancreatitis.
Severe acute pancreatitis is associated with an early increase in intestinal permeability and endotoxemia. Endotoxin is a potent stimulator for the production and release of procalcitonin and its components (calcitonin precursors; [CTpr]). The aim of this study is to evaluate the role of plasma CTpr as an early marker for gut barrier dysfunction in patients with acute pancreatitis. ⋯ In patients with acute pancreatitis, plasma concentrations of CTpr appear to reflect more closely the derangement in gut barrier function rather than the extent of systemic inflammation.
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Pancreatic fibrosis is a characteristic feature of alcoholic chronic pancreatitis. Recent studies suggest that activated pancreatic stellate cells (PSCs) are the major cell-type involved in pancreatic fibrogenesis. Cultured PSCs become activated when exposed to ethanol or its metabolite acetaldehyde (as indicated by increased alpha-smooth muscle actin [alpha-SMA] expression and increased collagen synthesis). However the intracellular signaling mechanisms responsible for ethanol- or acetaldehyde-induced PSC activation remain to be fully elucidated. One of the major signaling pathways known to regulate protein synthesis in mammalian cells is the mitogen-activated protein kinase (MARK) pathway. ⋯ (1) The MAP kinase pathway is induced in PSCs after exposure to ethanol or acetaldehyde and this induction is sustained for at least 24h. (2) The p38 MAPK pathway mediates the activation (as indicated by increased alpha-SMA expression) of PSCs by ethanol or acetaldehyde.
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Hypercytokinemia is known to occur in severe acute pancreatitis, suggesting that the production, deposition, and degradation of the extracellular matrix (ECM) occur actively as a result of the actions of the complicated cytokine network. ⋯ The results of our study suggest that the activity of the ECM catabolic enzyme MMP-1 and cytokines are related to the development of acute pancreatitis.