Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytokines and their endogenous antagonists are released from inflammatory cells during acute pancreatitis, in particular its severe form. They can be found early in the course of the disease as is shown in animal models and in endoscopic retrograde cholangio-pancreatography (ERCP) induced human pancreatitis. Cytokine measurements can predict the course of the disease. This can, however, be achieved using more simple parameters, such as clinical judgement and leucocyte elastase. Anticytokine strategies in the treatment of severe acute pancreatitis should be further evaluated since some positive effects have been found in experimental settings. Interleukin 10 or soluble TNF alpha-receptors may be good candidates. Plasmapheresis seems to change cytokine-anticytokines patterns and this also needs to be explored in controlled trials.
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PMID:Interleukins in acute pancreatitis. 886 70

Interleukin 10 (IL-10) recently emerged as an antiinflammatory cytokine that inhibits the secretion of proinflammatory cytokines by monocytes and/or macrophages and the release of free oxygen radicals. It has been reported that treatment with IL-10 decreases the severity of experimental pancreatitis, mainly by inhibiting cellular necrosis. The aim of this study was to evaluate the behavior of serum IL-10 in patients with acute pancreatitis and to explore the possibility of a relationship between this cytokine and severity of the disease. Forty-five patients with acute pancreatitis were studied. Acute pancreatitis was of biliary origin in 30 patients, due to alcohol abuse in 10, due to pancreas divisum in 1, and of unknown origin in the remaining 4. According to the Balthazar criteria, 19 patients had scores of A, B, or C and 25 had scores of D or E. Twelve healthy subjects were also studied as controls. Serum IL-10 was determined in all subjects on admission, and in acute pancreatitis patients also daily for the following four days using a commercial kit. Healthy subjects had no detectable serum levels of IL-10. In acute pancreatitis patients, serum IL-10 levels were increased on the first day of the disease and then progressively decrease in the following days. On the first day of the acute pancreatitis, patients with the mild disease had serum levels of IL-10 significantly higher than those with severe disease, whereas in the following days, no statistically significant difference was observed between the two groups. The elevation of IL-10 on the first day of the illness is more marked in patients with mild acute pancreatitis than in those with the severe form of the disease. The finding of low values of serum IL-10 in severe acute pancreatitis suggests that there may be altered down-regulation of the immune system response in these patients.
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PMID:Serum interleukin-10 in human acute pancreatitis. 924 48

Post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis has been suggested as a model for acute pancreatitis (AP), which allows evaluation of early alterations in the time course of the disease. The influence of the clinical course on procalcitonin (PCT), serum amyloid A (SAA), and several proinflammatory and inhibitory cytokines was evaluated in patients with AP following ERCP. Blood samples were prospectively collected from patients undergoing ERCP. The incidence of ERCP-induced pancreatic damage, defined as abdominal complaints, a threefold increase of serum lipase, and elevation of CRP from <10 to >20 mg/liter was 12.8% (12/94). Only mild clinical courses of acute pancreatitis were observed. PCT significantly increased in subjects with post-ERCP pancreatitis after 24 hr. However, PCT levels did not exceed 0.5 ng/ml in any patient. Interleukin-1 receptor antagonist (IL-1RA) began to differ from baseline 2 hr after ERCP, followed by interleukin-6 (IL-6, 6 hr), solubilized tumor necrosis factor-alpha receptor II (sTNF-alphaRII, 24 hr) and SAA (24 hr). Interleukin 10 (IL-10) showed marked interindividual variations with no obvious peak. Among all parameters evaluated, only peak values of IL-6 and IL-10 showed significant correlations with the reported pain score (r2 = 0.62/0.78), degree of ampullar irritation (r2 = NS/0.87), and the duration of ERCP (r2 = 0.58/0.76). No correlation was found with the volume of the injected contrast agent. We conclude that IL-10 and IL-6 appear to be useful to monitor patients after ERCP. The absence of any PCT elevation in the present study is in accordance with the clinical course of the patients who suffered from mild pancreatic damage without systemic or infectious complications.
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PMID:Diagnostic relevance of interleukin pattern, acute-phase proteins, and procalcitonin in early phase of post-ERCP pancreatitis. 972 66

The aim of the present review is to summarize the current knowledge regarding pharmacological prevention and treatment of acute pancreatitis (AP) based on experimental animal models and clinical trials. Somatostatin (SS) and octreotide inhibit the exocrine production of pancreatic enzymes and may be useful as prophylaxis against post endoscopic retrograde cholangiopancreatography pancreatitis (PEP). The protease inhibitor gabexate mesilate (GM) is used routinely as treatment to AP in some countries, but randomized clinical trials and a meta-analysis do not support this practice. Nitroglycerin (NGL) is a nitrogen oxide (NO) donor, which relaxes the sphincter of Oddi. Studies show conflicting results when applied prior to ERCP and a large multicenter randomized study is warranted. Steroids administered as prophylaxis against PEP has been validated without effect in several randomized trials. The non-steroidal anti-inflammatory drugs (NSAID) indomethacin and diclofenac have in randomized studies showed potential as prophylaxis against PEP. Interleukin 10 (IL-10) is a cytokine with anti-inflammatory properties but two trials testing IL-10 as prophylaxis to PEP have returned conflicting results. Antibodies against tumor necrosis factor-alpha (TNF-alpha) have a potential as rescue therapy but no clinical trials are currently being conducted. The antibiotics beta-lactams and quinolones reduce mortality when necrosis is present in pancreas and may also reduce incidence of infected necrosis. Evidence based pharmacological treatment of AP is limited and studies on the effect of potent anti-inflammatory drugs are warranted.
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PMID:Pharmacological approach to acute pancreatitis. 1885