Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lung injury is a common and severe complication in acute pancreatitis. The pathogenesis of which has not been completely understood. To explore the mechanism of lung injury, ST and FFA and PLA in bronchoalveolar perfusate, FFA and PLA in blood were measured; clinical symptoms and chest film were analysed; blood gas analysis was performed. The results indicated that lung injury mostly occurs in ABNP and less in AEP. Pulmonary edema and atelectasis are essential changes of lung injury. It is believed that FFA is an important factor responsible for pulmonary edema. PLA, which plays the most important role in lung injury, not only results in atelectasis by degradating the SA in alveolar, but also induces pulmonary edema. The main reason for the increase of ST is the degradation of SA in alveolar. The levels of FFA and PLA in the blood may indicate the severity of acute pancreatitis. However, it remains unknown whether the synthesis of SA in patient with acute pancreatitis is inhibited.
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PMID:[Clinical study of lung injury in acute pancreatitis]. 209 52

An increase in microvascular permeability may be important in the pathogenesis of acute pancreatitis. beta-adrenergic receptor agonist drugs are known to inhibit the increase in microvascular permeability induced by histamine and related vasoactive substances. These inflammatory mediators have been shown to be released during the course of experimental and human pancreatitis. We investigated the effect of isoproterenol and terbutaline sulfate on the development of acute edematous (AEP) and acute hemorrhagic (AHP) pancreatitis in a feline model of biliary pancreatitis. When given at the time of pancreatic insult, isoproterenol prevented the development of both AEP and AHP. Both isoproterenol and terbutaline sulfate reduced the severity of pancreatic inflammation, even when given up to 12 hours after the onset of AEP. Although neither drug was effective in treating established AHP, our findings suggest that, if given early in the course of the disease, they may be useful in preventing the progression of AEP to AHP.
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PMID:Treatment of acute pancreatitis with beta-adrenergic agonist drugs. 288 41

In acute pancreatitis, damage to the liver is an important aspect of multiorgan failure. In 28 dogs (20 with bile-trypsin induced acute experimental pancreatitis (AEP], 'total' and 'free' activity of lysosomal hydrolases: beta-glucuronidase, cathepsins and acid phosphatase in mitochondrial and lysosomal subfraction of the liver were determined 12 h or 24 h after the induction of AEP. The respiratory control ratio with sodium succinate as a substrate, using Clarck's electrode and uncoupler-dependent ATP-ase activity in mitochondrial subfraction, was assayed. Groups of dogs were treated or pretreated with prostacyclin (PGI2), 20 ng.kg-1.min-1 i.v. for 12 or 13 h. The relative free activity of hydrolases was significantly elevated in untreated AEP after 12 h and was partially normalized in AEP after 24 h or after 12 h followed by treatment and pretreatment with PGI2. Respiratory control ratio was twice lower than normal in AEP after 12 h and partially normalized after 24 h post PGI2 treatment. The relative free activity of lysosomal hydrolases was highly negatively correlated with respiratory control ratio. It was concluded, that during AEP in dogs the function of liver mitochondria and lysosomal stability are impaired. The significant correlation found between the mitochondrial and lysosomal lesions points to lysosomal-mitochondrial interactions in liver damage in AEP. Prostacyclin in the investigated dose partially prevents the mitochondrial and lysosomal lesions in liver in this disease.
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PMID:Lysosomal-mitochondrial interrelationships in damage to the liver in acute experimental pancreatitis in dogs. Treatment with prostacyclin (PGI2). 304 48

In 32 patients with acute pancreatitis (AEP = 15, ANP = 17), tumor necrosis factor (TNF) activity, oxygen-derived free radicals (OFR) and endotoxin contents were determined by L929 cell bioassay, Tetrabarbituric acid fluorometry and Limulus test respectively. The results showed that TNF and OFR elevated in patients with AP at the admission (P < 0.05 vs normal). The change of TNF and OFR responded to the clinical symptoms. TNF correlated to early multiple organ failure (MOF). In patients with late MOF, TNF and OFR were both the important factors. By measuring endotoxin, we found that endotoxemiae were not so important in early phase of the disease as in late phase, in which they made TNF and OFR released profusely.
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PMID:[The role of tumor necrosis factor in acute pancreatitis and associated multiple organ failure]. 778 Aug 14

Severe hypertriglyceridemia ( >1,000 -2,000 mg/dL) is known to cause acute pancreatitis (AP). If standard treatment regimen including absolute diet restriction regarding fats, use of lipid -lowering agents and combination of low molecular weight heparin with insulin is not effective, plasma exchange (PE) has emerged as an effective modality in rapidly lowering serum triglyceride levels and helping to treat and prevent hypertriglyceridemia-induced AEP. It has been shown to reduce triglyceride levels by an average of 61% after 1 session and provide rapid resolution of AP symptoms. However, the timing of PE in managing hypertriglyceridemia remains unevaluated. Randomized controlled trials on this specific topic are needed to be performed in the future.
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PMID:[Treatment of hypertriglyceridemia: plasma exchange]. 2420 32