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)

The purpose of this study was to analyse the clinical course of 410 patients of severe surgical infections (primary 251, postoperative 159) during recent 5 years and to evaluate the important background factors which make these patients serious. As a result, the following patients such as, (1) who have refractory primary infections, for example malignant lymphoma, severe pancreatitis etc. (2) whose infectious foci were uncontrolled. (3) who had finally complicated a septic MOF or DIC, seemed to be especially critical even though recent advanced surgical therapy. To improve these severe conditions, we believe to need a renewed approach like so called "multi-disciplinary therapy", additionally with both conventional antibiotics administration and drainage for infectious foci. Several methods such as, (1) rational nutrition management using indirect calorimetry. (2) plasma exchange for removing toxic substances such as bacterial toxins, chemical mediators etc, from circulating blood. (3) pharmacological block of these toxic substances, were shown. In terms of the harmful chemical mediators, we supposed that both PAF (platelet activating factor) and oxygen free radical were extremely important in septic conditions from previous clinico-experimental studies. Therefore the effects of those pharmacological blockers such as PAF antagonists, SOD, protease inhibitor in experimental endotoxin shock were discussed in detail.
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PMID:[Clinico-experimental analysis of backgrounds of the severe surgical infections]. 194 10

The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis was studied in a new model of acute hemorrhagic pancreatitis and cerulein-induced edematous pancreatitis in rats. Hemorrhagic pancreatitis was produced by administering two intraperitoneal doses of cerulein [40 micrograms/kg body weight (BW)] at 1-h intervals following water immersion stress applied for 5 h. Edematous pancreatitis was induced by injecting cerulein as described but without water immersion. Five hours after the first injection of cerulein, pancreatic edema and elevation of serum amylase level were more marked in the animals with hemorrhagic than with edematous pancreatitis. Five hours after the first injection of cerulein, marked hemorrhage and venous dilatation were observed only in those with hemorrhagic pancreatitis. Local pancreatic blood flow decreased to approximately 60% of control values in the animals with edematous pancreatitis, and to approximately 30% of control values in those with hemorrhagic pancreatitis. To evaluate the involvement of oxygen radicals, some rats received three intraperitoneal injections of superoxide dismutase (SOD 10,700 U/kg BW) and catalase (132,000 U/kg BW) beginning 15 min before the first injection of cerulein and repeated at 1-h intervals. No significant effect of free radical scavengers was observed on the edematous pancreatitis. However, in hemorrhagic pancreatitis, treatment with SOD and catalase completely suppressed the hemorrhage and venous dilatation of the pancreas, significantly reduced the pancreatic wet weight and the serum amylase level, and reduced the histologic alterations. However, after treatment with SOD and catalase, no differences were observed in local pancreatic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of oxygen-derived free radicals in hemorrhagic pancreatitis induced by stress and cerulein in rats. 750 65

Caerulein-induced acute pancreatitis in rats commonly complicated ARDS-like acute lung injury. Acute pancreatitis induced by caerulein in the circulating neutrophil-depleted rat by hydroxyrea or with the administration of SOD, CAT or Pentoxifylline, the wet lung weight, lung capillary endothelial permeability decrease significantly compared to the caerulein group (P < 0.05). There are no lung morphologic evidences of neutrophil sequestration, interstial edema, intralveolar hemorrhage that seen in caerulein infusion animals. But it has no effect against the development of acute pancreatitis. It suggested that neutrophil and neutrophil-derived oxygen radical are the important mediators of acute lung injury complicated by pancreatitis.
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PMID:[The role of pentoxifylline in acute lung injury complicated by pancreatitis]. 799 67

A proband with chylomicronemia, pancreatitis, and non-insulin-dependent diabetes (NIDDM) bears two different mutations in exon 3 of the lipoprotein lipase (LPL) gene: a missense mutation, 75Arg-->Ser, inherited through the paternal line and a truncation, 73Tyr-->Ter, through the maternal line. NIDDM appeared to be independently segregating. The R75S mutant was studied in extracts and media from transfected COS-1 cells. Detectable amounts of catalytically competent R75S LPL suggested destabilization of the active homodimer as with exon 5 mutants (Hata et al. 1992. J. Biol. Chem. 267:20132-20139). Hydrolysis of a short-chain fatty acid ester indicated that R75S does not directly affect activation of LPL by apoC-II. Subjects with NIDDM and wild-type LPL, and nondiabetic middle-aged carriers of the 73Tyr-->Ter truncation had moderate hypertriglyceridemia (260-521 mg/dl) and reduced high density lipoprotein cholesterol. A maternal aunt with NIDDM carried the truncation. Her phenotype (triglycerides of 5,300 mg/dl, eruptive xanthomatosis, and recurrent pancreatitis) was as severe as that in homozygotes or compound heterozygotes. We conclude: (a) diabetic carriers of dysfunctional LPL alleles are at risk for severe lipemia; and (b) the physiologic defects in NIDDM may be additive or synergistic with heterozygous LPL deficiency.
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PMID:Mutations in exon 3 of the lipoprotein lipase gene segregating in a family with hypertriglyceridemia, pancreatitis, and non-insulin-dependent diabetes. 832 86

Intraperitoneal injection of lipopolysaccharide (LPS) at a dose of 50 micrograms/kg increased the activity and the mRNA level of manganese superoxide dismutase (Mn-SOD) but did not change those of copper/zinc-SOD (Cu/Zn-SOD) in the rat pancreas. Both the formation of pancreatic edema and the elevation of serum amylase during caerulein pancreatitis were significantly relieved in the rats pretreated with LPS (50 micrograms/kg) compared with the rats without the pretreatment. These results support the view that superoxides play a key role in the pathogenesis of caerulein pancreatitis, and that Mn-SOD in the pancreas may work as a defense against the development of this disease.
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PMID:Lipopolysaccharide induces manganese superoxide dismutase in the rat pancreas: its role in caerulein pancreatitis. 855 79

The role of oxidative stress in acute pancreatitis was investigated by comparing the pathological features of caerulein pancreatitis between transgenic mice that overexpress human Cu/Zn-superoxide dismutase (SOD) and nontransgenic littermates. Both the elevation of serum amylase and the formation of pancreatic edema during the pancreatitis were significantly reduced in the transgenic mice compared with the nontransgenic littermates. In the transgenic mice, the pancreatitis-associated reduction of Cu/Zn-SOD activity in the pancreatic tissues was significantly smaller than that in the nontransgenic mice. These results provide direct evidence that the elevation of intracellular oxygen radicals is an important factor for the progress of acute edematous pancreatitis.
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PMID:Transgenic copper/zinc-superoxide dismutase ameliorates caerulein-induced pancreatitis in mice. 914 18

Reactive oxygen species (ROS), generated by infiltrating neutrophils, are considered as an important regulator in the pathogenesis and deveolpment of pancreatitis. A hallmark of the inflammatory response is the induction of cytokine gene expression, which may be regulated by oxidant-sensitive transcription factor, nuclear factor-kappaB (NF-KB). Present study aims to investigate whether neutrophils primed by 4beta-phorbol 12beta-myristate 13alpha-acetate (PMA) affect the productions of H2O2 and lipid peroxide (LPO), NF-kappaB activation and cytokine production in pancreatic acinar cells, and whether these alterations were inhibited by N-acetylcysteine (NAC) and superoxide dismutase (SOD). ROS generation in neutrophils increased by PMA, which was inhibited by NAC and SOD. The productions of H2O2, LPO and TNF-alpha were increased with the amounts of PMA-primed neutrophils added to acinar cells while the productions of H2O2, LPO and cytokines increased with time. PMA-primed neutrophils resulted in the activation of two species of NF-kappaB dimers (a p50/p65 heterodimer and a p50 homodimer). Both NAC and SOD inhibited neutrophil-induced alterations in acinar cells. In conclusion, ROS, generated by neutrophils, activates NF-kappaB, resulting in upregulation of inflammatory cytokines in acinar cells. Antioxidants such as NAC might be clinically useful antiinflammatory agents by inhibiting oxidant-mediated activation of NF-KB and decreasing cytokine production.
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PMID:NF-kappaB and cytokines in pancreatic acinar cells. 1098 15

Reactive oxygen species (ROS), generated by infiltrating neutrophils, are considered as an important regulator in the pathogenesis and development of pancreatitis. A hallmark of the inflammatory response is the induction of cytokine gene expression, which may be regulated by oxidant-sensitive transcription factor, nuclear factor-kappaB (NF-kappaB). Present study aims to investigate whether neutrophils primed by 4beta-phorbol 12beta-myristate 13alpha-acetate (PMA) affect the productions of H(2)O(2) and lipid peroxide (LPO), NF-kappaB activation and cytokine production in pancreatic acinar cells, and whether these alterations were inhibited by N-acetylcysteine (NAC) and superoxide dismutase (SOD). Neutrophils generated ROS by stimulation with PMA, which was inhibited by NAC and SOD. In acinar cells, PMA-primed neutrophils increased the productions of H(2)O(2), LPO, and cytokines both time and dose dependently. PMA-primed neutrophils resulted in the activation of two species of NF-kappaB dimers (a p50/p65 heterodimer and a p50 homodimer) in acinar cells. Both NAC and SOD inhibited neutrophil-induced, oxidant-mediated alterations in acinar cells. In conclusion, ROS, generated by neutrophils, activates NF-kappaB, resulting in upregulation of inflammatory cytokines in acinar cells. Antioxidants such as NAC might be useful antiinflammatory agents by inhibiting oxidant-mediated activation of NF-kappaB and decreasing cytokine production.
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PMID:Suppression of NF-kappaB activation and cytokine production by N-acetylcysteine in pancreatic acinar cells. 1103 20

AIM:To observe the changes in oxygen free radical (OFR) and the curative effect of traditional Chinese medicine Qing Yi Tang in acute necrotizing pancreatitis (ANP).METHODS:After induction of ANP by injection of sodium taurocholate into pancreatic duct, 16 dogs were randomly divided into control group and Chinese medicine group.Serum amylase, SOD and MDA were determined on postoperative day 1, 2, 4 and 7. The animals were sacrificed on day 7. SOD and MDA in organs were determined, and pathological changes in pancreas were observed.RESULTS: As compared with control group, the serum level of amylase (734U/L vs 2783U/L) and MDA (7.8nmol/ml vs 14.8nmol/ml) in Chinese medicine group were decreased on day 7 (P < 0.05), while SOD increased significantly (281nU/ml vs 55nU/ml, P < 0.01), and similar changes occurred in MDA and SOD in organs, especially in the pancreas; the pathological changes in the pancreas were alleviated as well.CONCLUSION: Qing Yi Tang is effective in clearing OFRs and alleviating pathological changes in ANP.
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PMID:Traditional Chinese medicine Qing Yi Tang alleviates oxygen free radical injury in acute necrotizing pancreatits. 1181 20

The assumption that the endoscopist is an important factor in outcome of ERCP is not easy to document. There are plenty of reasons for the difficulties in defining experience and skill of an endoscopist, and establishing suitable endpoints for their measurement. Suitable proxy variables are ERCP-frequency (ongoing volumes) and ERCP-experience (life-time volumes) of the endoscopist, as well as individual and institutional conditions. Important confounders are difficulty of ERCP, patient-related and procedure-related risk factors and risk-reducing factors. Endpoints should include success and (specific) complications of ERCP. Only few studies are available that analyse the influence of the endoscopist's skills on post-ERCP pancreatitis. Studies with a high preponderance of dominating patient-related risk factors for post-ERCP pancreatitis, e.g. suspect of SOD and unexplained abdominal pain, failed to prove such a dependence. On the other hand, evidence increases from studies with patient populations of more traditional indications for ERCP that suggests the existence of an association between ERCP-frequency of the endoscopist or ERCP-frequency of the environment and the incidence of post-ERCP pancreatitis and other complications. ERCP-experience measured in overall live-time volumes, however, does not seem to influence the risk of pancreatitis due to ERCP, although the data are very limited. During the ERCP-training of young endoscopists an impaired success rate appears more important than an increased complication rate. Nevertheless, all undesired outcomes of ERCP should be applied to the endpoints of quality assessment in ERCP-training. Further studies on this topic are needed. Since many variables significantly interact with the endpoints post-ERCP pancreatitis and complications of ERCP, a special study design appears indispensable to conclusively prove a relationship between an endoscopist's expertise and specific complications of ERCP.
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PMID:Post-ERCP pancreatitis: is the endoscopist's experience the major risk factor? 1243 84


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