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)

Therapy with oral 5-aminosalicylic acid for inflammatory bowel disease has been reported as effective and safe. We report two cases of biochemically proven mild acute pancreatitis occurring 2 and 14 days, respectively, after oral 5-aminosalicylic acid therapy was instituted for inflammatory bowel disease. A hypersensitivity mechanism might be involved, owing to possible erratic systemic absorption of the drug. We suggest clinical and biochemical monitoring for patients undergoing oral 5-aminosalicylic acid therapy in order to confirm its possible association with acute pancreatitis and to assess the actual incidence of such an adverse reaction.
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PMID:Acute pancreatitis during oral 5-aminosalicylic acid therapy. 239 Sep 34

We describe six patients with acute pancreatitis associated with chronic inflammatory bowel disease (IBD) and no other etiological factor of pancreatic disease in a series of 513 patients with IBD. Five of the 6 patients had Crohn's disease and one indeterminate colitis; four had simultaneous symptoms of active colitis. The pancreatis was not caused by drugs or duodenal involvement of IBD. Our study suggests that pancreatic disease is one of the extra-intestinal manifestations of IBD, in particular of Crohn's disease.
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PMID:Pancreatitis in patients with chronic inflammatory bowel disease. 231 41

Two patients with inflammatory bowel disease and no history of bilio-pancreatic disorders or alcoholism developed acute pancreatitis after therapy with sulfasalazine. The treatment lasted two months in the first case and four days in the second. The onset of pancreatic complications was heralded by jaundice; abdominal pain was a late symptom. The clinical course was dramatic in both cases, and one patient died. These findings agree with the hypothesis that sulfasalazine like other sulfonamidic compounds is a potentially pancreotoxic drug.
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PMID:Pancreatitis and pancreatic necrosis during sulfasalazine therapy. 287 81

Leukotrienes are potent mediators of inflammatory and allergic reactions involved, among others, in endotoxin action and shock, tissue trauma, acute liver injury, hepatorenal syndrome, inflammatory bowel disease, acute pancreatitis, and asthma. Studies on metabolism and analysis of these arachidonate metabolites in vivo are a prerequisite for an improved understanding of their role under physiological and pathophysiological conditions and for the development of inhibitors of leukotriene synthesis and of receptor antagonists. Leukotriene C4 and its metabolites, collectively termed the cysteinyl leukotrienes, are predominantly inactivated by the liver. Rapid hepatocellular uptake is followed by partial metabolic inactivation, comprising omega-oxidation and N-acetylation of leukotriene E4, and excretion into bile. A minor portion of the cysteinyl leukotrienes undergoes enterohepatic circulation. In all species investigated so far, hepatobiliary elimination of cysteinyl leukotrienes predominates over renal excretion. Analysis of the systemic production of cysteinyl leukotrienes in vivo has been accomplished by radioimmunological determination of species-characteristic index metabolites in bile after their separation by high-performance liquid chromatography. The mercapturate N-acetyl-leukotriene E4 is the index metabolite of choice in the rat. In man, leukotriene E4 is the predominant endogenous cysteinyl leukotriene in both bile and urine. The amounts of cysteinyl leukotrienes detected under various pathophysiological conditions may be sufficient to induce known phenomena associated with the respective disease. As shown under experimental conditions, inhibition of leukotriene synthesis or receptor antagonism can serve as therapeutic approaches.
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PMID:[The Heinrich-Wieland Prize presentation. Metabolism and analysis of leukotrienes in vivo]. 307 Jan 47

The sera of 59 patients with Crohn's disease (CD) and of 46 patients with ulcerative colitis (UC) were tested for autoantibodies (Aab) by indirect immunofluorescence with modern histochemical techniques using 19 different human tissues as antigenic substrates. Control collectives consisted of 19 patients with coeliac disease and of 100 healthy subjects. It was possible to demonstrate a specific marker for CD: Aab against exocrine pancreas (Pab) were present in 39% of the CD sera (UC 4%, coeliac disease 0%, healthy controls 3%). High Pab titres were only detectable in CD sera (29%). The CD-related autoantigen was demonstrated to be a component of normal pancreatic juice. Pab in CD were fundamentally different from those sometimes occurring in chronic and acute pancreatitis. It is suggested that CD is caused by autoimmune reactions against a component of pancreatic juice. Pab in CD correspond to Aab against intestinal goblet cells (Gab), which occurred exclusively in UC (28%). Pab and Gab, but obviously none of the other Aab investigated in this study, are of diagnostic value in chronic inflammatory bowel disease.
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PMID:Autoimmunity to pancreatic juice in Crohn's disease. Results of an autoantibody screening in patients with chronic inflammatory bowel disease. 332 99

Elevated serum and urine amylase and serum lipase values are not always diagnostic of an acute pancreatitis, on the account of the extrapancreatic production of these enzymes. A diagnostic improvement can be made by using the CAm/CCr ratio, but this index too is abnormal in some non pancreatic diseases. Since trypsin measurement seems to be more specific in the evaluation of pancreatic condition, serum trypsin-like immunoreactivity has been measured in 28 patients with acute pancreatitis, 95 patients with a wide spectrum of gastroenterological diseases and in 30 patients with severe chronic renal failure. 85 normal subjects were used as controls. Abnormally high serum trypsin-like immunoreactivity (TLI) values were detected in 100% of patients with acute pancreatitis, without any overlap with normal controls. TLI values above the upper normal limit were also found in 70% of patients with severe renal damage, while none of the patients with liver disease, biliary disease, peptic ulcer an inflammatory bowel disease had elevated TLI levels. In 29 patients with hyperamylasemia due to extra-pancreatic diseases serum trypsin-like immunoreactivity was always within the normal range. It is concluded that the determination of serum TLI is a sensitive and reliable tool in the diagnosis of an acute pancreatic inflammation, providing that a severe renal failure is excluded.
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PMID:Trypsin-like immunoreactivity in the diagnosis of acute pancreatitis. 616 10

Since recently adding Intralipid (IL) to our standard total parenteral nutrition (TPN) regimen for children with inflammatory bowel (IBD) disease, two children undergoing major intestinal resections have developed acute pancreatitis in the early postoperative period. Herein, we present the clinical summaries of these two patients, discuss the multifactoral etiologies of acute pancreatitis, and review the role of emulsified fat solutions in TPN in children with IBD.
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PMID:Pancreatitis and intravenous fat: an association in patients with inflammatory bowel disease. 641 38

Two patients with inflammatory bowel disease who developed acute pancreatitis within 21 days of commencing treatment with 6-mercaptopurine are presented. Both were inadvertently reexposed to the drug and developed recurrent pancreatitis within 3 hr of a single dose.
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PMID:6-Mercaptopurine-related pancreatitis in 2 patients with inflammatory bowel disease. 653 74

Cytokines are important immunoregulatory mediators. Their contribution to the pathogenesis of acute and chronic gastroenterological disorders is obvious. Increased expression of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor (TNF) can be detected in inflammatory bowel disease. During the last few years it has also been recognized that activated leukocytes have an important role in the multisystem involvement of acute pancreatitis. Activation of leukocytes is an early event during severe acute pancreatitis, and it may be a pathogenetic factor in the severity of the disease. The review summarizes the recent findings in the field of inflammatory cytokines with particular attention of TNF, IL-1, IL-6, and IL-8 during severe acute pancreatitis and underscores the role of the activated leukocytes in the pathogenesis of complicated acute pancreatitis.
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PMID:[Inflammatory mediators in acute pancreatitis (theoretical considerations)]. 765 17

While the knowledge concerning the role of the immune system in many internal disorders has grown rapidly in recent years, there are few methods to assess immune system activation in clinical practice. Measurement of urine neopterin, product of a metabolic pathway controlled by interferon-gamma, has been found useful in many clinical conditions. The present study concerns neopterin excretion in 157 patients with different internal disorders. As expected, we found an increase in urine neopterin in patients with malignant tumors, autoimmune disorders like systemic lupus erythematosus or inflammatory bowel disease, and infections. Elevated neopterin levels were also observed in acute pancreatitis and in acute myocardial infarction. In addition, significant correlations between urine neopterin and zinc and neopterin and copper excretion were found suggesting a physiological role of neopterin as urine antioxidant.
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PMID:Neopterin in the diagnosis of disorders associated with immune system activation. 815 11


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