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)

Rhodanese is one of the enzymes concerned in the detoxification of cyanide. Cassava intake and consequent cyanide toxicity are incriminated in the pathogenesis of goitre and calcific pancreatitis of tropics. So we studied the activity of rhodanese in these patients. 14 controls, 13 patients with pancreatitis and 12 with goitre were studied. The median (and range) of rhodanese in these groups were 82 (50-144), 110 (64-180) and 71 (22-160) units respectively. The serum rhodanese was significantly higher (P less than 0.05) in patients with pancreatitis when compared to the other groups. There was no significant difference between the serum rhodanese in patients with goitre and the controls. The presence of adequate amounts of rhodanese indicates that goitre and chronic pancreatitis are not produced by impaired cyanide detoxification.
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PMID:Serum rhodanese in goitre and calcific pancreatitis of tropics. 263 15

The appearance of vacuoles inside acinar cells characterizes an early stage of development in different models of acute pancreatitis and, possibly, also in human disease. The vacuoles have been shown to contain both digestive and lysosomal enzymes. This abnormal admixture may have important implications for the pathogenesis of pancreatitis because the lysosomal enzyme cathepsin B can activate trypsinogen and may, by this way, trigger pancreatic autodigestion. For the activation process of trypsinogen by cathepsin B, however, an acidic pH is required. This study, therefore, looked for evidence of vacuole acidification in two different models of acute pancreatitis. Edematous pancreatitis was induced in rats by hyperstimulation with cerulein and hemorrhagic pancreatitis was induced in mice by feeding a choline-deficient, ethionine-supplemented diet. Pancreatic acinar cells were isolated at different times after induction of pancreatitis and incubated with 50 microM of acridine orange to identify acidic intracellular compartments. As shown in previous work, zymogen granules are the main acidic compartment of normal acinar cells; they remained acidic throughout the course of pancreatitis in both models. Vacuoles became increasingly more frequent in both models as pancreatitis progressed. Throughout development of pancreatitis, vacuoles accumulated acridine orange indicating an acidic interior. Addition of a protonophore (10 microM monensin or 5 microM carbonyl cyanide m-chlorophenylhydrazone [CCCP] or a weak base (5 mM NH4Cl) completely and rapidly abolished acridine orange fluorescence inside both zymogen granules and vacuoles providing further evidence for an acidic interior. The acidification of vacuoles seen in two different models of pancreatitis may be an important requirement for activation of trypsinogen by cathepsin B and thus for the development of acute pancreatitis.
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PMID:Intracellular vacuoles in experimental acute pancreatitis in rats and mice are an acidified compartment. 333 39

We hypothesize that chronic cyanide toxicity may explain the occurrence of calcific pancreatitis in chronic alcoholic individuals in affluent Western nations and malnourished children and young adults in developing tropical regions. In alcoholic persons the source of cyanide is cigarette smoke, and in tropical countries the source could be cassava or other plants. The cyanide hypothesis is consistent with the known epidemiologic and metabolic characteristics of these two contrasting forms of pancreatitis. We believe that continued chronic cyanide poisoning could reinforce any independent effect of alcohol or malnutrition on the pancreas, resulting in an exaggerated and perhaps irreversible form of the disease.
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PMID:Chronic cyanide poisoning: unifying concept for alcoholic and tropical pancreatitis. 337 31

1-Cyano-2-hydroxy-3-butene (CHB) has been reported to cause cell death in rat pancreatic acini. In this report, we describe the time-dependent effects of CHB on mouse acinar cell apoptosis and the effects of CHB-induced acinar cell apoptosis on the severity of secretagogue-induced acute pancreatitis in mice. CHB administration to mice resulted in a time-dependent increase in pancreatic apoptosis, which was maximal 12 hours after CHB administration. The severity of pancreatitis was significantly reduced by prior CHB administration and maximal protection was observed when the caerulein injections were started 12 hours after CHB administration. These observations indicate that induction of apoptosis can reduce the severity of pancreatitis and they suggest that induction of pancreatic acinar cell apoptosis may be beneficial in the clinical management of acute pancreatitis.
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PMID:Induction of apoptosis in pancreatic acinar cells reduces the severity of acute pancreatitis. 961 Mar 87

Tropical pancreatitis is an uncommon cause of acute, and often chronic, relapsing pancreatitis. Patients present with abdominal pain, weight loss, pancreatic calcifications, and glucose intolerance or diabetes mellitus. Etiologies include a protein-calorie malnourished state, a variety of exogenous food toxins, pancreatic duct anomalies, and a possible genetic predisposition. Chronic cyanide exposure from the diet may contribute to this disease, seen often in India, Asia, and Africa. The pancreatic duct of these patients often is markedly dilated, and may contain stones, with or without strictures. The risk of ductal carcinoma with this disease is accentuated. Treatment may be frustrating, and may include pancreatic enzymes, duct manipulations at endoscopic retrograde cholangiopancreatography, octreotide, celiac axis blocks for pain control, or surgery via drainage and/or resection.
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PMID:Tropical pancreatitis. 1208 Feb 28