Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe pancreatitis and a pseudocyst occurred in a patient following accidental ingestion of an anticholinesterase insecticide, a substance not previously known to produce pancreatitis. Experiments were done to elucidate the mechanism. In one group of dogs the pancreatic duct was perfused and intraductal pressures were measured. The cholinesterase inhibitor 0,0-diethyl-0-(2-isopropyl-6-methyl-4-pyrimidinyl)phosphorothioate (25 mg/kg) caused a significant increase in the mean intraductal pressure from 12 +/- 2.4 to 27.8 +/- 5.9 cm saline. In a second group of dogs pancreatic secretory rates were measured. Anticholinesterase (75 mg/kg) in combination with secretin infusion (1 U/kg/hr) caused a significant increase in the secretin stimulated flow rate from 0.13 to 0.56 cc/min. Atropine (75 microgram/kg) abolished the anticholinesterase induced pressure and secretory rate increases. In a third group of dogs administration of cholinesterase inhibitor 75 mg/kg and secretin infusion 2 U/kg/hr resulted in acute pancreatic interstitial edema, acinar cell vacuolization, hyperamylasemia and hyperlipasemia. These results suggest that occurrence of pancreatitis as a complication of anticholinesterase insecticide intoxication is the result of hypersecretion and pharmacologic ductal obstruction.
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PMID:Pancreatitis as a complication of anticholinesterase insecticide intoxication. 42 52

We report the case of a 54-year-old male patient hospitalized for diarrhea and weight loss (8 kg over the previous three months). At admission, we observed pale oral and conjunctival mucosa and peripheral edema of the lower limbs. Stool frequency was 8-10 per day. Laboratory data were as follows: hemoglobin, 11 g/dL; total proteins, 4.3 g/dL; albumin, 2 g/dL; pseudocholinesterase, 1248 U/L; triglycerides, 54 mg/dL; serum cholesterol, 102 mg/dL; calcium, 7.9 mg/dL. Fecal fat was 8.2 g/24 hr. Fecal chymotrypsin (FCT) was 2.3 U/g. A duodenal probe was performed after administration of intravenous secretin and cerulein stimulation, and a contemporaneous mucosal biopsy was taken at the ligament of Treitz. Microscopic examination showed numerous Giardia lamblia in the fluid collected. Pancreatic enzyme activity in the duodenal fluid showed a severe reduction in lipase: 120 U/ml/min (normal value = 600 U/ml/min). Small bowel bacterial overgrowth was excluded by microbiologic examination of intestinal fluid. The patient was treated with metronidazole, leading to a complete remission of symptoms. Immediately after stopping treatment, the FCT was 15.2 U/g. Four months after hospitalization, the patient's weight had increased by 11 kg and he was asymptomatic; total proteins were 6.7 g/dL; albumin, 3.8 g/dL; triglycerides, 104 mg/dL; cholesterol, 152 mg/dL; pseudocholinesterase, 3,567 mg/dL; calcium, 10 mg/dL; steatorrhea was 3.6 g/24 hr and fecal chymotrypsin was 88 U/g. This case describes a severe, reversible impairment in pancreatic function leading to clinical malabsorption in the presence of Giardia infection.
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PMID:Secondary impairment of pancreatic function as a cause of severe malabsorption in intestinal giardiasis: a case report. 923 Jul 86