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)

A 44-year-old woman with C1q esterase inhibitor deficiency was seen in consultation for recurrent right upper quadrant abdominal discomfort, nausea, and vomiting. Each of these episodes was accompanied by concomitant peripheral edema. Initial diagnostic efforts were fruitless. In time, intermittent elevations in amylase and lipase developed, and a diagnosis of relapsing pancreatitis was made. We contend that the patient's recurrent acute pancreatitis is associated with her hereditary angioedema. Possible pathogenesis could involve intermittent intrapancreatic edema with partial ductal obstruction or loss of inhibition on the kallikrein-kinin system.
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PMID:Hereditary angioedema associated with pancreatitis. 143 59

A total of 25 patients with metastatic renal cancer were treated on a phase II protocol with 5 days of continuous-infusion fluorodeoxyuridine (FUDR), (0.1 mg/kg daily) together with high-dose oral leucovorin (100 mg 4 h) and daily x6 high-dose interferon-alpha 2b (30 x 10(6) IU/m2). Despite the good performance status of the patients and the inclusion of 14 previously untreated patients in the cohort, no response was observed among the 20 evaluable patients. Toxicities included high fever, moderate anemia, transient leukopenia, transient and mild elevations of transaminases, and moderate to severe nausea, vomiting, diarrhea, and mucositis. There were also two episodes each of confusion, fluid retention, and pancreatitis and one episode of increased creatinine levels. During the study three deaths occurred, two of which were possibly therapy-related. Despite previous reports of activity of FUDR in metastatic renal cancer, the present regimen cannot be recommended.
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PMID:Continuous-infusion fluorodeoxyuridine with leucovorin and high-dose interferon: a phase II study in metastatic renal-cell cancer. 146 58

Vomiting, abdominal pain and distension, common findings in children who receive bone marrow transplants (BMT), are usually attributed to chemo-irradiation and mucositis, universally found in these patients. We report seven children, 3.5% of BMT patients at our institutions, with these symptoms who were found to have mild to severe pancreatitis during conditioning for or after receiving BMT. All patients were receiving drugs known to cause pancreatitis, such as adrenocorticosteroids and sulfonamides as well as numerous putative pancreatotoxins such as cyclosporin A and cytosine arabinoside. Five of the seven patients had suffered from graft-versus-host disease. In patients who have received BMT, upper gastrointestinal symptoms should not be attributed to mucositis or chemo-irradiation without first testing for pancreatitis.
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PMID:Pancreatitis associated with bone marrow transplantation in children. 151 81

We report a patient with classical features of amiodarone hepatotoxicity who died of progressive liver failure. Throughout the course of his illness, he had epigastric pain, nausea, vomiting, and persistent mild to moderate elevation of amylase and lipase in his serum and peritoneal fluid. Pancreatitis due to amiodarone has not been reported. We raise the question of whether or not the pancreas is yet another organ subject to amiodarone toxicity and speculate as to possible pathogenesis. We suggest that patients on amiodarone who develop abnormal liver enzymes, nausea, vomiting, or abdominal pain be evaluated not only for hepatotoxicity, but for pancreatitis as well.
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PMID:Can pancreatitis be associated with amiodarone hepatotoxicity? 168 30

A 28-year-old woman with nausea, vomiting, and abdominal pain had been hospitalized elsewhere on 13 separate occasions over the year before this admission for similar episodes thought to be secondary to acute pancreatitis. She had undergone repeated work-ups including endoscopic retrograde cholangiopancreatography, computed tomographic scan, and exploratory laparotomy. There was a discrepancy between her unremarkable physical examination and extremely elevated amylase (3,210 U/L) which suggested nonpancreatic hyperamylasemia; normal serum pancreatic isoamylase, trypsinogen, and lipase confirmed this suspicion. The patient was noted to have self-induced vomiting in the hospital which she admitted was frequent behavior. her psychiatric disturbance was characterized as an atypical eating disorder. This case illustrates that hyperamylasemia in association with abdominal pain, nausea, and vomiting may not be secondary to pancreatitis and that use of a second serum marker (such as trypsinogen, lipase, or isoamylase) helps to establish a definitive diagnosis.
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PMID:Atypical eating disorder masquerading as recurrent acute pancreatitis: the value of multiple pancreatic serological markers. 168 31

A case of acute necrotizing pancreatitis in association with choledochal cyst is presented. Pancreatitis associated with choledochal cyst is probably caused by a biliary reflux into the pancreatic duct via a pancreatobiliary malunion, as the intraductal pressure of the cyst exceeds that of the pancreatic duct. Ampullar stenosis due to gallstones or inflammatory changes may increase the intraductal pressure. Bile with activated pancreatic enzymes refluxes into the pancreatic duct, and possibly results in acute pancreatitis. However, patients with choledochal cyst presenting with recurrent bouts of abdominal pain, vomiting, and fever have often been diagnosed as having acute pancreatitis because of hyperamylasemia, despite no evidence of pancreatitis at the time of surgery. At the time of bouts, they also show a slight elevation of serum bilirubin, and an increase in the degree of the choledochal dilatation that are possibly caused by biliary obstruction, not ampullar obstruction, due to suppurative cholangitis. The term "fictitious pancreatitis" or "pseudopancreatitis" in choledochal cyst appears to be appropriate. This clinical study shows that amylase in the biliary tract has ready access to the blood stream, probably through a sinusoidal pathway by cholangiovenous reflux, and a lymphatic pathway, via the Disse's space and denuded cyst wall, provided the biliary ductal pressure is increased.
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PMID:Pseudopancreatitis in choledochal cyst in children: intraoperative study of amylase levels in the serum. 169 Feb 81

A retrospective study of 76 children with hemolytic uremic syndrome (HUS) who were admitted to the Alberta Children's Hospital in Calgary. Alberta between January 1982 and December 1988 was undertaken to explore the gastrointestinal manifestations of the syndrome. The children (mean age of 4.0 +/- 3.1 years) presented primarily during the summer months with a microangiopathic hemolytic anemia (Hgb 94 +/- 26 g/L), thrombocytopenia (platelets 87 +/- 83 X 10(9)/L), and acute renal failure (oligoanuria with a BUN of 26 +/- 15 mmol/L, and a creatinine of 294 +/- 90 mumol/L). Forty-three children required dialysis for 10 +/- 17 days. The duration of hospitalization was 17 +/- 17 days. Four children died of complications attributable to HUS. The following symptoms and gastrointestinal manifestations of HUS were noted: fever (33%), vomiting (80%), abdominal discomfort/tenderness (59%), diarrhea (100%), hemorrhagic colitis (79%), rectal prolapse (13%), colonic stricture (3%), colonic perforation (1%), intussusception (1%), indirect hyperbilirubinemia (49%), and elevated hepatocellular enzymes (58%). Of the last 29 children studied, 19 (66%) had elevated levels of amylase and lipase in the presence of acute renal failure, and six (21%) had a marked elevation of lipase (more than four times normal) with additional supportive evidence of pancreatitis. The additional supportive evidence included persistent elevation of lipase after the resolution of acute renal failure in four children, a marked increment in lipase in association with abdominal pain and an abnormal ultrasound of the pancreas after the initiation of oral feeding in a fifth child, and pancreatic exocrine and endocrine necrosis at autopsy in a sixth child.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gastrointestinal manifestations of hemolytic uremic syndrome: recognition of pancreatitis. 170 51

The role of operative intervention for hereditary pancreatitis, a rare form of chronic parenchymal destruction, is unclear. To determine whether surgical therapy is safe and provides prolonged symptomatic relief, the authors reviewed the management of 22 adults (11 men, 11 women) with hereditary pancreatitis treated surgically between 1950 and 1989. Hereditary pancreatitis was defined as a family history of two or more relatives with pancreatitis and clinical, biochemical, or radiologic evidence of pancreatitis. The mean ages at onset of symptoms and at operation were 15 years (range, 3 to 52 years) and 31 years (range, 18 to 54 years), respectively. Pain was the primary indication for operation in all patients. Additional symptoms included nausea, vomiting (73%), weight loss (55%), and diarrhea (41%). Ductal dilatation was present in 68%, pancreatic parenchymal calcifications in 73%, pseudocysts in 36%, and splenic vein thrombosis in 18%. Primary operations included ductal drainage in 10 patients, pancreatic resection alone in three, resection with drainage in three, cholecystectomy plus sphincteroplasty in two, cholecystectomy with or without common bile duct exploration in two, pancreatic abscess drainage in one, and pseudocyst drainage in one. There were no perioperative deaths, and the morbidity rate was 14% (intra-abdominal abscess, wound infection, and urinary tract infection). Symptoms recurred in nine patients. Severity prompted reoperation in five. Secondary operations included pancreatic resection in three, pseudocyst excision in one, and pancreaticolithotomy in one. Follow-up to date is complete and extends for a median of 85 months. Eighteen patients (82%) are clinically improved or asymptomatic. Symptoms have persisted in four patients, and two patients have died of pancreatic carcinoma. Two patients died of unrelated causes. Surgical therapy for patients with hereditary pancreatitis selected on the basis of the traditional indications for surgical treatment of chronic pancreatitis is safe and efficacious.
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PMID:The surgical spectrum of hereditary pancreatitis in adults. 173 48

Recurrent abdominal pain in an adolescent population is a frequent complaint. However, diseases of the pancreas, and especially chronic pancreatitis, in this age group are extremely uncommon. One type of pancreatitis, fibrosing pancreatitis, has been reported in only 14 previous pediatric patients, five of whom were over 12 years of age. We report an additional 12-year-old female with this condition. This case serves to remind us that fibrosing pancreatitis needs to be considered in any adolescent patient with chronic abdominal pain, recurrent vomiting, weight loss, steatorrhea, and painless obstructive jaundice.
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PMID:Chronic fibrosing pancreatitis in a 12-year-old female. 175 9

N-(2,2-Diphenylethyl)adenosine (DPEA) has been identified as a potential antipsychotic agent acting via stimulation of adenosine receptors. The projected human therapeutic dose, based on animal studies, is 2-3 mg/kg. DPEA has been tested for potential toxicity in mice, rats, dogs and monkeys. Following single oral doses, median lethal dose values were approximately 10-fold greater in rats than in mice, although similar clinical signs including reduced activity, prostration, and necrosis of the tail were seen in both species. DPEA was well tolerated at daily doses up to 40 mg/kg in rats for 2 weeks. A no observed effect level (NOEL) was not identified in the dog or monkey studies. Reduced activity, dacryorrhea, ptosis, hypothermia, necrosis of the tail, and death occurred in rats given 120 and 160 mg/kg. Pathologic changes consisted of pancreatitis, gastric erosion/ulceration, lymphocyte depletion of the thymus, and pulmonary congestion and hemorrhage at 80 mg/kg or greater. In dogs, sporadic emesis was noted at 12.5 mg/kg and greater, and significant pathologic changes consisted of coronary arteritis associated with myocardial lesions and lymphocyte depletion at 25 and 50 mg/kg, pancreatic acinar necrosis at 50 mg/kg, and renal tubular degeneration at 12.5 mg/kg and greater. Emesis and depression were noted at 25 and 50 mg/kg in monkeys. Renal tubular dilatation and degeneration at 25 and 50 mg/kg were noted in the monkeys. These studies demonstrated that DPEA produced a range of adverse effects in common laboratory animal species.
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PMID:Preclinical toxicity studies of an adenosine agonist, N-(2,2-diphenylethyl) adenosine. 187 77


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