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Case reports of 2 patients who developed pancreatitis and hyperlipidemia while using oral contraceptives are presented. The 1st patient had been taking Ovulen for 2 years when severe abdominal pain suddenly developed. Initially cholecystitis was diagnosed. Symptoms subsided within 1 week but recurred 2 months later, when the white blood count was increased to 16,400/cubic mm. Serum was grossly lipemic with a triglyceride level of 3500 mg% and serum cholesterol 560 mg%. 3 days later triglycerides had fallen to 400 mg% and cholesterol to 270 mg%. Cholecystography was normal. The pain had subsided. Symptoms have not recurred since stopping use of Ovulen. The 2nd patient was admitted with severe abdominal pain of 48 hours duration. Similar attacks of pain had occurred previously but had been of short duration. She had been taking Ovulen for 3 years. White blood count was increased to 18,000. Serum was grossly lipemic. Serum glyceride concentration was 7000 mg% and cholesterol 1200 mg%. Afer 3 days triglycerides were 500 mg% and cholesterol 475 mg%. Pancreatitis was diagnosed. Therapy was Ryles tube suction, atropine, intravenous saline, and a broad spectrum antibiotic. Symptoms subsided in 10 days. The hyperlipidemia is thought to have been a primary condition causing the pancreatitis. [Patients known to have such a condition should avoid use of oral contraceptives.
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PMID:Hyperlipidaemia and pancreatitis associated with oral contraceptive therapy. 118 40

A case of pancreatic ascites is reported and compared with 55 previously reported cases. A 42-year-old black male chronic alcoholic presenting with abdominal pain was found at operation to have chronic pancreatitis with no pseudocyst formation or overt duct disruption, in contrast to the majority of cases reported. The diagnosis and differentiation from cirrhosis of the liver were based on the operative findings, elevated serum amylase level, ascitic fluid amylase value, and protein content. Surgical exploration alone has proven beneficial--the patient has done well in the past 2 years with no recurrence of the ascites and continued weight gain. The clinical course was compatible with pancreatitis although the radiographic and angiographic studies were not diagnostic. It is suggested that the clinical entity of pancreatic ascites occurs more often than reported and a workup for it should be done even in the face of unconvincing radiographic and angiographic evidence.
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PMID:Pancreatic ascites. A case report and review of the literature. 120 11

Eight-four patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) were randomized to receive 100 micrograms of octreotide intravenously immediately prior to ERCP, and 100 micrograms subcutaneously 45 min after the initial dose, or placebo. Amylase, lipase, and glucose were measured and clinical assessment was performed before, and 2 and 24 h after, ERCP. We define clinical pancreatitis as the combination of elevated amylase or lipase with abdominal pain and tenderness. Interim analysis in 84 patients revealed an 11% incidence of clinical pancreatitis in the control group and 35% in the treatment group (p < 0.01). There were no differences in either group with respect to sphincterotomy, gender, age, duration of ERCP, number of cannulations of the pancreatic duct, degree of duct injection, or the volume of contrast injected. Analysis of group differences stratified by sphincterotomy revealed the following: 1) In patients who did not undergo a sphincterotomy, there was a significantly higher rate of pancreatitis in the treatment group [10/17 (59%) versus 1/17 (6%) RR 10.0 (95% CI 1.4-69.8)]. 2) Sphincterotomy reduced the rate of pancreatitis in patients who received octreotide from 10/17 (59% no sphincterotomy), to 3/20 (15% sphincterotomy) (p = 0.01), which equals the rate in patients who received placebo and underwent sphincterotomy [4/25 (16%)]. 3) Although the incidence of pancreatitis was higher in the treatment group, octreotide may reduce the severity of pancreatitis measured by the number of days NPO (Wilcoxon rank sum, p = 0.02), length of stay after ERCP (p = 0.13), the number of days of pain (p = 0.11), and the degree of amylase elevation (p = 0.04). We conclude that: 1) Octreotide appears to increase the incidence of pancreatitis when given prophylactically for diagnostic ERCP. 2) Although pancreatitis was more common in the octreotide group, it was less severe than the placebo group. 3) Sphincterotomy may afford protection against pancreatitis in patients who received octreotide. 4) We cannot recommend the use of prophylactic octreotide during diagnostic or therapeutic ERCP.
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PMID:A multicenter, randomized, controlled trial to evaluate the effect of prophylactic octreotide on ERCP-induced pancreatitis. 836 55

To determine whether the lipase:amylase ratio differentiates alcoholic from nonalcoholic pancreatitis, we conducted a retrospective review of charts with the diagnosis of acute pancreatitis at the George Washington University Medical Center between January 1988 and July 1990. A total of 446 charts were reviewed. For a patient to be included in the subsequent analysis, the following criteria were met: 1) the patient had typical symptoms of pancreatitis, 2) serum amylase and lipase were analyzed on admission, and 3) a computerized tomographic (CT) scan or ultrasound of the abdomen was obtained within 72 h of admission. Forty-seven charts satisfied the requirements for inclusion in the study. Data collected from the charts included history of alcohol consumption, age, sex, race, admission serum amylase and serum lipase (from this the amylase:lipase ratio was calculated), peak serum amylase and serum lipase, and number of days of abdominal pain before admission. Patients with alcoholic pancreatitis had significantly lower serum amylase levels and significantly higher lipase:amylase ratios than those with nonalcoholic pancreatitis (p < 0.01). There was no difference in the serum lipase between the groups. The higher the lipase:amylase ratio, the greater the specificity of alcohol as the etiology of acute pancreatitis. Only patients with alcoholic acute pancreatitis had lipase:amylase ratios > 5.0 (sensitivity 31%, specificity 100%). Our data point to the clinical utility of the lipase:amylase ratio in differentiating alcoholic from nonalcoholic acute pancreatitis. Prospective studies will be needed to confirm the clinical utility of this ratio.
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PMID:The admission serum lipase:amylase ratio differentiates alcoholic from nonalcoholic acute pancreatitis. 128 Apr 5

Five hundred patients with successful pancreatogram between 1982 and 1990, 8 patients (1.6%) were found to have complete pancreas divisum. The sex distribution was equal (4 men, 4 women), and the average age was 42.5 years (22-77 years). No increased incidence of pancreas divisum in any of the three groups: a group with pancreatitis, a group with unexplained upper abdominal pain, and an incidental group (obstructive jaundice, gall bladder disease, abdominal mass, miscellaneous). These findings show that pancreas divisum is a normal anatomic variant with an incidence of 1.6 per cent in Thai patients, and is seldom a cause of pancreatic symptoms.
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PMID:Pancreas divisum: incidence and clinical evaluation in Thai patients. 130 37

The occurrence of rhabdomyolysis and acute renal failure associated with cytomegaloviral infection is rare. A 27-year-old housewife was admitted to our hospital with complaints of thirst, muscle weakness, abdominal pain and oliguria. There was no past history of diabetes, drinking, fever or drug habituation and a negative family history. Laboratory tests revealed myoglobinuria, hyper-pancreatic type amylaseuria, hyperglycemia, azotemia and highly increased creatine phosphokinase in the plasma. She was treated with hemodialysis and insulin therapy. Serological studies showed a 4-fold increase in cytomegalovirus antibody titers 4 weeks after admission. Muscle biopsy specimens showed hyaline degeneration and infiltration of T cell lymphocytes in the muscle. Renal biopsy specimens showed acute tubular necrosis and some myoglobin casts. No cytomegalovirus antigen was found in renal specimens by immunofluorescence study. From these results, it was determined that a systemic cytomegalovirus infection triggered pancreatitis which caused diabetic ketoacidosis, rhabdomyolysis and acute renal failure.
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PMID:Cytomegalovirus infection associated with acute pancreatitis, rhabdomyolysis and renal failure. 131 48

Villous neoplasms of the main pancreatic duct are uncommon. Two cases of neoplasm of the main cephalic pancreatic duct in 61- and 42-year-old patients presenting with long standing (10 and 12 years) history of abdominal pain are reported. In both cases, duodenal fistula was present and mucus was observed by endoscopy at the fistula and major papilla levels. Endoscopic retrograde pancreatography showed a stricture of the main pancreatic duct in the pancreatic head. In one case, with incomplete stricture, pancreatic ducts disclosed typical features of chronic obstructive pancreatitis and contained mucus casts. Histologic examination of total and proximal duodenopancreatectomy showed a villous neoplastic pattern with focal malignant changes within the main pancreatic duct. The adjacent pancreatic tissue showed signs of stromal invasion without lymph node or nervous infiltration. Glandular parenchyma was atrophic in the pancreatic body and tail, with extensive fibrosis, and the pancreatic duct depicted signs of nonpapillary hyperplasia. Histochemical study disclosed a predominant sialomucin secretion by villous adenoma and sulfomucin secretion by epithelial cells lining the accessory or main caudal pancreatic ducts. These results lead us to suggest a possible relationship between villous adenoma of ducts and pancreatic adenocarcinoma.
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PMID:[Villous tumors of the Wirsung's duct and pancreatic intraductal adenocarcinoma: interrelation or accidental association?]. 136 60

Because pancreatitis has been reported frequently in adults with human immunodeficiency virus infection, we sought to determine the incidence of pancreatitis in children with acquired immunodeficiency syndrome by reviewing all records of children with AIDS, their serum amylase and lipase levels, and the factors associated with pancreatitis through a case-control analysis. During a 6-year period pancreatitis developed in 9 (17%) of 53 pediatric patients with AIDS. Six children had vertical transmission of infection and three patients had acquired HIV infection through contaminated blood products. Pancreatitis developed at a median age of 5.2 years (range 1.2 to 20 years). All patients had vomiting and abdominal pain. When the patients were first seen, lipase values were elevated more than amylase values (p = 0.028). Amylase and lipase levels declined at comparable rates. In the case-control analysis, pentamidine isethionate was significantly associated with pancreatitis (p = 0.02); the risk was greater in patients who received pentamidine isethionate and had absolute CD4 T-lymphocyte counts less than 100 cells/mm3 (p = 0.001). Infections associated with the onset of pancreatitis included cytomegalovirus (4), Cryptosporidium (1), Pneumocystis carinii pneumonia (3), and Mycobacterium avium intracellulare (1). Coinfection with cytomegalovirus was associated with a protracted course in four children. Ultrasonographic examination demonstrated biliary ductal dilatation 6 months after the onset of pancreatitis in one child. Seven children have died at a mean of 8 months after the initial onset of pancreatitis; the one living child has survived 5 months from the onset of pancreatitis. We conclude that pancreatitis is common in pediatric patients with AIDS and may be related to pentamidine isethionate exposure, especially when absolute CD4 T-lymphocyte counts are less than 100 cells/mm3. Serum amylase levels do not always accurately predict the onset of pancreatitis; serum lipase levels should be measured in children with symptoms. The onset of pancreatitis in an HIV-infected child is a poor prognostic indicator.
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PMID:Pancreatitis in pediatric human immunodeficiency virus infection. 137 Sep 62

In macroamylasemia, a macromolecular complex consisting of amylase linked to immunoglobulins circulates in the plasma and usually causes benign hyperamylasemia with low or normal amylasuria. Macroamylasemia is extremely rare in pediatric patients as it has been described in only four patients. We report herein the case of a 5-year-old girl with abdominal pain and macroamylasemia. To recognize macroamylase, we used agar gel electrophoresis, PEG precipitation, and fast protein liquid chromatography (FPLC). In our case, FPLC was found to be the most reliable method for the identification of the macromolecular complex. Macroamylasemia is merely a biochemical abnormality that is not associated with any kind of pathology. Its identification is therefore essential in order to avoid a wrong diagnosis, i.e., pancreatitis, with consequent inappropriate therapies.
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PMID:Macroamylasemia in a 5-year-old girl. 137 23

This study evaluates the effect of the long acting somatostatin analogue octreotide on biochemical and clinical parameters of endoscopic retrograde cholangiopancreatography (ERCP) induced pancreatitis. Altogether 245 patients were randomised to receive either octreotide or isotonic saline. Octreotide (100 micrograms) was administered intravenously five minutes before ERCP and subcutaneously 45 minutes after ERCP. There were no significant differences in the median serum amylase and lipase activities at baseline, eight, and 24 hours after ERCP. Five patients (2%) developed clinical pancreatitis--three in the octreotide and two in the placebo groups. Excluding patients who developed pancreatitis, 43 (18%) developed abdominal pain after ERCP--21 in the octreotide and 23 in the placebo groups. There were no significant differences in the median serum amylase and lipase values between the treatment groups. None of the 52 patients who had therapeutic interventions developed pancreatitis. This study suggests that octreotide may not protect against ERCP induced pancreatitis.
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PMID:Does the somatostatin analogue octreotide protect against ERCP induced pancreatitis? 138 99


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