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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a patient with an eating disorder and hyperamylasemia originating from the salivary glands, who developed pancreatitis with a huge pancreatic pseudocyst. A 40-year-old woman was referred for the treatment of an eating disorder that had persisted for 9 years. She was admitted with abdominal pain, diarrhea, and nausea. She had bilateral parotid enlargement with marked elevation of total serum amylase level (3288 IU/l; normal range, 60-220) and an isolated increase of salivary isoamylase activity. After her symptoms resolved, oral intake of food was commenced. She subsequently complained of abdominal pain; this was associated with a slight elevation of serum pancreatic isoamylase and lipase levels, and a huge pancreatic pseudocyst was detected. Percutaneous drainage of the pseudocyst was successful. Endoscopic retrograde cholangiopancreatography demonstrated irregularity of the pancreatic duct. Based on these findings, the final diagnosis was parotid enlargement and acute exacerbation of chronic pancreatitis associated with a pancreatic pseudocyst in a patient with an eating disorder.
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PMID:Pancreatic pseudocyst associated with eating disorder. 965 29

A 25 year-old woman experienced a sudden onset of epigastralgia with nausea, and consulted our hospital. Because the abdominal pain did not subside with medication, she was hospitalized. On physical examination she had a slight tenderness of the right upper abdominal quadrant. Laboratory studies disclosed increases in the serum alkaline phosphatase, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and serum amylase levels. Abdominal ultrasonography, computed tomography, and endoscopic retrograde cholangiopancreatography revealed choledocholithiasis and a pancreatic duct which originated from the common bile duct. A common bile duct stone was removed with a basket catheter after an endoscopic sphincterotomy was performed. Since an anomalous union of a pancreatobiliary duct is a high risk factor of gallbladder cancer, laparoscopic cholecystectomy was perfomed. The post-operative course was uneventful and she was discharged on the twentieth post-operative day. In a microscopical examination of the resected specimen, a pyloric type gastric mucosa was clearly evident in the submucosa, while the remaining gallbladder demonstrated chronic cholecystitis. Some cases of heterotopic gastric mucosa in the gallbladder come from metaplasia, and metaplasia is also one of the most important factors in the carcinogenesis of gallbladder cancer. In conclusion, the present case is the first report of gastric mucosa with an anomalous union of the pancreatobiliary duct. Heterotopic gastric mucosa in the gallbladder may be one of the causes of gallbladder cancer, and close attention should, therefore, be paid to any occurrence of heterotopic gastric mucosa in this region.
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PMID:Heterotopic gastric mucosa in a gallbladder with an anomalous union of the pancreatobiliary duct: a case report. 984 91

We report herein the cases of two women, aged 34 years and 39 years, respectively, found to have hyperinsulinemic hypoglycemia after presenting with a history of episodes of temporary loss of consciousness, nausea, and fainting. Under the suspected diagnosis of insulinoma, localization procedures were carried out, but no tumor was found. In both patients, a definite gradient in insulin concentration was found in the pancreas by percutaneous transhepatic or intraoperative portal venous sampling, and a misdiagnosis of insulinoma of the pancreatic body was made. During exploratory laparotomy no tumor was palpable in the pancreas, and intraoperative ultrasonography showed no low echoic mass in the pancreas. A distal pancreatectomy was performed in both patients, and histopathological examination of the resected specimens revealed graded slight hyperplasia of the islet cells.
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PMID:Nesidioblastosis with hyperinsulinemic hypoglycemia in adults: report of two cases. 1021 70

Hereditary Pancreatitis (HP), is an autosomal dominant trait, which presents with recurrent attacks of abdominal pain, and is the most common cause of chronic relapsing pancreatitis in children. In addition to recurring episodes of intense epigastric pain, patients have nausea, vomiting, and anorexia, and typically show elevated serum amylase levels during the acute episode that can rapidly decline in convalescence. Complications of long-standing disease include features of chronic pancreatitis, such as pancreatic pseudo-cyst, exocrine and endocrine failure, parenchymal calcification, and pancreatic cancer. A large family from Virginia, which was originally studied by Katwinkle and Lapey in 1973, was re-ascertained through a new proband. Linkage studies in this family mapped the gene to the 7q35 region, with similar results being reported simultaneously by two other groups. A pathogenic G to A transition mutation in exon 3 of the cationic trypsinogen (CT) gene, which had previously been mapped to this region, was found both in our family as well as other families from North America. Many other conditions can produce abdominal symptoms that are often mis-attributed to the disease in HP families. An affected member of our family in whom the mutation was confirmed by direct sequencing of exon 3 of the cationic trypsinogen gene requested diagnostic testing on his 4-year-old son because of onset of severe abdominal pain and vomiting. Screening for the mutation in this child did not reveal the pathogenic G to A change. These results prevented unnecessary invasive diagnostic procedures and treatment in this child. The pre-symptomatic testing of high risk individuals could, thus, have a significant impact on the well being of both affected and normal family members.
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PMID:Implications of molecular diagnostic testing in families with hereditary pancreatitis. 1046 47

Acute pancreatitis is one of the complications associated with severe primary and secondary hypertriglyceridemia. The frequency of hypertriglyceridemia in patients with pancreatitis ranges from 4 to 53%. The elevation in serum triglycerides probably induces the release of free fatty acids, responsible for the pancreatic damage. During a three year study, nine patients with acute pancreatitis due to hypertriglyceridemia were followed up at the University Hospital of Federal University and at the "Hospital Monte Sinai" (Juiz de Fora, MG, Brazil). Suggestive clinical manifestations, especially superior abdominal pain, nausea, vomiting and ileus, were found in all the patients; however, only three showed elevated serum amylase levels. All had triglyceride levels above 1000 mg/dl (11.3 mmol/L). The evolution after clinical treatment was good in eight patients (two needed parenteral nutrition). The only death observed was due to shock and acute respiratory distress, refractory to clinical management. The maintenance treatment aimed at withdrawing the predisposing conditions and reduction of the triglyceride levels prevented recurrence of acute pancreatitis episodes during the 23 months of follow-up.
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PMID:[Hyperlipemic pancreatitis: clinical course]. 1051 73

A case of erythropoietic protoporphyria associated with severe hepatic dysfunction and acute pancreatitis is reported. The patient, a 33-year-old man, was admitted to our hospital complaining of upper abdominal pain, nausea, and vomiting of 3 days' duration. Laboratory tests on admission demonstrated liver dysfunction, anemia, and thrombocytopenia. On the third hospital day, the intensity of the upper abdominal pain increased, concomitantly with elevated levels of serum amylase. Ultrasonography and computed tomography scanning revealed a slightly enlarged pancreas. During this episode, he also complained of various neurological symptoms, including reduced mental alertness, weakness of extremities, constipation, profound sweating, and urinary retention. Porphyrin studies demonstrated markedly elevated erythrocyte and fecal protoporphyrin levels. Laparoscopic findings obtained after the attack subsided were compatible with porphyric liver cirrhosis. We therefore concluded that neurologic disorders and acute pancreatitis could develop in patients with erythropoietic protoporphyria with severe liver dysfunction.
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PMID:Erythropoietic protoporphyria with severe liver dysfunction and acute pancreatitis. 1083 76

The use of protease inhibitors such as ritonavir to treat HIV-infected individuals has been associated with lipodystrophy, combined hyperlipidemias, and hypertriglyceridemia-induced pancreatitis. We report here on the treatment by plasmapheresis of a HIV-patient who presented with a rapid onset of severe ritonavir-induced hypertriglyceridemia complicated with an acute pancreatitis. A 35-year-old HIV-1 positive male following 3 weeks of ritonavir treatment presented with nausea, abdominal pain, a distended abdomen, and the following laboratory values: amylase (238 U/L), lipase (864 U/L), total cholesterol (27.1 mmol/L), and triglycerides (62.9 mmol/L). Following two plasmaphereses, the levels of total cholesterol, triglycerides, lipase, and amylase declined drastically and the patient was discharged home after 4 days with lipid and pancreatic enzyme levels within the reference range. To our knowledge, this is the first case of pancreatitis due to a PI-induced hyperlipidemia in a HIV-patient treated with plasmapheresis in an acute setting.
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PMID:Plasmapheresis in the treatment of an acute pancreatitis due to protease inhibitor-induced hypertriglyceridemia. 1174 45

We report tamoxifen-induced hypertriglyceridemia and asymptomatic acute pancreatitis in a 51 year-old women with type 2 diabetes mellitus and stage III-b infiltrative ductal carcinoma, admitted to the hospital with weakness, oliguria and glucose dysregulation. On admission, there was no fever, abdominal or back pain, rebound tenderness, nausea, or vomiting. Following 1 year of tamoxifen treatment, triglycerides increased from 400 to 1344 mg/dl (blood urea nitrogen 52 mg/dl, creatinine 2.0 mg/dl, glucose 341 mg/dl). Hypertriglyceridemia was considered to be due to either diabetic dyslipidemia and/or tamoxifen. On computerized tomography, pancreatic enlargement, heterogenity, hypodensity and a pancreatic pseudocyst (5 x 7.5 cm diameter) were found. Acute pancreatitis was suspected, and serum amylase level was found to be increased (273 IU/L). Tamoxifen was discontinued and gemfibrozil was started. Triglycerides decreased to 301 mg/dl and amylase decreased to 66 IU/L a week later and remained normal thereafter. This case indicates that tamoxifen-induced hypertriglyceridemia may cause acute pancreatitis without classical symptoms which might be due to autonomic neuropathy in diabetic patients. Effects on lipid metabolism should be considered and triglycerides should be closely followed in patients on tamoxifen.
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PMID:Asymptomatic acute pancreatitis due to tamoxifen-induced severe hypertriglyceridemia in a patient with diabetes mellitus and breast cancer. 1212 Aug 88

Endoscopic retrograde cholangiopancreatography (ERCP), together with its substantial therapeutic capabilities, carries a higher potential for complications than other endoscopic procedures. Common major complications specific to pancreaticobiliary instrumentation include pancreatitis, post-sphincterotomy hemorrhage, perforation, and cholangitis with or without systemic sepsis. Two patients underwent therapeutic ERCP for recurrent episodes of abdominal pain and elevation of hepatobiliary enzymes. Endoscopic sphincterotomy was difficult and prolonged. The calculi were successfully extracted by sweeping the choledochus with a balloon-tipped catheter or basket in both cases. The patients experienced postprocedure diffuse abdominal pain unassociated with nausea or vomiting. Laboratory data showed normal serum amylase and lipase 2, 6, and 18 h after the end of procedure, a fall in hematocrit level, and an increase of indirect bilirubin and lactic dehydrogenase. The abdominal pain subsided in 4 to 6 h. The hematocrit level remained stable during the next 3 days, and the patients were very well when discharged. Examination of glucose-6-phosphate dehydrogenase (G-6PD) enzyme levels in red cells 20 days later showed complete enzyme deficiency. This report highlights the importance of examining G-6PD deficiency in patients with post-ERCP abdominal pain, normal serum amylase and lipase, and laboratory findings of hemolysis.
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PMID:Hemolysis caused by G-6PD deficiency after a difficult and prolonged therapeutic endoscopic retrograde cholangiopancreatography. 1272 87

Systemic lupus erythematosus presenting as acute pancreatitis is rare. We report a case of a 12-year-old girl with a 1-year history of systemic lupus erythematosus who developed active pancreatitis. The pancreatitis was first manifested by nausea, vomiting, fever, and abdominal pain. Elevated serum amylase (578 U/L) and lipase levels (5588 U/L), and pancreatic enlargement on ultrasound and computerized tomography confirmed the diagnosis. She responded well to high-dose corticosteroid. The high titer of antinuclear antibodies (1:1280) and low level of complement components (C3, 42.9 mg/dL; C4, 2.3 mg/dL) during the pancreatitis attack suggested that the pancreatitis may have been due to systemic lupus erythematosus exacerbation and not related to drug therapy.
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PMID:Systemic lupus erythematosus-related acute pancreatitis: a case report. 1458 68


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