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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Hyperamylasemia, which has been reported in patients with the eating disorders anorexia nervosa and bulimia, generally has been thought to result from pancreatitis. To evaluate the mechanisms of hyperamylasemia, we measured amylase, lipase, and isoamylase activity in 17 consecutive patients admitted to the eating disorder unit. Six patients had elevated amylase activity, and 5 of these 6 had isolated increases in salivary isoamylase activity. Six other patients had normal serum total amylase activity but modest elevations in the salivary isoamylase fraction. No patient developed clinical evidence of pancreatitis during hospitalization. Thus, the hyperamylasemia in patients with anorexia and bulimia often is caused by increased salivary-type amylase activity. The appropriate diagnostic test for hyperamylasemia in patients with anorexia or bulimia is the simple measurement of serum lipase or pancreatic isoamylase activity. If these levels are found to be normal, further tests to exclude pancreatitis are unnecessary.
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PMID:Hyperamylasemia in patients with eating disorders. 243 40

Between 1978 and 1985, we conducted a prospective study of 21 patients who survived several attacks of pancreatitis and were diagnosed as having primary hyperlipidemia. None of the patients suffered from chronic alcoholism, primary diabetes, or cholelithiasis or was receiving prolonged steroid therapy. Lowering of plasma lipid values toward normal was achieved in all patients following a program of combined dietary and drug (bezafibrate) therapy. Five patients had recurrent episodes of pancreatitis during the treatment program. These patients were diagnosed subsequently as suffering from bulimia and were all given cognitive behavioral therapy. One patient died following an attack of pancreatitis. An underlying eating disorder should be suspected in patients who relapse after treatment for pancreatitis and hyperlipidemia. Multidisciplinary treatment should be used in these patients to improve therapeutic efficacy and uncover behavioral patterns that have a direct impact on their life expectancy.
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PMID:Bulimia. An underlying behavioral disorder in hyperlipidemic pancreatitis: a prospective multidisciplinary approach. 382 58

Bulimia is an episodic compulsive urge to overeat often followed by recurrent attempts to lose weight by self-induced vomiting. Seven young women with this eating disorder and associated benign bilateral painless parotid enlargement are described. The glandular swelling was generally intermittent, with parotid enlargement usually developing 2 to 6 days after a binge overeating episode had stopped. Several had hypokalemic alkalosis and a moderate elevation in serum amylase levels. None had clinical evidence of pancreatitis, and a parotid gland biopsy in one patient was normal. The clinician should be alerted to the association of benign parotid enlargement with this syndrome.
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PMID:Benign parotid enlargement in bulimia. 616 Jul 96

Acute pancreatitis developed in an 18-year-old woman after multiple episodes of bulimia. The pancreatitis was severe and the patient developed a pseudocyst. Eating disorders may be associated with acute pancreatitis, and so we review the literature on this possibility.
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PMID:Acute pancreatitis associated with bulimia. 658 19

Anorexia nervosa (AN) and bulimia nervosa (BN) are potentially fatal eating disorders which primarily affect adolescent females. Differentiating eating disorders from primary gastrointestinal (GI) disease may be difficult. GI disorders are common in eating disorder patients, symptomatic complaints being seen in over half. Moreover, many GI diseases sometimes resemble eating disorders. Inflammatory bowel disease, acid peptic diseases, and intestinal motility disorders such as achalasia may mimic eating disorders. However, it is usually possible to distinguish these by applying the diagnostic criteria for eating disorders and by obtaining common biochemical tests. The primary features of AN are profound weight loss due to self starvation and body image distortion; BN is characterized by binge eating and self purging of ingested food by vomiting or laxative abuse. GI complications in eating disorders are common. Recurrent emesis in BN is associated with dental abnormalities, parotid enlargement, and electrolyte disturbances including metabolic alkalosis. Hyperamylasemia of salivary origin is regularly seen, but may lead do an erroneous diagnosis of pancreatitis. Despite the weight loss often seen in eating disorders, serum albumin, cholesterol, and carotene are usually normal. However, serum levels of trace metals such as zinc and copper often are depressed, and hypophosphatemia can occur during refeeding. Patients with eating disorders frequently have gastric emptying abnormalities, causing bloating, postprandial fullness, and vomiting. This usually improves with refeeding, but sometimes treatment with pro-motility agents such as metoclopromide is necessary. Knowledge of the GI manifestations of eating disorders, and a high index of suspicion for one condition masquerading as the other, are required for the correct diagnosis and management of these patients.
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PMID:Gastrointestinal and nutritional aspects of eating disorders. 840 9

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 26-year-old woman with an eating disorder presented to the emergency department with severe abdominal pain following binge eating. A plain film X-ray demonstrated a huge dilatation of the stomach with a high air-fluid level. Serum amylase was 2,265 IU/L, and serum lipase was 2,001 IU/L. Abdominopelvic computed tomography scan revealed a massive gastric dilatation and completely compressed duodenum. The distended right colonic loop and small bowel loops were reduced to the pelvic area and the displaced small bowel and mesenteries tightly pulled on the mesenteric vasculature. After nasogastric tube decompression and irrigation, her abdominal pain subsided. On the 15th day after admission, a follow-up abdominopelvic computed tomography scan demonstrated mild edematous changes of the pancreas compatible with pancreatitis.
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PMID:Acute gastric dilatation and acute pancreatitis in a patient with an eating disorder: solving a chicken and egg situation. 2142 80