Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperamylasemia and parotid hypertrophy are conditions found in bulimic patients. The authors studied serum amylase levels in 56 underweight anorectics, 24 weight-recovered anorectics, 23 normal-weight bulimics, and 31 volunteer women. Normal-weight bulimic patients had significantly higher admission serum amylase values (mean +/- SE = 73.4 +/- 8.0 IU/L) than controls (40.8 +/- 2.4 IU/L). Additionally, the serum amylase test distinguished between restrictor anorectics (N = 31, 44.7 +/- 4.7 IU/L) and bulimic anorectics (N = 25, 68.8 +/- 8.6 IU/L, p less than .05) with a high degree of specificity and a fair degree of sensitivity. A subsample (N = 7) of bulimics showed twofold to fourfold increases in serum amylase values after a controlled period of binge eating and vomiting, whereas normal volunteers showed no change in serum amylase values (p less than .001) after ingesting a large meal. Serum amylase values declined significantly within 6 to 15 days of admission. However, after passes off the unit, serum amylase values returned to admission values, presumably as a result of binge-vomit episodes. The authors observe that modest increases of serum amylase values appear to be a consequence of binge-vomit behavior and suggest that serial serum amylase determination may be useful in monitoring the degree of patient abstinence in therapeutic programs.
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PMID:Hyperamylasemia and its relationship to binge-purge episodes: development of a clinically relevant laboratory test. 170 33

In a retrospective study of patients 18 years of age and younger over a 28-year period, 48 children had pancreatitis. Epigastric pain, nausea, and emesis were present in 90%. Hyperamylasemia was present in 34 children; elevated amylase/creatinine clearance ratio was helpful in diagnosing ten others. In four children, pancreatitis was diagnosed at laparotomy. Etiology of the pancreatitis was idiopathic in 16, drug-induced in 12, all of whom had received corticosteroids. Nine developed pancreatitis after blunt trauma; seven had obstruction of the pancreaticobiliary drainage system. Two children developed pancreatitis in association with sepsis, and two had recurrent hereditary pancreatitis. Thirty of the 48 patients were managed nonoperatively while operations were required in 18. Seven had drainage of pancreatic pseudocysts, four had a pancreatectomy, and four underwent laparotomy with debridement and drainage of necrotic pancreas. Bilioenteric bypass procedures were performed to prevent recurrent pancreatitis in three patients; while duodenojenjunostomy sphincteroplasty and cholecystectomy were performed in one child each. Cure was achieved in 38 of 48 children treated for pancreatitis and its complications; each subsequently grew and developed normally. Hemorrhagic pancreatitis occurred in seven children, six of whom died. Seven deaths occurred, all in the medically treated group. Fifteen of the 18 children treated operatively did well in long-term follow-up. Although rare, pancreatitis is a serious cause of abdominal pain in childhood; almost half of the children will benefit from operation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Surgical management of pancreatitis in childhood. 361 58

The authors investigated the significance of vomiting for hyperamylasemia and sialadenosis in patients with bulimia nervosa. Hyperamylasemia was found in 61% of the bulimics and in 20% of the restrictor anorectics but in no patients with binge-eating syndrome. In more than three fourths of the bulimics there was a close positive correlation between the frequency of vomiting and total serum amylase levels. Both frequency and type of vomiting seem to be relevant to the extent of salivary gland enlargement. The significance of vomiting for the etiopathology of hyperamylasemia and for the diagnosis of eating disorders will be discussed.
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PMID:Significance of vomiting for hyperamylasemia and sialadenosis in patients with eating disorders. 768 85

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

Three cases of acute pancreatitis following transurethral resection of the prostate are reported. The incidence is rare. A review of perioperative data failed to disclose any unique factor except in 1 patient who had an underlying biliary tract disease. Hyperamylasemia or hyperlipaemia in association with abdominal pain and vomiting was noted in all patients to establish the diagnosis. Computed tomography also confirmed the existence of acute pancreatitis. One patient died of respiratory and renal failure. However, early diagnosis and prompt treatment are essential to reduce high mortality. In conclusion, acute pancreatitis should be considered as one of the differential diagnoses in the presence of abdominal pain with vomiting, azotemia or oliguria after transurethral resection of the prostate.
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PMID:Acute pancreatitis following transurethral resection of prostate. 850

Hyperamylasemia has been reported in more than 65% of patients with severe leptospirosis, and the true diagnosis of acute pancreatitis is complicated by the fact that renal failure can increase serum amylase levels. Based on these data we retrospectively analyzed the clinical and histopathological features of pancreas involvement in 13 cases of fatal human leptospirosis. The most common signs and symptoms presented at admission were fever, chills, vomiting, myalgia, dehydratation, abdominal pain and diarrhea. Trombocytopenia was evident in 11 patients. Mild increased of AST and ALT levels was seen in 9 patients. Hyperamylasemia was recorded in every patient in whom it was measured, with values above 180 IU/L (3 cases). All patients presented acute renal failure and five have been submitted to dialytic treatment. The main cause of death was acute respiratory failure due to pulmonary hemorrhage. Pancreas fragments were collected for histological study and fat necrosis was the criterion used to classify acute pancreatitis. Histological pancreatic findings were edema, mild inflammatory infiltrate of lymphocytes, hemorrhage, congestion, fat necrosis and calcification. All the patients infected with severe form of leptospirosis who develop abdominal pain should raise the suspect of pancreatic involvement.
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PMID:Pancreatic involvement in fatal human leptospirosis: clinical and histopathological features. 1476 28