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)

Sixty-one patients (1 to 18 1/2 years of age) with acute pancreatitis were evaluated. In over one third of cases, acute pancreatitis was one feature of a multisystem disease (Reye syndrome, sepsis, shock, hemolytic-uremic syndrome, viral infections). Other common causes included blunt trauma (15%), acquired or congenital structural defects (10%), metabolic diseases (10%), and drug toxicity (3%). In 25% of cases, no cause was identified. All conscious patients complained of abdominal pain, but the location, severity, and duration of pain were extremely variable. Vomiting was a common symptom. Ultrasonography was helpful in establishing the diagnosis and for assessment of complications such as pseudocyst formation. Endoscopic retrograde cholangiopancreatography was used to identify structural or anatomic lesions in patients with recurrent acute pancreatitis. Serum cationic trypsin(ogen) was superior to amylase in the early diagnosis of acute pancreatitis, and was more consistently elevated during the first 5 days in the hospital. Patients were managed conservatively with complete bowel rest, gastric decompression, intravenous fluid therapy, and pain relief. Pancreatic pseudocysts occurred in 10% of patients. There were 13 fatalities, all in patients with a severe multisystem disorder. Recurrences of acute pancreatitis were noted only in certain diagnostic groups: idiopathic pancreatitis, structural anomalies of the pancreaticobiliary tree, metabolic disorders, and (in a single patient) familial pancreatitis.
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PMID:Acute pancreatitis in childhood. 245 30

High levels of the serum free fatty acids (FFA) are found in Reye's syndrome (RS). While this is attributed to enhanced adipose tissue lipolysis, the possibility that intravascular lipolysis could augment this process was investigated by measuring lipase activity in sera from RS and other subjects. Ordinarily, lipolytic activity is not detectable in serum from unheparinized subjects. Significant lipolytic activities ranging from 1-3 mumol/ml serum per hour were detected in sera from 5 of the 7 RS patients studied. Similar activities were also found in sera from two other subjects one of whom was a long-term survivor of RS and the other who had recurrent bouts of biliary obstruction and encephalopathy. Lipase activity was negligible in the serum from 2 other RS patients, 4 other long-term survivors of RS, 2 siblings, one RS parent and in 20 disease controls including patients with influenza, diabetic ketoacidosis and cerebral edema, meningitis and febrile infections with diarrhea and vomiting. None of these individuals had received heparin. An inverse relationship was found between LPL and hepatic lipase (HL) activities. Glucose levels tended to correlate directly with LPL and inversely with HL activity. The basis for the presence of LPL activity in RS sera is not known but the presence of serum lipase activity in unheparinized patients supports the notion that the TG in the circulating lipoprotein particles probably also serve as another source of FFA in the sera of RS patients.
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PMID:Serum lipolytic activity in Reye's syndrome. 259 64

This is the case of a 29 year-old woman, admitted because of diarrhea and incoercible vomiting; later in the course of the disease she developed signs and symptoms of encephalopathy. The diagnosis of Reye's syndrome was made after death.
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PMID:[Reye's syndrome in adults. Presentation of a new case and review of the literature]. 269 55

To date, seven inborn errors of mitochondrial fatty acid oxidation have been identified. A total of about 100 patients in the world have been reported. Clinically the beta-oxidation defects are more often characterized by episodic hypoglycaemia leading to a coma mimicking Reye's syndrome. The hypoglycaemia is non-ketotic since the synthesis of ketone bodies is deficient. Periods of decompensation occur when carbohydrate supply is poor, e.g. prolonged fasting, vomiting, or increased caloric requirements, as and when lipid stores are used. Defects in beta-oxidation have also been reported to be one cause of sudden infant death syndrome. The diagnosis of these inborn errors is by biochemical investigation since where symptoms suggest such a defect, the precise aetiology cannot be assessed. The biochemical diagnosis is based firstly on identification of abnormal plasma and of urinary metabolites during acute attacks. Derivatives of the omega-oxidation and omega-1-oxidation of medium chain fatty acids have been identified, as well as acylglycine and acylcarnitine conjugates. These metabolites are nearly always absent when patients are in good clinical condition. Secondly, the diagnosis must be based on the identification of the enzymatic defects: this involves global assays which allow a localization of the 'level' of the defect (i.e. the oxidation of long, medium or short chain fatty acids) and specific measurement of enzyme activities (acyl-CoA dehydrogenases and electron carriers: ETF and ETF-DH). The diagnosis of these disorders is of prime importance because of the severity of the clinical symptoms. These can be prevented, in some cases, by an appropriate diet (a high carbohydrate, low fat diet, sometimes supplemented with L-carnitine). In other cases, genetic counselling can be offered.
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PMID:The inborn errors of mitochondrial fatty acid oxidation. 311 38

The authors describe an intoxication by Atractylis gummifera in a 7-year old boy who drunk an extract made from the plant's root as traditional medicine. He was admitted to the Hospital 2 days after ingestion, in coma stage II, with epigastric pain, vomiting and general anxiety. Laboratory findings showed severe hepatocellular damage and acute renal failure. In spite of all treatment and therapeutic efforts, the boy died 8 days after admission. A postmortem histopathological study of the liver confirmed the panlobular hepatic necrosis and allowed the differential diagnosis of the intoxication from Reye syndrome.
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PMID:Hepatotoxicity due to Atractylis gummifera-L. 323 May 99

A 40-year-old woman with a history of alcohol abuse, drug-related suicide attempts, and depression presented with a flu-like illness, vomiting, and changes in mentation. On admission, therapeutic blood levels of salicylates, trazadone, and acetaminophen were found. A tentative diagnosis of a psychotic crisis with possible superimposed drug overdose was made. The etiology of the patient's acute encephalopathy remained unclear until a plasma ammonia and liver biopsy established the diagnosis of Reye's syndrome. The patient was given supportive therapy and recovered completely.
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PMID:Adult Reye's syndrome. 327 49

A family is described in which the father and three (and probably all four) of his children had a decreased capacity for the oxidation of medium-chain fatty acids. One of the children suddenly died at the age of 16 months following an episode of a rapidly deteriorating Reye syndrome-like illness with hypoketotic hypoglycemia and dicarboxylic aciduria, but without any previous alarming symptoms. The eldest sibling had died at the age of 19 months under similar conditions. The other family members had always been healthy. On fasting, all affected family members accumulated in their plasma the medium-chain fatty acids octanoic, decanoic, and cis-4-decenoic acids. Their urinary organic acid excretion profile could be characterized as "dicarboxylic aciduria." A deficiency of medium-chain acyl-coenzyme A dehydrogenase was demonstrated in a postmortem liver sample of the index patient. Cultured fibroblasts from the father and the two healthy children had a decreased rate of [14C]octanoate oxidation. It is suggested that a deficiency of medium-chain acyl-coenzyme A dehydrogenase may lead to a life-threatening illness when other complicating factors such as diarrhea and vomiting result in an abnormal depletion of the body's glycogen stores. Careful monitoring of at-risk patients during a minor illness is necessary.
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PMID:Sudden child death and 'healthy' affected family members with medium-chain acyl-coenzyme A dehydrogenase deficiency. 378 30

Reye's syndrome (RS) is generally considered a childhood disease. We report our experience with RS in adults in the metropolitan Milwaukee area. Reye's syndrome was diagnosed in seven 18- to 46-year-old adults. The diagnostic criteria were as follows: viral prodrome followed by vomiting and encephalopathy without focal neurological signs, normal cerebrospinal fluid values, increased levels of serum aminotransferases (transaminase), prolonged prothrombin time, elevated blood ammonia levels, and characteristic microvesicular fatty liver and mitochondrial changes. None of the patients was hypoglycemic. The diagnosis of RS was entertained in 22 but confirmed in only seven patients. In cases of non-Reye's encephalopathy, drug ingestion presented as one of the most difficult differential diagnostic problems, which also included alcohol abuse, collagen vascular disease, and hepatitis B surface antigenemia. Clinical jaundice, distinctly uncommon in RS, was present in only one patient who presented to us in stage V coma. In adults, RS is more difficult to diagnose and should be suspected more frequently in patients with unexplained altered behavior following a viral illness and vomiting. Liver biopsy can be performed safely and is usually mandatory in adults. Patients with RS diagnosed during stage I or II coma and treated experienced an uneventful recovery.
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PMID:Reye's syndrome in adults. Diagnostic considerations. 380 May 31

Reye's syndrome is a potentially devastating neurologic illness seen predominantly in children following a viral prodrome. The cause is unknown. The clinical history and laboratory presentation are stereotypical and easy to recognize if the clinician considers the diagnosis. Neurologic dysfunction is characterized by lethargy, obtundation, persistent vomiting, agitated delirium, and coma. Death is secondary to severe cerebral swelling with elevation of intracranial pressure. Although no specific therapy has been clearly demonstrated to be superior in terms of outcome, most clinicians have adopted a management scheme aimed at lowering and controlling the elevated ICP. We have described the management protocol in use at the Children's Hospital of Philadelphia. The protocol is summarized in the Appendix for the convenience of the reader.
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PMID:Management of Reye's syndrome. 391 81

Clinicians and nurses should obtain a history of antecedent illness occurring within 2 weeks of the onset of vomiting. Ninety percent of school-age children will give a history of an antecedent illness (varicella or influenza-like respiratory illness) within 1 week of the onset of vomiting. The vomiting of Reye's syndrome is usually persistent, lasting for 24 to 96 hours before the onset of serious brain signs. We believe that any child with the history of flu or chickenpox within 1 week of the onset of vomiting, which lasts for more than 12 hours, and is unusually severe or is associated with lethargy, should have an SGPT (alanine aminotransferase). This laboratory measure is clearly elevated in most cases of Reye's syndrome.
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PMID:Management of Reye's syndrome: need for early diagnosis and intravenous treatment of stage I non-comatose cases. 402 67


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