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)

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

Sixty-eight bottle-fed babies under 9 months of age with mild acute gastroenteritis were observed to evaluate current feeding regimens following acute gastroenteritis in infancy. All babies were fed for 24 h with a glucose-electrolyte mixture (GEM) and then randomly assigned to either a gradual reintroduction to their normal milk, i.e., slow regrade; immediate return to full-strength formula; or a rapid regrade to a hypoallergenic whey hydrolysate formula. All groups were well matched for age, sex, ethnic origin, nutritional state, and degree of hydration. There was no significance difference in stool frequency or reducing substances, vomiting, and duration of hospital stay between the three groups. Many infants (6/24) refused to take the whey hydrolysate formula, presumably because of unpalatability. Weight gain was more rapid when full-strength milk was given. Clinical relapse developed in 12 (17%) of patients. An enteric pathogen was detected in eight of this group and cow's milk protein intolerance in three (one from each feeding group). No infant had clinically significant lactose intolerance, in marked contrast to previous experience at Queen Elizabeth Hospital. In this group of previously healthy, well-nourished babies with mild acute gastroenteritis, there was no advantage in regrading slowly to milk or a hypoallergenic formula. An immediate return to normal formula 24 h after GEM feeding was well tolerated and simpler for parents.
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PMID:Evaluation of infant feeding in acute gastroenteritis. 270 54

We initiated a prospective study of the dizzy patient to identify key factors on which a directed evaluation could be based. This study used a standardized history, physical examination, and basic laboratory evaluation totalling 66 items to assist collection of relevant clinical information on 125 patients. Diagnosis was based on the emergency physicians' diagnosis. This was modified when necessary based on one month of follow-up using diagnostic criteria adapted from previous studies. The most common disorder was some form of peripheral vestibular disorder, found in 54 patients (43%). These patients were typically vertiginous and were managed successfully as outpatients. Despite correlations with multiple factors, this diagnosis was best predicted by positive Nylen-Barany test with either vertigo, vomiting, or both with 94% specificity and 43% sensitivity. Potentially serious causes were identified, including medication-related, seizure, stroke, transient ischemic attacks, vertebral-basilar insufficiency, hypertension, pericarditis, arrhythmias, and all those requiring hospitalization. The best predictors, either older age, lack of vertigo, or neurologic deficit, could identify 86% of "serious" dizziness with 42% specificity. The following tests were of low yield and may be done in a directed manner based on a brief history: Valsalva, carotid stimulation, Romberg and Quix tests, mental status examination, complete blood count, serum electrolytes, and BUN. Our results do support routine testing of glucose in all patients and monitoring rhythm in patients age 45 and older. Such a directed approach could rapidly classify a significant number of dizzy patients and forego many time- and cost-intensive elements of provocative examination and laboratory testing.
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PMID:A directed approach to the dizzy patient. 272 92

Investigations were carried out in 1041 consecutive patients of acute pancreatitis, to correlate the prognosis with their symptoms and signs. It has been found that there were 15 symptoms and signs may be related to their prognosis; that is age over 60, high intake of fatty food immediately before attack, severe upper abdominal pain with vomiting, pulse rate over 100/min, pulse pressure below 2.6 kPa, peritoneal irritation, absence of peristaltic sounds, bloody ascites, serum electrolytes disorder, acidosis, more than 4000 ml of fluid were needed in first 24 h, serum calcium level below 1.9 mmol/L, blood glucose over 8.3 mmol/L, BUN over 7.0 mmol/L, and poor liver functions. If there are less than 4 positive signs, edematous pancreatitis may be present, 5 to 8 positive signs may be necrotizing pancreatitis with high risk of mortality and early operation is indicated, and more than 8 positive signs the prognosis will be very poor.
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PMID:[Diagnostic criteria and their relation to prognosis in acute pancreatitis]. 280 98

Between 6 and 28 weeks of gestation, 2-hour postprandial blood glucose determinations were performed on 66 pregnant patients who had no history of diabetes. Each patient received two methods of carbohydrate loading on separate occasions in a random, crossover fashion. One group received a 100-g carbohydrate meal and then a 50-g glucose load (Glucola). The order of the test regimens was reversed for the second group. The average 2-hour postprandial glucose value following a meal was 103.1 +/- 3.7 mg/dL, and the mean value for the 2-hour postprandial glucose following Glucola was 102.5 +/- 3.8 mg/dL. The difference in glucose values obtained with the two methods was not statistically significant. A 12% incidence of emesis was encountered after Glucola but none was encountered after the meal. The 100-g carbohydrate meal is recommended as the method of testing for glucose intolerance.
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PMID:Detection of glucose intolerance in pregnancy. 280 77

Nitulamide (ANANDRON (R] is an antiandrogen used as an adjuvant therapy in the treatment of advanced prostatic cancer. The effects of ingestion of high doses of nitulamide has not been so far reported. A 79 years old man was admitted 2 hours after the ingestion of 13 g of nitulamide (170 mg/kg or 43 times the therapeutic dose), in a suicide attempt. He was receiving nitulamide 300 mg/day for two weeks. On admission, he underwent immediately gastric lavage, followed by administration of oral activated charcoal and received an intravenous infusion of glucose in balanced salt solution. During the first 12 hours, the patient presented with moderate vomiting and diarrhoea. There was no change in the following parameters: blood cell count, plasma electrolytes, serum transaminases and serum bilirubin, arterial blood gases, plasma cortisol value, as compared to the pre-treatment values. Chest X ray was unchanged. Plasma concentrations were measured 2 hours, 3 hours, 12 hours, 24 hours, 48 hours and 72 hours after ingestion. The initial level reached 6 times the normal therapeutic range, then fell to 3.5 times at the 72th hour. The patient recovered rapidly and was discharged on the 4th day. Biologic parameters were controlled on 4th, 9th, 30th day and remained unchanged. Treatment was started again on the 30th day with nitulamide 150 mg/day. We did not notice any side effect previously described in daily administration of nitulamide: anemia, rise in serum transaminases, interstitial pneumopathy.
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PMID:[Absence of clinical and biological manifestations after massive absorption of nitulamide]. 281 Jan 41

Parenteral rehydration is mandatory if dehydration is severe, vomiting and anorexia prevails, peristalsis is abolished or consciousness disturbed. It has the aim to prevent a circulatory collapse, to fill up the deficit and maintain the requirement until oral feeding is restarted. The principles of parenteral rehydration did not change during the last 20 years. Initially a rapid infusion of isotonic Ringer's lactate solution is mandatory, which usually is followed by half isotonic Ringer's glucose solution. Hypertonic dehydration should be rehydrated very carefully and slowly. During 1976-1986 212 infants and children with severe dehydration were parenterally rehydrated in the Children's Hospital of Medical School Hannover. Dehydration was isotonic in 65.7%, hypertonic in 20.7%, and hypotonic in 13.6%. The parenteral rehydration lasted from 1 to 7 days and was longer necessary in the hypertonic and hypotonic than isotonic states. 4 infants with hypertonic dehydration showed cerebral complications, and 2 of them died. All other patients recovered quickly without acute sequelae.
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PMID:[Parenteral rehydration treatment of acute diarrhea]. 281 81

150 infants aged under 6 months and admitted to hospital with acute gastroenteritis were treated with rice water (RW), rice-based electrolyte solution (RES), and the glucose electrolyte solution (GES) recommended by the World Health Organisation. Two-thirds of the patients were moderately dehydrated and only 8% had positive stool culture. Vomiting, present in 11%, did not interfere with successful oral rehydration. Before treatment serum electrolytes and other biochemical variables were similar in the three groups. After 48 h of treatment the blood urea nitrogen and serum creatinine were lower (p less than 0.05) in the RW and RES group than in the GES group. Serum potassium was also lower in the RW than in the RES group. RW and RES were superior to GES in reducing the frequency and volume of stool output and in producing weight gain.
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PMID:Comparison of rice water, rice electrolyte solution, and glucose electrolyte solution in the management of infantile diarrhoea. 287 Mar 23

Since skeletal muscle is an important source of precursor for gluconeogenesis, it would not be surprising if carbohydrate metabolism was altered in some muscle disorders. We report a 7-10/12-year-old white male with congenital muscular dystrophy whose recurrent episodes of vomiting and dehydration were due to fasting hypoglycemia. He was found to have a blood glucose of 21 mg/dl with an episode of vomiting and dehydration. Diagnostic fasting replicated the symptoms and hypoglycemia. Associated laboratory findings included hypoalaninemia, ketonemia, and acidosis. With use of frequent feedings, there were no further episodes over 1-9/12 years of observation. To our knowledge this is the first report of hypoglycemia complicating muscular dystrophy. However, hypoglycemia may not be diagnosed because of the nonspecific nature of the symptoms. Hypoglycemia should be considered when children with reduced muscle mass develop otherwise unexplained vomiting.
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PMID:Hypoglycemia in a child with congenital muscular dystrophy. 292 68

The plasma beta-endorphin response to glucose ingestion was compared in 8 bulimics and 8 controls. The bulimics demonstrated a sustained elevation of plasma beta-endorphin unrelated to glucose ingestion throughout the 5-hour study period. It is hypothesized that such an elevation of beta-endorphin is the result of stress and that it may play an important role in the perpetuation of the binge-vomiting cycle.
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PMID:Plasma immunoreactive beta-endorphin in bulimics. 293 4


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