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)

A five-year-old girl presented with profound growth failure, lethargy, vomiting and acidosis. A diagnosis of Munchausen syndrome by proxy was made after the demonstration of egg albumin, diphenhydramine and phenothiazine metabolites in her urine. Growth improved dramatically, but a subsequent child in the family died of sudden infant death syndrome.
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PMID:Albuminuric growth failure. A case of Munchausen syndrome by proxy. 160 6

Sixty-three infants, aged from 1 to 4 months, were examined for gastroesophageal reflux (GER) using esophageal pH monitoring. Thirty were examined because of chronic vomiting, 21 were healthy controls examined for GER as part of a screening program for sudden infant death syndrome, and 12 had an acute respiratory disease (RD). The 24-h pH monitoring data were within normal ranges in 26 infants (20 controls, 2 babies with emesis, and 4 with RD). Data were abnormal in 37 infants (1 control, 28 infants with emesis, and 8 with RD). All babies were submitted during a fasting awake period to a 30-min chest physiotherapy session. In the three groups studied, the incidence of GER episodes detected by the pH probe was significantly higher during physiotherapy if compared (a) to the calculated mean incidence during a 30-min period of the 24-h investigation or (b) to the incidence during a fasting awake period such as that during which the physiotherapy was given (p less than 0.001; Wilcoxon rank-sum test). We conclude that chest physiotherapy significantly increases GER incidence. We therefore propose restricting chest physiotherapy to fasting periods. These data add to the confusion that already exists regarding the possible causal relationship between (acid) GER and respiratory disease.
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PMID:Esophageal pH monitoring data during chest physiotherapy. 191 48

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

Three to four hour polygraphic sleep studies were carried out in 10 infants, five with upper respiratory infection and five with metabolic alkalosis secondary to vomiting during and after recovery from illness. During upper respiratory infection, the main abnormality detected was brief (greater than 3 less than 6 seconds) or prolonged (greater than 6 seconds) attacks of obstructive apnoea. Other indices of apnoea were similar to recovery data. Gross body movements were also increased. In infants with metabolic alkalosis indices of central apnoea were significantly increased when compared with recovery or case control data. Prolonged (greater than 15 seconds) attacks of central apnoea and obstructive apnoea (greater than 6 seconds) were only observed during illness. Gross body movements and periodic breathing were also increased. These findings suggest that the functional consequences of apparently 'mild' illnesses in young infants may be greater than is generally suspected and perhaps relevant to mechanism(s) of death in sudden infant death syndrome.
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PMID:Sleep apnoea during upper respiratory infection and metabolic alkalosis in infancy. 378 86

Ultrasound is a new test proven to be sensitive in the demonstration of gastroesophageal reflux (GER). Following reflux seen with ultrasound various symptoms can be observed in physiological circumstances, and thereby a causal relationship between reflux and these symptoms can be observed in physiological circumstances, and thereby a causal relationship between reflux and these symptoms can be proven. We performed a study in 220 children suspected of GER to determine the incidence of sonographically demonstrated "symptomatic reflux" in different clinical groups: children with (1) vomiting only, (2) respiratory symptoms, (3) attack-like symptoms, and (4) pain and irritability. Overall, GER was demonstrated in 78% of all 209 children in whom technically satisfactory studies could be performed. This reflux was associated with symptoms in 32% of the cases. Symptomatic reflux was most frequent in group 3, which included children investigated for near-miss sudden infant death syndrome. The symptoms that were noted most frequently were vomiting, motor unrest, coughing, and wheezing. Apnea, bradycardia and attacks of unusual posturing could incidentally be related to reflux. Ultrasound is a cheap, simple, noninvasive, and physiological test to show clinically significant reflux.
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PMID:Symptomatic gastroesophageal reflux: diagnosis with ultrasound. 796 78

A 24 hour pH-metry was performed in children younger than 3 months divided in 4 groups: group 1: 37 infants who presented an apparent life-threatening event (ALTE), group 2: 45 infants with an ALTE and chronic digestive symptoms (recurrent vomiting), group 3: 33 infants with digestive symptoms only, group 4: 32 sudden infant death syndrome (SIDS) siblings. The percent duration of oesophageal pH below 4 (% pH < 4) was measured during 24 hours and 12 nocturnal hours (8 PM-8 AM). In addition the mean duration of nocturnal episodes of reflux (MDNR) was calculated (duration of pH < 4 per 12 nocturnal hours/number of reflux episodes). No significant difference was found in the 4 groups for % pH < 4. Nocturnal reflux was present in all groups (40% in group 1, 55% in group 2, 49% in group 3 and 63% in group 4). The MDNR was higher in group 1 (12.3 +/- 7.8 min) vs group 2 (6.8 +/- 5.1 min) and group 3 (6.7 +/- 3.2 min) (P < 0.05). High MDNR did not appear to be related to an history of ALTE since the MDNR in group 2 was identical to group 3. Nocturnal pH metry profile failed to show a relationship between gastro-oesophageal reflux and ALTE.
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PMID:[Comparative study of results of pH-metry in function of its indication in infants]. 839 74

Gastroesophageal reflux (GER) is one of the most frequent symptomatic clinical disorders affecting the gastrointestinal tract of infants and children. During the past 2 decades, GER has been recognized more frequently because of an increased awareness of the condition and also because of the more sophisticated diagnostic techniques that have been developed for both identifying and quantifying the disorder. Gastroesophageal fundoplication is currently one of the three most common major operations performed on infants and children by pediatric surgeons in the United States. Normal gastroesophageal function is a complex mechanism that depends on effective esophageal motility, timely relaxation and contractility of the lower esophageal sphincter, the mean intraluminal pressure in the stomach, the effectiveness of contractility in emptying of the stomach, and the ease of gastric outflow. More than one of these factors are often abnormal in the same child with symptomatic GER. In addition, in patients with GER disease, and particularly in those patients with neurologic disorders, there appears to be a high prevalence of autonomic neuropathy in which esophagogastric transit and gastric emptying are frequently delayed, producing a somewhat complex foregut motility disorder. GER has a different course and prognosis depending on the age of onset. The incompetent lower esophageal sphincter mechanism present in most newborn infants combined with the increased intraabdominal pressure from crying or straining commonly becomes much less frequent as a cause of vomiting after the age of 4 months. Chalasia and rumination of infancy are self-limited and should be carefully separated from symptomatic GER, which requires treatment. The most frequent complications of recurrent GER in childhood are failure to thrive as a result of caloric deprivation and recurrent bronchitis or pneumonia caused by repeated pulmonary aspiration of gastric fluid. Children with GER disease commonly have more refluxing episodes when in the supine position, particularly during sleep. The reflux of acid into the mid or upper esophagus may stimulate vagal reflexes and produce reflex laryngospasm, bronchospasm, or both, which may accentuate the symptoms of asthma. Reflux may also be a cause of obstructive apnea in infants and possibly a cause of recurrent stridor, acute hypoxia, and even the sudden infant death syndrome. Premature infants with respiratory distress syndrome have a high incidence of GER. Esophagitis and severe dental carries are common manifestations of GER in childhood. Barrett's columnar mucosal changes in the lower esophagus are not infrequent in adolescent children with chronic GER, particularly when Heliobacter pylori is present in the gastric mucosa. Associated disorders include esophageal dysmotility, which has been recognized in approximately one third of children with severe GER. Symptomatic GER is estimated to occur in 30% to 80% of infants who have undergone repair of esophageal atresia malformations. Neurologically impaired children are at high risk for having symptomatic GER, particularly if nasogastric or gastrostomy feedings are necessary. Delayed gastric emptying (DGE) has been documented with increasing frequency in infants and children who have symptoms of GER, particularly those with neurologic disorders. DGE may also be a cause of gas bloat, gagging, and breakdown or slippage of a well-constructed gastroesophageal fundoplication. The most helpful test for diagnosing and quantifying GER in childhood is the 24-hour esophageal pH monitoring study. Miniaturized probes that are small enough to use easily in the newborn infant are available. This study is 100% accurate in diagnosing reflux when the esophageal pH is less than 4.0 for more than 5% of the total monitored time.
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PMID:Gastroesophageal reflux in childhood. 853 88

In western countries, the sudden infant death syndrome (SIDS) is the leading cause of mortality in infants under one year of age. In an official statement on prevention from the French Ministry of Health, sleeping in the supine position or on the side is recommended for all infants unaffected by a particular medical condition. This clear restrictive recommendation is based on valid epidemiological data but raises questions in the minds of paediatricians and general practitioners since the most recent recommendations for treatment of gastro-oesophageal reflux indicate that the prone position at a 30 degrees angle is the first preventive measure to be taken. We present here an objective view point on this complex problem which others may find helpful in developing a sound approach to each individual case. First it must be emphasized that multiple factors are involved in SIDS. While the confirmed correlation between the supine sleeping position and reduced incidence of SIDS is a valid rationale for population-based preventive measures, it does not indicate any causal relationship. Secondly, epidemiological data is valid for a given geographical area but cannot be extrapolated to other areas without taking into account intercurrent factors such as soft bedding, use of feather-bed quilts, excessive bedroom temperature and passive smoking. The public campaign for the prevention of SIDS should be encouraged as an effective low-cost measure, but both physicians and parents should be aware of its multifactorial nature in order to avoid psychologically catastrophic consequences of the guilt syndrome. For infants with uncomplicated simple gastro-oesophageal reflux, a formerly well-known condition but currently less well tolerated by modern parents, it is essential to explain the physiological nature of the reflux to parents then to propose formula thickeners, antacids or prokinetic agents in particularly symtomatic cases. Sleeping in the 30 degrees prone position should not, in this particular case, be introduced as a preventive measure since the risk induced would probably be greater than the beneficial effect. For complicated reflux, after careful exploration and elimination of other causes of vomiting, treatment should be optimized first, followed by discussion on placing the infant in the 30 degrees prone position which should be considered as a therapeutic tool with the same risk of secondary effects as expected with drugs.
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PMID:[Position and sudden death of the infant]. 874 34

Cot death (sudden infant death syndrome) is one of the most common causes of death in the first year of life. Four cases with a pathological fear of cot death are presented. All the patients were depressed and in 2 cases the fear of cot death had an obsessional quality. In all cases there were complications during pregnancy (miscarriage, threatened abortion, recurrent vomiting in last trimester). In 1 case, the patient knew 3 mothers who had suffered cot deaths; in another, the infant was gravely ill in the neonatal period. Pathological fear of cot death can be recognised by the presence of two central features - overvigilance and excessive nocturnal checking of the baby's breathing. Therapeutic interventions are discussed.
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PMID:Pathological fear of cot death. 973 Jul 83

Staphylococcus aureus and Streptococcus pyogenes produce a lot of toxins, some of them responsible for specific diseases. Staphylococcal food poisoning is due to ingestion of enterotoxin containing food. Seven toxins have been isolated so far. Generalized exfoliative syndrome is related to exfoliatin. Young children are particularly affected. The disease consists in a cutaneous exfoliation usually limited with a favourable outcome. The mucus membranes are not involved. The nose or pharynx are the most usual portal of entry. Staphylococcus aureus is not grown from the bullae. Severe extensive forms have been observed particularly in neonates (Ritter's disease). Bullous impetigo is also due to exfoliatin. It consists in the presence of a restricted number of cloudy bullae, from which staphylococcus can be grown. It is a mild disease with a favourable outcome within a few days. Scarlet fever is related to the streptococcal erythrogenic toxins. The classic form of the disease is presently rare. This disease may be related to staphylococcus as a complication of arthritis, osteomyelitis or wound super-infection. Bacteremia is usual. Staphylococcal scarlet fever is not related to exfoliatin as previously believed, but to enterotoxins or TSST-1, so it seems to be an abortive form of toxic shock syndrome. Toxic shock syndrome is defined as a multi organ failure syndrome with a rapid onset, fever, rash followed by desquamation, vomiting and diarrhea, hypotension, conjunctivitis and strawberry tongue. The disease is related to an infection or colonisation with a toxin (TSST-1) producing strain of Staphylococcus aureus. Enterotoxins (mainly C) may be involved. The disease may occur in childhood, sometimes after superinfection of varicella. The mortality is low (5%) and mainly due to ARDS or cardiac problems. Erythrogenic toxins produced by Streptococcus pyogenes are involved in a streptococcal form of toxic shock syndrome with a quite similar presentation. In most cases however, a cutaneous or soft tissue infection is at the origin. Necrotizing fasciitis complicating varicella is a classic cause in children. Bacteremia is often observed. The mortality rate is as high as 60%. The streptococcal strains involved in north america use to produce the toxin erythrogenic A, the european cases seem to be more related to strains secreting the B toxin with a dysregulation of the mechanisms which control the secretion of the toxin. Staphylococcus strains producing the Panton and Valentine leucocidin are responsible for chronic or relapsing furonculosis and above all for a very severe necrotizing pneumonia observed in children and young adults presenting as an acute respiratory distress syndrome with leucopenia, hemoptysis and shock carrying a heavy mortality rate. Besides these specific diseases, staphylococcal and streptococcal toxins may be involved in some syndromes of unknown origin, in which the intervention of superantigens seems very likely. Kawasaki syndrome is among them as strains producing staphylococcal and streptococcal toxins have been grown from patients with Kawasaki syndrome. In the same way, the intervention of toxins is suspected in the determination of sudden infant death syndrome and atopic eczema.
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PMID:[Clinical aspects of streptococcal and staphylococcal toxinic diseases]. 1158 25


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