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)

Cyclical vomiting syndrome is an uncommon, disabling symptom complex of unknown cause, with features in common with migraine. It affects principally children and adolescents. Differential diagnosis and theories of pathogenesis are discussed. Therapy should be aimed at prophylaxis of vomiting bouts, 'switching off' episodes once they commence and preventing complications of established vomiting episodes. Families need rapid access to care to minimize morbidity and disruption to functioning.
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PMID:Cyclical vomiting syndrome. 779 26

Cyclic vomiting syndrome is an unusual cause of episodic emesis in children. It manifests as intermittent episodes of severe vomiting, similar in time of onset and duration, with no symptoms during the intervening period. Dehydration necessitating intravenous fluid therapy may occur. Most therapeutic maneuvers have proven unsuccessful. We report the use of erythromycin as a prokinetic agent in the treatment of cyclic vomiting in 20 children (9 boys, 11 girls). Many patients had mild associated abdominal pain with their vomiting. Thirteen patients had previously been given metoclopramide, but none responded. Two patients were mildly developmentally delayed. Twenty patients were given oral erythromycin ethylsuccinate, approximately 20 mg/kg/day, in 2-4 divided doses for 7 days. This dosage was repeated as needed when symptoms reappeared. Thirteen of 20 patients reported total resolution of symptoms when reevaluated at 2 and 6 months. All males responded, 4 of 13 responders were female, and all seven with partial or no response to therapy were female. This uncontrolled trial suggests that erythromycin may be a useful prokinetic agent in the treatment of cyclic vomiting syndrome in childhood. As the study was uncontrolled, placebo effect cannot be excluded. Case-controlled, double-blinded prospective trials should be considered to evaluate the effectiveness of erythromycin in cyclic vomiting syndrome.
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PMID:Treatment of cyclic vomiting in childhood with erythromycin. 814 93

Cyclic vomiting syndrome (CVS) is an unusual cause of episodic emesis in children. It manifests as intermittent episodes of severe vomiting, similar in time of onset and duration, with no symptoms during the intervening period. Dehydration necessitating intravenous fluid therapy may occur. Most therapeutic maneuvers have proven unsuccessful. We report the use of erythromycin as a prokinetic agent in the treatment of cyclic vomiting in 24 children (10 boys, 14 girls). Many patients had mild associated abdominal pain with their vomiting. Fourteen patients had previously been given metoclopramide but none responded. Two patients were mildly developmentally delayed. Twenty-four patients were given oral erythromycin ethylsuccinate, approximately 20 mg/kg/day, in two to four divided doses for 7 days. This dose was repeated as needed when symptoms reappeared. Eighteen of 24 patients reported total resolution of symptoms when re-evaluated at 2 and 6 months. All males responded, eight of 18 responders were female, and all six with partial or no response to therapy were female. This uncontrolled trial suggests that erythromycin may be a useful prokinetic agent in the treatment of CVS in childhood. Because the study was uncontrolled, placebo effect cannot be excluded. Case-controlled, double-blinded prospective trials should be considered to evaluate the effectiveness of erythromycin in CVS.
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PMID:Treatment of cyclic vomiting in childhood with erythromycin. 870 73

Lysinuric protein intolerance (LPI) is a rare autosomal recessive defect of cationic amino acid transport (CAA), relatively common in Finland and Italy. After weaning, LPI patients present poor feeding, vomiting and failure to thrive. A severe pulmonary complication and episodes of metabolic imbalance may lead to death. Prenatal diagnosis has not been available due to lack of either biochemical or molecular markers to be used in the fetal period. The LPI locus has recently been assigned to chromosome 14q12, very close to the T-cell receptor alpha-chain (TCRA) locus. We carried out a prenatal diagnosis for LPI by linkage analysis in one LPI Italian family after CVS. For the haplotype analysis 11 DNA markers from the LPI critical region were used (D14S742, D14S50, D14S283, five TCRA intragenic polymorphic sites, D14S990, MYH7 and D14S80). It was concluded that the haplotype analysis indicated that the fetus was healthy as he had inherited the two wild alleles of the LPI locus. After birth, the clearances of CAA were measured and found to be in the normal range, thus confirming the result of the prenatal diagnosis. The prenatal diagnosis of LPI can now be offered to families affected by LPI.
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PMID:Feasibility of prenatal diagnosis of lysinuric protein intolerance by linkage analysis: a case report. 1045 27

Cyclic vomiting syndrome is a disorder of unknown etiology that is characterized by its clinical pattern of rapid-fire, episodic (on-off) vomiting with interval wellness. The pattern is stereotypic within individuals and typified by a rapid onset during the night or early morning, rapid denouement, and associated symptoms of pallor, lethargy, anorexia, nausea, retching, vomiting, and abdominal pain. The vomiting appears to be triggered by a variety of physical and psychological stresses. The disorder usually begins in toddlers and resolves during adolescence. By definition, cyclic vomiting syndrome is an idiopathic disorder that requires exclusionary laboratory testing. Not only can it be mimicked by many specific disorders, eg, surgical, neurologic, endocrine, metabolic, renal, but within idiopathic cyclic vomiting syndrome there may be specific subgroups that have different mechanisms. Treatment options are improving at present and serotonergic agents have the most promise. Although the pathogenesis is unknown, there are now several tenable mechanisms including migraine, metabolic, neuroendocrine, and gastrointestinal. Cyclic vomiting syndrome may be a useful model for the study of emesis.
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PMID:Cyclic vomiting syndrome: features to be explained by a pathophysiologic model. 1049 33

Cyclical vomiting is an intermittent episodic disorder found most commonly in children. It bears considerable similarities to abdominal migraine and to migraine headaches. It has been proposed that cyclical vomiting is a form of or juvenile equivalent of migraine and that there is a spectrum of disease encompassing cyclical vomiting, abdominal migraine, and migraine headaches. There are considerable overlaps among the syndromes that support this concept. It seems, however, unlikely that all cases of cyclical vomiting are migranous in origin.
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PMID:Is cyclical vomiting an abdominal form of migraine in children? 1049 35

Nausea and vomiting are both elements of the system that evolved to defend the body against toxins accidentally ingested with the food. When they are induced by an ingested toxin, they are considered to be an appropriate response, but in many clinical settings (eg, anticancer chemotherapy, anesthesia and surgery, raised intracranial pressure) both responses are inappropriate in that the vomiting does not remove the cause and the nausea may lead to aversion to further treatment. Cyclic vomiting syndrome (CVS) is a particularly intense and prolonged example of inappropriate activation of this protective reflex. This review argues that insights into the pattern of emesis in CVS can be gained by examining the basic unit (quantum) of emesis, the emetic episode usually comprising retches followed by a vomit. Two (of several) possible mechanisms for the induction of the intense vomiting in CVS are discussed: (1) defects in intrinsic pathways (eg, opioid neurons) that may modulate the brain-stem emetic mechanisms, and (2) defects in the regulation of cellular mechanisms (eg, cAMP, ion channels) in cells at critical locations in the emetic pathway (eg, nucleus tractus solitarius, area postrema). If it is not possible to identify the causal mechanism of CVS, then will it be possible to treat CVS? This question is discussed in the context of the identification of universal or broad-spectrum antiemetic agents with recent preclinical studies with neurokinin-1 receptor antagonists reviewed to illustrate that such an approach is feasible.
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PMID:Cyclic vomiting syndrome: timing, targets, and treatment--a basic science perspective. 1049 37

Children with cyclic vomiting syndrome have a characteristic periodicity, and this could be due to abnormal gastric myoelectrical activity detectable by cutaneous electrogastrography (EGG). Fifteen children, aged 4-15 years, with CVS (eight symptomatic and seven asymptomatic at the time of study) underwent EGG and were compared to five normal and four disease control children. The relative tachygastria activity (RTA) or power ratio was calculated in each group. Five of the eight symptomatic CVS children showed marked episodes of tachygastria preprandially and all showed tachygastria postprandially. The asymptomatic CVS children showed tachygastria only postprandially after the test meal. RTA index and or power ratio of symptomatic children was significantly different from the asymptomatic CVS children (P = 0.001), normal (P = 0.007) and disease control children (P = 0.006). In a subsequent study, 2-hr gastric emptying 99mTc scintiscans were performed in 28 CVS children and compared to eight healthy control children. Twelve of 16 CVS children (75%) showed abnormal gastric emptying, and 7 of 28 (25%) showed abnormal EGG with significant tachygastria. The CVS children had significantly higher RTA both preprandially (P < 0.05) and postprandially (P < 0.05). Our results demonstrate that accelerated gastric rhythm was seen during the acute episodes of half of the CVS patients studied. Abnormal EGGs and higher RTA or power ratios were associated with delayed gastric emptying in the CVS children. Abnormal gastric myoelectrical activity may play a role in the pathogenesis of CVS syndrome.
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PMID:Electrogastrography in cyclic vomiting syndrome. 1049 42

Cyclic vomiting syndrome is an idiopathic disorder characterized by attacks of severe vomiting, interspersed with normal periods, and found in patients with a family history of migraine headaches. In this report, we investigated the characterization of the autonomic abnormalities in cyclic vomiting syndrome, contrasting them with values in pediatric population, as well as adults with migraine headache. We studied five groups: 41 normal pediatric controls (NPC), 12 patients with pediatric chronic vomiting (PCV), 15 patients with cyclic vomiting syndrome (CVS), 21 adults patients with migraine headaches (MHA), and 40 normal adult controls (NAC). We studied the sympathetic and cholinergic functions: two measures of sympathetic adrenergic function-vasoconstriction to cold and postural adjustment ratio; two measures of vagal cholinergic function--Valsalva ratio and ECG R-R interval; and one measure of total autonomic score. Comparisons were performed between and within groups by t tests and reported as mean +/- SEM. Although cholinergic function measures were lower in cyclic vomiting and migraine groups, the most distinct abnormality was low postural adjustment ratio in both cyclic vomiting and migraine groups vs normal pediatric and pediatric chronic vomiting groups. There was also a significant difference between cyclic vomiting and pediatric chronic vomiting groups (P < 0.05 in three other parameters). Cyclic vomiting syndrome is associated with distinctive adrenergic autonomic abnormalities similar to those in patients with migraine headaches and is usually characterized by a low postural adjustment ratio. These findings may have implications for both confirmation and diagnosis of cyclic vomiting syndrome.
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PMID:Autonomic function in cyclic vomiting syndrome and classic migraine. 1049 43

Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization. The effect of sulfated proteoglycans heparin and chondroitin sulfate was also tested on mast cell histamine secretion. Ileal brush border appeared intact in control animals, but was shorter and exhibited intercellular gaps after 30 min of acute immobilization stress. Mast cell activation in control rats was minimal, while stress induced obvious signs of activation as judged from disappearance of secretory granule electron dense contents. However, these intragranular changes were not accompanied by typical degranulation through exocytosis. Treatment of purified homogeneic rat peritoneal mast cells with 10(-4) M heparin or chondroitin sulfate 30 min prior to stimulation with 0.5 microg/ml compound 48/80 decreased histamine release by over 70% and 50% (P < 0.05), respectively. These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.
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PMID:Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans. 1049 45


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