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)

Two infants with lethargy, vomiting, convulsions, coma and marked metabolic acidosis were found to have very high concentrations of methylmalonic acid in their serum and urine. In vitro studies of fibroblasts demonstrated that the infants had different variants of methylmalonic acidemia.Vitamin B(12) was given in two different forms at 1 month of age and at 12 months of age. Each trial continued for 4 months but neither infant showed a clinical or biochemical response.In both infants hyperglycinemia, neutropenia and thrombocytopenia developed during acute metabolic crises only. Hypoglycemia was found in patient 2. Hyperammonemia was severe in patient 2 during acute crises but never appeared in patient 1. When clinically well, both infants continued to excrete abnormal amounts of methylmalonic acid in the urine and both had persistent compensated metabolic acidosis.Marked hyperuricemia developed in patient 1 at 18 months of age and led to progressive renal failure. Allopurinol therapy was necessary to keep the uric acid concentration within the normal range. Renal function returned to normal, as indicated by a marked increase in the renal clearance of creatinine and uric acid.Patient 1 is physically and mentally retarded, and has moderate hypotonia, hepatomegaly and persistent vomiting. Patient 2 has developed normally.The urine concentrations of methylmalonic acid in the four parents were normal.
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PMID:Methylmalonic acidemia: 6 years' clinical experience with two variants unresponsive to vitamin B12 therapy. 3 17

A neuropsychiatric syndrome developed in four patients 2 1/2-9 months after gastric partition for morbid obesity. Since the partition, all four patients had recurrent severe vomiting with severe weight loss (52 to 100 lb) and they had not had vitamin supplementation. Two patients had peripheral neuropathy along with confusion and memory loss of recent events. The other two had peripheral neuropathy alone. Vitamin B complex replacement was especially helpful in the management of these patients. Peripheral neuropathy completely resolved in one of the patients, whereas the other three patients were left with residual weakness in their extremities and two had recent memory loss. Awareness of this complication may result in early recognition and treatment in the postgastric partition patient.
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PMID:Neuropsychiatric syndromes after gastric partition. 630 87

A recently introduced rodenticide containing N-3-pyridylmethyl N'-p-nitrophenyl urea (PNU), Vacor, was accidently ingested by a 25-month-old child, resulting in acute vomiting, lethargy, seizures, and hypoglycemia, as well as chronic evidence of autonomic and peripheral neuropathy and glucose intolerance. Treatment with niacinamide (nicotinamide), may have been of benefit since all problems were resolved within three months of ingestion. This agent (PNU) is remarkably similar chemically and toxicologically to alloxan and streptozocin, both potent beta-cell toxins. These similarities are not only important in regard to the antodite for PNU, but they also suggest that the toxin m,y cause long-term endocrinologic, neurlogic, and oncologic problems.
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PMID:Accidental ingestion of Vacor rodenticide: the symptoms and sequelae in a 25-month-old child. 644 44

Tumour cell hypoxia is a recognized cause of resistance to radiotherapy. Using clinically relevant dose-fractionation schedules in a mouse tumour model, the addition of carbogen and nicotinamide to overcome chronic and acute hypoxia results in a marked increase in radioresponsiveness with a lower degree of sensitization in normal tissue. Carbogen and nicotinamide were added to the palliative radiation treatment given to six patients with locally advanced breast cancer. The aim of the pilot study was to determine if patients tolerated the addition of carbogen and nicotinamide and to assess if there was any increase in radiosensitivity of the skin. Patients received 30 Gy prescribed to the intersection dose in six fractions over 17/18 days with full skin bolus to the tumour. All patients were given 6 g of nicotinamide orally 90 min before radiation treatment. Carbogen breathing was started 5 min prior to treatment and continued during it. Patients tolerated the treatment well, with vomiting in one patient being the only side effect that could be related to the nicotinamide, and this settled with an anti-emetic. No increase in skin reaction was noted with the addition of carbogen and nicotinamide, and good tumour regression was achieved.
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PMID:Short communication: the addition of carbogen and nicotinamide to a palliative fractionation schedule for locally advanced breast cancer. 753 98

Nineteen patients with glioblastoma were treated with nicotinamide and carbogen and radiotherapy. Eight patients did not complete the protocol because of hepatic toxicity from phenytoin/nicotinamide drug interactions, persistent nausea or vomiting with nicotinamide, intolerance of the carbogen breathing apparatus, or other reason. In addition, early radiation neurotoxicity appeared increased.
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PMID:Tolerance of nicotinamide and carbogen with radiation therapy for glioblastoma. 921 96

Patients suffering from nausea and vomiting of pregnancy (NVP) frequently do not receive therapy, in part because of fears of adverse effects of medications on the fetus. Several vitamin-based and herbal therapies have been shown to be effective and safe. Two randomized trials of vitamin B(6) have shown a benefit in reducing NVP. Women taking periconceptional multivitamins are less likely to have severe NVP. The combination of vitamin B(6) and doxylamine (previously marketed in the United States as Bendectin) has been shown to be safe for the fetus and effective in reducing NVP. Ginger was shown, in 2 studies, to reduce NVP. Vitamin B(1) (thiamine) deficiency can lead to Wernicke's encephalopathy in women with severe NVP. Replacement is needed for all women with vomiting of more than 3 weeks' duration. Prophylaxis with multivitamins and therapy with B(6), with or without doxylamine, are safe and effective therapies for NVP.
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PMID:Overview of nausea and vomiting of pregnancy with an emphasis on vitamins and ginger. 1201 96

N-(3,5-Dichloro-pyrid-4-yl)-[1-(4-fluorobenzyl)-5-hydroxy-indole-3-yl]-glyoxylic acid amide (AWD 12-281) is a highly potent and selective phosphodiesterase 4 (PDE4) inhibitor that was designed to have a metabolic profile that was optimized for topical administration. The aim of the current study was to explore the pharmacological profile of intratracheally administered AWD 12-281 in different models of asthma and chronic obstructive pulmonary disease (COPD) in comparison with steroids. To assess the anti-inflammatory potential of AWD 12-281, the antigen-induced cell infiltration in bronchoalveolar lavage fluid (BALF) of Brown Norway rats was determined. AWD 12-281 (ID50 of 7 microg/kg i.t.) as well as beclomethasone (0.1microg/kg i.t.) suppresses late-phase eosinophilia when administered intrapulmonary. Furthermore, AWD 12-281 has also strong anti-inflammatory properties when tested in lipopolysaccharide-induced acute lung neutrophilia in Lewis rats (ID50 of 0.02 microg/kg i.t.), ferrets (ID50 of 10 microg/kg i.t.), and domestic pigs (2-4 mg/pig i.t. or 1 mg/kg i.v.). In pigs, AWD 12-281 was as effective as beclomethasone (0.4 mg/pig i.t.) and dexamethasone (0.28 mg/kg i.v.), although at 3 to 10 times the dosage. The bronchodilatory activity of AWD 12-281 was assessed in sensitized guinea pigs. AWD 12-281 (1.5 mg/kg i.t., 1-h pretreatment) inhibited allergen-induced bronchoconstriction by 68% (parameter airway resistance). In sensitized BP-2 mice AWD 12-281 abolished the allergen-induced bronchial hyperresponsiveness and eosinophilia in BALF, showing dose dependence. When given orally, i.v. or i.t., AWD 12-281 has a considerably lower emetic potential than cilomilast in ferrets and roflumilast in pigs. When given topically by inhalation, no emesis could be induced in dogs up to the highest feasible dose (15 mg/kg in 50% lactose blend). These results indicate that AWD 12-281 is a unique potential new drug for the topical treatment of asthma and COPD.
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PMID:In vivo efficacy in airway disease models of N-(3,5-dichloropyrid-4-yl)-[1-(4-fluorobenzyl)-5-hydroxy-indole-3-yl]-glyoxylic acid amide (AWD 12-281), a selective phosphodiesterase 4 inhibitor for inhaled administration. 1294 97

Nicotinamide is a potent radiosensitizer currently employed in the treatment of cancer of the bladder, head, and neck. Unfortunately, nicotinamide is also a potent emetic at the concentrations required for radiosensitization. Previously, we have demonstrated that nicotinamide-induced emesis is the direct result of decreased spontaneous peristaltic activity in the ileum. However, the effect of nicotinamide's metabolites on peristaltic activity have not been investigated, although several studies have unsuccessfully attempted to correlate the degree of emesis with the levels of the metabolites in plasma. Isolated rat ileum rings and rat tail arteries were perfused with oxygenated Krebs solution in an organ bath. Nicotinamide, 1-methynicotinamide, or N-oxide nicotinamide were introduced to the perfusate and changes in amplitude of spontaneous peristaltic activity or phenylephrine-induced vasoconstriction recorded. Nicotinamide inhibited peristalsis in the ileum and agonist-induced vasoconstriction in the rat tail arteries, as previously observed. However, the primary metabolites of nicotinamide were without effect. Gut smooth muscle and rat tail artery are sensitive to the relaxant effects of nicotinamide. The primary metabolites of nicotinamide are not vasoactive and do not blunt either spontaneous or agonist-induced contraction and are thus unlikely to contribute to the degree of emesis observed following nicotinamide administration.
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PMID:Metabolites of the radiosensitizer nicotinamide are unlikely to contribute to the degree of emesis observed with the parent drug. 1835 Nov 31

The effect of RCMF-magnetic therapy apparatus on signal substances was studied. The radioimmunoassay (RIA) suggested that the magnetic field increased beta-endorphin markedly in plasma. ELISA indicated that the magnetic field inhibited vomiting reaction induced by chemotherapy drug, with reversible decrease of serotonin (5-HT) level in brains, small intestine tissue and serum. Furthermore, the bioeffect of magnetic fields on 5-HT level presented a typical window effect and post-effect, and the inhibitory effect of magnetic field on the emesis was parallel to the decrease level of 5-HT. This result implied that the decrease of 5-HT might be the basis of rotating constant magnetic field (RCMF) inhibiting drug-induced emesis. The nitric acid reductase-spectrophotometry and nicotinamide adenine dinucleotide-diaphorase/arginine-vasopressin (AVP) cytochemistry technique showed that the magnetic field induced nitric oxide (NO) increase in hypothalamus and the high NO(A) level lasted for 3 hours. The results suggested that NO(A) increases after the treatment of the magnetic field in hypothalamus, which may result from strong expression of NO-ergic neuron in paraventricular hypothalamic nucleus (PVN), periventricular hypothalamic nucleus (PEN) and supraoptic nucleus (SON). The coexistence of NO and AVP may play an important role in the regulation of endocrine and neuroendocrine by the magnetic field. And our data also confirmed that the magnetic field increased the content of NO so strongly that high NO level lasted for 3 hours, also made neuropeptide Y (NPY) cell in medulla stained heavily.
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PMID:Molecular mechanism of effect of rotating constant magnetic field on organisms. 1872 1

Alcoholic ketoacidosis is an acute metabolic acidosis that typically occurs in people who chronically abuse alcohol and have a recent history of binge drinking, little or no food intake and persistent vomiting. Alcoholic ketoacidosis is a result of starvation with glycogen depletion and counter-regulatory hormone production, a raised nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+) ratio related to the metabolism of ethanol, and volume depletion resulting in ketogenesis. Alcoholic ketoacidosis is characterized by elevated serum ketone levels and a high anion gap. Once the diagnosis of alcoholic ketoacidosis is made, the mainstay of treatment is hydration with 5% dextrose in normal saline. With timely and aggressive intervention, the prognosis for a patient with alcoholic ketoacidosis is good.
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PMID:[Alcoholic ketoacidosis]. 1929 98


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