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)

With the increased use of various fluoride preparations for caries prevention, all dental personnel should know their potential toxicity and the margins of safety associated with their use. An understanding of the body's mechanisms for handling fluoride provides a rational basis for assessing the possible risks of excessive fluoride ingestion. Five to 10 grams of sodium fluoride is considered a Certainly Lethal Dose (CLD) for a 70 kg adult. One quarter of the CLD can be ingested without producing serious acute toxicity, and is known as the Safety Tolerated Dose (STD). CLDs and STDs for most commonly used fluoride agents and procedures show that they can be applied with little or no risk of adverse effects, as long as they are handled judiciously. If their use is abused, there is a risk of illness or even death. If amounts of fluoride close to the CLD are ingested, the speed of initiating proper treatment is critical for survival. Vomiting should be induced, if it is not spontaneous; fluoride-binding liquids, such as milk, administered; and the patient taken to the nearest hospital for emergency care. Frequent ingestion of low, but excessive quantities of fluoride during the period of tooth formation can lead to dental fluorosis. Particular concern is warranted for the ingestion of fluoride-containing toothpastes by young children and the inappropriate use of dietary fluoride supplements in communities with sufficient fluoride already present in drinking water. Parents should brush the teeth of preschool children or, at the very least, dispense only small amounts of toothpaste for them (a pea-size portion). Dentists and physicians should know the fluoride concentration of a patient's water supply before prescribing fluoride supplements. Fluoride preparations should be dispensed in appropriate quantities; labeled with suitable cautionary statements; packaged, when appropriate, with childproof closures or in tearproof materials; and stored in safe locations. Practitioners should use only FDA- or ADA- approved products, employ recommended methods for their delivery; know their toxicity; and be familiar with emergency measures for treating accidental overdosages. The risk of adverse effects is small, when fluorides are handled judiciously.
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PMID:The amounts of fluoride in current fluoride therapies: safety considerations for children. 659 May 78

Sulfiram, a drug applied topically to treat scabies, produces effects similar to those of disulfiram after subsequent ingestion of ethanol. Disulfiram, used in aversion therapy in the treatment of alcoholism, inhibits hepatic aldehyde dehydrogenase (ALDH) causing an accumulation of acetaldehyde after ethanol ingestion. The increased tissue levels of acetaldehyde cause a spectrum of undesirable side-effects including flushing, nausea, vomiting, and tachycardia, which are referred to as the disulfiram reaction. Previous studies have shown that in vitro sulfiram is a very weak inhibitor of ALDH, but solutions of sulfiram markedly increase in potency with time. In the present study, fresh solutions of sulfiram were exposed to fluorescent room light under ambient conditions and analyzed at timed intervals by HPLC. At least eight products, including disulfiram, were formed in the light-exposed sulfiram solutions, but not in solutions kept in the dark. Structural characterization of two of the photolysis products was obtained by on-line microbore HPLC-mass spectrometry (mu LC-MS) and on-line microbore HPLC-tandem mass spectrometry (mu LC-MS/MS) using continuous flow-liquid secondary ion mass spectrometry (CF-LSIMS) as the primary ionization method. Sulfiram was converted to disulfiram at an initial rate of 0.7%/hr, and the formation of disulfiram correlated with the increase in ALDH inhibition in vitro. The results of this investigation show that while sulfiram is a weak inhibitor of ALDH in vitro, it is readily photoconverted to disulfiram, a very potent inhibitor of ALDH, which may explain the adverse reaction to ethanol after sulfiram therapy.
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PMID:Photolysis of sulfiram: a mechanism for its disulfiram-like reaction. 798 3

Ethanol-induced emesis were investigated using Suncus murinus and the emetogenic mechanisms of ethanol were compared with those of cisplatin. Intraperitoneal injection of ethanol caused dose-dependent emesis with ED50 value of 22.3% (v/v) when injection volume was adjusted to 4 ml/kg. Intraperitoneal and subcutaneous injection of acetaldehyde also caused dose-dependent emesis (ED50 = 3.5% (v/v) with an extremely shorter latency (6% i.p.: 1.0 +/- 0.3 min cf. 40% ethanol: 13.0 +/- 1.9 min). Neither ethanol nor acetaldehyde caused emetic responses when injected intracerebroventricularly. Pretreatment with disulfiram, an inhibitor of liver aldehyde dehydrogenase, potentiated the emetogenic effects of ethanol. Surgical abdominal vagotomy, which blocks cisplatin-induced emesis completely, did not prevent ethanol-induced emesis. 5-HT3 receptor antagonists, which also cause complete inhibition of cisplatin-induced emesis, did not affect the responses. However, ethanol-induced emesis was prevented by the pretreatment with 8-hydroxy-2-(di-n-propylamino)tetrarin hydrobromide (8-OH-DPAT) and N-(2-mercaptopropionyl)-glycine (MPG) dose-dependently. The tackykinin NK1 receptor antagonist (+)-(2S, 3S)-3-(2-methoxybenzylamino)-2-phenyl-piperidine (CP-99,994) also attenuated ethanol-induced emesis. Taken together, these results suggest that 1) acetaldehyde is probably responsible for ethanol-induced emesis, 2) active site for ethanol maybe peripheral, 3) ethanol-induced emesis is mediated by free radicals, and 4) mechanism of ethanol-induced emesis and that caused by cisplatin are different in many respects, although in some they are similar and that the precise pathways remain to be identified. Therefore, the tolerance to emetogenic effects of cisplatin in alcoholic patients cannot be explained as a simple cross desensitization of the pathway.
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PMID:Ethanol-induced emesis in the house musk shrew, Suncus murinus. 901 Apr 80

Disulfiram is used in alcohol rehabilitation because it inhibits aldehyde dehydrogenase and consequently causes the disulfiram-ethanol reaction (vomiting, vertigo, anxiety, cardiovascular effects) after ingestion of alcoholic beverages. However, adverse effects on the central nervous system (for the most part psychotic reactions, acute organic brain syndrome, catatonia) may appear as a direct result of the drug itself. Disulfiram and its metabolite carbon disulfide inhibit dopamine beta-hydroxylase, increasing the levels of dopamine and reducing those of norepinephrine in the central nervous system. We observed direct disulfiram-induced toxicity on the central nervous system in 8 abstinent patients in whom a disulfiram-ethanol reaction had been excluded. Risk is increased when 1) excessive amounts of the drug are ingested; 2) the patient is already suffering from a major psychiatric illness; 3) the patient has anatomical brain lesions. In all cases observed, the toxic effects appeared in the first weeks and were reversed after suspension of the drug (except in one patient who died from severe bronchopulmonary infection). We thus suggest the following protocol: 1) physical examination and interview 3-4 weeks after initiation of treatment; 2) as a general rule, in abstinent patients, the lowest possible maintenance dosage should be administered. This strategy, despite the risk of underdosage, meets the goals inherent in an integrated medical and psychosocial approach to the treatment of alcoholism with which these patients seem better able to comply.
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PMID:[Collateral effects of disulfiram on the central nervous system in alcoholics that have become totally abstemious. Description of 8 cases]. 907 70

Hydrogen cyanamide is used in agriculture as a plant growth regulator and is applied to many deciduous plants to stimulate uniform budbreak after dormancy, resulting in uniform flowering and maturity. Hydrogen cyanamide is highly toxic, and adverse health effects from contact include severe irritation and ulceration of the eyes, skin, and respiratory tract. The substance also inhibits aldehyde dehydrogenase and can produce acetaldehyde syndrome (e.g., vomiting, parasympathetic hyperactivity, dyspnea, hypotension, and confusion) when exposure coincides with alcohol use. After Dormex (Degussa AG, Trostberg, Germany), a pesticide product containing hydrogen cyanamide (49% by weight), was introduced in Italy in 2000, a total of 23 cases of acute illness associated with exposure to this chemical were identified in early 2001. This led to a temporary suspension of sales and usage of Dormex on February 23, 2002, and strengthening of protective measures, as specified on the pesticide label when sales were resumed on June 20, 2003. This report describes 28 additional cases of hydrogen cyanamide-related illness that occurred during 2002-2004, 14 of which occurred after sales resumed. These illnesses suggest that the preventive measures adopted in Italy in 2003 to protect workers using hydrogen cyanamide are inadequate. Workers exposed to hydrogen cyanamide should be provided adequate information, training, personal protective equipment (PPE), and engineering controls.
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PMID:Update: hydrogen cyanamide-related illnesses--Italy, 2002-2004. 1585 60

We describe the development of enterovirus meningoencephalitis associated with increased adenosine deaminase in cerebrospinal fluid of a 12-year-old boy, a known case of hypogamaglobulinemia despite monthly replacement of IVIg.The patient was referred to our center with fever, headache and vomiting for 10 days. CSF analysis was compatible with aseptic meningoencephalitis but high CSF protein (>200mg/dl) and high level of adenosine deaminase in CSF (30IU/L) were against the diagnosis of simple viral meningoencephalitis. Nested PCR of CSF for entrovirus was positive. Treatment with daily high-dose IVIg was commenced, with significant clinical improvement. For patients with increased ADA and lymphocytic pleocytosis in CSF, differential diagnoses should include enteroviral meningitis. Antibodies, although crucial, cannot on their own prevent enteroviral infection in some hypogamaglbulinemic patients.
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PMID:A case of hypogammaglobulinemia with enteroviral meningoencephalitis, associated with increased adenosine deaminase in cerebrospinal fluid. 1967 42

This review updates the pharmacology, efficacy, safety, and tolerability of liraglutide, a glucagon-like peptide 1 (GLP-1) analog approved for the treatment of type 2 diabetes (T2DM) in January 2010. MEDLINE was searched (May 2009-January 1, 2011) for articles in English, using the terms liraglutide, NN2211, incretin mimetic, glucagon-like peptide (GLP)-1, and GLP-1 receptor agonist. Abstracts from key meetings (ADA 2009 and 2010, AACE 2010, EASD 2009, and EASD 2010) were also searched for relevant data. A GLP-1 analog with pharmacokinetic properties allowing once-daily administration via subcutaneous injection, liraglutide has shown clinical benefits when used as monotherapy or in combination. Liraglutide monotherapy has demonstrated efficacy in reducing hemoglobin A1c (A1C) and body weight, with low risk for hypoglycemic events. Liraglutide has also been studied in combination with metformin, glimepiride, and rosiglitazone for the treatment of T2DM. Extension studies within the Liraglutide Effects and Action in Diabetes clinical program have demonstrated the efficacy of liraglutide over 2 years of treatment. Overall, liraglutide has been shown to be well tolerated, with dose-dependent nausea, vomiting, and diarrhea being the most commonly reported adverse events in clinical trials. Extended dosing periods have demonstrated the durability of response of liraglutide with respect to glycemic control, lack of weight gain, and blood pressure benefits. Compared with exenatide and sitagliptin, liraglutide seems to offer greater improvements in A1C, fasting plasma glucose, and body weight. Adverse events commonly associated with liraglutide in clinical trials included nausea and hypoglycemia. Emerging data suggest that liraglutide may be a useful option for patients with T2DM.
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PMID:Liraglutide for the treatment of type 2 diabetes: a clinical update. 2173 32

Disulfiram treatment for alcohol dependence is used with acceptable outcomes. By inhibiting the aldehyde dehydrogenase enzyme, this treatment increases acetaldehyde concentration after the ingestion of alcohol causing an unpleasant disulfiram-alcohol reaction. Typical symptoms include flushing, headache, nausea, vomiting, sweating, vertigo, and lightheadedness. However, there have also been descriptions of more serious reactions including severe hypotension, arrhythmias, myocardial infarction, and cardiovascular collapse. We report a patient with a severe disulfiram-alcohol reaction marked by flushing, confusion, generalized malaise, epigastric pain, and hypotension. Cardiac biomarker and electrocardiographic changes were suggestive of non-ST-elevation myocardial infarction (NSTEMI). Left heart catheterization showed no angiographic evidence of coronary artery disease. Because of the frequency of alcohol dependence and its treatment with disulfiram, it is critical for physicians to be aware of these types of life-threatening complications.
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PMID:Disulfiram--alcohol reaction mimicking an acute coronary syndrome. 2474 56