Disulfiram
Alcohol Deterrents
Ditiocarb
Thiram
Aldehyde Dehydrogenase
Chlorzoxazone
Activity of disulfiram (bis(diethylthiocarbamoyl)disulphide) and ditiocarb (diethyldithiocarbamate) against metronidazole-sensitive and -resistant Trichomonas vaginalis and Tritrichomonas foetus. (1/242)
Clinical resistance of Trichomonas vaginalis to metronidazole is best correlated with MIC values measured under aerobic conditions. Under these conditions both disulfiram (bis(diethylthiocarbamoyl)disulphide), and its first mammalian metabolite, ditiocarb (diethyldithiocarbamate), showed high levels of activity against metronidazole-sensitive (disulfiram MIC, 0.1-0.7 microM; ditiocarb MIC, 0.3-9 microM) and -resistant (MICs 0.2-1.3 microM and 1.2-9 microM respectively) isolates. Tritrichomonas foetus was also sensitive-the MICs for seven metronidazole-sensitive isolates were 0.1-1.0 microM for disulfiram and 1.0-6.9 microM for ditiocarb; those for two highly metronidazole-resistant strains were 0.3-1.3 microM and 0.6-6 microM respectively. Under anerobic conditions most strains became highly resistant to both compounds. Surprisingly, disulfiram was consistently more active than ditiocarb. (+info)Clinical isoflurane metabolism by cytochrome P450 2E1. (2/242)
BACKGROUND: Some evidence suggests that isoflurane metabolism to trifluoroacetic acid and inorganic fluoride by human liver microsomes in vitro is catalyzed by cytochrome P450 2E1 (CYP2E1). This investigation tested the hypothesis that P450 2E1 predominantly catalyzes human isoflurane metabolism in vivo. Disulfiram, which is converted in vivo to a selective inhibitor of P450 2E1, was used as a metabolic probe for P450 2E1. METHODS: Twenty-two elective surgery patients who provided institutionally-approved written informed consent were randomized to receive disulfiram (500 mg orally, N = 12) or nothing (controls, N = 10) the evening before surgery. All patients received a standard isoflurane anesthetic (1.5% end-tidal in oxygen) for 8 hr. Urine and plasma trifluoroacetic acid and fluoride concentrations were quantitated in samples obtained for 4 days postoperatively. RESULTS: Patient groups were similar with respect to age, weight, gender, duration of surgery, blood loss, and delivered isoflurane dose, measured by cumulative end-tidal isoflurane concentrations (9.7-10.2 MAC-hr). Postoperative urine excretion of trifluoroacetic acid (days 1-4) and fluoride (days 1-3) was significantly (P<0.05) diminished in disulfiram-treated patients. Cumulative 0-96 hr excretion of trifluoroacetic acid and fluoride in disulfiram-treated patients was 34+/-72 and 270+/-70 micromoles (mean +/- SD), respectively, compared to 440+/-360 and 1500+/-800 micromoles in controls (P<0.05 for both). Disulfiram also abolished the rise in plasma metabolite concentrations. CONCLUSIONS: Disulfiram, a selective inhibitor of human hepatic P450 2E1, prevented 80-90% of isoflurane metabolism. These results suggest that P450 2E1 is the predominant P450 isoform responsible for human clinical isoflurane metabolism in vivo. (+info)A retinoic acid-inducible transgenic marker of sino-atrial development in the mouse heart. (3/242)
To study the specification of inflow structures in the heart we generated transgenic animals harboring the human alkaline phosphatase (HAP) gene driven by the proximal 840 bp of a quail SMyHC3 promoter. In transgenic mice, the SMyHC3-HAP reporter was expressed in posterior heart precursors at 8.25 dpc, in sinus venosa and in the atrium at 8.5 and 9.0 dpc, and in the atria from 10.5 dpc onwards. SMyHC3-HAP transgene expression overlapped synthesis and endogenous response to retinoic acid (RA) in the heart, as determined by antibodies directed against a key RA synthetic enzyme and by staining of RAREhsplacZ transgenic animals. A single pulse of all-trans RA administered to pregnant mice at 7.5, but not after 8.5, dpc induced cardiac dismorphology, ranging from complete absence of outflow tract and ventricles to hearts with reduced ventricles expressing both SMyHC3-HAP and ventricular markers. Blockade of RA synthesis with disulfiram inhibited RA-induced transcription and produced hearts lacking the atrial chamber. This study defines a novel marker for atrial-restricted transcription in the developing mouse heart. It also suggests that atrial-specific gene expression is controlled by localized synthesis of RA, and that exclusion of RA from ventricular precursors is essential for correct specification of the ventricles. (+info)Differential regulation of peptide alpha-amidation by dexamethasone and disulfiram. (4/242)
alpha-Amidation is essential for the function of many peptides in intercellular communication. This C-terminal modification is mediated in a two-step process by the hydroxylase and lyase activities of the bifunctional enzyme, peptidylglycine alpha-amidating monooxygenase (PAM). The first step, catalyzed by peptidylglycine-alpha-hydroxylating monooxygenase (PHM; EC 1.14.17. 3), is rate limiting in the process, and therefore subject to regulation. Dexamethasone and disulfiram (tetraethylthiuram disulfide; Antabuse) were used as in vivo treatments to study the regulation of PHM expression and activity in cardiac atrium. Our findings show that both dexamethasone and disulfiram treatment increase the activity of PHM in atrial tissue but that they do so by distinctly different mechanisms. Dexamethasone elevated tissue levels of PAM mRNA and protein concurrently, suggesting that glucocorticoids regulate PAM expression at the level of gene transcription. In contrast, disulfiram treatment, which depletes stores of alpha-amidated peptides, increased the specific activity of PHM without affecting the level of PAM expression. The catalytic efficiency of PHM was enhanced by raising the Vmax of the enzyme. Importantly, this increase in Vmax was retained through purification to homogeneity, indicating that either a covalent modification or a stable conformational change had occurred in the protein. These novel findings demonstrate that the rate-limiting enzyme in the bioactivation of peptide messengers is differentially regulated by transcriptional and post-transcriptional mechanisms in vivo. It is proposed that regulation of PHM's expression and catalytic efficiency serve as coordinated physiologic mechanisms for maintaining appropriate levels of alpha-amidating activity under changing conditions in vivo. (+info)Lack of single-dose disulfiram effects on cytochrome P-450 2C9, 2C19, 2D6, and 3A4 activities: evidence for specificity toward P-450 2E1. (5/242)
Disulfiram and its primary metabolite diethyldithiocarbamate are effective mechanism-based inhibitors of cytochrome P-450 2E1 (CYP2E1)1 in vitro. Single-dose disulfiram diminishes CYP2E1 activity in vivo and has been used to identify CYP2E1 participation in human drug metabolism and prevent CYP2E1-mediated toxification. Specificity of single-dose disulfiram toward CYP2E1 in vivo, however, remains unknown. This investigation determined single-dose disulfiram effects on human CYP 2C9, 2C19, 2D6, and 3A4 activities in vivo. In four randomized crossover experiments, volunteers received isoform-selective probes (oral tolbutamide, mephenytoin, dextromethorphan, or i.v. midazolam) on two occasions, 10 h after oral disulfiram or after no pretreatment (controls). Plasma and/or urine parent and/or metabolite concentrations were measured by HPLC or gas chromatography-mass spectrometry. CYP2C9, 2C19, 2D6, and 3A4 activities were determined from the tolbutamide metabolic ratio, 4'-hydroxymephenytoin excretion, and dextromethorphan/dextrorphan ratios in urine and midazolam systemic clearance, respectively. Midazolam clearance (670 +/- 190 versus 700 +/- 240 ml/min, disulfiram versus controls), dextromethorphan/dextrorphan metabolic ratio (0.013 +/- 0.033 versus 0.015 +/- 0.035), 4'-hydroxymephenytoin excretion (122 +/- 22 versus 128 +/- 25 micromol), and tolbutamide metabolite excretion (577 +/- 157 versus 610 +/- 208 micromol) were not significantly altered by disulfiram pretreatment, although the tolbutamide metabolic ratio was slightly diminished after disulfiram (60 +/- 17 versus 81 +/- 40, p <.05). Results show that single-dose disulfiram does not cause clinically significant inhibition of human CYP2C9, 2C19, 2D6, and 3A4 activities in vivo. When single-dose disulfiram is used as an in vivo probe for P-450, inhibition of drug metabolism suggests selective involvement of CYP2E1. Single-dose disulfiram should not cause untoward drug interactions from inhibition of other P-450 isoforms. (+info)The ethanol metabolite acetaldehyde inhibits the induction of long-term potentiation in the rat dentate gyrus in vivo. (6/242)
1. Ethanol has been reported to inhibit the induction of long-term potentiation (LTP) in the hippocampus. However, the correlation between the effects of ethanol in vivo and in vitro remained unclear. In addition, previous works have little considered the possibility that the effect of ethanol is mediated by its metabolites. To solve these problems, we investigated the effects of ethanol and acetaldehyde, the first metabolite in the metabolism of ethanol, on the induction of LTP at medial perforant path-granule cell synapses in the dentate gyrus of anaesthetized rats in vivo. 2. Oral administration of 1 g kg-1 ethanol significantly inhibited the induction of LTP, confirming the effectiveness of ethanol in vivo. 3. A lower dose of ethanol (0.5 g kg-1) failed to inhibit the induction of LTP in intact rats, but significantly inhibited LTP in rats treated with disulfiram, an inhibitor of aldehyde dehydrogenase, demonstrating that LTP is inhibited by acetaldehyde accumulation following ethanol administration. 4. Intravenous injection of acetaldehyde (0.06 g kg-1) significantly inhibited the induction of LTP. 5. The inhibitory effect of acetaldehyde on LTP induction was also observed when it was injected into the cerebroventricules, suggesting that acetaldehyde has a direct effect on the brain. The intracerebroventricular dose of acetaldehyde effective in inhibiting LTP induction (0.1 - 0.15 mg brain-1) was approximately 10 fold lower than that of ethanol (1.0 - 1.5 mg brain-1). 6. It is possible that acetaldehyde is partly responsible for memory impairments induced by ethanol intoxication. (+info)Duration of cytochrome P-450 2E1 (CYP2E1) inhibition and estimation of functional CYP2E1 enzyme half-life after single-dose disulfiram administration in humans. (7/242)
Disulfiram (DSF) is a mechanism-based inhibitor of cytochrome P-450 2E1 (CYP2E1), resulting in loss of CYP2E1 protein and activity, which may be useful in preventing CYP2E1-mediated xenobiotic toxicity. The duration of inhibition after a single DSF dose is, however, unknown. The purpose of this investigation was to determine this duration, and CYP2E1 formation and degradation rates, in humans. Oral chlorzoxazone (CLZ) was used as the selective in vivo probe for CYP2E1. Healthy subjects received CLZ to determine baseline CYP2E1 activity (CLZ plasma clearance and 6-hydroxychlorzoxazone fractional metabolic clearance). One week later, DSF (500 mg orally) was administered at bedtime, and CLZ administered the following morning and 3, 6, 8, 10, and 13 days after DSF. A terminal DSF metabolite, 2-thiothiazolidine-4 carboxylic acid, was also measured in each 24-h urine sample. The mean CLZ clearance and 6-hydroxychlorzoxazone fractional metabolic clearance on the first day declined to 10.2 and 5.5% of baseline values, indicating rapid and profound CYP2E1 inhibition. CYP2E1 activity returned to half that of control on day 3, and to baseline values on day 8. Assuming zero-order synthesis and first-order degradation, the in vivo CYP2E1 synthesis rate and degradation half-life was estimated to be 11 +/- 5 nmol/h and 50 +/- 19 h, respectively. Significant amounts of 2-thiothiazolidine-4 carboxylic acid were present only on day 1, suggesting that the return of in vivo CYP2E1 activity was not caused by inhibitor washout, but by enzyme resynthesis. Results regarding CYP2E1 disposition may be useful for modeling the effects of CYP2E1 inducers and inhibitors. For prevention of CYP2E1-mediated bioactivation, depending on protoxicant disposition, a second DSF dose might be necessary to completely prevent toxicity. (+info)Effect of diclofenac, disulfiram, itraconazole, grapefruit juice and erythromycin on the pharmacokinetics of quinidine. (8/242)
AIMS: In vitro studies suggest that the oxidation of quinidine to 3-hydroxyquinidine is a specific marker reaction for CYP3A4 activity. To assess the possible use of this reaction as an in vivo marker of CYP3A4 activity, we studied the involvement of cytochromes CYP2C9, CYP2E1 and CYP3A4 in the in vivo oxidative metabolism of quinidine. METHODS: An open study of 30 healthy young male volunteers was performed. The pharmacokinetics of a 200 mg single oral dose of quinidine was studied before and during daily administration of 100 mg diclofenac, a CYP2C9 substrate (n=6); 200 mg disulfiram, an inhibitor of CYP2E1 (n=6); 100 mg itraconazole, an inhibitor of CYP3A4 (n=6); 250 ml single strength grapefruit juice twice daily, an inhibitor of CYP3A4 (n=6); 250 mg of erythromycin 4 times daily, an inhibitor of CYP3A4 (n=6). Probes of other enzyme activities, caffeine (CYP1A2), sparteine (CYP2D6), mephenytoin (CYP2C19), tolbutamide (CYP2C9) and cortisol (CYP3A4) were also studied. RESULTS: Concomitant administration of diclofenac reduced the partial clearance of quinidine by N-oxidation by 27%, while no effect was found for other pharmacokinetic parameters of quinidine. Concomitant administration of disulfiram did not alter any of the pharmacokinetic parameters of quinidine. Concomitant administration of itraconazole reduced quinidine total clearance, partial clearance by 3-hydroxylation and partial clearance by N-oxidation by 61, 84 and 73%, respectively. The renal clearance was reduced by 60% and the elimination half-life increased by 35%. Concomitant administration of grapefruit juice reduced the total clearance of quinidine and its partial clearance by 3-hydroxylation and N-oxidation by 15, 19 and 27%, respectively. The elimination half-life of quinidine was increased by 19%. The caffeine metabolic index was reduced by 25%. Concomitant administration of erythromycin reduced the total clearance of quinidine and its partial clearance by 3-hydroxylation and N-oxidation by 34, 50 and 33%, respectively. Cmax was increased by 39%. CONCLUSIONS: The results confirm an important role for CYP3A4 in the oxidation of quinidine in vivo, and this applies particularly to the formation of 3-hydroxyquinidine. While a minor contribution of CYP2C9 to the N-oxidation of quinidine is possible, a major involvement of the CYP2C9 or CYP2E1 enzymes in the oxidation of quinidine in vivo is unlikely. (+info)Disulfiram is a medication used to treat chronic alcoholism. It works by inhibiting the enzyme acetaldehyde dehydrogenase, which is responsible for breaking down acetaldehyde, a toxic metabolite produced when alcohol is consumed. When a person taking disulfiram consumes alcohol, the buildup of acetaldehyde causes unpleasant symptoms such as flushing, nausea, palpitations, and shortness of breath, which can help discourage further alcohol use.
The medical definition of Disulfiram is:
A medication used in the treatment of chronic alcoholism, which works by inhibiting the enzyme acetaldehyde dehydrogenase, leading to an accumulation of acetaldehyde when alcohol is consumed, causing unpleasant symptoms that discourage further alcohol use. Disulfiram is available as a tablet for oral administration and is typically prescribed under medical supervision due to its potential for serious interactions with alcohol and other substances.
Alcohol deterrents, also known as alcohol deterrent devices or ignition interlock devices, are breathalyzer devices that are installed in vehicles to prevent a driver from starting the vehicle if their blood alcohol concentration (BAC) is above a certain limit. These devices are often used as a condition of license reinstatement for individuals who have been convicted of drunk driving or other alcohol-related offenses.
The driver must blow into the device, and if their BAC is above the programmed limit, the vehicle will not start. Some devices also require periodic rolling retests while the vehicle is in motion to ensure that the driver remains sober throughout the trip. The use of alcohol deterrents has been shown to reduce recidivism rates among drunk drivers and improve overall road safety.
I'm sorry for any confusion, but "Ditiocarb" is not a recognized medical term or abbreviation in standard medical or clinical contexts. It's possible that you may have made a typo or are referring to a term from a different field. If you have more information or if there's a specific context in which you encountered this term, I'd be happy to help further!
Thiram is not typically considered a medical term, but it is a chemical compound that has been used in some medical and healthcare settings. Thiram is an organic compound that belongs to the class of chemicals known as dithiocarbamates. It is primarily used as a fungicide to prevent fungal growth on crops such as potatoes, beans, and nuts.
In medical contexts, thiram has been used in some topical creams and ointments as an antifungal agent to treat skin conditions like athlete's foot and ringworm. However, its use in medicine is relatively limited due to concerns about its potential toxicity and environmental impact.
It is important to note that the use of thiram in topical medications has declined over time, and it is not commonly used in modern medical practice. Always consult with a healthcare professional for accurate information regarding medical treatments and therapies.
Aldehyde dehydrogenase (ALDH) is a class of enzymes that play a crucial role in the metabolism of alcohol and other aldehydes in the body. These enzymes catalyze the oxidation of aldehydes to carboxylic acids, using nicotinamide adenine dinucleotide (NAD+) as a cofactor.
There are several isoforms of ALDH found in different tissues throughout the body, with varying substrate specificities and kinetic properties. The most well-known function of ALDH is its role in alcohol metabolism, where it converts the toxic aldehyde intermediate acetaldehyde to acetate, which can then be further metabolized or excreted.
Deficiencies in ALDH activity have been linked to a number of clinical conditions, including alcohol flush reaction, alcohol-induced liver disease, and certain types of cancer. Additionally, increased ALDH activity has been associated with chemotherapy resistance in some cancer cells.
Thiocarbamates are a group of chemical compounds that contain a functional group with the structure R-S-CO-NH-R', where R and R' represent organic groups. They are commonly used as herbicides, fungicides, and nematocides in agriculture due to their ability to inhibit certain enzymes in plants and pests.
In a medical context, thiocarbamates have been studied for their potential therapeutic effects, particularly as anti-cancer agents. Some thiocarbamate derivatives have been found to inhibit the growth of cancer cells by interfering with microtubule dynamics or by inducing apoptosis (programmed cell death). However, more research is needed to fully understand their mechanisms of action and potential side effects before they can be widely used in clinical settings.
Chlorzoxazone is a muscle relaxant medication that works by helping to reduce muscle spasms. It does not directly affect the muscles themselves, but rather works on the central nervous system to help decrease the sensation of pain and allow the muscles to relax. Chlorzoxazone is often used in combination with physical therapy, rest, and other treatments for muscle injuries or disorders.
Like all medications, chlorzoxazone can have side effects, including dizziness, drowsiness, and upset stomach. It is important to follow your healthcare provider's instructions carefully when taking this medication, and to avoid activities that require alertness, such as driving or operating heavy machinery, until you know how the drug affects you.
It is worth noting that chlorzoxazone is a prescription medication, and should only be used under the guidance of a licensed healthcare provider. If you have any questions about this medication or its use, it is important to speak with your doctor or pharmacist for more information.
Aldehyde oxidoreductases are a class of enzymes that catalyze the oxidation of aldehydes to carboxylic acids using NAD+ or FAD as cofactors. They play a crucial role in the detoxification of aldehydes generated from various metabolic processes, such as lipid peroxidation and alcohol metabolism. These enzymes are widely distributed in nature and have been identified in bacteria, yeast, plants, and animals.
The oxidation reaction catalyzed by aldehyde oxidoreductases involves the transfer of electrons from the aldehyde substrate to the cofactor, resulting in the formation of a carboxylic acid and reduced NAD+ or FAD. The enzymes are classified into several families based on their sequence similarity and cofactor specificity.
One of the most well-known members of this family is alcohol dehydrogenase (ADH), which catalyzes the oxidation of alcohols to aldehydes or ketones as part of the alcohol metabolism pathway. Another important member is aldehyde dehydrogenase (ALDH), which further oxidizes the aldehydes generated by ADH to carboxylic acids, thereby preventing the accumulation of toxic aldehydes in the body.
Deficiencies in ALDH enzymes have been linked to several human diseases, including alcoholism and certain types of cancer. Therefore, understanding the structure and function of aldehyde oxidoreductases is essential for developing new therapeutic strategies to treat these conditions.
"Cocaine-Related Disorders" is a term used in the medical and psychiatric fields to refer to a group of conditions related to the use of cocaine, a powerful stimulant drug. These disorders are classified and diagnosed based on the criteria outlined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published by the American Psychiatric Association.
The two main categories of Cocaine-Related Disorders are:
1. Cocaine Use Disorder: This disorder is characterized by a problematic pattern of cocaine use leading to clinically significant impairment or distress, as manifested by at least two symptoms within a 12-month period. These symptoms may include using larger amounts of cocaine over a longer period than intended, persistent desire or unsuccessful efforts to cut down or control cocaine use, spending a great deal of time obtaining, using, or recovering from the effects of cocaine, and continued use despite physical or psychological problems caused or exacerbated by cocaine.
2. Cocaine-Induced Disorders: These disorders are directly caused by the acute effects of cocaine intoxication or withdrawal. They include:
* Cocaine Intoxication: Presents with a reversible syndrome due to recent use of cocaine, characterized by euphoria, increased energy, and psychomotor agitation. It may also cause elevated heart rate, blood pressure, and body temperature, as well as pupillary dilation.
* Cocaine Withdrawal: Occurs when an individual who has been using cocaine heavily for a prolonged period abruptly stops or significantly reduces their use. Symptoms include depressed mood, fatigue, increased appetite, vivid and unpleasant dreams, and insomnia.
Cocaine-Related Disorders can have severe negative consequences on an individual's physical health, mental wellbeing, and social functioning. They often require professional treatment to manage and overcome.
Cyanamide is a chemical compound with the formula NH2CN. It is a colorless, crystalline solid that is highly soluble in water and has an ammonia-like odor. Cyanamide is used as a reagent in organic synthesis and as a fertilizer.
In a medical context, cyanamide may be used as a drug to treat certain conditions. For example, it has been used as a muscle relaxant and to reduce muscle spasms in people with multiple sclerosis. It is also being studied as a potential treatment for alcohol dependence, as it may help to reduce cravings and withdrawal symptoms.
It is important to note that cyanamide can be toxic in high doses, and it should only be used under the supervision of a healthcare professional.
Disulfiram
Disulfiram-alcohol reaction
Disulfiram-like drug
Lofepramine
Alcohol flush reaction
Aversion therapy
Naari
List of dopaminergic drugs
Trimethoprim
Molecular and epigenetic mechanisms of alcoholism
Effervescent tablet
Alcohol in Russia
Acetaldehyde dehydrogenase
Amitriptyline
Dopamine beta-hydroxylase
Proteasome inhibitor
Professional practice of behavior analysis
Retinal dehydrogenase
Inkcap
Community reinforcement approach and family training
Alcohol intolerance
Metronidazole
Alcoholism
Sertraline
Coprinopsis variegata
Benznidazole
Sulfiram
CYP2E1
Mushroom poisoning
Sulfur vulcanization
Disulfiram - Wikipedia
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Take disulfiram6
- The patient should not take disulfiram for at least 12 hours after drinking. (medlineplus.gov)
- Take disulfiram exactly as directed. (medlineplus.gov)
- 1, 3 Those who do take disulfiram too soon may experience the aforementioned unpleasant effects and other types of illness. (withdrawal.net)
- 4(6) It's also important that those who choose to take disulfiram are aware of the side effects that will emerge should they drink while taking the medication. (withdrawal.net)
- People with severe heart disease or who are pregnant should not take disulfiram. (medicalnewstoday.com)
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Naltrexone10
- citation needed] Disulfiram is used as a second-line treatment, behind acamprosate and naltrexone, for alcohol dependence. (wikipedia.org)
- medical citation needed] Although disulfiram remained the most common pharmaceutical treatment of alcohol abuse until the end of the 20th century, today it is often replaced or accompanied with newer drugs, primarily the combination of naltrexone and acamprosate, which directly attempt to address physiological processes in the brain associated with alcohol abuse. (wikipedia.org)
- Naltrexone may cause liver problems, and using it with other medications that can also affect the liver such as disulfiram may increase that risk. (drugs.com)
- Randomization included assignment to 1 of 4 groups: (1) naltrexone alone, (2) placebo alone, (3) (open-label) disulfiram and (blinded) naltrexone, or (4) (open-label) disulfiram and (blinded) placebo. (psychiatrist.com)
- A healthcare professional may prescribe disulfiram to people who cannot take acamprosate or naltrexone. (medicalnewstoday.com)
- Naltrexone reduces the risk for hospitalization for alcohol use disorder (AUD), regardless of whether it is used alone or in conjunction with disulfiram or acamprosate, new research suggests. (medscape.com)
- Investigators analyzed 10-year data on more than 125,000 Swedish residents with AUD and found that naltrexone, used as monotherapy or combined with acamprosate or disulfiram, was associated with significantly lower risk for AUD hospitalization or all-cause hospitalization in comparison with patients who did not use AUD medication. (medscape.com)
- Previous research has shown that disulfiram, acamprosate, naltrexone, and nalmefene are efficacious in treating AUD, but most studies have been randomized controlled trials or meta-analyses, the authors write. (medscape.com)
- The within-individual analysis showed that naltrexone - whether used as monotherapy or adjunctively with disulfiram or acamprosate - "was associated with a significantly lower risk of AUD-related hospitalization, compared to those time periods in which the same individual did not use any AUD medication," the authors report. (medscape.com)
- Other medications used in the treatment of alcohol use disorder include disulfiram for enforced abstinence, naltrexone or topiramate to dampen cravings, and naloxone if opiate overdose is suspected. (medscape.com)
Aldehyde dehydrogenase5
- Disulfiram works by inhibiting the enzyme aldehyde dehydrogenase, causing many of the effects of a hangover to be felt immediately following alcohol consumption. (wikipedia.org)
- Disulfiram reduces the rate of oxidation of acetaldehyde by competing with the cofactor nicotinamide adenine dinucleotide (NAD) for binding sites on aldehyde dehydrogenase (ALDH). (medscape.com)
- The prolonged effects of disulfiram occur not only because the drug is slowly eliminated from the body but also because it irreversibly inhibits aldehyde dehydrogenase. (medscape.com)
- Disulfiram inhibits aldehyde dehydrogenase, the oxidative enzyme of acetaldehyde, a metabolite of alcohol. (johogo.com)
- Disulfiram is an aldehyde dehydrogenase inhibitor licensed for specialist use as an adjunct in the treatment of alcohol dependence. (uktis.org)
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Prescription4
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Active Ingredient1
- The active ingredient of Disulfiram is disulfiram or tetraethyl thiuram disulfide. (essentialhospitals.org)
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Effects of disulfiram3
- In considering disulfiram toxicity, a distinction must be made between the clinical manifestations of a disulfiram-ethanol reaction (DER) and the toxic effects of disulfiram itself. (medscape.com)
- The directly toxic effects of disulfiram include neurologic, cutaneous, and hepatotoxic sequelae in addition to the disulfiram-ethanol reaction. (medscape.com)
- 5 The aversive effects of disulfiram or Antabuse can range from mild to severe, depending on the amount of alcohol consumed in association with the particular therapeutic dose of disulfiram that a person takes. (withdrawal.net)
Reaction10
- When the dehydrogenase enzyme is inhibited, acetaldehyde builds up, causing unpleasant side effects (Disulfiram-alcohol reaction). (wikipedia.org)
- Under normal metabolism, alcohol is broken down in the liver by the enzyme alcohol dehydrogenase to acetaldehyde, which is then converted by the enzyme acetaldehyde dehydrogenase to a harmless acetic acid derivative (acetyl coenzyme A). Disulfiram blocks this reaction at the intermediate stage by blocking acetaldehyde dehydrogenase. (wikipedia.org)
- consequently, medical ethics dictate that patients must be fully informed about the disulfiram-alcohol reaction. (wikipedia.org)
- A reaction may occur for up to 2 weeks after disulfiram has been stopped. (medlineplus.gov)
- The disulfiram-ethanol reaction (DER) is due to increased serum acetaldehyde concentrations generated by the metabolism of ethanol by alcohol dehydrogenase in the liver. (medscape.com)
- Emergency department treatment of disulfiram-ethanol reaction (DER) is primarily supportive. (medscape.com)
- An increased serum acetaldehyde concentration is thought to be responsible for the unpleasant side effects associated with the disulfiram-ethanol reaction. (medscape.com)
- 5 In some cases, severe reactions require supportive medical care, and it is recommended that prescribing physicians advise patients taking disulfiram carry a medical alert card that details their use of disulfiram as well as the symptoms of a disulfiram and alcohol reaction. (withdrawal.net)
- Tricyclic antidepressants exacerbate symptoms of disulfiram alcohol reaction. (johogo.com)
- The autonomic instability resulting from the disulfiram-alcohol reaction, particularly when the reaction is severe, may pose a risk to both mother and fetus. (uktis.org)
Treat chronic alcoholism1
- Disulfiram is used to treat chronic alcoholism. (medlineplus.gov)
Tetraethylthiuram disulfide1
- Disulfiram (tetraethylthiuram disulfide [TETD]) has been used for more than 50 years as a deterrent to ethanol abuse in the management of alcoholism. (medscape.com)
Alcoholism5
- Disulfiram is a medication used to support the treatment of chronic alcoholism by producing an acute sensitivity to ethanol (drinking alcohol). (wikipedia.org)
- Disulfiram is not a cure for alcoholism, but discourages drinking. (medlineplus.gov)
- Disulfiram is frequently used in the treatment of alcoholism and has been reported to possess antiretroviral activity and can eject intrinsic zinc out of human immunodeficiency virus (HIV) nucleocapsid protein. (aspetjournals.org)
- Disulfiram is the brand name of the most widely used drug for the treatment of alcoholism. (essentialhospitals.org)
- Since then (1950), both disulfiram (Disulfiram®) and calcium cyanamide (Colme®) became the pharmacological treatment of choice for alcoholism. (essentialhospitals.org)
Disulfide4
- A method is described which allows the separate determination of carbon disulfide, free diethyldithiocarbamate and disulfides derived from disulfiram with adequate precision in 10 ml patient blood. (uni-regensburg.de)
- It is based on a spectrophotometric determination of a yellow compound formed by trapping carbon disulfide produced from diethyldithiocarbamate and disulfiram in an ethanolic solution of diethylamine and copper(II)-acetate. (uni-regensburg.de)
- Good quantitation of disulfiram and diethyldithiocarbamate in blood was achieved by trapping carbon disulfide produced when formic acid and cystein were added to the samples. (uni-regensburg.de)
- During daily administration of 200 mg disulfiram to humans, concentrations of zero to 0.6 [Ag carbon disulfide and 0.2 to 1.0 /ug diethyldithiocarbamate per ml blood were found using this method. (uni-regensburg.de)
Inhibits3
- Disulfiram irreversibly inhibits the oxidation of acetaldehyde by competing with the cofactor nicotinamide adenine dinucleotide (NAD) for binding sites on ALDH (see the image below). (medscape.com)
- Disulfiram also directly inhibits hepatic microsomal enzymes (cytochrome P450), in particular CYP2E1. (medscape.com)
- Disulfiram inhibits the metabolism of alcohol, causing increased levels of acetaldehyde, resulting in flushing, nausea, and multiple other noxious symptoms. (medscape.com)
Abstinence3
- 3 As such, disulfiram is largely prescribed to medically stable patients who are highly determined to avoid drinking and are fully aware that disulfiram is a type of aversion therapy that is used to support abstinence. (withdrawal.net)
- A gambling-group-by-disulfiram interaction was observed for abstinence, with problem-gambling features not associated with beneficial response to disulfiram ( z = 6.58, P = .01). (psychiatrist.com)
- A patient who is highly motivated to participate in an abstinence program may benefit from the use of disulfiram. (medscape.com)
Medications5
- Do not drink any alcoholic beverages (including wine, beer, and medications that contain alcohol such as cough syrup) while taking disulfiram, during the 12-hour period before you take your first dose, and for several weeks after stopping the drug. (medlineplus.gov)
- 1 One of the three FDA-approved medications used in the treatment of alcohol use disorder (AUD) is disulfiram, also known by its brand name, Antabuse. (withdrawal.net)
- As stated, disulfiram is one of three medications that are FDA-approved for the treatment of alcohol use disorder. (withdrawal.net)
- Based on cheap Disulfiram Generic Online education, Born into of her medications buy Antabuse Price of the based encryption algorithm only 9 percent case of a past medical, past speed up learning. (thahtaymin.com)
- We also know as the cheap Disulfiram effect to the alcoholic hypersensitivity caused by some medications (ketoconazole, griseofulvin, antibiotics) in the presence of alcohol. (essentialhospitals.org)
Symptoms7
- Cases of disulfiram neurotoxicity have also occurred, causing extrapyramidal and other symptoms. (wikipedia.org)
- Three patients, each of whom had required intensive open-ended antimicrobial therapy for control of the symptoms of chronic relapsing neurological Lyme disease and relapsing babesiosis, were able to discontinue treatment and remain clinically well for periods of observation of 6-23 months following the completion of a finite course of treatment solely with disulfiram. (canlyme.com)
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- We know by Disulfiram effect the set of adverse symptoms caused by alcohol consumption in the presence of disulfiram. (essentialhospitals.org)
- Due to these symptoms, Disulfiram exerts a deterrent effect with respect to alcohol consumption. (essentialhospitals.org)
Dosages2
- However, in most cases, this disruption is mild and presents itself as a 20-40% increase in the half-life of the compound at typical dosages of disulfiram. (wikipedia.org)
- How long disulfiram lasts largely depends on the dosages a person takes, how long they're taken the dosages for, and other individual factors. (withdrawal.net)
Ethanol3
- [ 3 ] Disulfiram blocks this enzyme, irreversibly inhibiting the oxidation of acetaldehyde and causing a marked increase in acetaldehyde concentrations after ethanol consumption. (medscape.com)
- For current guidelines on the management of disulfiram co-ingested with ethanol it is advisable to consult TOXBASE and contact UKTIS. (uktis.org)
- It contains active substance disulfiram bis(diethylthiocarbamoyl) which blocks alcohol dehydrogenase (ADH), the enzyme involved into metabolism of ethanol. (premiumpillsprice.com)
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- A person may begin taking disulfiram 12 hours after their last drink and should not drink alcohol while taking the medication. (medicalnewstoday.com)
Acetaldehyde3
- After alcohol intake under the influence of disulfiram, the concentration of acetaldehyde in the blood may be five to 10 times higher than that found during metabolism of the same amount of alcohol alone. (wikipedia.org)
- Ultimately, disulfiram reduces the rate of oxidation of acetaldehyde, causing a 5- to 10-fold increase in the concentration of acetaldehyde. (medscape.com)
- The Disulfiram effect is due to the accumulation of acetaldehyde in the body (one of the components resulting from the metabolism of alcohol). (essentialhospitals.org)
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