Concentration‐time profiles of ethanol and acetaldehyde in human volunteers treated with the alcohol‐sensitizing drug, calcium carbimide.

Jones, Alan Wayne; Neiman, Jack; Hillbom, Matti

doi:10.1111/j.1365-2125.1988.tb03293.x

Cited by 34 publications

(18 citation statements)

References 23 publications

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“…As stated earlier, some individuals naturally experience acetaldehyde-related flushing after ethanol exposure due to decreased ALDH activity attributed to genetic polymorphisms, with peak serum concentrations and effects of ethanol and acetaldehyde expected to occur within 1 hour after ingestion. 10,14 The flushing reaction in this case occurred roughly 3 hours after ethanol exposure, making it less likely that the patient was solely having an adverse effect to the ethanol alone. Based on pediatric-modified blood alcohol concentration (BAC) calculations described by Donovan, 15 our patient's peak BAC was estimated to have been 2 to 3 mg/dL after ingestion of the medication elixir based on its alcohol content (5% ethanol v/v), the dose volume (13.3 mL), and the patient's height and weight.…”

Section: Discussionmentioning

confidence: 93%

Disulfiram-like Reaction Involving Ceftriaxone in a Pediatric Patient

Small¹,

Bacher²,

Jost³

2018

The Journal of Pediatric Pharmacology and Therapeutics

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Several medications have been shown to cause disulfiram-like reactions in patients concomitantly exposed to ethanol, including specific cephalosporin antibiotics that possess a methylthiotetrazole substituent. Within the cephalosporin class, there are few reports of disulfiram-like reactions with ceftriaxone. This case report is the first to involve a pediatric patient, and it describes a mild but likely disulfiram-like reaction manifesting as facial flushing in an 8-year-old male upon receiving a ceftriaxone infusion preceded by a dose of prednisolone elixir (5% ethanol by volume) for presumed community-acquired pneumonia thought to be complicated by an asthma exacerbation. The patient's flushing resolved with intravenous diphenhydramine, did not reappear, and was diagnosed as an allergy to ceftriaxone. Upon further evaluation, a hypersensitivity reaction was considered unlikely, and the allergy history was revised. The patient's antibiotic treatment was switched to azithromycin without steroids, and he had no further issues. This case suggests there is benefit in increased monitoring of pediatric patients receiving certain cephalosporins along with alcohol-containing medications, and it demonstrates how disulfiram reactions can easily be misinterpreted as hypersensitivity reactions. Aside from just alcohol-cephalosporin interactions, this case underscores the need for general vigilance when using alcohol-containing drug preparations in pediatric patients in an effort to prevent adverse effects and potential drug interactions.

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Section: Discussionmentioning

confidence: 93%

Disulfiram-like Reaction Involving Ceftriaxone in a Pediatric Patient

Small¹,

Bacher²,

Jost³

2018

The Journal of Pediatric Pharmacology and Therapeutics

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“…After the placebo control treatment, the concentrations of acetaldehyde in plasma were barely measurable, whereas after blocking ALDH the concentrations were raised about 50-fold for several hours afterward. The subjects in this experiment complained of headache, tachycardia, and difficulties in breathing and these symptoms as well as a pronounced flush of the face lasted for several hours after the end of drinking [246] (Fig. 13.12).…”

Section: Pharmacokinetic and Pharmacodynamic Interactions…mentioning

confidence: 85%

“…Metronidazole and had no effect on the elimination of alprazolam [243], diazepam [244], lorazepam [243], or midazolam [245]. The same was true for the non-imidazole antifungal [226]; the terfenadine data are from Jurima-Romet et al [228]; and the tolbutamide data are from Back et al [434] agent, terbinafine, on midazolam [241] and triazolam [246] ( Their ability to do this followed the same potency ranking as was their effects on the pharmacokinetics, ketoconazole > itraconazole > fluconazole. Indeed, multiple doses of ketoconazole strongly enhanced the pharmacodynamic effects of triazolam and midazolam; triazolam was also strongly enhanced by itraconazole and fluconazole.…”

Section: Interactions With Imidazole Antifungal Agentsmentioning

confidence: 99%

“…The active substance in the mushroom was later identified as coprine, which is a naturally occurring inhibitor of hepatic ALDH [245]. Figure 13.9 shows a plot of the plasma concentration of acetaldehyde, estimated indirectly by analysis of breath, in one subject who participated in two drinking sessions [246]. The man drank the same small dose of ethanol (0.25 g/kg) with or without pretreatment with the ALDH inhibitor calcium carbimide (50 mg) given 60 min before drinking.…”

Section: Pharmacokinetic and Pharmacodynamic Interactions…mentioning

confidence: 99%

See 1 more Smart Citation

Handbook of Drug Interactions

Karalliedde¹,

Henry²

2012

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PrefaceAdverse drug reactions and drug interactions remain a major issue in 2011. During the second edition of our book, FDA reported greater than 370,000 serious adverse events in 2009 and more than 100,000 for the first quarter of 2010. The Adverse Event Reporting System is a database that gives computerized statistics used to support FDA's post-marketing safety surveillance for all approved drugs. A serious event is defined as requiring hospitalization, being life-threatening, causing disability or congenital anomalies, for example. Importantly, more than 63,000 deaths were recorded in 2009, and more than 20,000 occured during the first quarter of 2010.The second edition of Handbook of Drug Interactions: A Clinical and Forensic Guide has been updated to reflect new information and also includes new chapters of interest. In this respect, it is a continuation of the first edition and part of the ongoing story of drug-drug interactions.Pharmacogenomics is a rapidly growing field covering the genetic basis for individual variability in drug responses. This new section allows the reader to review important polymorphisms in drug metabolizing enzymes and applies the findings to forensic interpretation through interesting cases involving opiates.Although the section relating to central nervous system drugs encompasses a number of potential drugs with illicit use such as benzodiazepines and opiates, a chapter dealing exclusively with drugs of abuse has been added to the second edition. Cocaine, amphetamines, cannabis, flunitrazepam and GHB are now discussed. Alcohol and nicotine are still covered in the section related to environmental and social pharmacology.The existing chapters from the first edition have, in most cases, been updated and edited to reflect new data or bring out better tables and diagrams. More recent drugs and formulations are included. Recent references have been added for completeness. This volume emphasizes explanations when possible and covers both pharmacokinetic and pharmacodynamic drug interactions. The result, we hope, will continue to prove useful to health and forensic professionals as well as students.

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“…Additionally, clinical data from volunteers consuming alcohol in conjunction with an hepatic ALDH inhibitor showed systemic concentrations of acetaldehyde of up to 240 mM. 36,37 With the considerable extrahepatic dilution, this would suggest that intrahepatic and intrahepatocyte concentrations should be considerably higher.…”

Section: Discussionmentioning

confidence: 99%

Suicide gene therapy: conversion of ethanol to acetaldehyde mediated by human beta 2 alcohol dehydrogenase

et al. 2004

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Acetaldehyde (AcH) produced in the physiological metabolism of ethanol can be potentially toxic and immunomodulating. The antitumour activity of a suicide gene system using adenovirus delivered alcohol dehydrogenase (ADH) to convert ethanol to acetaldehyde inside cancer cells has been investigated in vitro and in vivo. In vitro experiments confirmed the toxicity of acetaldehyde to a number of tumour cell lines. Daudi lymphoma cells grown in normal media increased by Day 4 to 650% of their starting number, while those exposed to 250 mM, 500 mM and 1 mM acetaldehyde reached 138, 30 and 5% respectively. Adenocarcinoma cells appeared to be less sensitive with CMT-64 cells and HeLa cells numbering 105 and 53% of their starting number by Day 4 with 1 mM acetaldehyde. After transduction with an adenovirus containing the human ADH beta 2 cDNA, CMT-64 cells exposed to 20 mM ethanol had a reduction in number to 74% by Day 2 and to 36% by Day 4. In a preclinical model with Ad-ADH CMT-64 cells, mice exposed to daily pulses of ethanol for 5 days formed tumours only 30% on Day 6 and 42% on Day 13 of the volume of those in mice exposed to water.The ability of this easily administered suicide gene system to produce significant effects on cell proliferation in vivo suggests that further optimized development is warranted.

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Concentration‐time profiles of ethanol and acetaldehyde in human volunteers treated with the alcohol‐sensitizing drug, calcium carbimide.

Cited by 34 publications

References 23 publications

Disulfiram-like Reaction Involving Ceftriaxone in a Pediatric Patient

Disulfiram-like Reaction Involving Ceftriaxone in a Pediatric Patient

Handbook of Drug Interactions

Suicide gene therapy: conversion of ethanol to acetaldehyde mediated by human beta 2 alcohol dehydrogenase

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