Increase of alpha 1‐acid glycoprotein after treatment with amitriptyline.

Baumann, Pierre; Tinguely, D; Schöpf, Josef

doi:10.1111/j.1365-2125.1982.tb04942.x

Cited by 27 publications

(11 citation statements)

References 7 publications

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“…It increases plasma AGP, thus increasing methadone binding. (53,143,157) Amprenavir Decrease A 35% decrease of methadone plasma levels has been observed. An open label, within-subject pharmacokinetic study showed a 13% decrease in R-methadone AUC.Amprenavir may induce CYP P450 enzymes.…”

Section: Metabolism and Excretionmentioning

confidence: 95%

Methadone: a review of drug-drug and pathophysiological interactions

Kapur

Hutson²,

Chibber

et al. 2011

Critical Reviews in Clinical Laboratory Sciences

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Numerous established and potential drug interactions with methadone are clinically important in people treated with methadone either for addiction or for chronic pain. Methadone users often have comorbidities and are prescribed drugs that may interact with methadone. Methadone is extensively metabolized by cytochrome P450 (CYP) 3A4 and to a lesser extent by CYP 1A2, 2D6, 2D8, 2C9/2C8, 2C19, and 2B6. Eighty-six percent of methadone is protein bound, predominately to α1-acid glycoprotein (AGP). Polymorphisms in or interactions with CYPs that metabolize methadone, changes in protein binding, and other pathophysiological conditions affect the pharmacokinetic properties of methadone. It is critical for health care providers who treat patients on methadone to have adequate information on the interactions of methadone with other drugs of abuse and other medications. We set out to describe drug-drug interactions as well as physiological and pathophysiological factors that may impact the pharmacokinetics of methadone. Using MEDLINE, we conducted a systematic search for papers and related abstracts published between 1966 and June 2010. Keywords that included methadone, drug-drug interactions, CYP P450 and AGP identified a total of 7709 papers. Other databases, including the Cochrane Database of Systematic Reviews and Scopus, were also searched; an additional 929 papers were found. Final selection of 286 publications was based on the relevance of each paper to the topic. Over 50 such interactions were found. Interactions of methadone with other drugs can lead to increased or decreased methadone drug levels in patients and result in potential overdose or withdrawal, respectively. The former can contribute to methadone's fatality. Prescribers of methadone and pharmacists should enquire about any new medications (including natural products and over-the-counter medications) periodically, and especially when an otherwise stable patient suddenly experiences drug craving, withdrawal or intoxication.

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Section: Metabolism and Excretionmentioning

confidence: 95%

Methadone: a review of drug-drug and pathophysiological interactions

Kapur

Hutson²,

Chibber

et al. 2011

Critical Reviews in Clinical Laboratory Sciences

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“…Depressive patients receiving long term amitriptyline treatment also exhibit elevated ai-acid 453 Andreasen (1973); Ghoneim & Pandya (1975) Tavares-Almeida et al ) Bruni et al (1980) Tavares-Almeida et al (1985 glycoprotein concentrations (Baumann et al 1982). The link between hepatic microsomal oxidase induction caused by some drugs and increased alacid glycoprotein concentrations in serum (and possibly in hepatocytes) is still obscure.…”

Section: Effect Of Drugsmentioning

confidence: 97%

Free Drug Concentration Monitoring in Clinical Practice

Svensson

Woodruff

Baxter

et al. 1986

Clinical Pharmacokinetics

169

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Recent advances in techniques to determine free drug concentrations have lead to a substantial increase in the monitoring of this parameter in clinical practice. The majority of drug binding to macromolecules in serum can be accounted for by association with albumin and alpha 1-acid glycoprotein. Albumin is the primary binding protein for acidic drugs, while binding to alpha 1-acid glycoprotein is more commonly observed with basic lipophilic agents. Alterations in the concentrations of either of these macromolecules can result in significant changes in free fraction. Diseases such as cirrhosis, nephrotic syndrome and malnourishment can result in hypoalbuminaemia. Burn injury, cancer, chronic pain syndrome, myocardial infarction, inflammatory diseases and trauma are all associated with elevations in the concentration of alpha 1-acid glycoprotein. Treatment with a number of drugs has also been shown to increase alpha 1-acid glycoprotein serum concentrations. A wide variety of biological fluids have been examined for their ability to provide an estimation of free drug concentration at receptor sites. The most useful fluid for estimating free drug concentrations appears to be plasma or serum, with subsequent treatment of the sample to separate free and bound drug by an appropriate technique. The two most widely used methods are equilibrium dialysis and ultrafiltration. Of these two, ultrafiltration has the greatest utility clinically because it is rapid and relatively simple. The major difficulty associated with this method involves the binding of drug to the ultrafilters, but significant progress has been made in solving this problem. Several authors have endorsed the routine use of free drug concentration monitoring. Data examining the clinical usefulness of free drug concentration monitoring for phenytoin, carbamazepine, valproic acid, disopyramide and lignocaine (lidocaine) are reviewed. While available evidence suggests that free concentrations may correlate with clinical effects better than total drug concentrations, there are insufficient data to justify the recommendation of the routine use of free drug concentration monitoring for any of these agents at present.

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“…The last may be associated either with lignocaine or with other components of the aerosol preparation, such as flavouring agents, propellants, and other constituents. Amitriptyline is known to increase AAG concentrations (Baumann et al, 1982). If lignocaine has a similar effect, its characterization might contribute to the understanding of the pharmacokinetics of this important drug.…”

Section: Discussionmentioning

confidence: 99%

“…This may be of importance when AAG-altering drugs are taken for long-term therapy. Amitriptyline is known to increase serum concentrations of AAG, with altered amitriptyline protein binding as a result (Baumann et al, 1982). It is possible that many drugs will be found to alter serum AAG concentrations in a similar fashion.…”

Section: Introductionmentioning

confidence: 99%

Cimetidine does not increase alpha 1‐acid glycoprotein serum concentrations.

Parish

Gotz

Mehta

1988

Brit J Clinical Pharma

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Serum concentrations of a1-acid glycoprotein (AAG) were studied in six healthy, male volunteers before and after administration of cimetidine, 300 mg by mouth every 6 h for 2 days. Serum AAG concentrations were measured at three different times during the first day, i.e. before cimetidine administration, and on the fourth and sixth days, after commencing cimetidine administration. Neither cimetidine treatment nor time of day contributed significantly to differences in serum AAG concentration, and no interaction of these factors was observed. It is concluded that altered drug-AAG binding as a result of cimetidine therapy is not likely to be an important mechanism contributing to cimetidine drug interactions.

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Increase of alpha 1‐acid glycoprotein after treatment with amitriptyline.

Cited by 27 publications

References 7 publications

Methadone: a review of drug-drug and pathophysiological interactions

Methadone: a review of drug-drug and pathophysiological interactions

Free Drug Concentration Monitoring in Clinical Practice

Cimetidine does not increase alpha 1‐acid glycoprotein serum concentrations.

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