Lack of effect of smoking on the metabolism and pharmacokinetics of quinidine in patients.

Edwards, David J.; Axelson, James E.; Visco, John P.; Vanevery, S.; Slaughter, Richard L.; Lalka, David

doi:10.1111/j.1365-2125.1987.tb03057.x

Cited by 12 publications

(3 citation statements)

References 8 publications

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“…Previous studies with quinidine have shown that cigarette smoking does not induce any of the main pathways for quinidine metabolism [34,35]. This gave contrasting results to our study on quinine and may be accounted for by the differences in subjects of the previous study [34].…”

Section: Discussioncontrasting

confidence: 83%

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Cigarette smoking enhances the elimination of quinine

Wanwimolruk

Wong

Coville

et al. 1993

Brit J Clinical Pharma

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The pharmacokinetics of a single dose (600 mg) of quinine sulphate were examined in a group of non-smokers (n = 10) and in heavy cigarette smokers (n = 10). The mean (± s.d.) oral clearance of quinine in smokers (0.189 ± 0.075 1 h-1 kg-1) was significantly greater than in non-smokers (0.107 ± 0.045 1 h-1 kg-, P < 0.01). The unbound clearance of quinine which reflects activity of the drug-metabolizing enzyme, was considerably greater (1.5-fold) in the smokers than in the non-smoker subjects. The mean elimination half-life of quinine in smokers was 7.5 ± 1.4 (s.d.) h, significantly shorter (P < 0.005) than the mean value in non-smokers (12.0 ± 3.1 h). These results suggest that cigarette smoking enhances the elimination of quinine. The clinical significance of these findings is unknown but they indicate the need for caution in the administration of quinine to patients who are heavy cigarette smokers.

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Section: Discussioncontrasting

confidence: 83%

“…This gave contrasting results to our study on quinine and may be accounted for by the differences in subjects of the previous study [34]. Their subjects were patients with cardiac diseases, older age and only five smokers were examined.…”

Section: Discussionmentioning

confidence: 61%

Cigarette smoking enhances the elimination of quinine

Wanwimolruk

Wong

Coville

et al. 1993

Brit J Clinical Pharma

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“…The pH of each sample was adjusted to 7.40 ± 0.05 with 0.5 N H3PO4 since it had previously been reported that the free fraction of at least some lipophilic bases is highly dependent on the hydrogen ion activity in serum (McNamara et al, 1981). Samples were subsequently centrifuged for 15 min in a temperature controlled unit (250 C) at 1250 g. The concentration of quinidine was measured in the ultrafiltrates using a modification (Edwards et al, 1987) of a previously reported h.p.l.c. method (Drayer et al, 1977).…”

Section: Methodsmentioning

confidence: 99%

Lack of effect of treatment with human recombinant‐tumour necrosis factor (HrTNF) on the binding of quinidine to alpha 1‐acid glycoprotein (AGP).

Barnett

et al. 1989

Brit J Clinical Pharma

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Tumour necrosis factor (TNF) is known to be a key mediator in the acute phase response and its administration has been shown to cause a five fold increase in serum oti-acid glycoprotein (AGP) concentration in the rat. Since, in man, plasma AGP level determines the protein binding of many important drugs (e.g. narcotic analgesics, phenothiazines, antiarrhythmics, calcium channel blockers) likely to be given to patients who will be treated with TNF, it is important to determine if TNF treatment of humans causes a similar increase in AGP concentration and drug binding. Therefore, the plasma protein binding of quinidine and the serum level of AGP were studied over a 4 day period in each of five cancer patients who were treated with human recombinant-tumour necrosis factor (HrTNF) using a dosage schedule of 6-8 x 10+5 units/M2 daily for 5 days. It was observed that the quinidine binding ratio (the quotient of bound and free concentration in plasma) was highly correlated with the plasma concentration of AGP (r = 0.818) and that the mean pretreatment AGP concentration in the patients was about three times that found in normal subjects. However, no effects of the TNF treatment regime used in the present study could be demonstrated on either plasma AGP concentration or quinidine free fraction. These observations allow the tentative conclusion that HrTNF does not cause a significant increase in serum AGP level in cancer patients whose baseline AGP concentration is high. However, further study of the relationship between TNF treatment and serum AGP level is needed.

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Clinical Implications of the Competitive Inhibition of the Debrisoquin-Metabolizing Isozyme by Quinidine

Caporaso¹,

Shaw²

1991

Arch Intern Med

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Lack of effect of smoking on the metabolism and pharmacokinetics of quinidine in patients.

Cited by 12 publications

References 8 publications

Cigarette smoking enhances the elimination of quinine

Cigarette smoking enhances the elimination of quinine

Lack of effect of treatment with human recombinant‐tumour necrosis factor (HrTNF) on the binding of quinidine to alpha 1‐acid glycoprotein (AGP).

Clinical Implications of the Competitive Inhibition of the Debrisoquin-Metabolizing Isozyme by Quinidine

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