Cigarette smoking enhances the elimination of quinine

Wanwimolruk, Sompon; Wong, S. M.; Coville, P. F.; Viriyayudhakorn, Somchai; Thitiarchakul, Supachai

doi:10.1111/j.1365-2125.1993.tb00424.x

Cited by 33 publications

(15 citation statements)

References 30 publications

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“…The pharmacokinetic parameters of quinine obtained in this study (Table 1) were comparable with those previously reported [22][23][24][25][26]. Results from ANOVA revealed that there were no period effects among the three treatments studied.…”

Section: Resultssupporting

confidence: 89%

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Marked enhancement by rifampicin and lack of effect of isoniazid on the elimination of quinine in man.

Wanwimolruk

Kang

Coville

et al. 1995

Brit J Clinical Pharma

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The effect of rifampicin and isoniazid pretreatment on the pharmacokinetics of quinine after a single oral dose (600 mg quinine sulphate) was studied in nine healthy young Thai male volunteers using a three-way randomized crossover design. Subjects were studied over three 2 day periods, during which they received no pretreatment, or pretreatment with daily 600 mg p.o. rifampicin for 2 weeks, or isoniazid 300 mg p.o. daily for 1 week, prior to quinine administration. The mean (+ s.d.) clearance (CL/F) of quinine coadministered with rifampicin (0.87 ± 0.35 1 h-1 kg-') was significantly greater than that of quinine alone (0.14 ± 0.05 1 h-1 kg-'). The mean difference in clearance from the control treatment was 0.73 1 h-1 kg-', with 95% confidence interval (C.I.) of 0.48 to 0.98. The unbound clearance (CLu/F) of quinine, which reflects the activity of the drug-metabolizing enzymes, was considerably greater (6.9-fold) in subjects when rifampicin was coadministered with quinine than that of quinine alone (6.9 ± 3.6 vs 1.0 ± 0.5 1 h-1 kg-'; the 95% C.I. for the mean difference was 3.3 to 8.5). The mean elimination half-life of quinine when coadministered with rifampicin (5.5 ± 3.0 h) was significantly shorter than when quinine was given alone (11.1 ± 3.0 h; the 95% C.I. for the mean difference was -8.6 to -2.6). In contrast to rifampicin, pretreatment for 1 week with 300 mg oral isoniazid had no significant effects on the pharmacokinetics of quinine. These results indicate that rifampicin pretreatment caused a marked increase (6.2-fold) in the clearance of quinine, possibly due to enzyme induction. The extent to which the elimination of quinine is enhanced by the concomitant administration of rifampicin is likely to have important clinical consequences. Although the clinical significance of these findings is unknown, they indicate the need for caution in the administration of quinine to patients who are concurrently taking rifampicin as an anti-tuberculosis medication.

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Section: Resultssupporting

confidence: 89%

“…The elimination half-life (ti,2,z), renal clearance (CLR), apparent oral clearance (i.e. CL/F) and unbound oral clearance (CLU/F) relative to the bioavailability (F) of quinine were estimated as described previously [22]. Cmax and tm.…”

Section: Pharmacokinetic Analysismentioning

confidence: 99%

Marked enhancement by rifampicin and lack of effect of isoniazid on the elimination of quinine in man.

Wanwimolruk

Kang

Coville

et al. 1995

Brit J Clinical Pharma

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“…The pharmacokinetics and pharmacodynamics of drugs mainly metabolized by CYP1A are known to be influenced by smoking (5-7). Smoking has also been suggested to induce CYP3A in 2 in vitro studies (45,46) and in a small clinical study on quinine-a known CYP3A substrate (47). Other studies, however, have not confirmed the influence of smoking on CYP3A (48)(49)(50).…”

Section: Discussionmentioning

confidence: 99%

Influence of Smoking on the Pharmacokinetics and Toxicity Profiles of Taxane Therapy

Graan

Loos

Friberg

et al. 2012

Clinical Cancer Research

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Purpose: Cigarette smoke is known to interact with the metabolism of several anticancer drugs. It may also affect the incidence and severity of adverse events and efficacy of chemotherapy. The main objective of this study was to examine the effects of smoking on the pharmacokinetics and toxicities of patients treated with docetaxel or paclitaxel.Experimental Design: Smoking status, toxicity profiles, and pharmacokinetic parameters (calculated by nonlinear mixed-effect modeling population analysis) were determined in 566 patients (429 nonsmokers and 137 smokers) treated with docetaxel or paclitaxel.Results: Smokers treated with docetaxel showed less grade IV neutropenia (35% vs. 52%; P ¼ 0.01) than nonsmokers. Smokers treated with paclitaxel had less grade III-IV leukopenia than nonsmokers (12% vs. 25%; P ¼ 0.03), and the white blood cell (WBC) nadir was lower in nonsmokers (median, 2.7 Â 10 9 /L; range, 0.05 Â 10 9 to 11.6 Â 10 9 /L) than in smokers (median, 3.3 Â 10 9 /L; range 0.8 Â 10 9 to 10.2 Â 10 9 /L; P ¼ 0.02). Of interest, significantly lower WBC counts and absolute neutrophil counts at baseline were seen in nonsmoking patients treated with paclitaxel (P ¼ 0.0001). Pharmacokinetic parameters were similar in smokers and nonsmokers for both taxanes.Conclusion: Cigarette smoking does not alter the pharmacokinetic determinants of docetaxel and paclitaxel. Smokers treated with docetaxel and paclitaxel have less neutropenia and leukopenia, but further research is warranted to elucidate this potential protective effect.

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“…17,33 Elimination of a single dose of quinine sulfate, an antimalarial medication structurally similar to chloroquine and hydroxychloroquine, was found to be enhanced with cigarette smoking. 41 As these antimalarial agents are partly metabolized via the cytochrome P450 enzyme system and as the constituents of cigarette smoke are known potent inducers of cytochrome P450, it has been hypothesized that the resistance of CLE to antimalarials might be explained by a modification of the metabolism of these drugs. 33,42 It is well established that low blood hydroxychloroquine concentrations are associated with SLE disease activity, are a strong predictor of exacerbations, 43 and may help to diagnose poor adherence.…”

Section: Association Between Smoking and Increased Disease Activity Imentioning

confidence: 99%

Hydroxychloroquine and smoking in patients with cutaneous lupus erythematosus

Ezra

Jorizzo

2012

Clinical and Experimental Dermatology

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SummaryAntimalarials, such as chloroquine and hydroxychloroquine, have been used to treat cutaneous and systemic lupus erythematosus for decades with excellent therapeutic efficacy. Smoking seems to inhibit the therapeutic efficacy of antimalarials when treating cutaneous lupus erythematosus (CLE), but the reason behind this observation is unclear. In addition, antimalarials have been associated with several potentially serious adverse effects, including irreversible loss of vision. The aim of this literature review is to discuss the evidence for how cigarette smoking interferes with antimalarial efficacy in the treatment of CLE. Evidence-based data with long-term follow-up will allow determination of the aetiology for diminished antimalarial response, and enable selection of the best treatment to maximize long-term remission in CLE.

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Cigarette smoking enhances the elimination of quinine

Cited by 33 publications

References 30 publications

Marked enhancement by rifampicin and lack of effect of isoniazid on the elimination of quinine in man.

Marked enhancement by rifampicin and lack of effect of isoniazid on the elimination of quinine in man.

Influence of Smoking on the Pharmacokinetics and Toxicity Profiles of Taxane Therapy

Hydroxychloroquine and smoking in patients with cutaneous lupus erythematosus

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