Fluconazole (Diflucan) Interactions
- Alfentanil
- Alosetron
- Amitriptyline
- Amphotericin B
- Aprepitant
- Aripiprazole
- Astemizole
- Atorvastatin
- Bexarotene
- Bortezomib
- Bosentan
- Budesonide
- Buprenorphine
- Caffeine
Calcium-Channel Blockers
- Celecoxib
- Cevimeline
- Chlordiazepoxide
- Cilostazol
- Cimetidine
- Cisapride
- Clomipramine
- Clonazepam
- Clorazepate
- Cyclosporine
- Darifenacin
- Diazepam
- Dihydroergotamine
- Dofetilide
- Doxercalciferol
- Eplerenone
- Ergotamine
- Ethinyl Estradiol; Levonorgestrel
- Fentanyl
- Flurazepam
- Fluvastatin
- Fosphenytoin
- Galantamine
- Gefitinib
- Glipizide
- Green Tea
- Guarana
- Haloperidol
- Hydrochlorothiazide, HCTZ
- Imatinib, STI-571
- Imipramine
- Irbesartan
- Levobupivacaine
- Levomethadyl
- Lovastatin
- Methadone
- Methysergide
- Midazolam
- Modafinil
- Nevirapine
- Nystatin
Oral contraceptives
- Paricalcitol
- Phenytoin
- Pimozide
- Prazepam
- Quazepam
- Ramelteon
- Rifabutin
- Rifampin
- Saquinavir
- Simvastatin
- Sirolimus
- Sufentanil
Sulfonylureas
- Tacrolimus
- Terfenadine
- Testosterone
- Theophylline, Aminophylline
- Tipranavir
- Triazolam
- Valdecoxib
- Voriconazole
- Warfarin
- Went Yeast, Monascus purpureus
- Zidovudine, ZDV
- Zonisamide
Fluconazole (Diflucan) Interactions
Fluconazole significantly inhibits the metabolism of celecoxib via 2C9. Fluconazole at 200 mg per day resulted in a two-fold increase in celecoxib plasma concentration after a single 200 mg dose of celecoxib. Celecoxib should be introduced at the lowest recommended dose in patients receiving fluconazole. In this crossover study, ketoconazole 200 mg daily did not alter the pharmacokinetics of celecoxib; however, one of about 45 subjects exhibited abnormally high celecoxib plasma concentrations.
The combined use of amphotericin B with azole antifungals is controversial. Although it is rare for these classes of drugs to be used together, such combinations have been initiated in patients with serious, resistant fungal infections. For the most part, the combinations represent duplication of therapy whenever the drugs are used by similar routes (e.g., systemic or topical routes). There are in vitro and in vivo data in the literature to support neutral effects for the combination of azole antifungals with amphotericin B against various fungal species or even antagonism of amphotericin B efficacy versus the use of amphotericin alone. Mechanistically, the azole antifungals inhibit the synthesis of the fungal sterol ergosterol, while the therapeutic actions of polyene antifungals, such as amphotericin B, result from binding to ergosterol. Theoretically, azole antifungals could interfere with the action of amphotericin B by depleting polyene binding sites. More data are needed to determine if combination treatment is beneficial, detrimental or provides no advantage in clinical infections. Whenever possible, azole antifungals should not be coadministered with amphotericin B until more data are available to indicate improved outcomes with co-treatment, unless coadministration represents attempts to resolve serious recalcitrant infection. In addition, clinicians should be alert for therapeutic failure if amphotericin B therapy was immediately preceded by therapy with azole antifungals; some data indicate that azole antifungal pretreatment may affect therapeutic response to amphotericin B.
Although it is rare for nystatin and azole antifungals to be used together, such combinations have been initiated in patients with resistant fungal infections or multiple-site infections. For the most part, the combinations represent duplication of therapy whenever the drugs are used by similar routes (e.g., systemic, vaginal or topical routes) and are usually avoided. Azole antifungals inhibit the synthesis of the fungal sterol ergosterol, while the therapeutic actions of polyene antifungals, such as nystatin, result from binding to ergosterol. Theoretically, azole antifungals could interfere with the action of nystatin by depleting polyene binding sites. However, topical preparations or mouthwashes containing nystatin may be used concurrently with azole antifungals in selected patients.
Closely monitor patients receiving azole antifungals concomitantly with warfarin. In post-marketing experience, bleeding events have been reported in association with increases in prothrombin time in patients receiving fluconazole concurrently with warfarin. Fluconazole appears to exert dose-dependent effects on warfarin metabolism. Fluconazole administered at low doses may affect warfarin hepatic metabolism only slightly while higher doses may significantly increase INR values. Careful monitoring of anticoagulation in patients receiving fluconazole and warfarin is recommended, especially in patients receiving warfarin prior to the addition of fluconazole therapy.
The combined use of fluconazole and cisapride is contraindicated. Cisapride is metabolized by cytochrome P-450 3A4 and fluconazole is an inhibitor of this isoenzyme. In patients receiving fluconazole 200 mg daily and cisapride 20 mg four times daily starting 7 days after beginning fluconazole, fluconazole significantly increased the AUC of cisapride following both single and multiple doses of cisapride. Fluconazole significantly increased the QTc interval; torsade de pointes has been reported. The potential exists for a similar drug interaction between fluconazole and terfenadine, although high doses of fluconazole (e.g., 400-800 mg/day) appear to be necessary for the interaction to be clinically significant. Nevertheless, coadministration of terfenadine is contraindicated in patients receiving fluconazole 400 mg/day or higher. Finally, similar caution should be observed during concomitant administration of fluconazole with astemizole.
Fluconazole may inhibit the metabolism of cyclosporine, sirolimus, and tacrolimus and lead to increased concentrations. Renal transplant patients stabilized on cyclosporine for at least 6 months and on a stable cyclosporine dose for at least 6 weeks received fluconazole 200 mg PO qd for 14 days. Fluconazole caused significant increases in cyclosporine AUC, Cmax, Cmin, and a significant reduction in apparent cyclosporine clearance. Plasma cyclosporine concentrations should be monitored closely if fluconazole is added. There have been reports of nephrotoxicity in patients to whom fluconazole and tacrolimus have been coadministered. Renal function in these patients should be carefully monitored.
Fluconazole can decrease the metabolism of phenytoin. A mean increase of 88% in phenytoin serum AUC has been seen in some normal male volunteers taking both fluconazole and phenytoin. Concentrations of phenytoin should be carefully monitored if fluconazole is added. A similar interaction would be expected with fosphenytoin.
Uveitis has been reported with concomitant use of fluconazole and rifabutin. Since fluconazole has been shown to significantly increase rifabutin AUC, it is likely that the development of uveitis is directly associated with rifabutin plasma concentrations. Because HIV-infected patients are likely to be receiving rifabutin and fluconazole concomitantly, these patients should be monitored for this adverse reaction. Limited data suggest that the risk of MAC bacteremia is lowered when fluconazole is added to rifabutin.
Rifampin is a potent enzyme inducer and can increase the metabolism of fluconazole. Administration of fluconazole 200 mg PO after 15 days of rifampin 600 mg PO daily to 8 healthy male volunteers resulted in a significant decrease in fluconazole AUC and a significant increase in fluconazole apparent oral clearance. The AUC was reduced by about 23% and the apparent oral clearance was increased by about 32%. Fluconazole half-life decreased from approximately 33 hours to approximately 27 hours. The dose of fluconazole may need to be increased in patients also receiving rifampin to assure adequate fluconazole plasma concentrations. Although available data are inconclusive, rifabutin may be less likely than rifampin to interact with fluconazole in this manner.
Fluconazole can inhibit the clearance of some benzodiazepines. Fluconazole can increase midazolam serum concentrations. After administration of oral midazolam with fluconazole, there was a significant increase in midazolam concentrations and psychomotor effects. The interaction was more pronounced after oral fluconazole than with intravenous fluconazole. Clinicians should be alert to the possibility of an exaggerated or a prolonged response to midazolam in patients receiving fluconazole. In a study of fluconazole with triazolam, fluconazole increased triazolam Cmax, area-under-the-curve, and half-life and potentiated the pharmacodynamic effects of triazolam. Fluconazole could theoretically inhibit CYP3A4 metabolism of other oxidized benzodiazepines (e.g., alprazolam, chlordiazepoxide, clonazepam, clorazepate, diazepam, estazolam, flurazepam, prazepam, quazepam).
Typically voriconazole would not be used in combination with other systemic azole antifungal agents due to similar mechanisms of action and indications for use (duplicate therapies). Fluconazole has the potential to exhibit multiple hepatic cytochrome P450 interactions with voriconazole. Serum concentrations of voriconazole or fluconazole may increase or decrease.
Limited data suggest that testosterone concentrations increase during fluconazole administration. It appears that fluconazole doses of 200 mg/day or greater are more likely to produce this effect than doses of 25-50 mg/day. The clinical significance of this interaction is unclear at this time. Although data are not available, a similar reaction may occur with voriconazole. Both fluconazole and voriconazole are inhibitors of CYP3A4, the hepatic microsomal isoenzyme responsible for metabolism of testosterone.
Thiazide diuretics may decrease the renal clearance of fluconazole. Coadministration of fluconazole and hydrochlorothiazide for 10 days in normal volunteers (n=13) resulted in a significant increase in fluconazole AUC and Cmax compared to fluconazole given alone. There was a mean increase in fluconazole AUC and Cmax of 45% and 43% ± 31% (range: 19 to 122%), respectively. These changes are attributed to a mean reduction in renal clearance of 30%. Dosage adjustments do not appear to be necessary during combined therapy with fluconazole and thiazides.
Cilostazol is extensively metabolized by the CYP3A4 and CYP2C19 hepatic isoenzyme and appears to have pharmacokinetic interactions with many medications that are potent inhibitors of these isoenzymes. Ketoconazole has been shown to increase both cilostazol AUC and Cmax when administered concurrently; other azole antifungals are likely to affect cilostazol AUC and Cmax. In some studies, coadministration of these agents with cilostazol resulted in increased incidences of adverse effects, such as headache. When significant CYP3A4 and/or CYP2C19 inhibitors are administered concomitantly with cilostazol, the cilostazol dosage should be reduced by 50%.
Modafinil is significantly metabolized by the CYP3A4 hepatic microsomal enzyme system. Azole antifungals are significant inhibitors of this isoenzyme and may reduce the clearance of modafinil. However, modafinil is also an inducer of the hepatic microsomal CYP3A4 isoenzyme, therefore, drug interactions due to CYP3A4 enzyme inhibition by other medications may be complex and difficult to predict.
Fluconazole may decrease the systemic clearance of alfentanil, buprenorphine, fentanyl, levomethadyl, methadone, or sufentanil . Prolonged duration of opiate action, increased sedation, respiratory depression or other opiate side effects may occur. Close monitoring of patients is warranted. One placebo-controlled study evaluated the effects of intravenous and oral fluconazole on the pharmacokinetics and pharmacodynamics of intravenous alfentanil. The clearance of alfentanil was reduced 55% by fluconazole and alfentanil-induced subjective effects were also increased.
Irbesartan is a substrate of the CYP 2C9 isoenzyme. Fluconazole (CYP2C9 inhibitor) has been reported to increase the AUC of irbesartan by 63%. Drugs that inhibit the cytochrome CYP 2C9 isoenzyme in vitro should be used cautiously in patients receiving irbesartan until further data are available regarding the clinical significance of theoretical drug interactions. Clinically significant interactions between irbesartan and inhibitors of CYP 2C9 metabolism have not been reported to date.
Fluconazole inhibits the hepatic cytochrome P450 isoenzyme 3A4 (CYP3A4) in vitro; the manufacturers of pimozide consider the concomitant use of inhibitors of CYP3A4 to be contraindicated. There are rare reports of QT prolongation, ventricular arrhythmia and sudden death when a CYP3A4 inhibitor was added to the drug regimen in patients on pimozide.
Levobupivacaine is metabolized by cytochrome P450 (CYP) isoenzymes 3A4 and 1A2. Fluconazole inhibits CYP3A4 and may inhibit the metabolism of levobupivacaine. Concurrent administration of fluconazole and levobupivacaine may result in increased systemic levels of levobupivacaine resulting in toxicity.
Fluconazole may decrease the clearance of calcium-channel blockers (e.g., diltiazem, felodipine, and verapamil) via inhibition of CYP3A4 metabolism.
Bexarotene is extensively metabolized by the CYP3A4 hepatic isoenzyme. When significant CYP3A4 inhibitors like fluconazole are administered concomitantly with bexarotene, the health care professional may need to observe the patient for increased toxicity from bexarotene. Due to low systemic exposure to bexarotene after low to moderate intense gel regimens, clinically significant metabolic drug interactions are unlikely with bexarotene gel.
Fluconazole may theoretically increase dofetilide plasma concentrations via inhibition of CYP3A4 metabolism, and therefore, be used with caution with dofetilide. The concomitant use of dofetilide and ketoconazole or itraconazole is specifically contraindicated; this interaction significantly increases dofetilide plasma concentrations with the potential risk of associated arrhythmias.
Cevimeline is metabolized by cytochrome P450 (CYP) 3A4 and CYP2D6. Concurrent administration of inhibitors of these enzymes, such as fluconazole, may lead to increased cevimeline plasma concentrations.
Alosetron is partially metabolized by cytochrome P450 3A4 (CYP3A4). Concurrent administration of inhibitors of these enzymes, such as fluconazole may lead to increased alosetron plasma concentrations.
Zonisamide is metabolized by cytochrome P450 3A4 (CYP3A4). Concurrent administration of inhibitors of these enzymes, such as fluconazole may lead to increased zonisamide plasma concentrations.
Hepatic CYP3A4 is partially responsible for the metabolism of galantamine. The bioavailability of galantamine may be increased when coadministered with fluconazole, which inhibits CYP3A4.
Fluconazole should be used cautiously in patients taking certain ergot alkaloids. Fluconazole may reduce the metabolism of ergotamine, dihydroergotamine or methysergide via inhibition of the hepatic CYP3A4 isoenzyme, potentially increasing the risk of ergot-related side effects.
Concurrent use of itraconazole with haloperidol has resulted in increased serum haloperidol concentrations; inhibition of haloperidol metabolism is the suspected mechanism of the interaction. Neurologic side effects have been noted clinically in some patients as a result of impaired haloperidol elimination. Similar interactions may occur with either fluconazole, ketoconazole, or voriconazole.
During concomitant administration with fluconazole 400 mg/day in 12 HIV-infected patients, the clearance of zidovudine, ZDV, was reduced by 43%, while the area under the concentration-time curve (AUC) was increased by 74% (range: 54-98%). The half-life of zidovudine was increased from 1.5 to 3.4 hours during fluconazole administration. Fluconazole also was reported to have increased zidovudine AUC by about 20% in 13 volunteers with AIDS or ARC who were stable on a zidovudine for at least two weeks. Although the clinical significance of this interaction has not been established, patients receiving fluconazole with zidovudine should be closely monitored for zidovudine-induced adverse effects, especially hematologic toxicity. Zidovudine dosage reduction may be considered.
Fluconazole may inhibit the metabolism of imatinib, STI-571 via cytochrome P450 3A4. Increased imatinib serum levels and toxicity may result with concurrent use of fluconazole. Close monitor patients for any signs of toxicity. There was a significant increase in imatinib Cmax and AUC when given with another systemic azole antifungal (i.e., ketoconazole).
Fluconazole has been reported to increase the effects of amitriptyline, perhaps through inhibition of the hepatic microsomal CYP2C19 or CYP3A4 isoenzymes. In at least one case, the interaction resulted in an increased incidence of TCA-related side effects, like dizziness and syncope. Monitor for an increased response to amitriptyline if fluconazole is coadministered. Because of similar metabolic pathways, other TCAs that may be affected include clomipramine and imipramine, but specific data are lacking.
Concomitant single dose administration of valdecoxib 20 mg with multiple doses of fluconazole produced a significant increase in exposure of valdecoxib. Plasma exposure (AUC) to valdecoxib was increased 62% when given with fluconazole. Significant increases in valdecoxib plasma levels are associated with fluid retention.
Coadministration of bosentan with ketoconazole, a potent CYP3A4 inhibitor, increased the plasma concentrations of bosentan by approximately 2-fold. No dosage adjustment of bosentan is needed, however, the potential for increased bosentan effects should be monitored. Although data are lacking, fluconazole (CYP3A4 inhibitor) could also increase bosentan plasma concentrations via CYP3A4 inhibition.
Fluconazole should be used cautiously with oral sulfonylureas because blood glucose response may be altered in diabetic patients. The combination of fluconazole and either glipizide, glyburide, tolbutamide or glimepiride has resulted in significant increases in the AUC and Cmax of these sulfonylureas in healthy volunteers; however, individual patients may have greater or lesser changes in these pharmacokinetic parameters. One fatality due to hypoglycemia has been reported with combined use of fluconazole and glyburide. Fluconazole reduces the metabolism of these sulfonylureas resulting in increases in their plasma concentrations. Blood glucose concentrations should be monitored during fluconazole treatment; patients should be aware of the symptoms of hypoglycemia. In some cases, dosage adjustment of the sulfonylurea may be necessary.
Fluconazole is an inhibitor of the hepatic CYP3A4 isoenzyme. Due to fluconazole’s inhibition CYP3A4, the drug may increase serum concentrations of eplerenone. Increased eplerenone levels may lead to a risk of developing hyperkalemia and hypotension; monitor for signs and symptoms in patients receiving fluconazole and eplerenone concurrently. If these medications are to be given concurrently, the initial eplerenone dose should not exceed 25 mg/day PO.
Increased aripiprazole blood levels are expected when aripiprazole is coadministered with inhibitors of CYP3A4 such as fluconazole. A dosage adjustment of aripiprazole is necessary when these drugs are used concomitantly, and conversely, when fluconazole is discontinued in a patient taking aripiprazole.
Fluconazole has been shown to inhibit the clearance of caffeine by 25%. The clinical significance of these interactions has not been determined. During concomitant fluconazole therapy, it may be prudent to limit caffeine-containing medications, foods including chocolate, products such as guarana, and beverages (e.g., coffee, green tea, other teas, and colas) in an effort to minimize caffeine related side effects such as nausea and tremor.
Concomitant administration of aprepitant with strong CYP3A4 inhibitors, such as systemic azole antifungals may lead to elevated serum concentrations of aprepitant. Coadminister these drugs with caution. In clinical trials, ketoconazole has been shown to increase the AUC of aprepitant by 5-fold. The clinical significance of elevated aprepitant serum concentrations is unknown. Systemic fluconazole is a less potent CYP3A4 inhibitor relative to ketoconazole, but might produce a similar interaction.
Agents that inhibit cytochrome P450 (CYP) 3A4 may increase the exposure to bortezomib and increase the risk for toxicity; however, bortezomib is also metabolized by other CYP isoenzymes. Therefore, the clinical significance of concurrent administration of bortezomib with fluconazole is not known.
Gefitinib is metabolized significantly by cytochrome P450 (CYP) 3A4. Substances that are potent inhibitors of cytochrome P450 (CYP) 3A4 activity, such as fluconazole in doses > 200 mg/day, decrease the metabolism of gefitinib and increase gefitinib concentrations. This increase may be clinically relevant as adverse reactions to gefitinib are related to dose and exposure; therefore caution should be used when administering high doses of fluconazole with gefitinib.
Fluconazole is an inhibitor of CYP2C9, and has the potential to inhibit the metabolism of fluvastatin (major CYP2C9 substrate).
The risk of developing myopathy, rhabdomyolysis, and acute renal failure is increased if lovastatin or simvastatin is administered concomitantly with CYP3A4 inhibitors including the systemic azole fungals (e.g., fluconazole). Since compounds in went yeast, Monascus purpureus/red yeast rice claim to have HMG-CoA reductase inhibitor activity, went yeast/red yeast rice should not be used in combination with fluconazole. Atorvastatin is also metabolized by CYP3A4, and may interact similarly.
In a pharmacokinetic study, fluconazole was found to increase nateglinide’s AUC by 48% and increase nateglinide half-life from 1.6 to 1.9 hours. The increases may be due to fluconazole’s inhibition of CYP2C9, which has been shown to participate in nateglinide’s metabolism in vitro. However, this interaction is not associated with any clinically relevant effects and blood glucose levels are not significantly affected.
Fluconazole inhibits CYP3A4 and increases the plasma concentration of saquinavir. This interaction has not been found to produce clinically relevant effects, although some patients might experience an increase in saquinavir-related adverse effects if saquinavir and fluconazole are coadministered.
Tipranavir concentrations are increased when coadministered with fluconazole; fluconazole doses > 200 mg per day are not recommended to be given with tipranavir.
When fluconazole and nevirapine are coadministered, nevirapine Cmax, AUC, and Cmin increase by 100%. The risk of nevirapine induced hepatotoxicity may increase with this combination. If concomitant use of fluconazole and nevirapine is necessary, use caution and closely monitor patients for nevirapine-associated toxicity.
Fluconazole increases the serum concentrations of theophylline. In one study (manufacturer data), the pharmacokinetics of theophylline were determined from a single IV dose of aminophylline (6 mg/kg) before and after fluconazole 200 mg PO qd for 14 days in 16 normal male volunteers. Significant increases in theophylline AUC, Cmax, and half-life were reported with a corresponding decrease in clearance. The mean ± SD theophylline AUC increased 21 ± 16%; the Cmax increased 13 ± 17%; and theophylline clearance decreased 16 ± 11%. Theophylline half-life increased from 6.6 ± 1.7 hours to 7.9 ± 1.5 hours. Serum theophylline concentrations should be monitored closely if fluconazole is added.
Fluconazole tablets, administered concomitantly with oral contraceptives containing either ethinyl estradiol; levonorgestrel or ethinyl estradiol; norethindrone, have resulted in an overall mean increase in ethinyl estradiol, levonorgestrel, and norethindrone serum concentrations compared to placebo. However, in some patients there are decreases up to 47% and 33% of ethinyl estradiol and levonorgestrel concentrations, respectively. Minimal decreases (<5%) in norethindrone AUC have been noted in several individuals. The available data indicate that the decreases in some individual ethinyl estradiol, levonorgestrel, and norethindrone AUC values with fluconazole treatment are likely due to random variation. While there is evidence that fluconazole can inhibit the metabolism of ethinyl estradiol and levonorgestrel, there is no evidence that fluconazole is a net inducer of ethinyl estradiol or levonorgestrel metabolism. The clinical significance of these effects is unknown.
Concomitant administration of fluconazole 100 mg PO and hydrochlorothiazide, HCTZ 50 mg PO for 10 days in 13 normal volunteers resulted in a significant increase in fluconazole AUC and Cmax compared to fluconazole alone. There was a mean ± SD increase in fluconazole AUC and Cmax of 45 ± 31% and 43 ± 31%, respectively. These changes were attributed to a mean ± SD reduction in fluconazole renal clearance of 30 ± 12%.
Administration of 20 ml of Maalox® (aluminum hydroxide; magnesium hydroxide) to 14 normal male volunteers immediately prior to a single oral dose of fluconazole 100 mg had no effect on the absorption or elimination of fluconazole.
Significant decreases in the AUC and Cmax of fluconazole were noted following administration of fluconazole 50 mg PO given two hours after a single dose of cimetidine 400 mg PO to six healthy male volunteers. However, fluconazole pharmacokinetics and bioavailability were not affected when fluconazole 200 mg PO as a single dose was given with cimetidine 600 mg to 900 mg IV over a 4-hour period in healthy male volunteers.
An open-label, randomized, three-way crossover study evaluated the interaction between a single 800 mg oral dose of fluconazole and a single 1200 mg oral dose of azithromycin. There was no significant pharmacokinetic interaction between the two agents.
Fluconazole, an inhibitor of CYP3A4, may decrease the metabolism of darifenacin and increase serum concentrations. Patients should be monitored for increased anticholinergic effects if these drugs are used concomitantly; dosage adjustments of darifenacin may be necessary.
Fluconazole is an inhibitor of CYP3A4. Care should be taken when dosing paricalcitol, a CYP3A4 substrate, with fluconazole; dose adjustments of paricalcitol may be required. Plasma iPTH and serum calcium and phosphorous concentrations should be closely monitored if a patient taking paricalcitol initiates or discontinues therapy with fluconazole.
The AUC and Cmax of ramelteon after a single 16 mg dose was increased by approximately 150% when administered with fluconazole (a CYP2C9 inhibitor). Ramelteon should be administered with caution in subjects taking strong CYP2C9 inhibitors such as fluconazole. The patient should be monitored closely for toxicity from ramelteon.
Doxercalciferol is converted in the liver to 1,25-dihydroxyergocalciferol, the major active metabolite, and 1-alpha, 24-dihydroxyvitamin D2, a minor metabolite. Although not specifically studied, cytochrome P450 enzyme inhibitors including systemic azole antifungals may inhibit the 25-hydroxylation of doxercalciferol, thereby decreasing the formation of the active metabolite and thus, decreasing efficacy. Patients should be monitored for a decrease in efficacy if systemic azole antifungals are coadministered with doxercalciferol.
Plasma levels of orally administered budesonide may increase during coadministration of CYP3A4 inhibitors such as fluconazole. A dose reduction should be considered. Toxicity may occur, particularly excessive HPA-axis suppression. Theoretically, inhibition of CYP3A4 may be clinically significant for inhaled forms of budesonide, including budesonide nasal spray (Rhinocort® Aqua™).
[ Last revised: 1/12/2006 10:02:00 AM ]
References
. Gericke KR. Possible interaction between warfarin and fluconazole. Pharmacotherapy 1993;13:508-9.
. Wells PS, Holbrook AM, Crowther NR et al. Interaction of warfarin with drugs and food. Ann Intern Med 1994;121:676-83.
. Havlir DV, Dube MP, Sattler FR et al. Prophylaxis against disseminated Mycobacterium avium complex with weekly azithromycin, daily rifabutin, or both. N Engl J Med 1996;335:392-8.
. Trapnell CB, Narang PK, Li R et al. Increased plasma rifabutin levels with concomitant fluconazole therapy in HIV-infected patients. Ann Intern Med 1996;124:573-6.
. Narang PK, Trapnell CB, Schoenfelder JR et al. Fluconazole and enhanced effect of rifabutin prophylaxis. N Engl J Med 1994;330:1316-7.
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