Desogestrel And Ethinyl Estradiol And Ethinyl Estradiol

Concomitant Use with Hepatitis C Virus (HCV) Combination Therapy - Liver Enzyme Elevation Co-administration of VIORELE ® with HCV drug combinations containing ombitasvir/paritaprevir/ritonavir, with or without dasabuvir is contraindicated, due to potential for ALT elevations (see WARNINGS , RISK OF LIVER ENZYME ELEVATIONS WITH CONCOMITANT HEPATITIS C TREATMENT).

Concomitant Use with Hepatitis C Virus (HCV) Combination Therapy - Liver Enzyme Elevation Co-administration of VIORELE ® with HCV drug combinations containing ombitasvir/paritaprevir/ritonavir, with or without dasabuvir is contraindicated, due to potential for ALT elevations (see WARNINGS , RISK OF LIVER ENZYME ELEVATIONS WITH CONCOMITANT HEPATITIS C TREATMENT).

Co-administration is contraindicated due to potential for ALT elevations.

Concomitant Use with Hepatitis C Virus (HCV) Combination Therapy - Liver Enzyme Elevation Co-administration of VIORELE ® with HCV drug combinations containing ombitasvir/paritaprevir/ritonavir, with or without dasabuvir is contraindicated, due to potential for ALT elevations (see WARNINGS , RISK OF LIVER ENZYME ELEVATIONS WITH CONCOMITANT HEPATITIS C TREATMENT).

Concomitant Use with Hepatitis C Virus (HCV) Combination Therapy - Liver Enzyme Elevation Co-administration of VIORELE ® with HCV drug combinations containing ombitasvir/paritaprevir/ritonavir, with or without dasabuvir is contraindicated, due to potential for ALT elevations (see WARNINGS , RISK OF LIVER ENZYME ELEVATIONS WITH CONCOMITANT HEPATITIS C TREATMENT).

Co-administration is not recommended due to potential for ALT elevations.

Combined hormonal contraceptives significantly decrease plasma concentrations of lamotrigine, which may reduce seizure control; dosage adjustments may be necessary.

Reduced efficacy and increased incidence of breakthrough bleeding and menstrual irregularities associated with concomitant use.

May increase plasma ethinyl estradiol concentrations, possibly by inhibition of conjugation.

Possible association with reduced efficacy and breakthrough bleeding, though less marked than with rifampin.

HIV protease inhibitor that may decrease plasma concentrations of estrogen and/or progestin, potentially diminishing contraceptive effectiveness.

Induces CYP3A4 and may decrease plasma concentrations of desogestrel and ethinyl estradiol, potentially diminishing contraceptive effectiveness and increasing breakthrough bleeding.

May increase plasma ethinyl estradiol concentrations, possibly by inhibition of conjugation.

HIV protease inhibitor that may increase plasma concentrations of estrogen and/or progestin.

Co-administration increases AUC of ethinyl estradiol by approximately 20-25%.

Similar association with reduced efficacy and breakthrough bleeding suggested, though less marked than with rifampin.

HCV protease inhibitor that may decrease plasma concentrations of estrogen and/or progestin, potentially diminishing contraceptive effectiveness.

Induces CYP3A4 and may decrease plasma concentrations of desogestrel and ethinyl estradiol, potentially diminishing contraceptive effectiveness and increasing breakthrough bleeding.

Similar association with reduced efficacy and breakthrough bleeding suggested, though less marked than with rifampin.

Bile acid sequestrant that significantly decreases the AUC of ethinyl estradiol, potentially diminishing contraceptive effectiveness.

Oral contraceptives may inhibit metabolism of cyclosporine, increasing its plasma concentrations.

HIV protease inhibitor that may decrease plasma concentrations of estrogen and/or progestin, potentially diminishing contraceptive effectiveness.

Non-nucleoside reverse transcriptase inhibitor that may increase plasma concentrations of estrogen and/or progestin.

Induces CYP3A4 and may decrease plasma concentrations of desogestrel and ethinyl estradiol, potentially diminishing contraceptive effectiveness and increasing breakthrough bleeding.

CYP3A4 inhibitor that may increase plasma hormone concentrations of desogestrel and ethinyl estradiol.

HIV protease inhibitor that may decrease plasma concentrations of estrogen and/or progestin, potentially diminishing contraceptive effectiveness.

CYP3A4 inhibitor that may increase plasma hormone concentrations of desogestrel and ethinyl estradiol.

Possible association with reduced efficacy and breakthrough bleeding, though less marked than with rifampin.

HIV protease inhibitor that may increase plasma concentrations of estrogen and/or progestin.

CYP3A4 inhibitor that may increase plasma hormone concentrations of desogestrel and ethinyl estradiol.

CYP3A4 inhibitor that may increase plasma hormone concentrations of desogestrel and ethinyl estradiol.

HIV protease inhibitor that may decrease plasma concentrations of estrogen and/or progestin, potentially diminishing contraceptive effectiveness.

HIV protease inhibitor that decreases plasma concentrations of estrogen and/or progestin.

HIV protease inhibitor that may decrease plasma concentrations of estrogen and/or progestin, potentially diminishing contraceptive effectiveness.

Non-nucleoside reverse transcriptase inhibitor that may decrease plasma concentrations of estrogen and/or progestin, potentially diminishing contraceptive effectiveness.

Induces CYP3A4 and may decrease plasma concentrations of desogestrel and ethinyl estradiol, potentially diminishing contraceptive effectiveness and increasing breakthrough bleeding.

Similar association with reduced efficacy and breakthrough bleeding suggested, though less marked than with rifampin.

Induces CYP3A4 and may decrease plasma concentrations of desogestrel and ethinyl estradiol, potentially diminishing contraceptive effectiveness and increasing breakthrough bleeding.

Similar association with reduced efficacy and breakthrough bleeding suggested, though less marked than with rifampin.

Oral contraceptives may inhibit metabolism of prednisolone, increasing its plasma concentrations.

Induces CYP3A4 and may decrease plasma concentrations of desogestrel and ethinyl estradiol, potentially diminishing contraceptive effectiveness and increasing breakthrough bleeding.

Co-administration increases AUC of ethinyl estradiol by approximately 20-25%.

Induces CYP3A4 and may decrease plasma concentrations of desogestrel and ethinyl estradiol, potentially diminishing contraceptive effectiveness and increasing breakthrough bleeding.

Induces CYP3A4 and may decrease plasma concentrations of desogestrel and ethinyl estradiol, potentially diminishing contraceptive effectiveness and increasing breakthrough bleeding.

HCV protease inhibitor that may decrease plasma concentrations of estrogen and/or progestin, potentially diminishing contraceptive effectiveness.

Possible association with reduced efficacy and breakthrough bleeding, though less marked than with rifampin.

Oral contraceptives may inhibit metabolism of theophylline, increasing its plasma concentrations.

HIV protease inhibitor that may decrease plasma concentrations of estrogen and/or progestin, potentially diminishing contraceptive effectiveness.

Induces CYP3A4 and may decrease plasma concentrations of desogestrel and ethinyl estradiol, potentially diminishing contraceptive effectiveness and increasing breakthrough bleeding.

CYP3A4 inhibitor that may increase plasma hormone concentrations of desogestrel and ethinyl estradiol.

Celecoxib is a CYP2C9 substrate that may interact with desogestrel metabolism. Clinical relevance of this interaction is unknown.

Diclofenac is a CYP2C9 substrate that may interact with desogestrel metabolism. Clinical relevance of this interaction is unknown.

Co-administration of VIORELE ® and glecaprevir/pibrentasvir is not recommended due to potential for ALT elevations.

Glipizide is a CYP2C9 substrate that may interact with desogestrel metabolism. Clinical relevance of this interaction is unknown.

Ibuprofen is a CYP2C9 substrate that may interact with desogestrel metabolism. Clinical relevance of this interaction is unknown.

Since desogestrel is mainly metabolized by the cytochrome P450 2C9 enzyme (CYP 2C9) to form etonogestrel, the active progestin, there is a possibility of interaction with CYP 2C9 substrates or inhibitors (such as: ibuprofen, piroxicam, naproxen, phenytoin, fluconazole, diclofenac, tolbutamide, glipizide, celecoxib, sulfamethoxazole, isoniazid, torsemide, irbesartan, losartan, and valsartan).

Isoniazid is a CYP2C9 substrate that may interact with desogestrel metabolism. Clinical relevance of this interaction is unknown.

Since desogestrel is mainly metabolized by the cytochrome P450 2C9 enzyme (CYP 2C9) to form etonogestrel, the active progestin, there is a possibility of interaction with CYP 2C9 substrates or inhibitors (such as: ibuprofen, piroxicam, naproxen, phenytoin, fluconazole, diclofenac, tolbutamide, glipizide, celecoxib, sulfamethoxazole, isoniazid, torsemide, irbesartan, losartan, and valsartan).

Naproxen is a CYP2C9 substrate that may interact with desogestrel metabolism. Clinical relevance of this interaction is unknown.

Co-administration of VIORELE ® and glecaprevir/pibrentasvir is not recommended due to potential for ALT elevations.

Piroxicam is a CYP2C9 substrate that may interact with desogestrel metabolism. Clinical relevance of this interaction is unknown.

Since desogestrel is mainly metabolized by the cytochrome P450 2C9 enzyme (CYP 2C9) to form etonogestrel, the active progestin, there is a possibility of interaction with CYP 2C9 substrates or inhibitors (such as: ibuprofen, piroxicam, naproxen, phenytoin, fluconazole, diclofenac, tolbutamide, glipizide, celecoxib, sulfamethoxazole, isoniazid, torsemide, irbesartan, losartan, and valsartan).

COCs have been shown to decrease plasma concentrations of acetaminophen, clofibric acid, morphine, salicylic acid, temazepam and lamotrigine.

Since desogestrel is mainly metabolized by the cytochrome P450 2C9 enzyme (CYP 2C9) to form etonogestrel, the active progestin, there is a possibility of interaction with CYP 2C9 substrates or inhibitors (such as: ibuprofen, piroxicam, naproxen, phenytoin, fluconazole, diclofenac, tolbutamide, glipizide, celecoxib, sulfamethoxazole, isoniazid, torsemide, irbesartan, losartan, and valsartan).

Since desogestrel is mainly metabolized by the cytochrome P450 2C9 enzyme (CYP 2C9) to form etonogestrel, the active progestin, there is a possibility of interaction with CYP 2C9 substrates or inhibitors (such as: ibuprofen, piroxicam, naproxen, phenytoin, fluconazole, diclofenac, tolbutamide, glipizide, celecoxib, sulfamethoxazole, isoniazid, torsemide, irbesartan, losartan, and valsartan).

Since desogestrel is mainly metabolized by the cytochrome P450 2C9 enzyme (CYP 2C9) to form etonogestrel, the active progestin, there is a possibility of interaction with CYP 2C9 substrates or inhibitors (such as: ibuprofen, piroxicam, naproxen, phenytoin, fluconazole, diclofenac, tolbutamide, glipizide, celecoxib, sulfamethoxazole, isoniazid, torsemide, irbesartan, losartan, and valsartan).