Interaction between Griseofulvin and Ethinylestradiol
Major
Metabolism
| ID | DDInter843 and DDInter692 |
| Interaction | RECOMMENDED: Limited clinical data suggest that griseofulvin may reduce the efficacy of contraceptive hormones. The proposed mechanism is accelerated clearance of the hormones due to induction of hepatic CYP450 enzymes by griseofulvin. |
| Management | Women using low-dose hormonal contraceptives should be advised of the risk of breakthrough bleeding and unintended pregnancy during concomitant therapy with griseofulvin. Because griseofulvin has been shown to be teratogenic in animal studies and is capable of inducing aneuploidy (abnormal segregation of chromosomes following cell division) in mammalian cells in vitro and in vivo, it is particularly important that patients not become pregnant during treatment. Therefore, additional methods of birth control should be used during and for one month after griseofulvin therapy. Input from a gynecologist or similar expert on adequate contraception, including emergency contraception, should be sought as needed. Intrauterine systems are unlikely to be significantly affected because of their local action. |
| References | |
| Alternative for Griseofulvin |
D01B
D01A
More
|
| Alternative for Ethinylestradiol |
G03A
L02A G03C
More
|
Potential Metabolism Interactions
Substrate-Substrate Interaction：If more than one drug is metabolized by the same CYP, it is possible that its metabolism is inhibited because of the competition between the drugs. That means, it can be useful to lower the dosage of the drugs in the drug-cocktail because they remain longer in the organism than in monotherapy.
Inhibitor-Inhibitor Interaction：Combining two or more inhibitors of one CYP, should be compensated by lowering the dosage of these drugs because the metabolism is reduced and the drugs remain longer in the organism than in monotherapy. Not adapting the dosage bears the risk of even more side effects.
Inhibitor-Substrate Interaction：Combining drugs that have inhibitory effect and are substrates of one particular CYP, should be compensated by lowering the dosage. They rest longer in the organism than in monotherapy. Not adapting the dosage bears the risk of even more side effects.