Loette Drug Interactions

Interactions between ethinyl estradiol (EE) and other substances may lead to decreased or increased serum EE concentrations, respectively.
Concomitant use with the medicinal products containing ombitasvir/paritaprevir/ritonavir and dasabuvir, with or without ribavirin may increase the risk of ALT elevations (see Contraindications and Special warnings: Hepatic neoplasia/liver disease/hepatitis C under Precautions).
Therefore, COC users must switch to an alternative method of contraception (e.g., progestagen-only contraception or non-hormonal methods) prior to starting therapy with anti-viral HCV medicinal products such as ombitasvir, paritaprevir, ritonavir, dasabuvir. COCs can be restarted 2 weeks following completion of treatment with an anti-viral HCV medicinal product.
Decreased EE serum concentrations may cause an increased incidence of breakthrough bleeding and menstrual irregularities and may possibly reduce efficacy of the COC.
During concomitant use of EE-containing products and substances that may lead to decreased EE serum concentrations, it is recommended that a nonhormonal back-up method of birth control (such as condoms and spermicide) be used in addition to the regular intake of Loette. In the case of prolonged use of such substances COCs should not be considered the primary contraceptive.
After discontinuation of substances that may lead to decreased EE serum concentrations, use of a nonhormonal back-up method is recommended for at least 7 days. Longer use of a back-up method is advisable after discontinuation of substances that have lead to induction of hepatic microsomal enzymes, resulting in decreased EE serum concentrations. It may sometimes take several weeks until enzyme induction has completely subsided, depending on dosage, duration of use and rate of elimination of the inducing substance.
Examples of substances that may decrease serum EE concentrations: Any substance that reduces gastrointestinal transit time, and therefore, EE absorption.
Substances that induce hepatic microsomal enzymes, such as rifampicin, rifabutin, barbiturates, primidone, phenylbutazone, phenytoin, dexamethasone, griseofulvin, topiramate, some protease inhibitors, modafinil.
Hypericum perforatum, also known as St. John's Wort, and ritonavir* (possibly by induction of hepatic microsomal enzymes).
Examples of substances that may increase serum EE concentrations: Atorvastatin.
Competitive inhibitors for sulfation in the gastrointestinal wall, such as ascorbic acid (vitamin C) and paracetamol (acetaminophen).
Substances that inhibit cytochrome P450 3A4 isoenzymes such as indinavir, fluconazole, and troleandomycin*.
Troleandomycin may increase the risk of intrahepatic cholestasis during co-administration with COCs.
EE may interfere with the metabolism of other drugs by inhibiting hepatic microsomal enzymes, or by inducing hepatic drug conjugation, particularly glucuronidation. Accordingly, plasma and tissue concentrations may either be increased (e.g., cyclosporine, theophylline, corticosteroids) or decreased (e.g., lamotrigine).
In patients treated with flunarizine, use of oral contraceptives has been reported to increase the risk of galactorrhea.
There have been reports of pregnancy when COCs were co-administered with certain antibiotics (e.g., ampicillin and other penicillins, tetracyclines).
The prescribing information of concomitant medications should be consulted to identify potential interactions.
*Although ritonavir is an inhibitor of cytochrome P450 3A4, treatment with ritonavir has been shown to decrease EE serum concentrations (see previously mentioned).
Interference with laboratory and other diagnostic tests: Effects on laboratory parameters: The use of COCs may cause certain physiologic changes that may be reflected in the results of certain laboratory tests, including biochemical parameters of liver function (including a decrease in bilirubin and alkaline phosphatase), thyroid function (increased total T₃ and T₄ due to increased TBG, decreased free T₃ resin uptake), adrenal function (increased plasma cortisol, increased cortisol binding globulin, decreased dehydroepiandrosterone sulfate (DHEAS), and renal function (increased plasma creatinine and creatinine clearance); plasma levels of (carrier) proteins, such as corticosteroid-binding globulin and lipid/lipoprotein fractions; parameters of carbohydrate metabolism; parameters of coagulation and fibrinolysis; decreased serum folate levels.