Interaction between Ginkgo biloba and Antithrombin Alfa
Moderate Synergy

ID DDInter819 and DDInter104
Interaction Ginkgo may potentiate the risk of bleeding associated with anticoagulants, platelet inhibitors, and thrombolytic agents. Ginkgolide B, a component of ginkgo, inhibits platelet-activating factor by displacing it from its receptor-binding site, resulting in reduced platelet aggregation.
Management Patients should consult a healthcare provider before taking any herbal or alternative medicine. In general, consumption of ginkgo should be avoided during use of coagulation-modifying agents and at least two weeks prior to surgery. In patients who have used this herb extensively prior to receiving anticoagulation, antiplatelet or thrombolytic therapy, the potential for an interaction should be considered. Close clinical and laboratory observation for hematologic complications is recommended. Patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools.
References
Alternative for Ginkgo biloba N06D
Alternative for Antithrombin Alfa -

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.