Warfarin

Ranitidine can modestly increase warfarin plasma levels and INR by inhibiting CYP2C9-mediated warfarin metabolism, though the magnitude is smaller than with cimetidine.

Cephalexin may enhance the anticoagulant effect of warfarin, with case reports describing INR elevation during concurrent therapy, likely through disruption of vitamin K-producing gut flora.

Clindamycin may enhance the anticoagulant effect of warfarin by disrupting vitamin K-producing gut flora, leading to unpredictable INR elevations and increased bleeding risk during and shortly after the antibiotic course.

Trimethoprim (alone or in combination as TMP-SMX) increases warfarin's anticoagulant effect through CYP2C9 inhibition, raising INR and bleeding risk.

Hydroxychloroquine may potentiate the anticoagulant effect of warfarin, raising INR and the risk of bleeding complications.

Colchicine may increase bleeding risk when combined with warfarin; isolated case reports suggest possible INR elevation, though the mechanism is not well characterized.

Regular or high-dose acetaminophen can potentiate the anticoagulant effect of warfarin, leading to INR elevation and increased bleeding risk, even though single analgesic doses carry a lower risk.

Semaglutide slows gastric emptying, potentially reducing and delaying oral warfarin absorption, leading to variable changes in INR that complicate anticoagulation management.

Simvastatin modestly potentiates warfarin anticoagulation, leading to small but potentially clinically relevant INR increases.

Levothyroxine enhances the catabolism of vitamin K-dependent clotting factors, amplifying warfarin's anticoagulant effect and raising the risk of bleeding when thyroid replacement is initiated or doses are increased.

Azithromycin can potentiate the anticoagulant effect of warfarin, leading to elevated INR and increased bleeding risk during and shortly after the antibiotic course.

Sertraline can modestly increase warfarin anticoagulation through weak CYP2C9 inhibition combined with SSRI-mediated platelet serotonin depletion.

Fluoxetine increases warfarin plasma levels via CYP2C9 inhibition and may independently impair platelet function, raising hemorrhagic risk.

Corticosteroids have a complex and variable interaction with warfarin; high doses may increase bleeding risk via GI mucosal effects while also affecting clotting factor synthesis.

Rosuvastatin increases warfarin plasma concentrations through inhibition of CYP2C9, potentially leading to supratherapeutic INR values.

Ciprofloxacin consistently enhances warfarin's anticoagulant effect, raising INR and increasing the risk of bleeding complications.

Doxycycline may enhance warfarin's anticoagulant effect, particularly in patients whose vitamin K intake is already limited.

Celecoxib, a selective COX-2 inhibitor, can inhibit CYP2C9-mediated warfarin metabolism and may increase GI bleeding risk, though platelet function is less impaired than with non-selective NSAIDs.

Valproic acid can displace warfarin from plasma protein binding sites and may inhibit platelet aggregation, increasing bleeding risk.