DQ-1 Protonix and drug-drug interactions with Warfarin for treatment of GI ulcer and deep vein thrombosis with elevated INR The background of this study includes a patient who was at high risk for ulcers and was prescribed Pantoprazole which is commonly used as prophylaxis of ulcers (Chandelia & Dubey, 2016). The patient was also taking Warfarin daily due to a discovery of a deep vein thrombosis of the circumflex vein, common femoral vein, superficial vein, and popliteal vein (Chandelia & Dubey, 2016). This patient was also in the ICU (Chandelia & Dubey, 2016). Initially, heparin was started on this patient and the healthcare team was able to keep the INR within normal limits of their heparin protocol (Chandelia & Dubey, 2016). However, when switching to Warfarin with a standard dose of 0.2 mg/kg (8mg/day) for this patient to maintain an INR of 2.5, there were some issues associated with it. On day 3 the INR came back elevated at 6.0, so there was a reduction of warfarin by 20% (Chandelia & Dubey, 2016). After two days, the INR was still elevated at 5.0, and another reduction by 20% without success (Chandelia & Dubey, 2016). At this time the healthcare team decided to look at the medications and foods the patient was eating. First, the healthcare team decided to compile a list of the patient's medications and foods and found that the patient was not receiving any garlic, mango, papaya or fish (Chandelia & Dubey, 2016). The patient's medications were ceftriaxone, vancomycin, and pantoprazole, but the team was unable to stop the antibiotics, so they decided to stop the pantoprazole. After three days post discontinuation of pantoprazole, the INR had dropped to 1.4 without any change in the dose of warfarin (Chandelia & Dubey, 2016). Most importantly, at this point, the healthcare team had to increase the warfarin dose back to the original 8mg/day to get the patient's INR into the therapeutic range (Chandelia & Dubey, 2016). There was an 87.5% reduction in the dose of warfarin when given with pantoprazole (Chandelia & Dubey, 2016). The rationale behind the drug to drug interaction is that warfarin undergoes metabolism by CYP1A2, CYP2C19, and CYP3A4 (Crader, Johns & Arnold, 2019). Pantoprazole has been shown to strongly inhibit CYP2C9 activity (Chandelia & Dubey, 2016). This metabolite inhibition and interaction is what causes the low metabolism of warfarin and leads to the elevated INR (Crader, Johns & Arnold, 2019). An alternate therapy suggested would be to use heparin subcutaneous injections through the hospital and at home until they need for pantoprazole has been resolved (Chandelia & Dubey, 2016). The issue is that the first and second-line proton pump inhibitors are inhibitors of CYP2C9 (Chandelia & Dubey, 2016). In this scenario, the only drug change that can occur is with warfarin to heparin and/or Lovenox (Chandelia & Dubey, 2016). Thought behind this is that in patients who can't tolerate oral warfarin, due to side effects, they c ...