PRASUGREL Drug Interactions
Also known as: PRASUGREL
Prasugrel is an antiplatelet medication that helps prevent blood clots. It works by making your platelets less sticky, reducing the risk of serious heart problems like heart attack or stroke, especially after a procedure to open blocked heart arteries (PCI) for conditions like acute coronary syndrome.PRASUGREL has 10 documented drug interactions in our database, including 0 contraindicated, 10 major, 0 moderate, and 0 minor interactions.
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Contraindicated
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Moderate
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Minor
Combining naproxen with prasugrel significantly increases your risk of serious bleeding, especially from the stomach or intestines. Your doctor will likely avoid this combination.
Mechanism
Naproxen, an NSAID, inhibits cyclooxygenase, reducing prostaglandin synthesis and impairing platelet aggregation. Prasugrel is an antiplatelet agent that irreversibly inhibits the P2Y12 receptor on platelets. The concurrent use of these two drugs leads to additive antiplatelet effects and increased gastrointestinal mucosal damage, significantly elevating bleeding risk.
Clinical Management
Patients are at a substantially increased risk of serious bleeding events, including gastrointestinal hemorrhage, intracranial hemorrhage, and other site-specific bleeding. The risk of major GI bleeding can be several-fold higher compared to antiplatelet therapy alone. This combination should generally be avoided due to the high risk of bleeding. If an NSAID is absolutely necessary, consider alternative pain management strategies or use the lowest effective dose for the shortest duration, with close monitoring for bleeding signs. Proton pump inhibitor co-prescription is recommended if NSAID use is unavoidable.
Combining etodolac with prasugrel significantly increases your risk of bleeding, including serious internal bleeding. This combination should generally be avoided.
Mechanism
Etodolac, an NSAID, inhibits cyclooxygenase-1 (COX-1), which reduces thromboxane A2 production and impairs platelet aggregation. Prasugrel is an antiplatelet agent that irreversibly inhibits the P2Y12 ADP receptor on platelets, preventing their activation and aggregation. The concurrent use of both drugs leads to an additive antiplatelet effect, severely compromising hemostasis.
Clinical Management
Patients are at a substantially increased risk of serious bleeding events, including gastrointestinal bleeding (e.g., ulcers, hemorrhage), intracranial hemorrhage, and other forms of systemic bleeding. The risk of major GI bleeding can be several-fold higher compared to either drug alone, potentially leading to anemia, hospitalization, and even death. This combination should be avoided due to the high risk of bleeding. If an NSAID is absolutely necessary, consider alternative pain management strategies or a COX-2 selective inhibitor with caution and close monitoring for bleeding. If co-administration is unavoidable, use the lowest effective dose of the NSAID for the shortest duration possible, and monitor closely for signs of bleeding. Proton pump inhibitor prophylaxis should be considered to reduce GI bleeding risk.
Combining aspirin with prasugrel significantly increases your risk of bleeding, including serious and life-threatening bleeding episodes, because both medications thin your blood.
Mechanism
Aspirin irreversibly inhibits cyclooxygenase-1 (COX-1), preventing thromboxane A2 production and platelet aggregation. Prasugrel is a prodrug that, once metabolized, irreversibly binds to the P2Y12 receptor on platelets, inhibiting ADP-induced platelet activation and aggregation. The concurrent use of two antiplatelet agents leads to a synergistic inhibition of platelet function.
Clinical Management
This combination substantially elevates the risk of bleeding, including gastrointestinal bleeding, intracranial hemorrhage, and other major bleeding events. Patients may experience bruising, nosebleeds, blood in urine or stool, or prolonged bleeding from cuts. The risk of major bleeding can be several-fold higher compared to monotherapy. Avoid concurrent use of aspirin and prasugrel unless the benefits clearly outweigh the risks, such as in specific acute coronary syndromes where dual antiplatelet therapy (DAPT) is indicated. If co-administration is unavoidable, monitor patients closely for signs of bleeding, perform regular blood counts, and educate them on bleeding precautions. Consider proton pump inhibitor co-therapy to reduce gastrointestinal bleeding risk.
Taking ibuprofen with prasugrel significantly increases your risk of serious bleeding, especially in the stomach or intestines. You should avoid this combination unless specifically directed by your doctor.
Mechanism
Ibuprofen, a non-steroidal anti-inflammatory drug (NSAID), inhibits cyclooxygenase (COX) enzymes, which reduces prostaglandin synthesis and impairs platelet aggregation. Prasugrel is an antiplatelet medication that irreversibly blocks the P2Y12 ADP receptor on platelets, preventing their activation and aggregation. The combined antiplatelet effects of both drugs lead to a synergistic increase in bleeding risk.
Clinical Management
The primary clinical effect is a significantly increased risk of bleeding, including gastrointestinal (GI) bleeding, intracranial hemorrhage, and other serious bleeding events. The risk of GI bleeding can be several-fold higher compared to either drug alone, potentially leading to anemia, hospitalization, or even death. This combination should generally be avoided due to the high risk of serious bleeding. If pain relief is needed, consider alternative analgesics such as acetaminophen. If an NSAID is deemed absolutely necessary, use the lowest effective dose for the shortest duration, and monitor closely for signs of bleeding. Proton pump inhibitors (PPIs) may be co-prescribed to reduce GI bleeding risk, but do not eliminate it.
Combining indomethacin with prasugrel significantly increases your risk of serious bleeding, especially from the stomach or intestines. This combination should generally be avoided.
Mechanism
Indomethacin, a nonsteroidal anti-inflammatory drug (NSAID), inhibits cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis which impairs gastric mucosal protection and platelet aggregation. Prasugrel is an antiplatelet agent that irreversibly inhibits the P2Y12 ADP receptor on platelets, preventing platelet activation and aggregation. The combined effect of impaired gastric protection and dual antiplatelet activity leads to a synergistic increase in bleeding risk.
Clinical Management
The primary clinical effect is a substantially increased risk of serious bleeding, particularly gastrointestinal bleeding, which can manifest as ulcers, melena, hematemesis, or even life-threatening hemorrhage. Other bleeding events like epistaxis, hematuria, or bruising are also more likely. The risk of major GI bleeding can be several-fold higher compared to either drug alone. This combination should be avoided whenever possible. If indomethacin is absolutely necessary, consider alternative pain management strategies or a COX-2 selective NSAID with concurrent proton pump inhibitor (PPI) therapy, though significant bleeding risk remains. Closely monitor for any signs of bleeding. If co-administration is unavoidable, use the lowest effective dose of indomethacin for the shortest duration.
Combining celecoxib with prasugrel significantly increases your risk of bleeding, especially from the stomach or intestines. This combination should generally be avoided due to the heightened bleeding risk.
Mechanism
Celecoxib, an NSAID, inhibits prostaglandin synthesis, which can impair gastric mucosal protection and inhibit platelet aggregation. Prasugrel is a potent antiplatelet agent that irreversibly inhibits the P2Y12 receptor on platelets, preventing platelet activation and aggregation. The concurrent use of both drugs leads to an additive antiplatelet effect and increased gastrointestinal toxicity, substantially raising the risk of bleeding.
Clinical Management
The primary clinical effect is a significantly increased risk of bleeding, including serious and life-threatening events such as gastrointestinal hemorrhage, intracranial hemorrhage, or other major bleeding. Studies show that combining NSAIDs with antiplatelets can increase the risk of major bleeding by 2-4 fold compared to antiplatelet therapy alone. Avoid concomitant use of celecoxib and prasugrel due to the substantial increase in bleeding risk. If an NSAID is absolutely necessary, consider alternative pain management strategies or discuss safer options with your doctor. If no alternatives exist, use the lowest effective dose for the shortest duration, and monitor closely for signs of bleeding such as black, tarry stools, easy bruising, or unusual bleeding.
Combining piroxicam with prasugrel significantly increases your risk of serious bleeding, including stomach bleeding. This combination should generally be avoided.
Mechanism
Piroxicam, a non-selective NSAID, inhibits cyclooxygenase-1 (COX-1), reducing platelet aggregation and impairing the integrity of the gastrointestinal mucosa. Prasugrel is a potent P2Y12 platelet inhibitor, irreversibly blocking ADP-induced platelet aggregation. The combined antiplatelet effects and GI mucosal damage lead to a synergistic increase in bleeding risk.
Clinical Management
Patients are at a substantially increased risk of serious bleeding events, including gastrointestinal hemorrhage, intracranial hemorrhage, and other major bleeding. The risk of major GI bleeding can be several-fold higher compared to either drug alone, potentially leading to hospitalization, transfusions, or even death. This combination should generally be avoided due to the high risk of serious bleeding. If an NSAID is absolutely necessary, consider a COX-2 selective NSAID (e.g., celecoxib) at the lowest effective dose for the shortest duration, along with a proton pump inhibitor (PPI) for gastroprotection. Closely monitor for any signs of bleeding (e.g., black stools, easy bruising, nosebleeds).
Combining meloxicam with prasugrel significantly increases your risk of serious bleeding, including stomach bleeding. This combination should generally be avoided.
Mechanism
Meloxicam, a non-steroidal anti-inflammatory drug (NSAID), inhibits prostaglandin synthesis, which can impair the protective mucosal barrier in the gastrointestinal tract and inhibit platelet aggregation. Prasugrel is a potent antiplatelet agent that irreversibly blocks the P2Y12 receptor on platelets, preventing platelet activation and aggregation. The concurrent use of these agents results in additive antiplatelet effects and increased gastrointestinal damage, leading to a substantially elevated risk of bleeding.
Clinical Management
The primary clinical effect is a significantly increased risk of bleeding, particularly gastrointestinal bleeding (e.g., ulcers, hemorrhage), but also bleeding from other sites. This risk can be several-fold higher compared to monotherapy. Symptoms may include black, tarry stools, vomiting blood, or unusual bruising. Avoid concurrent use of meloxicam and prasugrel due to the high risk of serious bleeding. If an NSAID is absolutely necessary, consider alternative pain management strategies or a short course of a COX-2 selective NSAID with concomitant proton pump inhibitor (PPI) therapy, though the bleeding risk remains significant. Closely monitor for signs and symptoms of bleeding if co-administration cannot be avoided.
Combining diclofenac with prasugrel significantly increases your risk of bleeding, especially in the stomach or intestines. This combination should generally be avoided.
Mechanism
Diclofenac, a non-steroidal anti-inflammatory drug (NSAID), inhibits cyclooxygenase enzymes, reducing prostaglandin synthesis and impairing platelet aggregation. Prasugrel is an antiplatelet agent that irreversibly inhibits the P2Y12 ADP receptor on platelets, preventing platelet activation and aggregation. The concurrent use of these agents results in additive antiplatelet effects and increased gastrointestinal mucosal damage, leading to a substantially elevated bleeding risk.
Clinical Management
Patients taking diclofenac and prasugrel concurrently face a significantly elevated risk of major bleeding events, including gastrointestinal hemorrhage, intracranial hemorrhage, and other site-specific bleeding. The risk of GI bleeding can be several times higher compared to taking either drug alone, potentially leading to anemia, hospitalization, or life-threatening complications. This combination should generally be avoided due to the high risk of major bleeding. If an NSAID is absolutely necessary, consider alternative pain management strategies or a COX-2 selective NSAID for the shortest duration possible, along with a proton pump inhibitor (PPI) for gastroprotection. Closely monitor for any signs of bleeding (e.g., black stools, easy bruising, nosebleeds) and hemoglobin levels. Discuss with the prescribing physician to assess the risk-benefit and explore safer alternatives.
Combining ketorolac with prasugrel significantly increases your risk of bleeding, including serious internal bleeding. This combination should generally be avoided.
Mechanism
Ketorolac, a non-steroidal anti-inflammatory drug (NSAID), inhibits cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis and impairing platelet aggregation. Prasugrel is an antiplatelet medication that irreversibly inhibits the P2Y12 ADP receptor on platelets, preventing their activation and aggregation. The concurrent use of these agents results in additive antiplatelet effects.
Clinical Management
The primary clinical effect is a substantially increased risk of bleeding, including gastrointestinal bleeding, intracranial hemorrhage, and other serious bleeding events. Studies show a significantly elevated risk of major bleeding when NSAIDs are co-administered with antiplatelet agents, potentially increasing the risk by 2 to 4 times compared to antiplatelet monotherapy. This combination should generally be avoided due to the high risk of bleeding. If an NSAID is absolutely necessary, consider a COX-2 selective inhibitor for the shortest duration possible, but even then, close monitoring for bleeding is essential. Alternative pain management strategies that do not increase bleeding risk, such as acetaminophen or opioids, should be prioritized. Patients must be educated on signs of bleeding.
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