Methotrexate toxicity

Methotrexate toxicity is an acute or chronic adverse clinical state resulting from supratherapeutic exposure to, or impaired elimination of, the antifolate antimetabolite methotrexate Pathophysiologically driven by the competitive inhibition of dihydrofolate reductase and subsequent depletion of reduced folates necessary for DNA and RNA synthesis, toxicity characteristically manifests with severe mucositis, gastrointestinal ulceration, myelosuppression presenting as pancytopenia, acute kidney in...

Methotrexate toxicity is an acute or chronic adverse clinical state resulting from supratherapeutic exposure to, or impaired elimination of, the antifolate antimetabolite methotrexate Commonly arising in patients treated for autoimmune diseases due to accidental daily rather than weekly dosing, or in oncologic populations receiving high-dose intravenous chemotherapy, it predominantly damages rapidly dividing tissues and organs responsible for drug clearance

Commonly arising in patients treated for autoimmune diseases due to accidental daily rather than weekly dosing, or in oncologic populations receiving high-dose intravenous chemotherapy, it predominantly damages rapidly dividing tissues and organs responsible for drug clearance

Pathophysiologically driven by the competitive inhibition of dihydrofolate reductase and subsequent depletion of reduced folates necessary for DNA and RNA synthesis, toxicity characteristically manifests with severe mucositis, gastrointestinal ulceration, myelosuppression presenting as pancytopenia, acute kidney injury from tubular crystalluria, and potential hepatotoxicity or pneumonitis

Pathophysiologically driven by the competitive inhibition of dihydrofolate reductase and subsequent depletion of reduced folates necessary for DNA and RNA synthesis, toxicity characteristically manifests with severe mucositis, gastrointestinal ulceration, myelosuppression presenting as pancytopenia, acute kidney injury from tubular crystalluria, and potential hepatotoxicity or pneumonitis

Pathophysiologically driven by the competitive inhibition of dihydrofolate reductase and subsequent depletion of reduced folates necessary for DNA and RNA synthesis, toxicity characteristically manifests with severe mucositis, gastrointestinal ulceration, myelosuppression presenting as pancytopenia, acute kidney injury from tubular crystalluria, and potential hepatotoxicity or pneumonitis