Core59: Drug-induced adverse reaction: thrombosis

🧫 High-yield / 要点：Drug-induced thrombosis is classically caused by estrogens/SERMs, COX-2 inhibitors, fibrinolysis inhibitors, plus EPO, JAK inhibitors, and some NSAIDs.

Drug classes and mechanisms / 薬剤クラスと機序

Drug group	Mechanism	Examples
Fibrinolysis inhibitors	Inhibit plasmin, which would break down thrombi	ε-aminocaproic acid, tranexamic acid
Estrogens / SERMs	Increase hepatic synthesis of coagulation factors	Estradiol, ethinylestradiol, raloxifene, tamoxifen
Selective COX-2 inhibitors	Shift PGI2 (endothelial COX-2) vs TXA2 (platelet COX-1) balance toward prothrombotic state	Celecoxib, rofecoxib
NSAIDs	Prothrombotic effect through prostaglandin balance	Ibuprofen, diclofenac
JAK kinase inhibitors	Associated with increased thrombosis risk	Tofacitinib, baricitinib
Agents acting on hematopoiesis	Increase red cell mass/viscosity	Erythropoietin / EPO

Key concept / 重要概念

• Thrombosis risk increases when drugs:
  • Reduce clot breakdown, e.g. fibrinolysis inhibitors.
  • Increase clotting factor synthesis, e.g. estrogens.
  • Shift prostaglandin balance toward TXA2 dominance, e.g. COX-2 inhibitors.
  • Increase blood viscosity, e.g. EPO.

Remember / 覚え方

• Estrogens/SERMs → more clotting factors
• COX-2 inhibitors → PGI2/TXA2 imbalance → thrombosis
• Tranexamic acid (antifibrinolytic) → thrombotic risk
• EPO and JAK inhibitors also raise thrombosis risk