A patient on fluoroquinolone therapy for a urinary tract infection develops tendon rupture. The sub-mechanism responsible for fluoroquinolone-induced tendinopathy involves:
- A Chelation of magnesium ions within tenocyte extracellular matrix, disrupting collagen cross-linking and triggering matrix metalloproteinase activation ✓
- B Direct inhibition of DNA gyrase in tenocytes leading to apoptosis
- C Competitive antagonism of vitamin K-dependent coagulation factors reducing tendon vascularity
- D Inhibition of cyclooxygenase-2 in tenocytes causing prostaglandin deficiency
Explanation
Fluoroquinolones chelate divalent cations, particularly Mg2+, which are essential cofactors for matrix metalloproteinase (MMP) inhibitors (TIMPs) and collagen fibril assembly. This chelation activates MMPs and simultaneously impairs collagen cross-linking, causing degradation of tendon extracellular matrix. Additionally, fluoroquinolones induce mitochondrial dysfunction and oxidative stress in tenocytes. Risk factors include age >60, concurrent corticosteroids, and renal failure. The Achilles tendon is most frequently affected. This is a class effect of all fluoroquinolones.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.