What is the mechanism of fluoroquinolone(FQ)-induced tendonopathy?

An uncommon but serious side effect of FQs (e.g. ciprofloxacin, levofloxacin, and moxifloxacin) is Achilles tendon rupture.   A putative mechanism for this adverse effect is inhibition of host mitochondrial components (1). Recall that mitochondria, the ATP-generating machine within our cells, are thought to be archaic bacterial ancestors that have co-evolved with us. Quinolones are inhibitors of bacterial gyrases and topoisomerases and also appear to be associated with DNA degradation of the mitochondria in some mammalian cells. In vitro, FQs appear to have a tropism for mitochondria in tenocytes, chondrocytes, and osteoblasts.   Thus, it is possible that at least in some patients (e.g. those ≥60 years of age, on higher doses of corticosteroids, or with several renal disease or other idiosyncratic factors) the mitochondrial damage is sufficient to cause serious injury to the Achilles tendon (2).

1. Barnhill AE, Brewer MT, Carlson SA. Adverse effects of antimicrobials via predictable or idiosyncratic inhibition of host mitochondrial components. Antimicrob Agents Chemother 2012;56:4046-4051.

2. Shakibaei M, Stahlmann R. Ultrastructure of Achilles tendon from rats after treatment with fleroxacin. Arch Toxicol 2001;75:97-102.

What is the mechanism of fluoroquinolone(FQ)-induced tendonopathy?

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