A 30-year-old woman with myasthenia gravis (MG) is intubated with respiratory failure. She was recently started on ciprofloxacin for a urinary tract infection. Which mechanism explains this drug-related exacerbation?
- A Ciprofloxacin acts as a competitive antagonist at nicotinic acetylcholine receptors
- B Ciprofloxacin inhibits acetylcholinesterase, increasing acetylcholine and causing a depolarizing block
- C Fluoroquinolones impair neuromuscular transmission by blocking presynaptic voltage-gated calcium channels and reducing acetylcholine release ✓
- D Ciprofloxacin enhances anti-AChR IgG production through molecular mimicry
Explanation
Fluoroquinolones can precipitate or worsen myasthenic crises by inhibiting presynaptic voltage-gated calcium channels, reducing calcium-dependent acetylcholine vesicle release into the neuromuscular junction. This presynaptic mechanism combined with the already-diminished post-synaptic AChR density in MG leads to critical neuromuscular blockade. They are listed as contraindicated or use-with-caution agents in MG. Other implicated antibiotics include aminoglycosides, macrolides, and clindamycin.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.