A 60-year-old asthmatic stabilized on oral theophylline is started on ciprofloxacin for a urinary tract infection. Two days later she develops nausea, tremor and sinus tachycardia. The mechanism responsible is:

• A Ciprofloxacin inhibition of CYP1A2, reducing theophylline clearance ✓
• B Additive phosphodiesterase inhibition producing excess cyclic AMP
• C Displacement of theophylline from plasma protein binding sites
• D Ciprofloxacin induction of hepatic glucuronidation enzymes

Explanation

Theophylline is metabolized largely by CYP1A2, and ciprofloxacin is a clinically important inhibitor of that enzyme. Co-administration raises theophylline concentrations and produces classic toxicity: nausea, vomiting, tremor, tachycardia and arrhythmias. The same interaction applies to tizanidine, which is contraindicated with ciprofloxacin. Enoxacin is an even stronger CYP1A2 inhibitor, while moxifloxacin interacts minimally. Protein binding displacement is irrelevant here since theophylline is only about 40 percent bound.

Reference: Katzung Basic and Clinical Pharmacology, 15th ed.

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