Levofloxacin induced myasthenia crisis

Patients with myasthenia gravis (MG) may suffer a worsening of symptoms upon exposure to a variety of medications. The relationship between MG and medication effects is complex. Some medications (such as penicillamine and α‐interferon) appear to cause MG occasionally, while other drugs (such as aminoglycoside antibiotics and quinine) may lead to MG symptoms by simply unmasking a pre‐existing mild case. In patients with known MG, there is a long list of drugs that are reported to be associated with increased weakness.¹ Myasthenic crisis is a life threatening situation in which the weakness arising from MG is severe enough to cause respiratory failure necessitating intubation.² This case report describes the development of myasthenic crisis and respiratory depression following the use of levoflaxacin in a patient with no previous diagnosis of MG.

A 45 year old male patient was diagnosed with atypical pneumonia at the emergency department (ED) to which he presented with a complaint of coughing and expectoration, and was given a prescription for levofloxacin. He re‐presented with severe respiratory difficulty 36 hours after commencing the medication. He was attached to a mechanical ventilator and intubated in the ED with a diagnosis of severe respiratory insufficiency. With the patient's tensilon test result proving positive and a decremental response shown on electromyogram, he was diagnosed with MG. Thymoma was determined using computed tomography, and thymectomy performed. Pridostigmine and steroid treatment was initiated. He was removed from the ventilator on the third day and discharged in a healthy condition on the 10th day.

Fluoroquinolones are widely used antibiotics, and have relatively few side effects. The most common adverse reactions are nausea, abdominal discomfort, headache, and dizziness. Rarely, hallucinations, delirium, and seizures have occurred. There are reports of the exacerbation of MG by ciprofloxacin, norfloxacin, and penfloxacin, ofloxacin, and trovafloxacin.³,⁴ The occurrence of increased myasthenic weakness shortly after the start of fluoroquinolone treatment and the rapid improvement after withdrawal of the antibiotic in each reported case are consistent with a fluoroquinolone block of neuromuscular transmission. Fluoroquinolones reduce the amplitude of the miniature endplate potentials.⁴

Although similar effects of floroquinolones have been reported previously, no case involving levoflaxacin, which is prescribed on a widespread basis, has been reported. This case shows that, like other quinolones, levofloxacin may also have a symptom triggering effect in subclinical MG and may even lead to myasthenic crises.