Air-flow limitation in myasthenia gravis. The effect of acetylcholinesterase inhibitor therapy on air-flow limitation.

Abstract

In a survey of 21 patients with myasthenia gravis receiving regular acetylcholinesterase inhibitor therapy, 8 were found to have air-flow limitation associated with their antimyasthenic therapy. In 6 of these subjects, detailed assessments were made of the effect of antimyasthenic therapy on airways function. Pyridostigmine was given together with either placebo or the anticholinergic bronchodilator ipratropium bromide (72 micrograms) by inhalation administered double blind on 2 consecutive days. Airways resistance (Raw) increased significantly after pyridostigmine and placebo inhaler (0.49 +/- 0.13 kPa/L/s basal versus 0.60 +/- 0.13 kPa/L/s at 2 h; mean +/- SEM, p less than 0.05), whereas a significant decrease in Raw followed the combination of pyridostigmine with ipratropium bromide (0.57 +/- 0.08 kPa/L/s basal versus 0.41 +/- 0.07 kPa/L/s at 2 h, p less than 0.05). Thus, acetylcholinesterase inhibitor therapy in subjects with myasthenia gravis with airflow limitation led to significant increase in airways resistance that could be completely reversed by the inhalation of the muscarinic receptor blocker ipratropium bromide.