Respiratory mucus hypersecretion (bronchorrhea): A case discussion—possible mechanism(s) and treatment

Abstract

The mechanism(s) underlying mucus hypersecretion (bronchorrhea) and the treatment of this condition are poorly understood. We have previously demonstrated that erythromycin inhibited mucus secretion from human airways and from secretory epithelial cells in vitro. We encountered a patient with airway obstruction marked by severe bronchorrhea, who previously had responded only to inhaled bronchodilators and high-dose prednisone. Many attempts to wean him from prednisone had failed. During the course of his disease, he had developed an IgG antibody to vasoactive intestinal peptide, had increased amounts of mucus secreted by his respiratory epithelial cells, and demonstrated hyperreactive airways as measured by methacholine challenge provocation test. Erythromycin was added to his therapy. The effect of erythromycin treatment was quite dramatic and included clinical and laboratory improvement. After a short trial of erythromycin, the patient tolerated low, every-other-day doses of prednisone. There was a significant reduction in the volume of his bronchorrhea, a major decrease in the epithelial mucins in his total expectorated mucus, complete inhibition of his airway hyperresponsiveness to inhaled methacholine, and significant reduction in the level of IgG antibody to vasoactive intestinal peptide. This response was specific for erythromycin since other antibiotics did not have any clinical, biochemical, or physiologic effects. We conclude that erythromycin may play a role in the treatment of patients with bronchorrhea and may have a steroid-sparing effect. Additional studies with larger numbers of patients are indicated.