Nonasthmatic Eosinophilic Bronchitis

Nonasthmatic eosinophilic bronchitis is a cause of chronic cough in which there is eosinophilic airway inflammation without variable airflow obstruction or airway hyperresponsiveness. It accounts for about 10 to 30% of cases of chronic cough referred to specialists.

Patients are of any age, and the cough is dry or with scant sputum, lasting over 8 weeks. It responds quickly to inhaled corticosteroid, which is its main distinguishing feature, and it does not progress to asthma in most.

Pathophysiology. Eosinophils and mast cells infiltrate the bronchial mucosa and release mediators that sensitise cough receptors, yet the smooth muscle is spared, so spirometry and bronchial challenge are normal. Triggers include inhaled allergens, occupational sensitisers (latex, isocyanates, flour dust), and sometimes no trigger is found.

Chronic cough with throat irritation, usually worse in the day, with a normal chest examination and no wheeze or breathlessness. Ask about allergen and workplace exposure, drugs (angiotensin converting enzyme inhibitors), smoking and reflux, and travel to areas where parasitic infection is common.

Haemoptysis, weight loss, fever, night sweats, hoarseness and abnormal examination findings point away from this diagnosis and need prompt investigation.

• Spirometry with bronchodilator testing normal, with peak flow variability under 20%, and a negative methacholine or mannitol challenge.
• Induced sputum eosinophil count of 3% or more (the definitive test, in specialist centres). Where sputum is not available, FeNO over 25 ppb in adults supports it and blood eosinophils over 300 cells/microlitre are suggestive.
• Chest radiograph (normal), and further imaging if the cough persists after treatment.
• Exclude drug causes, upper airway cough syndrome and reflux on history and response.
• In areas with parasitic disease, stool and blood tests for helminths, since tissue invasive helminths can cause eosinophilic airway disease.

Differential diagnosis.

• Cough variant asthma
• Upper airway cough syndrome
• Gastro oesophageal reflux
• Angiotensin converting enzyme inhibitor cough
• Parasitic infection with eosinophilia
• Pulmonary tuberculosis or lung cancer in smokers or with alarm features
• Eosinophilic granulomatosis with polyangiitis

• Avoid the allergen or occupational exposure. Stop angiotensin converting enzyme inhibitors.
• Inhaled corticosteroid: budesonide 400 micrograms twice daily or fluticasone propionate 500 micrograms twice daily, with a spacer, for 2 to 4 weeks. Cough usually improves within 1 to 2 weeks. Continue for 3 to 6 months or longer if cough returns on stopping.
• When the response is poor or the cough is severe: prednisolone 20 to 30 mg orally daily for 1 to 2 weeks, then inhaled therapy.
• Relapse occurs in a half of cases after stopping, and long term low dose inhaled corticosteroid (budesonide 200 to 400 micrograms daily) is used for those who relapse.
• A leukotriene receptor antagonist (montelukast 10 mg daily) is sometimes used in those who cannot use inhaled corticosteroid.
• Treat parasitic infection when found, for example albendazole 400 mg as a single dose or ivermectin 200 micrograms/kg as a single dose, chosen by the organism found.

Monitoring. Review at 4 weeks for cough control and then at 3 months, with repeat FeNO or sputum eosinophils when available. Watch for later development of asthma with symptoms and spirometry.

Referral and escalation. Refer to a respiratory specialist when the cough persists beyond 8 weeks of treatment, sputum induction is needed, or an occupational cause is suspected.