A reappraisal of nasal saline solution use in chronic sinusitis.

concept that chronic inflammation of foregut structures can be associated with airway inflammation and damage struck a cord with us since we have noted a striking excess of cases of treated hypothyroidism among a population of patients with idiopathic chronic cough 2 and in nonsmoking patients with fixed airflow obstruction. 3 Hypothyroidism is usually due to autoimmune destruction of the thyroid gland and is associated with intrathy-roid lymphocytic infiltration. We have shown that idiopathic chronic cough is associated with a BAL lymphocytosis 2 and have suggested that this is due to homing of activated lymphocytes from the primary site of autoimmune inflammation to embryo-logically related structures such as the airways. 2– 4 The mechanism of airway inflammation and damage in autoimmune thyroid disease, and perhaps in chronic hepatitis C infection, may be analogous to that thought to be responsible for airway complications of inflammatory bowel disease. The concepts that inflam-matory bowel disease and autoimmune thyroid disease are associated with airway disease, and that the pathogenesis is similar and not related to thyroid hormone status, are supported by a recent study 4 showing a twofold to threefold excess of cough, sputum production, and breathlessness, and a remarkably similar profile of respiratory symptoms, among a cohort of patients with inflammatory bowel disease and among another cohort with treated autoimmune thyroid disease. One important difference between the primary sites of inflammation in chronic hepatitis C infection and autoimmune thyroid disease is that the former condition is treatable. The findings of Kanazawa et al 1 with interferon therapy raise the interesting possibility that treatment may modify the airway consequences of chronic inflammation of the foregut. The search is on for other treatable causes of chronic foregut inflammation that might be relevant to airway diseases. COPD is associated with peptic ulcer disease, 5 so one possibility worth investigating is that chronic gastric inflammation secondary to Helicobacter pylori infection is a potentially modifiable factor underlying the amplified immune response to cigarette smoking and other pollutants that characterizes COPD. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). References 1 Kanazawa H, Hirata K, Yoshikawa J. Accelerated decline of lung function in COPD patients with chronic hepatitis C virus infection: a preliminary study based on small numbers of patients. Chest 2003; 123:596 –599 2 Birring SS, Brightling CE, Symon FA et al. Idiopathic chronic cough: association with organ …