Affiliations: Glenfield Hospital Leicester, UK,
Osaka City University Osaka, Japan
Correspondence to: Surinder Birring, MB, ChB, Institute for Lung Health, Department of Respiratory Medicine, Glenfield Hospital, Leicester, LE3 9QP, United Kingdom; e-mail: email@example.com
To the Editor:
Kanazawa et al (February 2003)1–
reported an accelerated decline of lung function in COPD patients with concomitant hepatitis C infection. They have suggested that the airway disease may be related to the underlying chronic inflammatory disorder. The 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 cough2–
and in nonsmoking patients with fixed airflow obstruction.3
Hypothyroidism is usually due to autoimmune destruction of the thyroid gland and is associated with intrathyroid lymphocytic infiltration. We have shown that idiopathic chronic cough is associated with a BAL lymphocytosis2
and have suggested that this is due to homing of activated lymphocytes from the primary site of autoimmune inflammation to embryologically 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 inflammatory 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 study4
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 al1
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.
We thank Dr. Birring for an interest regarding our study (February 2003).1–
Hepatitis C virus (HCV) infection is a major cause of chronic liver disease. However, it has previously been reported that chronic HCV infection is associated with several other syndromes, including cardiomyopathy2–
and proliferative glomerulonephritis.3–
Therefore, we speculated that there is also an interaction between chronic HCV infection and some pulmonary disorders. Birring et al suggest that airway disease may be related to the underlying chronic inflammatory disorder.4–
We were very interested in their concepts. In our previous study,5
we discussed the role of T lymphocytes in airway inflammation in asthmatic patients with chronic HCV infection. They also emphasized that idiopathic chronic cough with hypothyroidism and inflammatory bowel disease is due to the homing of activated lymphocytes from the primary site of inflammation to embryologically related structures such as airways. However, we did not have any data that chronic inflammation of the foregut structure can be associated with airway inflammation. In future studies, we will examine the relationships between chronic inflammation of the foregut structure and airway inflammation according to their concepts.
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