Published ahead of print on October 9, 2003, doi:10.1164/rccm.200304-558OC Am. J. Respir. Crit. Care Med., Volume 169, Number 2, January 2004, 174-179 A more recent version of this article appeared on January 15, 2004
Submitted on April 22, 2003 Airway Inflammation and Infection in Congenital Bilateral Absence of the Vas DeferensMarita Gilljam1,1 Respiratory Medicine and Allergology, Sahlgrenska University Hospital, Goteborg University, Goteborg, Sweden, 2 Adult Cystic Fibrosis Centre, St Michael's Hospital, Toronto, Ontario, Canada; Medicine, Division of Respirology, University of Toronto, Toronto, Ontario, Canada, 3 Toronto General Hospital Reseach Institute, Toronto, Ontario, Canada; Medicine, Division of Respirology, University of Toronto, Toronto, Ontario, Canada, 4 Diagnostic Laboratories and Pathobiology, St Michael's Hospital, Toronto, Ontario, Canada, 5 Research Institute, Hospital For Sick Children, Toronto, Ontario, Canada; Pediatrics, University of Toronto, Toronto, Ontario, Canada, 6 Medicine, Division of Respirology, University of Sherbrooke, Sherbrooke, Quebec, Canada, 7 Research Institute, Hospital For Sick Children, Toronto, Ontario, Canada; Medical and Molecular Genetics, University of Toronto, Toronto, Ontario, Canada * To whom correspondence should be addressed. E-mail: tullise{at}smh.toronto.on.ca.
In cystic fibrosis (CF), airway disease begins early in life. Bacteria and elevated levels of neutrophils and inflammatory mediators have been detected in bronchoalveolar lavage (BAL) fluid from infants with CF. Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) are common in men with congenital bilateral absence of the vas deferens (CBAVD) and it has been suggested that this syndrome represent a mild form of CF. We hypothesized that men with CBAVD also have subclinical pulmonary disease. Bronchoscopy with BAL with viral and quantitative bacterial cultures and analyses of total and differential cell count, cytokines and free neutrophil elastase was performed in 8 men with CBAVD, who had mutations in CFTR and intermediate or elevated sweat chloride levels, and in 4 healthy controls. There was light growth of Staphylococcus aureus in 1/8 and small numbers of gram-negative bacteria in 6/8 men with CBAVD and in one control subject. BAL cell counts and neutrophil elastase were within the normal range. IL-8 and TNF Key words: Cystic fibrosis, bronchoalveolar lavage, inflammation, infection, cystic fibrosis transmembrane conductance regulator
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levels were higher for CBAVD than for controls. These data suggest that mutations in CFTR in men with CBAVD, in addition to causing infertility, lead to subclinical bacterial pulmonary infection and inflammation consistent with mild CF.
