Botha, Phil; Fisher, Andrew J.
Department of Cardiopulmonary Transplantation, Freeman Hospital, Newcastle upon Tyne, United Kingdom, Newcastle University, Institute for Cellular Medicine, Framlington Place, Newcastle upon Tyne, United Kingdom
None of the authors have a financial relationship with a commercial entity that has an interest in the subject of the presented manuscript.
Address correspondence to: Phil Botha, Newcastle University, 3rd Floor William Leech, Framlington Place, Newcastle upon Tyne, NE2 4HH, United Kingdom.
E-mail: [email protected]
Received 21 April 2008.
Accepted 9 May 2008.
We read with interest the letter by Vos and colleagues. The authors have demonstrated a similar association between pseudomonas aeruginosa (PA) colonization and the development of bronchiolitis obliterans syndrome (BOS) in lung transplant recipients in their center. Their finding of disparate effects of de novo colonization (in those with airways free of PA pretransplant) and persistence of colonization (in those shown to be colonized with the organism pretransplant) is interesting and in contrast to the observations made in our study (1). The authors noted a strong correlation between persistent colonization in patients with cystic fibrosis (CF) and the development of BOS, and a statistically nonsignificant effect for de novo colonization. Colonization of the lower respiratory tract with PA is a common finding in lung transplant recipients with CF (71%–88%) and occurs relatively early after transplantation in this patient group (1, 2). The association demonstrated by Vos and colleagues would lead one to expect a higher incidence of BOS and/or shorter freedom from BOS in lung transplant recipients with CF than in other patient groups. This is clearly not the case, as survival after lung transplantation for CF is significantly better than in any other diagnostic category (3) and the incidence of BOS has been similar (4) or lower (5) in past studies. There is therefore no evidence to date that recipients with CF get BOS earlier or live longer with BOS. This remains a fundamental limitation to the findings described by the Leuven group. However, the authors correctly pointed out that infection or colonization with mixed Pseudomonads has been demonstrated to correlate with airway neutrophilia and raised inflammatory markers. The disparate nature of our findings may simply reflect small patient numbers in both studies, and the complicated nature of the interaction between PA and the airway. We hope further studies with greater numbers of patients in these subgroups will illuminate the true nature of this intriguing association.
Phil Botha
Andrew J. Fisher
Department of Cardiopulmonary Transplantation
Freeman Hospital
Newcastle upon Tyne, United Kingdom
Newcastle University
Institute for Cellular Medicine
Framlington Place, Newcastle upon Tyne, United Kingdom
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