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Associate Professor of Medicine, University of Texas Health Science Center at San Antonio, and Medical Director of Lung Transplantation, South Texas Veterans Health Care System, Audie L. Murphy Memorial Veterans Hospital Division.
Correspondence to: Stephanie M. Levine, MD, FCCP, Department of Medicine, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78284-7885; e-mail: evines@uthscsa.edu.
Bronchiolitis obliterans (BO) remains the leading cause of long-term morbidity and mortality following lung transplantation and is thought to be chronic lung allograft rejection.1 It is estimated that up to 50% of lung transplant recipients surviving beyond the third posttransplant month will develop BO.2 BO is characterized clinically by limitation to airflow and pathologically by obliterative bronchiolitis, and is thought to be related to recurrent acute rejection and/or infection. Due to the poor sensitivity of transbronchial biopsy for the diagnosis of BO, the bronchiolitis obliterans syndrome (BOS) staging system was established by the International Society for Heart and Lung Transplantation.3 This staging system is based on airflow limitation (a percent change from a baseline posttransplant FEV1 as obtained on formal clinic spirometry) with or without the diagnostic histologic finding of BO. Inherent to the BOS diagnosis is the exclusion of other causes of graft dysfunction by bronchoscopy, such as acute rejection, infection, and anastomotic complications.
Once BOS is established, the condition is difficult to reverse. What one can hope for is stabilization or a reduction in the rate of decline of pulmonary function with treatment to include the following: corticosteroids, cytolytic agents, and immunosuppressive agents such as mycophenolate mofetil, or tacrolimus, or alternate delivery mechanisms of older immunosuppressive agents, ie, aerosolized cyclosporine.4 5 6
The early and accurate diagnosis of BOS may allow stabilization of pulmonary function at a higher level. However, the diagnosis of BOS remains difficult since numerous other graft complications can occur resulting in a decline in pulmonary function mimicking BOS. Available diagnostic tests, in general, have variable sensitivity and lack the specificity for the diagnosis of BOS.
In the early stages of BOS, the chest radiograph typically is normal, but as BOS progresses, the chest radiograph may reveal volume loss and/or fibrosis. Recently, the utility of high resolution CT in the diagnosis of BOS has revealed a correlation, with findings of bronchiectasis and airway dilatation consistent with small airway obstruction and BO.7 Mosaic perfusion patterns and airtrapping on end expiratory high resolution CT scan have also been reported to be sensitive findings for BO. In the large majority of patients, these radiographic findings develop well after the decline in FEV1.
The sensitivity of transbronchial biopsies for diagnosis of BO varies from 15 to 78%, and the specificity varies from 75 to 93% in various studies.8 More importantly, bronchoscopy is required in the diagnosis of BOS primarily to exclude other causes of airflow obstruction. BAL is usually not helpful in the diagnosis of BOS. Lung biopsy may be considered the "gold standard" for the diagnosis of BO but has its own associated morbidity and mortality and is not regularly performed.
Thus, pulmonary function testing is strongly relied upon as one of the earliest tests for detection of a graft complication such as BOS. While the staging of BOS is primarily based on a decline in FEV1, several studies have indicated that a decrease in forced expiratory flow at 25 to 75% of vital capacity is also a sensitive marker for the onset of BOS and may actually occur earlier than a decline in FEV1.9 To date, all of these data have been collected and reported on clinic-based spirometric testing performed at the transplant center or the pulmonologist's office.
Along these lines, the article in this issue of CHEST by Finkelstein and colleagues (see page 120) retrospectively examines the staging of BOS using home spirometry. The concept of home spirometry is not a new one in the field of lung transplantation, as patients are typically advised to record home spirometry measurements once or twice a day and to report persistent decrements in these numbers to their lung transplant centers or pulmonologist.10 11 There are inherent problems with home spirometry, such as intermittent or noncompliance with daily or twice daily testing, difficulty with interpretation of the data points, and patient denial and rationalization when decrements in function are obtained. In the study by Finkelstein and colleagues, the investigators analyzed home spirometric data sent weekly to the data center via telephone from the patient's home. Declines that persisted from 1 to 3 days were correlated with concurrent clinic spirometry to determine BOS staging. The authors found that home spirometry may detect a decline in pulmonary function significantly earlier than clinic spirometry and may be a reliable and safe alternative to frequent clinic-based pulmonary function testing in lung transplant recipients.
The use of home spirometry for detection of BOS may not preclude a visit to the local pulmonologist or transplant center to undergo a bronchoscopy to exclude alternate diagnoses. What it may allow is the diagnosis of BOS to be made earlier and more conveniently for those patients who live great distances from transplant centers. Hopefully, this could have an impact on graft and patient survival. Other potential ramifications of such a protocol could be reduced cost by negating the need to perform frequent clinic spirometries and traveling to the office for spirometry, although a cost analysis was not performed by these authors. Earlier diagnosis and treatment of BOS could also result in the use of less expensive and less toxic immunosuppressive agents and therapies and allow earlier outpatient treatment. Furthermore, in the age of concerns regarding insurance reimbursement, this study may be of importance to present to the insurance companies that are reluctant to reimburse for home spirometers for lung transplant patients.
Whether or not the use of home spirometry reaches widespread use in the lung transplantation community for detection of BOS remains to be determined. Also, it remains to be seen whether a several month lead time in the diagnosis of BOS will translate to earlier stabilization of pulmonary function, a less limited patient, and improved survival. For now, this article provides promise for the use of home spirometry for an earlier, easier, reliable, and potentially more fiscally responsible detection of this devastating complication of lung transplantation.
References
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