MIXED (NEUTROPHIL-RICH) INTERSTITIAL PNEUMONITIS IN BIOPSY SPECIMENS OF LUNG ALLOGRAFTS - A CLINICOPATHOLOGICAL EVALUATION

Citation
Jw. Mcdonald et al., MIXED (NEUTROPHIL-RICH) INTERSTITIAL PNEUMONITIS IN BIOPSY SPECIMENS OF LUNG ALLOGRAFTS - A CLINICOPATHOLOGICAL EVALUATION, Chest, 113(1), 1998, pp. 117-123
Citations number
11
Categorie Soggetti
Respiratory System","Cardiac & Cardiovascular System
Journal title
ChestACNP
ISSN journal
00123692
Volume
113
Issue
1
Year of publication
1998
Pages
117 - 123
Database
ISI
SICI code
0012-3692(1998)113:1<117:M(IPIB>2.0.ZU;2-J
Abstract
Study objectives: Mixed interstitial pneumonitis (MIP), defined herein as a diffuse neutrophil-rich inflammatory infiltrate within the inter stitial tissues, is an uncommon finding that is not a standard manifes tation of acute or chronic rejection. This study examines the clinical significance of MIP in lung allograft recipients at St, Louis Univers ity Hospital. Design: We retrospectively reviewed surgical pathology r eports from a selected 50-month period, and identified MIP reported in 13 transbronchial biopsy specimens in lung transplant recipients, rep resenting 4.7% of all lung allograft biopsy specimens seen during this 4-year period. Biopsy specimens with MIP were examined to confirm the presence of a neutrophil-rich interstitial infiltrate and other assoc iated histopathologic findings. The culture results, cytopathologic fi ndings, and clinical charts of the affected patients were also reviewe d. Measurements and results: The detection of MIP at some point in a p atient's posttansplant course was found to be associated with a signif icantly shorter (p<0.01) survival, when compared to lung allograft rec ipients who did not show this finding. A total of seven lung allograft recipients (23% of total) showed MIP at some point in their posttrans plant course, Four of the seven (57%) were actively smoking following lung transplantation, compared to 0 of 22 patients who did not show MI P. Six of the 13 MIP biopsy specimens were associated with positive cu ltures. In no case did MIP coexist with the conventional histologic pa tterns of acute or chronic rejection, MIP also did not correlate with levels of immunosuppressive therapy or with the incidence of rejection at other times in the patients' posttransplant courses. Conclusions: We found no evidence that MIP represents an unusual form of acute or c hronic rejection. Instead, it appears to represent a response to acute injury, similar to other injury patterns (hyaline membranes, organizi ng pneumonia) in transplant recipients. Exposure to tobacco smoke is l ikely to have played a role in the development of MIP in at least some cases, Because patients with MIP had a significantly shorter posttran splant survival, MIP may usefully identify lung allograft recipients a t risk for an adverse outcome.