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Radiation Pneumonitis in Lung Cancer Patients - The Neglected Patient-Related Variables

2005; Elsevier BV; Volume: 63; Linguagem: Inglês

10.1016/j.ijrobp.2005.07.391

1879-355X

Andrea Bezjak, V. Soyfer, Qijian Yi, A. Sun, G.C. Kane, Jerome M. Waldron, J. Cho, W. Wells, Debbie Payne,

Lung Cancer Research Studies

Purpose/Objective: Limited radiation tolerance of lung tissue remains a challenge in radiation (RT) treatment of patients (pts) with lung cancer. Most attention has been given to treatment-related variables that influence the development of RT pneumonitis, particularly RT dose and volume of lung receiving a certain dose. A number of pt-related factors are known to be relevant to the development and clinical severity of RT pneumonitis, most notably pts pre-existing lung function. There is evidence from animal experiments, and limited information from humans, that some frequently prescribed medications may module the risk of developing RT pneumonitis. To determine the potential protective role of concurrent medications, specifically glucocorticoids, angiotensin converting enzyme (ACE) inhibitors and/or NSAIDs (non-steroidal anti-inflammatory drugs) including aspirin, on development of RT pneumonitis in pts treated by radical RT for non-small cell lung cancer (NSCLC). Materials/Methods: Incidence and severity of RT pneumonitis were retrospectively analyzed for 142 NSCLC pts treated by RT to doses > 60 Gy (with or without chemotherapy) at Princess Margaret Hospital between 1999 and 2003. One of the variables of interest was administration of concurrent medications, specifically glucocorticoids, ACE inhibitors and/or NSAIDs. Pneumonitis was retrospectively scored according to modified RTOG/EORTC pulmonary toxicity grading. Results: Overall incidence of clinically significant (grade 2–5) RT pneumonitis was 26%. Of 77 pts who received concurrent medications in any combinations, 14 (18.2%) developed Grade >2 RT pneumonitis, as compared to 23/65 (35.4%) of pts who were not on these medications (p=0.02). The strongest protective effect was observed with ACE inhibitors, with 3/24 (12.5%) of pts on ACE inhibitors showing evidence of > grade 2 RT pneumonitis, as compared to 34/118 (28.8%) of pts not taking that medication (p=0.097). The difference was present but less marked for steroids (5/23 (21.7%) of pts on steroids showing >grade 2 RT pneumonitis, vs 32/119 (26.9%) of pts not on steroids) and NSAIDS (10/51 (19.6%) vs 27/91 (29.7%). On univariate analysis, presence of chronic lung disease, concurrent chemotherapy and smoking status were not correlated with clinically significant RT pneumonitis, and neither was fraction size (> 2 Gy/ fr vs <2Gy/fr). On multivariate analysis, the effect of concurrent medications persisted after adjustment for smoking, fractionation size, preexisting lung disease and concurrent chemotherapy. Conclusions: Pts who are on medications with potentially protective mechanism on lung tissue may have lower incidence of RT lung toxicity. If these findings are confirmed, they may be a reason why the current methods of trying to predict the risk of RT pneumonitis from a given RT plan are inaccurate, as they focus on treatment-related variables and ignore potentially important patient-related factors, which may be easily modifiable. It is important both to document concurrent medications, and to pursue these findings with confirmatory studies, in order to try to module the risk of RT and improve the therapeutic ratio.