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Clinical Investigations: CANCER |

Changes in Airway Responsiveness Following Mantle Radiotherapy for Hodgkin’s Disease*

Giovanni Rolla, MD, FCCP; Umberto Ricardi, MD; Paola Colagrande, MD; Daniela Nassisi, MD; Luca Dutto, MD; Giovanni Chiavassa, MD; Caterina Bucca, MD
Author and Funding Information

*From the Department of Biomedical Sciences and Human Oncology (Drs. Rolla, Colagrande, Dutto, Chiavassa, and Bucca), the Radiotherapy Division (Drs. Ricardi and Nassisi), University of Torino, Torino, Italy.

Correspondence to: Caterina Bucca, MD, Associate Professor in Clinical Pathophysiology, Department of Biomedical Sciences and Human Oncology, University of Torino, Via Genova 3, 10126 Torino, Italy



Chest. 2000;117(6):1590-1596. doi:10.1378/chest.117.6.1590
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Study objectives: To investigate whether mantle radiotherapy (MRT) for the lung, through its proinflammatory effects, can induce an increase in airway responsiveness.

Design: Follow-up of the changes in lung function and methacholine responsiveness in patients 1, 6, 12, and 24 months after they underwent MRT.

Patients: Thirteen nonasthmatic patients with bulky Hodgkin’s lymphoma who were scheduled for MRT.

Measurements and results: Chest radiographs, lung function tests, methacholine thresholds of the bronchi (the provocative dose of methacholine causing a 10% fall in FEV1[ PD10]) and central airway (the provocative dose of methacholine causing a 25% fall in the maximal mid-inspiratory flow[ PD25MIF50]), and the provocative dose of methacholine causing five or more coughs (PDcough) were serially assessed. One month after patients underwent MRT, there were significant decreases in PD10 (mean [± SEM], 2,583 ± 414 μg to 1,512 ± 422 μg, respectively; p < 0.05), PD25MIF50 (mean 2,898 ± 372 μg to 1,340 ± 356 μg, respectively; p < 0.05), and PDcough (mean 3,127 ± 415 μg to 1,751 ± 447 μg; p < 0.05), which were independent of the decrease in FEV1 and reversed within 6 months in all patients but three. Six months after undergoing MRT, four patients showed radiation-induced lung injury (RI) on chest radiographs, which subsequently evolved into fibrosis. These patients had greater decreases in vital capacity, FEV1, MIF50, and methacholine thresholds than those without RI, and this persisted up to 2 years after they had undergone MRT. One year after the patients underwent MRT, a close relationship was found overall between the change in FEV1 and those in both PD10 (r = 0.733; p = 0.004) and PD25MIF50 (r = 0.712; p = 0.006).

Conclusions: MRT triggers an early transient increase in airway responsiveness, which reverses spontaneously. In patients with RI, the persistence of airway dysfunction long after undergoing MRT may depend on airway remodeling from radiation fibrosis.

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