Changes in Airway Responsiveness Following Mantle Radiotherapy for Hodgkin's Disease

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 FEV 1 [PD 10 ]) and central airway (the provocative dose of methacholine causing a 25% fall in the maximal mid-inspiratory flow [PD 25 MIF 50 ]), 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 PD 10 (mean [± SEM], 2,583 ± 414 μg to 1,512 ± 422 μg, respectively; p 25 MIF 50 (mean 2,898 ± 372 μg to 1,340 ± 356 μg, respectively; p 1 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, FEV 1 , MIF 50 , 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 FEV 1 and those in both PD 10 (r = 0.733; p = 0.004) and PD 25 MIF 50 (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.