Showing papers on "Radiation-induced lung injury published in 2005"

Radiation pneumonitis and pulmonary fibrosis in non-small-cell lung cancer: pulmonary function, prediction, and prevention.

Abstract: Although radiotherapy improves locoregional control and survival in patients with non-small-cell lung cancer, radiation pneumonitis is a common treatment-related toxicity. Many pulmonary function tests are not significantly altered by pulmonary toxicity of irradiation, but reductions in D(L(CO)), the diffusing capacity of carbon monoxide, are more commonly associated with pneumonitis. Several patient-specific factors (e.g. age, smoking history, tumor location, performance score, gender) and treatment-specific factors (e.g. chemotherapy regimen and dose) have been proposed as potential predictors of the risk of radiation pneumonitis, but these have not been consistently demonstrated across different studies. The risk of radiation pneumonitis also seems to increase as the cumulative dose of radiation to normal lung tissue increases, as measured by dose-volume histograms. However, controversy persists about which dosimetric parameter optimally predicts the risk of radiation pneumonitis, and whether the volume of lung or the dose of radiation is more important. Radiation oncologists ought to consider these dosimetric factors when designing radiation treatment plans for all patients who receive thoracic radiotherapy. Newer radiotherapy techniques and technologies may reduce the exposure of normal lung to irradiation. Several medications have also been evaluated for their ability to reduce radiation pneumonitis in animals and humans, including corticosteroids, amifostine, ACE inhibitors or angiotensin II type 1 receptor blockers, pentoxifylline, melatonin, carvedilol, and manganese superoxide dismutase-plasmid/liposome. Additional research is warranted to determine the efficacy of these medications and identify nonpharmacologic strategies to predict and prevent radiation pneumonitis.

Cytokine profiling for prediction of symptomatic radiation-induced lung injury

Abstract: Purpose: To analyze plasma cytokine profiles before the initiation of radiation therapy to define a cytokine phenotype that correlates with risk of developing symptomatic radiation-induced lung injury (SRILI). Methods and Materials: Symptomatic radiation-induced lung injury was evaluated in 55 patients (22 with SRILI and 33 without SRILI), according to modified National Cancer Institute common toxicity criteria. These plasma samples were analyzed by the multiplex suspension bead array system (Bio-Rad Laboratories; Hercules, CA), which included the following cytokines: interleukin (IL)-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12p70, IL-13, IL-17, granulocyte/macrophage colony-stimulating factor, interferon-γ, monocyte chemotactic protein 1, macrophage inflammatory protein 1β, tumor necrosis factor α, and granulocyte colony-stimulating factor. Results: Significant differences in the median values of IL-8 were observed between patients with and without SRILI. Patients who did not develop SRILI had approximately fourfold elevated levels of IL-8 as compared with patients who did subsequently develop SRILI. Significant correlations were not found for any other cytokine in this study, including transforming growth factor β1. Conclusions: Patients with lower levels of plasma IL-8 before radiation therapy might be at increased risk for developing SRILI. Further studies are necessary to determine whether IL-8 levels are predictive of SRILI in a prospective trial and whether this marker might be used to determine patient eligibility for dose escalation.

[Exploration of serum endothelin-1 as a marker of early radiation lung injury].

Abstract: AIM: To explore the possibility of endothelin-1(ET-1) as a serological marker of early diagnosis and progression of radiation induced lung injury. METHODS: One hundred and ninety female rats were randomly divided into control group (group C) and experimental groups, namely, radiation group (group R), fluvastatin treatment group (group Flu), retinoic acid treatment group (group Ra) and dexemethasone treatment group (group Dex). The chests of rats in experimental groups were exposed to radiation by linear accelerator after anesthesia. The radiation dose for each rat was 15Gy, 2Gy per minute, and radiation distance was 1 meter. The next day after radiation, fluvastatin (20 mg·kg~(-1)·d~(-1)) was administered orally in group Flu, retinoic acid (20 mg·kg~(-1)·d~(-1)) in group Ra and dexemethasone (3.33 mg·kg~(-1)·d~(-1)) in group Dex. The rats in group C and group R were medicated with the equal volume of normal saline. On the 5th, 15th, 30th, and 60th day after radiation, five rats were randomly chosen from each group respectively. The sera were harvested by decapitation or cardiopuncture and at the same time, lung tissues were cut off. The levels of serum ET-1 and LN were detected by radioimmunological assay(RIA). The pathologic changes of lung tissue were observed under light microscope. RESULTS: Compared to the control group, serum ET-1 level began to increase on the 5th day after exposure to radiation and reached the peak on the 60th day in group R. The levels of laminin and hyaluronic acid began to rise on the 30th day and the 60th day respectively. The elevation of serum ET-1 level in group R was obviously earlier than that in other groups and correlated to extent of lung injury. CONCLUSION: The serum ET-1 can be used as a marker of early diagnosis and dynamic changes of radiation lung injury.