Abstract

Radiation-induced acute and chronic lung toxicity is one of the important adverse events that has a negative influence on quality of life. It is widely accepted today that there are important factors such as personal sensibility and genetic differences between patients which effect both treatment response and treatment toxicity. In this study, the influence of gender differences on acute lung toxicity due to radiotherapy is investigated. Accordingly, it is examined if there is a relation between gender and histopathologically proven vasculitis and pneumonia in the lung tissues of male and female rats that are sacrificed 6 weeks after radiotherapy. It is concluded that the gender differences in rats have no effect on lung toxicity.

Highlights

  • Radiotherapy (RT) plays an important role in the treatment of many tumors which exist in and around thorax

  • Radiation pneumonia usually develops within 4–12 weeks after RT and it can cause hypoxia, cough, dyspnea, fever and exhaustion, and can be fatal [1]

  • The development of RT-induced changes were statistically higher in the RT-male and RT-female groups as compared to the control groups (RT-induced pneumonitis: RT-male and control male, p 0.004, RT-female and control female, p 0.01; Vasculitis: RT-male and control male, p 0.009, RT-female and control female, p 0.08), as expected (Tables 2 & 3)

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Summary

Introduction

Radiotherapy (RT) plays an important role in the treatment of many tumors which exist in and around thorax. Radiation pneumonia is the main dose-limiting toxicity in thoracic radiotherapy. Radiation pneumonia usually develops within 4–12 weeks after RT and it can cause hypoxia, cough, dyspnea, fever and exhaustion, and can be fatal [1]. Histopathological findings seen after radiotherapy are defined as “diffuse alveolar damage” [2]. In this period, besides endothelial changes which cause an increase in capillary vascular permeability, protein exudation in alveolar spaces and alveolar wall oedema are observed. Thrombosis and consecutively intra-alveolar haemorrhage can develop in vessels that have focal necrosis. Fibroblastic proliferation and collagen accumulation occur both in intra-alveolar spaces and insterstitium. Alveolar septum thickening and fibrosis become obvious in a couple of weeks [5].

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