Occurrence of pneumonitis following radiotherapy of breast cancer – A prospective study

Abstract

Aimof this study is to determine the temporal resolution of therapy-induced pneumonitis, and to assess promoting factors in adjuvant treated patients with unilateral mammacarcinoma.Patients and methodsA total of 100 post-surgery patients were recruited. The cohort was treated by 2 field radiotherapy (2FRT; breast and chest wall, N = 75), 3 field radiotherapy (3FRT; + supraclavicular lymphatic region, N = 8), or with 4 field radiotherapy (4FRT; + parasternal lymphatic region, N = 17). Ninety-one patients received various systemic treatments prior to irradiation. Following an initial screening visit post-RT, two additional visits after 12 and 25 weeks were conducted including radiographic examination. In addition, general anamnesis and the co-medication were recorded. The endpoint was reached as soon as a pneumonitis was developed or at maximum of six months post-treatment.ResultsA pneumonitis incidence of 13% was determined. Of 91 patients with prior systemic therapy, 11 patients developed pneumonitis. Smoking history and chronic obstructive pulmonary disease (COPD) appeared to be positive predictors, whereas past pneumonia clearly promoted pneumonitis. Further pneumonitis-promoting predictors are represented by the applied field extensions (2 field radiotherapy [2FRT] < 3 field radiotherapy [3FRT] < 4 field radiotherapy [4FRT]) and the type of combined initial systemic therapies. As a consequence, all of the three patients in the study cohort treated with 4FRT and initial chemotherapy combined with anti-hormone and antibody protocols developed pneumonitis. A combination of the hormone antagonists tamoxifen and goserelin might enhance the risk for pneumonitis. Remarkably, none of the 11 patients co-medicated with statins suffered from pneumonitis.ConclusionsThe rapidly increasing use of novel systemic therapy schedules combined with radiotherapy (RT) needs more prospective studies with larger cohorts. Our results indicate that contribution to pneumonitis occurrence of various (neo)adjuvant therapy approaches followed by RT is of minor relevance, whereas mean total lung doses of >10 Gy escalate the risk of lung tissue complications. The validity of potential inhibitors of therapy-induced pneumonitis as observed for statin co-medication should further be investigated in future trials.

Is prone free breathing better than supine deep inspiration breath-hold for left whole-breast radiotherapy? A dosimetric analysis

“…The heart priority type would represent patients with history of heart disease, presenting cardiovascular comorbidity, or receiving cardiotoxic therapy such as doxorubicin or trastuzumab, thus requiring most heart protection [ 27 ]. The lungs priority type would apply to patients with higher age or a history of pulmonary disease [ 9 , 57 ]. The PTVs priority type would be patients at a high risk of local relapse, such as large tumors or negative hormone receptor status [ 58 ].…”

Acute toxicity of normofractionated intensity modulated radiotherapy with simultaneous integrated boost compared to three-dimensional conformal radiotherapy with sequential boost in the adjuvant treatment of breast cancer

“…No patient was symptomatic. There is few data for comparison, however Vasiljevic et al [25] conducted a prospective study of 100 patients with follow-up CT-scans at 13 and 24 weeks after RT. They identified 13 patients with features suggestive of pneumonitis, all of which had mild respiratory symptoms.…”

Prospective Long-Term Follow-Up of Pulmonary Diffusion Capacity Reduction Caused by Dose-Dense Chemotherapy in Patients with Breast Cancer

“…The prophylactic use of growth factor support might also have contributed to the DLCO reduction, as it has been known to exacerbate chemotherapy-related pulmonary toxicity through activation of neutrophils and a proinflammatory cytokine response [22]. In addition, our patients received paclitaxel, which may cause pulmonary toxicity such as pulmonary infiltrates and hypersensitivity reactions and, in rare cases, pneumonitis [23, 24]. The mechanism for hypersensitivity is thought to be non-IgE-mediated given that most reactions occur during the first and second doses [25].…”