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E. Troost



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    P1.08 - Poster Session 1 - Radiotherapy (ID 195)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Radiation Oncology + Radiotherapy
    • Presentations: 1
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      P1.08-022 - Number of pathologic nodes in regions closest to the oesophagus is the strongest predictor for esophagitis in small cell lung cancer patients treated with concurrent chemo-radiation: an analysis of 170 patients. (ID 2711)

      09:30 - 09:30  |  Author(s): E. Troost

      • Abstract

      Background
      Radiation esophagitis grade III caused by chemo-radiation for small-cell lung cancer is a burden for patients and thus of concern to radiation oncologists. Neutropenia and radiation dose to the esophagus are known treatment factors influencing the rate of esophagitis during treatment, but currently the only factors that can be discussed with the patient at diagnosis are the choice of concurrent versus sequential chemo-radiation and the radiation dose fractionation schedule. In order to build predictive models to more accurately tailor treatment and advise patients on treatment options, more prognostic factors known at the moment of diagnosis are needed.

      Methods
      Analysis of all patients in our prospective database with stage I-III SCLC referred for concurrent chemo-radiotherapy between 5-2004 and 1-2012. All patients were PET-staged and received 45 Gy in 1.5 Gy fractions twice daily to the tumour and PET-or pathologically proven positive lymph nodes. Chemotherapy consisted of carboplatin-etoposide given concurrently with radiotherapy. All pathological lymph node regions were noted for each patient. Based on the Mountain Dressler atlas, the lymph node regions closest to the oesophagus were designated ``high risk`` regions for esophagitis, namely: 1R, 1L, 3P, 4L, 7, 8 and 9. Toxicity was scored according to CTC AE 3.0. Univariate analysis was done using the Chi-square test, reporting for p-value the Fischer exact Test for small numbers of events. Multivariate analysis was done using logistic regression. .

      Results
      170 patients were included in the present analysis. Thirty-seven (20%) patients developed grade III esophagitis. In univariate analysis the number of nodal regions (0, 1-4, ≥5) (p=0.02) and the number of high risk nodal regions (0, 1-2, ≥3) (p=0.001) had a significant effect on the risk of grade III esophagitis whereas the location of the primary tumour or having a T4 tumour did not. In multivariate analysis including age, gender and T4 tumour, the number of pathological nodal stations lost significance. In the multivariate analysis using age, gender, T4 tumour and the ``high risk`` count (0, 1-2, ≥3 areas) having nodes in ≥3 high risk areas was the only significant factor (p=0.002), with a hazard ratio (HR) of 7.4 for developing oesophagitis grade III (95% CI for HR: 2.2-25.2). The absolute rates of esophagitis grade III were: 5/51 (10%), 19/91 (21%), 12/28 (43%) for patients with respectively 0, 1-2 and ≥3 pathological high risk nodal areas.

      Conclusion
      In this series of stage I-III small cell lung cancer treated with radical chemo-radiation, the strongest predictor for esophagitis grade III known at diagnosis is the presence of nodal disease in ``high-risk regions`` 1R, 1L, 3P, 4L, 7, 8 and 9. Analysis of the correlation of this finding with the dose to the esophagus (Dmax/ Dmean) is ongoing and will also be presented at the conference.

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    P3.24 - Poster Session 3 - Supportive Care (ID 160)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Supportive Care
    • Presentations: 1
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      P3.24-029 - Progression of radiation induced esophageal stenosis in a non-small cell lung cancer (NSCLC) patient treated with sorafenib (ID 1882)

      09:30 - 09:30  |  Author(s): E. Troost

      • Abstract

      Background
      Sorafenib is an orally available multikinase inhibitor with antiproliferative and anti-angiogenic activity. Reported oral adverse events of any grade are stomatitis/mucositis (11-38%, mostly ≤ CTC-AE grade 2), oral mucosal pain and dysphagia in the absence of clinical lesions. Sorafenib is under investigation in NSCLC. We report a patient who developed symptomatic progression of an esophageal stenosis during sorafenib treatment.

      Methods
      not appicable

      Results
      Case: A 67-year old male presented at the outpatient clinic with dysphagia CTC-AE grade 3. He was diagnosed with a cT3N3M1a (oligometastatic adenocarcinoma, KRAS mutated) NSCLC in January 2011 for which he was treated with concurrent chemoradiotherapy. Treatment was complicated with grade 3 radiation esophagitis (confirmed with duodenogastroscopy) for which he was treated with a feeding tube and proton pump inhibition. Because of remaining grade 1 dysphagia, duodenogastroscopies were performed in August 2011 and February 2012. A stable relative stenosis of the upper esophagus was found, easy to pass with the duodenogastroscope. Because of progressive disease he was subsequently treated with erlotinib/ pemetrexed (September 2011, study) and docetaxel monotherapy (August 2012). February 2013 he progressed again with subsequent participation in a phase II study with sorafenib 400 mg BID and metformin 1000 mg BID. Within three weeks he developed dysphagia for solid foods. A chest computed tomography showed no external compression of the esophagus and no tumor progression. Duodenogastroscopy revealed a stenosis with ulceration in the upper part of the esophagus, passing the stenosis was only possible with a baby-duodenogastroscope. Because of swallowing problems, sorafenib was temporarily stopped and placement of a percutaneous feeding tube was planned. However, two days after stopping sorafenib, his dysphagia completely resolved and food passage was normal. So, ten days later sorafenib was restarted with dose reduction (200 mg BID). After restarting sorafenib his dysphagia returned with grade 3 within six weeks. Again, sorafenib was temporarily stopped and in a couple of days his dysphagia resolved. After another restart of sorafenib at the latter dose he again developed dysphagia, but this time manageable.

      Conclusion
      We present a patient who developed a grade 3 stenosis of the esophagus during treatment with sorafenib which clinically resolved shortly after stopping sorafenib but reoccurred after rechallenge with sorafenib at a lower dose. Dysphagia resolved again after stopping the sorafenib with again complaints after restarting. No other explanation was found (e.g. progression of malignancy, external compression). 1.5 year before, after concurrent chemoradiotherapy, he was diagnosed with a relative stenosis of the upper esophagus, but this remained stable until sorafenib treatment was started. He scored 8/13 points on the Naranjo score, making sorafenib a probable cause of the stenosis. The underlying mechanism is unknown. A possible explanation is sorafenib inhibition of the VEGF and MAP-kinase pathway. These pathways are both involved in the process of mucosal defense and repair, and it could be that blocking this pathway combined with sensitization by previous irradiation caused progression of the stenosis. This case stresses the importance of being aware of unusual side effects of medication and taking into account possible interactions with previous treatments.