Musaddiq J Awan1, Abdallah S R Mohamed2, Jan S Lewin3, Charles A Baron4, G Brandon Gunn5, David I Rosenthal6, F Christopher Holsinger7, David L Schwartz8, Clifton D Fuller9, Katherine A Hutcheson10. 1. Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77082, United States; Department of Radiation Oncology, Case Western Reserve University Hospitals, Cleveland, OH 44106, United States. Electronic address: muawan@gmail.com. 2. Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77082, United States; Department of Clinical Oncology, Faculty of Medicine, The University of Alexandria, Alexandria, Egypt. Electronic address: abdallah.sherif@alexmed.edu.eg. 3. Department of Head & Neck Surgery, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, United States. Electronic address: jlewin@mdanderson.org. 4. Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77082, United States. Electronic address: cbaron@wesleyan.edu. 5. Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77082, United States. Electronic address: gbgunn@mdanderson.org. 6. Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77082, United States. Electronic address: dirosenthal@mdanderson.org. 7. Department of Head and Neck Surgery, Department of Otolaryngology, Stanford University, Stanford, CA 94305, United States. Electronic address: holsinger@stanford.edu. 8. Department of Radiation Oncology, The University of Texas Southwestern, Dallas, TX, United States. Electronic address: dschwartz516@gmail.com. 9. Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77082, United States. Electronic address: cdfuller@mdanderson.org. 10. Department of Head & Neck Surgery, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, United States. Electronic address: karnold@mdanderson.org.
Abstract
BACKGROUND AND OBJECTIVES: Late radiation-associated dysphagia (late-RAD) is a rare delayed toxicity, in oropharyngeal cancer (OPC) survivors. Prevention of late-RAD is paramount because the functional impairment can be profound and refractory to standard therapies. The objective of this analysis is to identify candidate dosimetric predictors of late-RAD and associated lower cranial neuropathies after radiotherapy (RT) or chemo-RT (CRT) for OPC. MATERIALS AND METHODS: An unmatched retrospective case-control analysis was conducted. Late-RAD cases were identified among OPC patients treated with definitive RT or CRT. Controls were selected with minimum of 6 years without symptoms of late-RAD. Dysphagia-aspiration related structures (DARS) and regions of interest containing cranial nerve paths (RCCNPs) were retrospectively contoured. Dose volume histograms were calculated. Non-parametric bivariate associations were analyzed with Bonferroni correction and multiple logistic regression models were fit. RESULTS: Thirty-eight patients were included (12 late-RAD cases, 26 controls). Median latency to late-RAD was 5.8 years (range: 4.5-11.3 years). Lower cranial neuropathies were present in 10 of 12 late-RAD cases. Mean superior pharyngeal constrictor (SPC) dose was higher in cases relative to controls (median: 70.5 vs. 61.6 Gy). Mean SPC dose significantly predicted late-RAD (p = 0.036) and related cranial neuropathies (p = 0.019). RCCNPs did not significantly predict late-RAD or cranial neuropathies. CONCLUSIONS: SPC dose may predict for late-RAD and related lower cranial neuropathies. These data, and those of previous studies that have associated SPC dose with classical dysphagia endpoints, suggest impetus to constrain dose to the SPCs when possible.
BACKGROUND AND OBJECTIVES: Late radiation-associated dysphagia (late-RAD) is a rare delayed toxicity, in oropharyngeal cancer (OPC) survivors. Prevention of late-RAD is paramount because the functional impairment can be profound and refractory to standard therapies. The objective of this analysis is to identify candidate dosimetric predictors of late-RAD and associated lower cranial neuropathies after radiotherapy (RT) or chemo-RT (CRT) for OPC. MATERIALS AND METHODS: An unmatched retrospective case-control analysis was conducted. Late-RAD cases were identified among OPC patients treated with definitive RT or CRT. Controls were selected with minimum of 6 years without symptoms of late-RAD. Dysphagia-aspiration related structures (DARS) and regions of interest containing cranial nerve paths (RCCNPs) were retrospectively contoured. Dose volume histograms were calculated. Non-parametric bivariate associations were analyzed with Bonferroni correction and multiple logistic regression models were fit. RESULTS: Thirty-eight patients were included (12 late-RAD cases, 26 controls). Median latency to late-RAD was 5.8 years (range: 4.5-11.3 years). Lower cranial neuropathies were present in 10 of 12 late-RAD cases. Mean superior pharyngeal constrictor (SPC) dose was higher in cases relative to controls (median: 70.5 vs. 61.6 Gy). Mean SPC dose significantly predicted late-RAD (p = 0.036) and related cranial neuropathies (p = 0.019). RCCNPs did not significantly predict late-RAD or cranial neuropathies. CONCLUSIONS:SPC dose may predict for late-RAD and related lower cranial neuropathies. These data, and those of previous studies that have associated SPC dose with classical dysphagia endpoints, suggest impetus to constrain dose to the SPCs when possible.
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