Posttreatment FDG-PET Uptake in the Supraglottic and Glottic Larynx Correlates With Decreased Quality of Life After Chemoradiotherapy

Ken Dornfeld, Shane Hopkins, Joel Simmons, Douglas R. Spitz, Yusuf Menda, Michael Graham, Russell Smith, Gerry Funk, Lucy Karnell, Michael Karnell, Maude Dornfeld, Min Yao, John Buatti

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Purpose: Inflammation and increased metabolic activity associated with oxidative stress in irradiated normal tissues may contribute to both complications following radiotherapy and increased glucose uptake as detected by posttherapy fluorodeoxyglucose (FDG)-PET imaging. We sought to determine whether increased glucose uptake in normal tissues after chemoradiotherapy is associated with increased toxicity. Methods and Materials: Consecutive patients with locoregionally advanced head and neck cancers treated with intensity-modulated radiation therapy and free of recurrence at 1 year were studied. FDG-PET imaging was obtained at 3 and 12 months posttreatment. Standardized uptake value (SUV) levels were determined at various head and neck regions. Functional outcome was measured using a quality of life questionnaire and weight loss and type of diet tolerated 1 year after therapy. A one-tailed Pearson correlation test was used to examine associations between SUV levels and functional outcome measures. Results: Standardized uptake value levels in the supraglottic and glottic larynx from FDG-PET imaging obtained 12 months posttreatment were inversely associated with quality of life measures and were correlated with a more restricted diet 1 year after therapy. SUV levels at 3 months after therapy did not correlate with functional outcome. Increases in SUV levels in normal tissues between 3 and 12 months were commonly found in the absence of recurrence. Conclusion: Altered metabolism in irradiated tissues persists 1 year after therapy. FDG-PET scans may be used to assess normal tissue damage following chemoradiotherapy. These data support investigating hypermetabolic conditions associated with either inflammation, oxidative stress, or both, as causal agents for radiation-induced normal tissue damage.

Original languageEnglish (US)
Pages (from-to)386-392
Number of pages7
JournalInternational Journal of Radiation Oncology Biology Physics
Issue number2
StatePublished - Jun 1 2008

All Science Journal Classification (ASJC) codes

  • Radiation
  • Oncology
  • Radiology Nuclear Medicine and imaging
  • Cancer Research


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