131I treatment for thyroid cancer and risk of developing primary hyperparathyroidism: A cohort study

Chien Mu Lin, Pat Doyle, Yu Tse Tsan, Chang Hsing Lee, Jung Der Wang, Pau Chung Chen

研究成果: 雜誌貢獻文章

5 引文 (Scopus)

摘要

Purpose: To evaluate the association between 131I therapy for thyroid cancer and risk of developing primary hyperparathy roidism. Methods: This was a nationwide population-based cohort study of patients with thyroid cancer diagnosed during the period 1997-2008. The data were obtained from the Taiwan National Health Insurance Research dataset. The cumulative 131I dose in each patient was calculated. Hazard ratios (HRs) were calculated using a proportional hazards model to estimate the effect of 131I therapy on the risk of developing primary hyperparathyroidism in the cohort. Results: A total of 8,946 patients with thyroid cancer were eligible for the final analysis. Among these patients, 8 developed primary hyperparathyroidism during the follow-up period that represented 38,248 person-years giving an incidence rate of 20.9 per 105 person-years. 131I was used in the treatment of 6,153 patients (68.8 %) with a median cumulative dose of 3.7 GBq. The adjusted HRs were 0.21 (95% CI 0.02-1.86) and 0.46 (95% CI 0.10-2.10) for those receiving a cumulative 131I dose of 0.1-3.6 GBq and ≥3.7 GBq, respectively, compared to no therapy. The risk of developing primary hyperparathyroidism did not increase with increasing 131I dose (test for trend p =0.51). No interaction was found between 131I dose and age (p =0.94) or 131I dose and sex (p = 0.99). Conclusion: 131I treatment for thyroid cancer did not increase risk of primary hyperparathyroidism during a 10-year follow-up in this study population. Further research with a longer follow-up period is needed to assess late adverse effects beyond 10 years.

原文英語
頁(從 - 到)253-259
頁數7
期刊European Journal of Nuclear Medicine and Molecular Imaging
41
發行號2
DOIs
出版狀態已發佈 - 2014

指紋

Primary Hyperparathyroidism
Thyroid Neoplasms
Cohort Studies
Therapeutics
National Health Programs
Taiwan
Proportional Hazards Models
Research
Population
Incidence

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

引用此文

131I treatment for thyroid cancer and risk of developing primary hyperparathyroidism : A cohort study. / Lin, Chien Mu; Doyle, Pat; Tsan, Yu Tse; Lee, Chang Hsing; Wang, Jung Der; Chen, Pau Chung.

於: European Journal of Nuclear Medicine and Molecular Imaging, 卷 41, 編號 2, 2014, p. 253-259.

研究成果: 雜誌貢獻文章

Lin, Chien Mu ; Doyle, Pat ; Tsan, Yu Tse ; Lee, Chang Hsing ; Wang, Jung Der ; Chen, Pau Chung. / 131I treatment for thyroid cancer and risk of developing primary hyperparathyroidism : A cohort study. 於: European Journal of Nuclear Medicine and Molecular Imaging. 2014 ; 卷 41, 編號 2. 頁 253-259.
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abstract = "Purpose: To evaluate the association between 131I therapy for thyroid cancer and risk of developing primary hyperparathy roidism. Methods: This was a nationwide population-based cohort study of patients with thyroid cancer diagnosed during the period 1997-2008. The data were obtained from the Taiwan National Health Insurance Research dataset. The cumulative 131I dose in each patient was calculated. Hazard ratios (HRs) were calculated using a proportional hazards model to estimate the effect of 131I therapy on the risk of developing primary hyperparathyroidism in the cohort. Results: A total of 8,946 patients with thyroid cancer were eligible for the final analysis. Among these patients, 8 developed primary hyperparathyroidism during the follow-up period that represented 38,248 person-years giving an incidence rate of 20.9 per 105 person-years. 131I was used in the treatment of 6,153 patients (68.8 {\%}) with a median cumulative dose of 3.7 GBq. The adjusted HRs were 0.21 (95{\%} CI 0.02-1.86) and 0.46 (95{\%} CI 0.10-2.10) for those receiving a cumulative 131I dose of 0.1-3.6 GBq and ≥3.7 GBq, respectively, compared to no therapy. The risk of developing primary hyperparathyroidism did not increase with increasing 131I dose (test for trend p =0.51). No interaction was found between 131I dose and age (p =0.94) or 131I dose and sex (p = 0.99). Conclusion: 131I treatment for thyroid cancer did not increase risk of primary hyperparathyroidism during a 10-year follow-up in this study population. Further research with a longer follow-up period is needed to assess late adverse effects beyond 10 years.",
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AU - Chen, Pau Chung

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N2 - Purpose: To evaluate the association between 131I therapy for thyroid cancer and risk of developing primary hyperparathy roidism. Methods: This was a nationwide population-based cohort study of patients with thyroid cancer diagnosed during the period 1997-2008. The data were obtained from the Taiwan National Health Insurance Research dataset. The cumulative 131I dose in each patient was calculated. Hazard ratios (HRs) were calculated using a proportional hazards model to estimate the effect of 131I therapy on the risk of developing primary hyperparathyroidism in the cohort. Results: A total of 8,946 patients with thyroid cancer were eligible for the final analysis. Among these patients, 8 developed primary hyperparathyroidism during the follow-up period that represented 38,248 person-years giving an incidence rate of 20.9 per 105 person-years. 131I was used in the treatment of 6,153 patients (68.8 %) with a median cumulative dose of 3.7 GBq. The adjusted HRs were 0.21 (95% CI 0.02-1.86) and 0.46 (95% CI 0.10-2.10) for those receiving a cumulative 131I dose of 0.1-3.6 GBq and ≥3.7 GBq, respectively, compared to no therapy. The risk of developing primary hyperparathyroidism did not increase with increasing 131I dose (test for trend p =0.51). No interaction was found between 131I dose and age (p =0.94) or 131I dose and sex (p = 0.99). Conclusion: 131I treatment for thyroid cancer did not increase risk of primary hyperparathyroidism during a 10-year follow-up in this study population. Further research with a longer follow-up period is needed to assess late adverse effects beyond 10 years.

AB - Purpose: To evaluate the association between 131I therapy for thyroid cancer and risk of developing primary hyperparathy roidism. Methods: This was a nationwide population-based cohort study of patients with thyroid cancer diagnosed during the period 1997-2008. The data were obtained from the Taiwan National Health Insurance Research dataset. The cumulative 131I dose in each patient was calculated. Hazard ratios (HRs) were calculated using a proportional hazards model to estimate the effect of 131I therapy on the risk of developing primary hyperparathyroidism in the cohort. Results: A total of 8,946 patients with thyroid cancer were eligible for the final analysis. Among these patients, 8 developed primary hyperparathyroidism during the follow-up period that represented 38,248 person-years giving an incidence rate of 20.9 per 105 person-years. 131I was used in the treatment of 6,153 patients (68.8 %) with a median cumulative dose of 3.7 GBq. The adjusted HRs were 0.21 (95% CI 0.02-1.86) and 0.46 (95% CI 0.10-2.10) for those receiving a cumulative 131I dose of 0.1-3.6 GBq and ≥3.7 GBq, respectively, compared to no therapy. The risk of developing primary hyperparathyroidism did not increase with increasing 131I dose (test for trend p =0.51). No interaction was found between 131I dose and age (p =0.94) or 131I dose and sex (p = 0.99). Conclusion: 131I treatment for thyroid cancer did not increase risk of primary hyperparathyroidism during a 10-year follow-up in this study population. Further research with a longer follow-up period is needed to assess late adverse effects beyond 10 years.

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