Endocrinology and Metabolism

Original Articles

Thyroid
Evaluation of Iodine Status among Korean Patients with Papillary Thyroid Cancer Using Dietary and Urinary Iodine: Ji Yeon Choi, Joon-Hyop Lee, YoonJu Song; Endocrinol Metab. 2021;36(3):607-618. Published online June 21, 2021; DOI: https://doi.org/10.3803/EnM.2021.1005

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Background
Concerns have been raised regarding thyroid disorders caused by excessive iodine in Koreans, who have iodine-rich diets. This study evaluated iodine status using dietary iodine intake and urinary iodine in papillary thyroid cancer (PTC) patients.
Methods
Dietary data of PTC patients were assessed using a 24-hour recall and food frequency questionnaire (FFQ), and urinary iodine concentrations (UICs) were also obtained. To compare the iodine status of PTC patients, Korean adults with or without thyroid disease from the Korea National Health and Nutrition Examination Survey, which had 24-hour recall data and urinary iodine measurements, were analyzed.
Results
The median daily iodine intake by 24-hour recall was 341.7 μg/day in PTC patients, similar to the levels of other Korean adults. Based on UICs, the prevalence of excessive iodine was 54.4% in PTC patients, which was similar to the prevalence among subjects with thyroid disease (55.4%) but slightly higher than that in subjects without thyroid disease (47.7%). Based on dietary iodine by 24-hour recall, the prevalence of excessive iodine intake was 7.2%, which was higher than that among subjects with (4.4%) or without (3.9%) thyroid disease. The dietary iodine intake based on 24-hour recall was closely correlated with the UIC (r=0.4826) in PTC patients, but dietary iodine by FFQ was not significantly correlated with either 24-hour recall or UIC-based dietary iodine.
Conclusion
Excessive iodine intake was more common in PTC patients than in subjects without thyroid disease. Further longitudinal research is necessary to elucidate the role of dietary iodine in PTC.

Citations

Citations to this article as recorded by

Dietary and Urinary Iodine in Relation to Thyroid Cancer Risk: A Meta-Analysis
Shitao Li, Hengxu Yu
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Bach Viet HOANG, Thuy Thi TRAN, Anh Tran Mai LE, Tien Thi Hong NGUYEN, Dung Thi NGUYEN, Huong Thi LE
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Yasmin G. Nagashima, Aline A. Soares, Grasiela Piuvezam, Camila X. Alves, Kleyton S. Medeiros, José Brandão‐Neto, Márcia M. G. D. Lopes
Journal of Human Nutrition and Dietetics.2026;[Epub] CrossRef
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Dorothy Bundi, Peter Chege, Regina Kamuhu
International Journal of Nutrition and Food Sciences.2024; 13(5): 209. CrossRef
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Hengqiang Zhao, Jin Hu, Le Cui, Yiping Gong, Tao Huang
Frontiers in Endocrinology.2023;[Epub] CrossRef
Effect of iodine restriction on short-term changes in thyroid function in patients with subclinical hypothyroidism
Obin Kwon, Dong Yeob Shin, Eun Jig Lee
Journal of Nutrition and Health.2022; 55(2): 250. CrossRef
Iodine nutrition and papillary thyroid cancer
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Frontiers in Nutrition.2022;[Epub] CrossRef

Thyroid
Effect of Cigarette Smoking on Thyroid Cancer: Meta-Analysis: Joon-Hyop Lee, Young Jun Chai, Ka Hee Yi; Endocrinol Metab. 2021;36(3):590-598. Published online May 26, 2021; DOI: https://doi.org/10.3803/EnM.2021.954

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Abstract PDF Supplementary Material PubReader ePub

Background
Although smoking is generally carcinogenic, its effect on thyroid cancers is still subject to controversy. The purpose of this study was to summarize the role of smoking in relation to thyroid cancer occurrence.
Methods
We performed a meta-analysis of 24 eligible studies: 21 case-control studies and three prospective cohort studies. The summary odds ratio (OR) and 95% confidence interval (CI) of all studies were acquired based on random effect model. Further subgroup analyses were conducted according to gender, histological type of thyroid cancer, and smoking status of patients for the case-control studies.
Results
The summary effect size indicated a negative association of smoking for thyroid cancer (OR, 0.798; 95% CI, 0.681 to 0.935). From the subgroup analyses for the case-control studies, reduced risk of thyroid cancer was observed in both men (OR, 0.734; 95% CI, 0.553 to 0.974) and women (OR, 0.792; 95% CI, 0.700 to 0.897). The protective effect of smoking was observed in studies in which thyroid cancer was limited to differentiated thyroid cancers (DTCs) (OR, 0.798; 95% CI, 0.706 to 0.902).
Conclusion
Our results suggests that smoking may have a protective effect on thyroid cancer, especially on DTCs. Further studies with larger sample sizes should be conducted in elucidating the dose and time dependent effect of smoking on thyroid cancer with specific focus on the types of thyroid cancers.

Citations

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Review Article

Miscellaneous
Rare PTH Gene Mutations Causing Parathyroid Disorders: A Review: Joon-Hyop Lee, Munkhtugs Davaatseren, Sihoon Lee; Endocrinol Metab. 2020;35(1):64-70. Published online March 19, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.1.64

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Abstract PDF PubReader ePub

Since parathyroid hormone (PTH) was first isolated and its gene (PTH) was sequenced, only eight PTH mutations have been discovered. The C18R mutation in PTH, discovered in 1990, was the first to be reported. This autosomal dominant mutation induces endoplasmic reticulum stress and subsequent apoptosis in parathyroid cells. The next mutation, which was reported in 1992, is associated with exon skipping. The substitution of G with C in the first nucleotide of the second intron results in the exclusion of the second exon; since this exon includes the initiation codon, translation initiation is prevented. An S23P mutation and an S23X mutation at the same residue were reported in 1999 and 2012, respectively. Both mutations resulted in hypoparathyroidism. In 2008, a somatic R83X mutation was detected in a parathyroid adenoma tissue sample collected from a patient with hyperparathyroidism. In 2013, a heterozygous p.Met1_Asp6del mutation was incidentally discovered in a case-control study. Two years later, the R56C mutation was reported; this is the only reported hypoparathyroidism-causing mutation in the mature bioactive part of PTH. In 2017, another heterozygous mutation, M14K, was detected. The discovery of these eight mutations in the PTH gene has provided insights into its function and broadened our understanding of the molecular mechanisms underlying mutation progression. Further attempts to detect other such mutations will help elucidate the functions of PTH in a more sophisticated manner.

Citations

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