- Retraction: Expression of RET in Thyroid Diseases of a Korean Population.
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Si Hoon Lee, Soon Won Hong, Woo Chul Moon, Myoung Ryur Oh, Jin Kyung Lee, Bong Soo Cha, Chul Woo Ahn, Kyung Rae Kim, Sung Kil Lim, Hyun Chul Lee
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J Korean Endocr Soc. 2008;23(1):70. Published online February 1, 2008
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- Management Guidelines for Patients with Thyroid Nodules and Thyroid Cancer.
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Won Bae Kim, Tae Yong Kim, Hyuk Sang Kwon, Won Jin Moon, Jae Bok Lee, Young Sik Choi, Seok Ki Kim, Sun Wook Kim, Ki wook Chung, Jung Hwan Baek, Byung Il Kim, Do Joon Park, Dong Gyu Na, Jun Ho Choe, Jae Hoon Chung, Hye Seung Jung, Jeong Han Kim, Kee Hyun Nam, Hang Seok Chang, Woong Youn Chung, Soon Won Hong, Suck Joon Hong, Jeong Hyun Lee, Ka Hee Yi, Young Suk Jo, Ho Cheol Kang, Minho Shong, Jin Woo Park, Jong Ho Yoon, Seong Joon Kang, Kwang Woo Lee
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J Korean Endocr Soc. 2007;22(3):157-187. Published online June 1, 2007
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DOI: https://doi.org/10.3803/jkes.2007.22.3.157
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3,412
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- No abstract available.
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So Won Oh, Sohyun Park, Ari Chong, Keunyoung Kim, Ji-In Bang, Youngduk Seo, Chae Moon Hong, Sang-Woo Lee Nuclear Medicine and Molecular Imaging.2024;[Epub] CrossRef - Nuclear Medicine Imaging in Differentiated Thyroid Cancer: Summary of the Korean Thyroid Association Guidelines 2024 from Nuclear Medicine Perspective, Part-I
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Eun Kyung Lee International Journal of Thyroidology.2024; 17(2): 259. CrossRef - 2023 Korean Thyroid Association Management Guidelines for Patients with Thyroid Nodules
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Young Joo Park, Young Shin Song, Ka Hee Yi International Journal of Thyroidology.2018; 11(1): 1. CrossRef - Decreasing Disease-Specific Mortality of Differentiated Thyroid Cancer in Korea: A Multicenter Cohort Study
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Yun Mi Choi, Won Gu Kim, Hyemi Kwon, Min Ji Jeon, Minkyu Han, Tae Yong Kim, Young Kee Shong, Sang Mo Hong, Eun‐Gyoung Hong, Won Bae Kim Cancer.2017; 123(24): 4808. CrossRef - Surgical Treatment Guidelines for Patients with Differentiated Thyroid Cancer: The Korean Association of Thyroid and Endocrine Surgeons (KATES) Guidelines Taskforce
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Byung Il Kim Journal of Korean Medical Science.2016; 31(Suppl 1): S59. CrossRef - 2016 Revised Korean Thyroid Association Management Guidelines for Patients with Thyroid Nodules and Thyroid Cancer
Ka Hee Yi, Eun Kyung Lee, Ho-Cheol Kang, Yunwoo Koh, Sun Wook Kim, In Joo Kim, Dong Gyu Na, Kee-Hyun Nam, So Yeon Park, Jin Woo Park, Sang Kyun Bae, Seung-Kuk Baek, Jung Hwan Baek, Byung-Joo Lee, Ki-Wook Chung, Yuh-Seog Jung, Gi Jeong Cheon, Won Bae Kim, International Journal of Thyroidology.2016; 9(2): 59. CrossRef - Sonographic Index for Extrathyroidal Extension of Papillary Thyroid Carcinoma
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- Reversible Pituitary Dysfunction in a Patient with Cushing's Syndrome due to Adrenal Adenoma.
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Jee Hyun Kong, Kyung Wook Kim, Hei Jin Kim, Ji Sun Nam, Jin A Park, Jong Sook Park, Chul Sik Kim, Byung Soo Moon, Soon Won Hong, Chul Woo Ahn, Kyung Rae Kim
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J Korean Endocr Soc. 2006;21(2):146-152. Published online April 1, 2006
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DOI: https://doi.org/10.3803/jkes.2006.21.2.146
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- A 45-year-old woman who complained of weight gain and irregular menstruation was diagnosed as having Cushing's syndrome due to a 3 cm sized left adrenal adenoma. She underwent left adrenalectomy, and she also underwent combined anterior pituitary tests before and 9 months after the surgery. The growth hormone and adrenocorticotropic hormone levels failed to respond to hypoglycemia before the surgery, but their responses recovered after the surgery. Cortisol and thyroid stimulating hormone failed to respond to hypoglycemia and thyrotropin releasing hormone (TRH) before the surgery, respectively, but these were improved after the surgery. Luteinizing hormone, follicle stimulating hormone, and prolactin adequately responded to gonadotropin-releasing hormone and TRH, respectively, before and after the surgery. However, the basal levels of these hormones were higher after adrenalectomy, suggesting that hypercortisolemia had a significant influence on all the pituitary hormones.
- A Case of Multiple Endocrine Neoplasia Type 1 with Papillary Thyroid Carcinoma.
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Hai Jin Kim, Chul Sik Kim, Hyun Chul Je, Jina Park, Jong Suk Park, Jee Hyun Kong, Eun Seok Kang, Chul Woo Ahn, Bong Soo Cha, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Hang Suk Jang, Soon Won Hong
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J Korean Endocr Soc. 2006;21(1):79-84. Published online February 1, 2006
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DOI: https://doi.org/10.3803/jkes.2006.21.1.79
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2,076
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- This is the first report of papillary thyroid carcinoma combined with multiple endocrine neoplasia type 1 (MEN 1). It is an hereditary syndrome characterized by neoplastic disorders such as pituitary adenoma, parathyroid adenoma or hyperplasia and pancreatic neuroendocrine tumor, such as gastrinoma just like in our case. But sometimes pheochromocytoma, mucosal ganglioneuromas, lipoma, forgut carcinoid and thyroid disease could be accompany the disease, but coincidental papillary thyroid carcinoma was never reported before in Korea. Herein we represent a 39-year-old woman who manifested typical features of MEN 1 with coincidental papillary thyroid carcinoma. Despite with definite family history of MEN 1, her genetic analysis of DNA had not found any germline mutation in MEN 1 gene. Unidentified culprit gene unable further genetic study of finding LOH (loss of heterogeneity) in 11q13, the possible explanation of papillary thyroid carcinoma as a new component of MEN 1. As we have experienced a case of MEN 1 combined with papillary thyroid carcinoma, we report it with the review of literature.
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- A Case of Multiple Endocrine Neoplasia Type I with Atypical Clinical Course
Yun Sun Choi, Youn Sun Bai, Bon Jeong Ku, Young Suk Jo, Young Kun Kim, Heung Kyu Ro, Minho Shong Journal of Korean Endocrine Society.2008; 23(4): 266. CrossRef
- A Case of Acromegaly Caused by Double Pituitary Adenomas.
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Hai Jin Kim, Chul Sik Kim, Jong Suk Park, Jina Park, Jee Hyun Kong, Ji Sun Nam, Chul Woo Ahn, Bong Soo Cha, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Soon Won Hong
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J Korean Endocr Soc. 2006;21(1):53-57. Published online February 1, 2006
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DOI: https://doi.org/10.3803/jkes.2006.21.1.53
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- Acromegaly is a clinical syndrome, which is caused by an excess of growth hormone (GH), most commonly secreted from a pituitary solitary adenoma. However, our patient had bilateral GH-secreting pituitary tumors, the incidence of which has been reported in only 1.3 to 1.69% of all acromegalic patients. A 59-year-old female, with no family history of pituitary adenomas, demonstrated an increased level of serum insulin-like growth factor-1 (IGF-1), and GH not suppressed after 75 g oral glucose loading. On a preoperative MRI, only one pituitary tumor, measuring 1.1 x 0.7 cm, could be observed using sellar MRI. After surgical resection of the tumor, her headache and myalgia were sustained, and the IGF-1 level was still in a high titer. Therefore, a follow-up sellar MRI was taken, and a 0.6 x 0.7 cm sized newly growing pituitary tumor was found on the other side. With a retrospective review of radiological examinations, the patient was found to have bilateral tumors. The 0.3 cm sized tumor on the left was too small to be detected on the preoperative MRI. As the patient preferred medical treatment after surgery, she was treated with sandostatin analogues. Acromegaly with bilateral GH-secreting pituitary tumors, is a very rare disease, with no previous case having been reported in Korea. Herein, we report the case with a review of the literature.
- A Case of Follicular Thyroid Carcinoma Developed in Pendred Syndrome.
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So Hun Kim, Ji Young Jung, Sung Jae Shin, So Young Park, Si Hoon Lee, Yoo Mee Kim, Yu Mie Rhee, Soon Won Hong, Bong Soo Cha, Chul Woo Ahn, Kyung Rae Kim, Sung Kil Lim, Hyun Chul Lee
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J Korean Endocr Soc. 2004;19(4):411-418. Published online August 1, 2004
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- Pendred syndrome is an autosomal recessive genetic disorder, which is characterized by sensorineural hearing loss, goiter and a positive perchlorate discharge test. It is caused by mutations of the PDS gene, and its clinical characteristics vary widely. The thyroid function in most cases is normal, or shows only mild hypothyroidism. In Pendred syndrome, there is an organification defect that leads to defective thyroid hormone synthesis, followed by chronic TSH stimulation. Herein is reported a case of a follicular thyroid carcinoma associated with Pendred syndrome. To our knowledge, this is the first case reported in Korea. The patient presented with a huge anterior neck mass, sensorineural hearing loss and a positive perchlorate discharge test. Fine needle aspiration cytology suggested malignancy of the thyroid, and a total thyroidectomy, with central compartment node dissection, was performed. The pathology from the thyroid mass showed a poorly differentiated follicular thyroid carcinoma
- Expression of RET in Thyroid Diseases of a Korean Population.
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Si Hoon Lee, Soon Won Hong, Woo Chul Moon, Myoung Ryur Oh, Jin Kyung Lee, Bong Soo Cha, Chul Woo Ahn, Kyung Rae Kim, Sung Kil Lim, Hyun Chul Lee
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J Korean Endocr Soc. 2003;18(2):140-152. Published online April 1, 2003
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- BACKGROUND
Activation of the RET proto-oncogene, located on the long arms of chromosome 10, contributes to the development of thyroid cancers in two different ways. Somatic rearrangements of RET with variable genes of activation are frequently found in papillary thyroid carcinomas. And Ggerm-line point mutations are responsible for the development of medullary thyroid carcinoma and the multiple endocrine neoplasia type 2(MEN2). There are several conflicting reports on the influences of RET expression and RET/PTC rearrangements on the clinical outcome of thyroid cancer. Therefore, we performed an examination of RET expression and RET/PTC-1, -2, -3 rearrangements in papillary thyroid carcinomas and other thyroid diseases. METHODS: Twenty-six papillary thyroid carcinomas(PTCs), three follicular thyroid carcinomas (FTCs), one anaplastic thyroid carcinoma(ATC), five follicular adenomas(FAs), nineteen hyperplasias, and two normal thyroid tissues were included in this study. RT-PCR and immunohistochemistry analysis were done to identify RET gene, RET/PTC rearrangements, and ret RET protein expression. RESULTS: By RT-PCR, 89.4% of PTCs, 100% of FTCs, and 62.1% of hyperplasias expressed the RET gene, but no RET was observed in ATCs, FAs, and normal thyroid tissues. RET/PTC-1, -2,-3 rearrangements were not detected in any specimens. Immunohistochemical results revealed that 76.9% of PTCs, 50% of FAs, 52.3% of hyperplasias, and 20.6% of normal thyroid tissues expressed the RET ret protein, but FTCs and ATCs did not. Most PTCs showed strong cytoplasmic positivity in RET ret immunostaining, but the positive non- PTCs expressed weak and membranous staining. Overall, the two methods for detecting RET gene, RT-PCR and immunohistochemistry showed similar results. CONCLUSION: The RET gene was highly expressed in PTCs. In contrast to the previous reports of that theRET gene expression of RET gene is being limited to PTCs, RET was also expressed in hyperplasias, Fas, and normal thyroid tissues. However, the pattern and the degree of expression of the RET ret protein in non- PTCs were are different from those in PTCs.
- A Case of Osteosarcoma induced Oncogenic Osteomalacia Detected by MRI.
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Sung Kil Lim, Young Duk Song, Hyun Chul Lee, Kap Bum Huh, Ki Hyun Park, Kyung Rae Kim, Soon Won Hong, Jae Hyun Nam, Jong In Yook, Byung Joo Choi, Mi Kyung Kim, Kyu Ho Shin
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J Korean Endocr Soc. 1999;14(2):401-409. Published online January 1, 2001
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- Oncogenic osteomalacia is a syndrome characterized by phosphaturia, hypophosphatemia, decreased 1,25-dihydroxyvitamin D level and specific signs and symptoms of osteomalacia. It is associated with the presence of neoplasm originated from mesenchyme. Until now, less than 100 cases of oncogenic osteomalacia have been reported. The pathophysiology of oncogenic osteomalacia has not been fully understood, but it has been suggested that a certain substance released by tumor may inhibit not only la-hydroxylase activity and reduce 1,25-dihydroxyvitamin D level in part, but directly inhibit reabsorption of phosphate. And then, reduced phosphaturia, hypophosphatemia and eventually osteomalacia develop. We report a case of osteosarcoma induced oncogenic osteomalacia detected by MRI in 59 year old woman.
- Two Cases of Aplastic Anemia Following Propylthiouracil.
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Hong Seung Kim, Choon Hee Chung, Hee Sun Kim, Mi Duk Lee, Young Hak Shim, Soon Won Hong
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J Korean Endocr Soc. 1998;13(2):258-263. Published online January 1, 2001
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- Aplastic anemia is characterized by a failure of blood cell production resulting in varying degrees of pancytopenia with a markedly hypocellular bone marrow. Most cases of aplastic anemia are acquired, but the disease may also occur as the result of inherited abnormalities. In 50-65% of cases, however, the etiology is unknown. For acquired forms of aplastic anemia, a variety of causative factors, including radiation, viruses, chemicals and drugs, have been implicated. Antithyroid drugs(Carbimazole, Methimazole, Propylthiouracil) are usually listed among agents associated with the development of agranulocytosis, but aplastic anemia rarely follows their use. The first case of aplastic anemia followmg propylthiouracil was reported by Marte~lo et al. in 1967 and the second case was by Aksoy and Erdem in 1968. Recently, we experienced two cases of aplastic anemia following propylthiouracil therapy due to Graves disease, so we report here these cases with literature review.
- A Case of Giant Adrenal Adenoma Presenting Primary Aldosteronism.
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Ji Hyun Lee, Bong Soo Cha, Moon Suk Nam, Young Duk Song, Sung Kil Lim, Hyun Chul Lee, Kap Bum Huh, Hyung Chan Suh, Young Hwa Choi, Jae Min Park, Jung Soo Park, Soon Won Hong, Dong Hwan Shin
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J Korean Endocr Soc. 1996;11(3):348-354. Published online November 7, 2019
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- Primary aldosteronism is a syndrome chracterized by hypokalemic alkalosis and hypertension. Small sized adrenal cortical adenomas have been the major cause of this syndrome in most of the patients. However, if the adrenal mass is larger than 6cm in diameter and with irregular consistency, malignancy is more favored. We experienced a patient who had a giant adrenal adenoma with primary aldosteronism. A 24-year-old female presented with hypertension, hypokalemia, low plasma renin, and high plasrna aldosterone levels, was found to have a 6×5.5×5 cm sized left adrenal tumor by MRI. Her clinical laboratory feature did not revealed any evidence of Cushing's syndrome or pheochromocytoma. Preoperatively adrenal carcinoma presenting pure adrenal aldosteronism was suspected due to large size and heterogenous signal character of the adrenal mass in radiologic study. At operation well encapsulated, round giant adrenal tumor weighing 65gm(4.5×4×4 cm) was removed. There was no evidence of metastasis with return of adrenal function to normal after surgery. Benign adrenal adenoma was confirmed by the gross morphology and the histologic features.
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