Skip Navigation
Skip to contents

Endocrinol Metab : Endocrinology and Metabolism

clarivate
OPEN ACCESS
SEARCH
Search

Author index

Page Path
HOME > BROWSE ARTICLES > Author index
Search
Soo Kee Min  (Min SK) 2 Articles
A Case of Hashimoto's Thyroiditis with Transient T3-Thyrotoxicosis Induced by Hydatidiform Mole.
Ji Youn Yoo, Hong Ju Moon, Cheol Young Park, Seong Jin Lee, In Kyung Jeong, Eun Gyung Hong, Gi Weon Oh, Hyeon Kyu Kim, Doo Men Kim, Jae Myung Yoo, Sung Hee Ihm, Moon Gi Choi, Hyung Joon Yoo, Sung Woo Park, Soo Kee Min
J Korean Endocr Soc. 2005;20(3):294-298.   Published online June 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.3.294
  • 1,923 View
  • 19 Download
  • 1 Crossref
AbstractAbstract PDF
Human chorionic gonadotropin(HCG) is a member of the glycoproteins family synthesized by the placenta, which consists of 2 noncovalently joined subunits(alpha(alpha) and beta(beta)). The alpha- and beta-subunits have a structural homology with the alpha- and beta-subunits of TSH and LH. The thyrotropic action of HCG results from its structural similarity to TSH, so beta-HCG can bind to the TSH receptor in the thyroid gland. A high level of HCG accompanied by an increased thyroid hormone level, can be observed in gestational trophoblastic disease (GTD), such as a hydatidiform mole or a choriocarcinoma, but the clinical symptoms of hyperthyroidism are rarely observed. We experienced a case of Hashimoto's thyroiditis, where the patient was diagnosed with T3-thyrotoxicosis, which had initially been induced by excess beta-HCG due to an H-mole; after evacuation of the H-mole, the condition was diagnosed as hypothyroidism. It has been speculated that a patient with Hashimoto's thyroiditis could have hyperthyroidism, induced by beta-HCG, due to an H-mole

Citations

Citations to this article as recorded by  
  • Transient T3 toxicosis associated with Hashimoto’s disease
    Sarah Jaroudi, Meredith Gavin, Kathryn Boylan, Alan N. Peiris
    Baylor University Medical Center Proceedings.2019; 32(1): 80.     CrossRef
Close layer
A Case of Apical Hypertrohic Cardiomyopathy Associated with Pheochromocytoma.
Joon Ho Moon, Sung Woo Park, Sung Hee Ihm, Cheol Young Park, Ki Won Oh, Cheol Soo Choi, Seong Jin Lee, In Kyung Jung, Eun Gyung Hong, Hyeon Kyu Kim, Doo Man Kim, Jae Myung Yoo, Moon Gi Choi, Hyung Joon Yoo, So Young Ku, Soo Kee Min
J Korean Endocr Soc. 2004;19(5):522-527.   Published online October 1, 2004
  • 1,134 View
  • 18 Download
AbstractAbstract PDF
Pheochromocytomas often present with cardiovascular manifestations, such as arrhythmia, angina pectoris and acute myocardial infarction and so on. Both dilated and nonobstructive hypertrophic cardiomyopathies are also rare complications of pheochromocytomas. In hypertrophic cardiomyopathy, an apical variant form constitutes about 25% of cases in Japan, but only 1 to 2% of those in non-Japanese populations, including Korea. The cause of apical hypertrophic cardiomyopathy (AHC) remains unknown. Recently, some cases of AHC associated with pheochromocytomas have been reported, with catecholamine thought to be an important cause. AHC associated with a pheochromocytoma has never been previously reported in Korea. Herein is reported our experience of a case of apical hypertrophic cardiomyopathy associated a pheochromocytoma with a review of the literature
Close layer

Endocrinol Metab : Endocrinology and Metabolism