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
Hyun Joo Lee  (Lee HJ) 7 Articles
Retraction: Contributing Factors to Different Natural Courses of Posttansplantation Diabetes Mellitus in Renal Allograft Recipients.
Kyu Yeon Hur, Myoung Soo Kim, Jae Hyun Nam, Eun Seok Kang, Hyun Joo Lee, So Hun Kim, Bong Soo Cha, Chul Woo Ahn, Soon Il Kim, Yu Seun Kim, Hyun Chul Lee
J Korean Endocr Soc. 2007;22(6):479.   Published online December 1, 2007
DOI: https://doi.org/10.3803/jkes.2007.22.6.479
  • 1,521 View
  • 21 Download
PDF
Close layer
Contributing Factors to Different Natural Courses of Posttansplantation Diabetes Mellitus in Renal Allograft Recipients.
Kyu Yeon Hur, Myoung Soo Kim, Jae Hyun Nam, Eun Seok Kang, Hyun Joo Lee, So Hun Kim, Bong Soo Cha, Chul Woo Ahn, Soon Il Kim, Yu Seun Kim, Hyun Chul Lee
J Korean Endocr Soc. 2006;21(5):373-381.   Published online October 1, 2006
DOI: https://doi.org/10.3803/jkes.2006.21.5.373
  • 1,998 View
  • 22 Download
  • 2 Crossref
AbstractAbstract PDF
BACKGROUND
New onset diabetes is a major complication after kidney transplantation. However, the natural course of posttransplantation diabetes mellitus (PTDM) remains unclear. The aim of this study was to demonstrate the detailed natural courses of PTDM according to the onset and persistency of hyperglycemia, and to investigate risk factors for development of different courses of PTDM in renal allograft recipients. METHODS: A total of 77 renal allograft recipients without previously known diabetes were enrolled and performed a serial 75 g oral glucose tolerance test at 0, 1, and 7 years after kidney transplantation. Patients were classified according to the onset and persistency of PTDM: early PTMD (E-PTDM), late PTDM (L-PTDM), persistent PTDM (P-PTDM), transient PTMD (T-PTDM), and non-PTDN (N-PTDM). RESULTS: The incidence of each group was as follows: E-PTDM, 39%; L-PTDM, 11.7%; P-PTDM, 23.4% T-PTDM, 15.6%; N-PTDM, 49.3%. Tacrolimus and female gender were associated with the development of E-PTDM. Among E-PTDM, age at transplantation was a high risk factor for the development of P-PTDM. Higher BMI at year1 was associated with the development of L-PTDM. CONCLUSION: Different risk factors were associated with various natural courses of PTDM. Since old age and female gender are not modifiable risk factors, it may be important to modify immunosuppressive therapy regimens for the prevention of E-PTDM and control of body weight for L-PTDM.

Citations

Citations to this article as recorded by  
  • Efficacy and Safety of Gemigliptin in Post-Transplant Patients With Type 2 Diabetes Mellitus
    Jaehyun Bae, Youjin Kim, Yongin Cho, Minyoung Lee, Ji-Yeon Lee, Yong-ho Lee, Byung-Wan Lee, Bong-Soo Cha, Dong Jin Joo, Kyu Ha Huh, Myoung Soo Kim, Yu Seun Kim, Eun Seok Kang
    Transplantation Proceedings.2019; 51(10): 3444.     CrossRef
  • Post-transplantation Diabetes Mellitus
    Kun-Ho Yoon
    Journal of Korean Endocrine Society.2006; 21(5): 370.     CrossRef
Close layer
A Case of Multiple Endocrine Neoplasia Type 1 with Mutation in MENIN Gene.
Se Eun Park, Eun Seok Kang, Hyun Joo Lee, So Hun Kim, Mi Young Do, Shin Ae Kang, Seung Jin Han, Hyeong Jin Kim, Chul Woo Ahn, Bong Soo Cha, Sung Kil Lim, Kyung Rae Kim, Il Jin Kim, Hyun Chul Lee
J Korean Endocr Soc. 2005;20(1):71-77.   Published online February 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.1.71
  • 2,041 View
  • 22 Download
  • 6 Crossref
AbstractAbstract PDF
Multiple endocrine neoplasia type 1(MEN 1) is an autosomal dominantly inherited syndrome, characterized by the combined occurrence of tumors of the parathyroid glands, endocrine pancreas, and anterior pituitary gland. The MENIN gene, which is a kind of tumor suppressor gene, is located at the chromosomal locus 11q13. It consists of one untranslated exon and nine exons encoding the menin protein. We report a case of a 22-yearss-old woman with MEN type 1, who was proven to have a mutation in the MENIN gene. The patient was admitted because of repeated hypoglycemia. The fasting plasma glucose level was 32mg/dL. Seventy two hours fasting test showed an the insulin/glucose ratio as 0.33. Endoscopic ultrasonography detected multiple masses on the pancreas. The arterial -stimulated venous sampling(ASVS) with calcium showed sudden step up of insulin at the head and tail portions of the pancreas. The sellar MRI showed a pituitary mass that produced prolactin. Instead of a pathologic diagnosis from operational specimen, the genetic analysis revealed a mutation in the MENIN 1 gene(exon 2, 200~201insAGCCC).

Citations

Citations to this article as recorded by  
  • Genetic and Epigenetic Analysis in Korean Patients with Multiple Endocrine Neoplasia Type 1
    Yoon Jung Chung, Sena Hwang, Jong Ju Jeong, Sun Yong Song, Se Hoon Kim, Yumie Rhee
    Endocrinology and Metabolism.2014; 29(3): 270.     CrossRef
  • A Case of Familial Multiple Endocrine Neoplasia Type 1 with a Novel Mutation in theMEN1Gene
    Min Jung Kim, Eun Hee Kim, Mi-Seon Shin, Joo Hui Kim, Hee Kyung Na, Seong Joon Park, Sang Ah Lee, Eun Hee Koh, Woo Je Lee, Ki Ho Song, Joong-Yeol Park, Ki-Up Lee, Gu-Hwan Kim, Han-Wook Yoo, Min-Seon Kim
    Endocrinology and Metabolism.2011; 26(2): 171.     CrossRef
  • Somatic Mutational Analysis of MEN1 and Phenotypic Correlation in Sporadic Parathyroid Tumors
    Young Su Chae, Hee Jin Kim, Sun Wook Kim, Myung-Chul Chang
    Journal of the Korean Surgical Society.2009; 76(1): 15.     CrossRef
  • Multiple Endocrine Neoplasia Type 1 with Multiple Leiomyomas Linked to a Novel Mutation in the MEN1 Gene
    Heekyoung Choi, Sehyun Kim, Jae-Hoon Moon, Yoon Hee Lee, Yumie Rhee, Eun Seok Kang, Chul Woo Ahn, Bong Soo Cha, Eun Jig Lee, Kyung Rae Kim, Hyun Chul Lee, Seon Yong Jeong, Hyun Ju Kim, Sung-Kil Lim
    Yonsei Medical Journal.2008; 49(4): 655.     CrossRef
  • A Case of Familial Multiple Endocrine Neoplasia Type 1 with MEN1 Gene Mutation
    Young Eun Jo, Yong-Jun Choi, Yun Kyung Kim, Sang Mi Ahn, Sun Hye Jung, Hae Jin Kim, Dae Jung Kim, Kwan Woo Lee, Ji-Hee Hong, Seon-Yong Jeong, Hyon J Kim, Yoon-Sok Chung
    Journal of Korean Endocrine Society.2007; 22(1): 68.     CrossRef
  • A Case of Familial Multiple Endocrine Neoplasia with MEN1 Gene Mutation
    Hye-Young Sung, Yeon-Joo Chun, Hyeug Lee, Bum Jun Kwon, Kun Woo Park, Jung Min Lee, Sung Dae Moon, Sang Ah Chang, Je-Ho Han
    Journal of Korean Endocrine Society.2006; 21(6): 560.     CrossRef
Close layer
Adiponectin Gene Polymorphism and Carotid Artery Intima-Media thickness in Type 2 Diabetes.
Eun Seok Kang, So Young Park, So Hun Kim, Hyun Joo Lee, Kyu Yeon Hur, Seung Jin Han, Se Eun Park, Hyeong Jin Kim, Chul Woo Ahn, Bong Soo Cha, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee
J Korean Endocr Soc. 2005;20(1):29-39.   Published online February 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.1.29
  • 1,779 View
  • 18 Download
AbstractAbstract PDF
BACKGROUND
The aim of this study was to examine the association between the common polymorphisms of the adiponectin gene(ACDC) and the intima-media thickness(IMT) of the common carotid arteries in type 2 diabetic patients. METHODS: The B mode ultrasound examination of carotid artery was performed on 133 type 2 diabetic patients. The carotid IMT was calculated using the Intimascope computer program. The SNP45 and SNP276 of the ACDC were examined. RESULTS: There was no significant difference in the carotid IMT among the SNP45 genotypes(0.66+/-0.18mm for TT, 0.71+/-0.12mm for TG and 0.64+/-0.15mm for GG, P=NS). Subjects carrying the SNP276 GG genotype had a markedly lower serum adiponectin concentration than those carrying the TT genotype(3.35+/-2.00microgram/mL vs. 4.98+/-2.24microgram/mL, P=0.029) The carotid IMT was significantly higher in patients with the SNP276 GG genotype than those with the TT genotype (0.70+/-0.17mm vs. 0.59+/-0.13mm, P=0.032). Patients with the +45GG/+276GG genotype combination showed significantly higher mean carotid IMT than the other genotype combinations(0.78+/-0.09mm vs. 0.71+/-0.15mm, P=0.013) CONCLUSIONS: These results suggest that the adiponectin gene, SNP276 is associated with the carotid IMT in type 2 diabetic patients. Further studies are will be needed to confirm these genotypephenotype associations.
Close layer
A Case of Thyroid Papillary Cancer Associated with Familial Adenomatous Polyposis.
Sung Jae Shin, Hyun Joo Lee, So Hun Kim, Wan Sub Shim, Sihoon Lee, Yoo Mee Kim, Yumie Rhee, Tae Il Kim, Bong Soo Cha, Hyun Chul Lee, Sung Kil Lim
J Korean Endocr Soc. 2004;19(2):209-216.   Published online April 1, 2004
  • 1,042 View
  • 19 Download
AbstractAbstract PDF
Familial adenomatous polyposis (FAP) is an autosomal dominant syndrome, typically characterized by multiple colorectal adenomas and increased incidence of colorectal carcinomas if left untreated. It is caused by germline mutations of the adenomatous polyposis coli (APC) gene, which has been mapped on chromosome 5q21, and is accompanied by various benign and malignant extracolonic manifestations. The prevalence of thyroid tumors developing in patients with FAP is about 1~2%, are associated with FAP and have certain characteristics; mean age of tumor diagnosis at less than 30 years of age, the pathology is the papillary histiotype in more than 90% of cases, including a so-called cribriform- morular pattern, and multifocality is a frequent feature. In a genetic analysis, thyroid cancer in FAP usually has a mutation in the 5-portion of exon 15 between 778 and 1309, on chromosome 5q21. Also, the ret/PTC (especially ret/PTC1 and ret/PTC3) and p53 genes are thought probably to be associated with thyroid cancer in FAP patients. A case of familial adenomatous polyposis, accompanied by thyroid papillary cancer, was experienced in a 29 year-old female. She had hundreds of adenomas throughout the entire colon and congenital hypertrophy of the retinal pigment epithelium (CHRPE). The pathological finding of thyroid cancer was revealed as a mixture of cribriform, trabecular and papillary patterns. In a genetic analysis, she and her brother had a germline mutation of the APC gene at codon 1309. In Korea, there has been no previous case of cribriform-morular pattern and familial genetic analysis in FAP associated with thyroid cancer. Therefore, this case is reported, with a review of the literature
Close layer
A Case of Adrenal Cortical Carcinoma with Liver Metastasis.
Hyun Joo Lee, Myung Soo Kim, Hyo Kyoung Park, Dae Jung Kim, Yu Mie Rhee, Chul Woo Ahn, Jae Hyun Nam, Bong Soo Cha, Young Duk Song, Sang Won Han, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh
J Korean Endocr Soc. 2003;18(2):232-238.   Published online April 1, 2003
  • 1,371 View
  • 19 Download
AbstractAbstract PDF
An adrenal cortical carcinoma is a rare malignancy associated with poor prognosis. On diagnosis, most patients present with large tumor masses, which are often detected at an advanced stage. The most effective treatment is a complete resection, which is the only curative treatment for adrenal cortical carcinomas. The most important prognostic factor is a successful resection of the primary tumor, as long as it is low-grade and has not spread to distant sites. However, with advanced adrenal cortical carcinomas, with distant metastasis, there is no strict effective treatment program, and the prognosis is poor. The case of a 50-year-old female patient, presenting with an adrenal cortical carcinoma and Cushing's syndrome, who had a long-term survival of 78 months, is reported. The mass was completely resected on diagnosis, but 16 months later liver metastasis was discovered. She had received chemotherapy, with cisplatin, etoposide and bleomycin, for the liver metastasis for a period of 15 months, but with no response, furthermore, the size had increased after 10 months. Afterward, she received her 10th session of intrahepatic artery cisplatin chemotherapy and her 3rd hepatic artery embolization. Although the patient had a large degree of liver metastasis, this was tolerated. The tumor mass is presently not aggravated, and she still survives after 78 months.
Close layer
A Case of Klinefelter's Syndrome with Rathke's Cleft Cyst.
Hyun Joo Lee, Hyo Kyoung Park, Dae Jung Kim, Yu Mie Rhee, Chul Woo Ahn, Sang Soo Jung, Jae Hyun Nam, Bong Soo Cha, Young Duk Song, Sung Kil Lim, Kyung Rae Kim, Yong Koo Park, Hyun Chul Lee, Kap Bum Huh
J Korean Endocr Soc. 2002;17(4):564-571.   Published online August 1, 2002
  • 1,070 View
  • 23 Download
AbstractAbstract PDF
Klinefelter's syndrome is one of the most common forms of primary hypogonadism presenting with gynecomastia, azospermia and increased follicle-stimulating hormone. It is well known that this syndrome has an increased incidence of neoplasia, especially breast cancer and extragonadal germ cell tumors. However, it is rarely associated with an intracranial tumor of maldevelopmental origin, especially in the suprasellar area. We report, for the first time, a case of Klinefelter's syndrome, with a Rathke's cleft cyst is the patient was a 32-year-old male who was known to have an incidentaloma form brain computed tomography, which was clinically diagnosed as a suprasellar tumor. After operating, the suprasellar mass was confirmed as a Rathke's cleft cyst, and his hormonal abnormality, an elevated level of follicle-stimulating hormone, was not normalized. Therefore, we performed chromosomal analysis, and diagnosed Klinefelter's syndrome with the XXY karyotype.
Close layer

Endocrinol Metab : Endocrinology and Metabolism