Endocrinology and Metabolism

Je Ho Han (Han JH)

16 Articles

Endocrine Research
Functional Identification of Compound Heterozygous Mutations in the CYP17A1 Gene Resulting in Combined 17α-Hydroxylase/17,20-Lyase Deficiency: Eun Yeong Mo, Ji-young Lee, Su Yeon Kim, Min Ji Kim, Eun Sook Kim, Seungok Lee, Je Ho Han, Sung-dae Moon; Endocrinol Metab. 2018;33(3):413-422. Published online September 18, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.3.413

5,304 View
67 Download
2 Web of Science
2 Crossref

Background

We previously reported a patient with congenital adrenal hyperplasia (CAH) with compound heterozygous mutations in the cytochrome P450 17A1 (CYP17A1) gene. One allele had a p.His373Leu and the other a new p.Glu383fsX36 mutation. The aim of this study was to investigate the functional properties of a new allele present in a compound heterozygote of CYP17A1.

Methods

To understand how p.His373Leu and p.Glu383fsX36 affect P450c17 enzymatic activity, wild type and mutant CYP17A1 cDNAs were cloned into flag-tagged pcDNA3 vector and introduced into human embryonic kidney cells 293T (HEK293T) cells. Protein expression levels of CYP17A1 were then analyzed. And the activities of 17α-hydroxylase and 17,20-lyase of CYP17A1 were evaluated by measuring the conversion of progesterone to 17α-hydroxyprogesterone and of 17α-hydroxypregnenolone to dehydroepiandrosterone, respectively. In addition a computer model was used to create the three-dimensional structure of the mutant CYP17A1 enzymes.

Results

Production of the p.His373Leu mutant protein was significantly lower than that of the wild type protein, and the p.Glu383fsX36 protein was hardly produced. Similarly the enzymatic activity derived from the p.His373Leu mutant vector was significantly lower than that obtained from the wild type vector, and little activity was obtained from the p.Glu383fsX36 vector. Three-dimensional modeling of the enzyme showed that p.His373 was located in region important for heme-binding and proper folding. Neither the p.His373Leu nor the p.Glu383fsX36 mutant protein formed a heme-binding structure.

Conclusion

Enzyme activity measured in both mutants disappeared completely in both 17α-hydroxylase and 17,20-lyase. This result accounts for the clinical manifestations of the patient with the compound heterozygous CYP17A1 mutations.

Citations

Citations to this article as recorded by

A rare case of 17α-hydroxylase/17, 20-lyase deficiency: Clinical and genetic findings and follow-up outcomes
Li-Zhen Dai, Hong Ma, Jian-Fang Ke, Chen-Shi Lin, Yanling Huang, Yuan Tian, Danling Chen
Women's Health.2022;[Epub] CrossRef
Novel mutations of the CYP17A1 gene in four Chinese 46,XX cases with partial 17a-hydroxylase/17,20-lyase deficiency
Yanjie Xia, Panlai Shi, Junke Xia, Huijuan Zhang, Lijun Xu, Xiangdong Kong
Steroids.2021; 173: 108873. CrossRef

A Case of Ectopic Neurohypophysis Presenting with Hypogonadism.: In Woon Baek, Ji Hyun Kim, Guk Jin Lee, Kyoung Eun Lee, Hae Lim Lee, Hye Won Lee, Nam Yong Kim, Yon Kwon Ihn, Seung Hyun Ko, Seung Hwan Lee, Je Ho Han; Endocrinol Metab. 2011;26(1):67-71. Published online March 1, 2011; DOI: https://doi.org/10.3803/EnM.2011.26.1.67

2,735 View
27 Download
2 Crossref

Abstract PDF

Pituitary stalk interruption and ectopic neurohypophysis seen on magnetic resonance Imaging (MRI) are often associated with either isolated growth hormone (GH) deficiency or combined anterior pituitary hormone deficiency, but their pathogenesis is not clear and the clinical data regarding these anatomical defect is limited. We experienced a 23-year-old male with the absence of secondary sexual characteristics and this was accompanied with pituitary stalk dysgenesis and ectopic neurohypophysis. He received growth hormone for a year when he was 12 years old due to his short stature. Sella MRI showed no visible pituitary stalk with minimal high signal change, suggesting ectopic neurohypophysis. The combined pituitary stimulation test revealed blunted responses of growth hormone, follicle stimulating hormone and luteinizing hormone. For the hypogonadotropic hypogonadism, the patient was given testosterone intramuscularly and he gradually developed secondary sexual characteristics. We concluded that the hypogonadism and growth hormone deficiency in this patient was caused by hypopituitarism due to pituitary stalk dysgenesis and ecopic nuerohypophysis.

Citations

Citations to this article as recorded by

MRI of ectopic posterior pituitary gland with dysgenesis of pituitary stalk in a patient with hypogonadotropic hypogonadism
Ashim Kumar Lahiri, Ramanivas Sundareyan, David Jenkins, Anjumara Nilak
Radiology Case Reports.2018; 13(4): 764. CrossRef
Hypothalamic Hypopituitarism Caused by Pituitary Stalk Dysgenesis
Seong-Ju Lee, Hye-Jin Yoon, A-Reum Cho, Yoo-Jin Um, Keun-Young Park, Dong-Mee Lim, Byung-Joon Kim
Korean Journal of Medicine.2013; 85(4): 420. CrossRef

A Case of Sporadic Medullary Thyroid Cancer with RET G691S Polymorphism.: Min Kyu Kang, Jung Min Lee, Ji Hyun Kim, Min Young Lee, Ji Hyun Kim, Sung Dae Moon, Je Ho Han, Sang Ah Chang; J Korean Endocr Soc. 2009;24(4):293-297. Published online December 1, 2009; DOI: https://doi.org/10.3803/jkes.2009.24.4.293

2,235 View
27 Download

Abstract PDF: Sporadic medullary thyroid carcinoma (MTC) is the most common form of MTC and somatic RET proto-oncogene mutations account for approximately 25% of the patients with sporadic MTC. However, other pathogeneses of sporadic MTC are still unclear. Not only RET mutation, but also polymorphisms of RET may have an association with sporadic MTC. We herein describe the association of MTC and RET proto-oncogene polymorphism. A 51-year-old man was diagnosed with MTC, which was incidentally found on a thyroid sonogram. The patient underwent total thyroidectomy and genetic mutational analysis of the RET gene. Genetic testing detected a polymorphism in codon 691 (G691S) on exon 11 of the RET proto-oncogene. His son and daughter had the same polymorphism. We report on this case along with a review of the related literature on RET gene polymorphism of sporadic MTC.

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; J Korean Endocr Soc. 2006;21(6):560-566. Published online December 1, 2006; DOI: https://doi.org/10.3803/jkes.2006.21.6.560

2,366 View
31 Download
3 Crossref

Abstract PDF

Multiple endocrine neoplasia type 1 (MEN 1) is an autosomal dominant disorder that's characterized by the combined occurrence of primary hyperparathyroidism, endocrine pancreatic tumors and anterior pituitary adenomas, but such manifestations as carcinoid tumors, adrenal adenoma and lipoma are also seen. We report here on a case of a 52-years old man with MEN type 1. He had a parathyroid adenoma, empty sella and a non-functioning pancreatic and adrenal mass. On the genetic analysis, he was proven to have a mutation in the MEN1 gene (exon 2, 200-201, INS AGCCC). On the family study for the mutation, one of his siblings and his son proved to have the same mutation.

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
Endocrine Diseases in Diabetes Mellitus
Yongsoo Park
Hanyang Medical Reviews.2012; 32(4): 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

The Effect of Oxidative Stress on the Proliferation and Differentiation of Human Bone Marrow Stromal Cell-Derived Osteoblasts.: Eun Sook Oh, Ki Hyun Baek, Won Young Lee, Ki Won Oh, Hye Soo Kim, Je Ho Han, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Moo Il Kang; J Korean Endocr Soc. 2006;21(3):222-232. Published online June 1, 2006; DOI: https://doi.org/10.3803/jkes.2006.21.3.222

2,414 View
20 Download
1 Crossref

Abstract PDF

BACKGROUND
The objectives of our study were to assess the effects of oxidative stress on the proliferation, differentiation and apoptosis of human bone marrow stromal cell (BMSC)-derived osteoblasts and to explore pathways by which osteoblast cell apoptosis was induced. METHODS: Mononuclear cells including BMSCs were cultured to osteoblastic lineage. Different doses of hydrogen peroxide (H2O2) were added to the culture media. The colony forming units-fibroblastic (CFU-Fs) were stained with crystal violet and alkaline phosphatase (ALP). The MTT assay was done to see the effect of H2O2 on cell viability. The effect of H2O2 on osteocalcin gene expression was determined by RT-PCR. The matrix calcification measurement was performed. FACS analysis was performed to determine the osteoblasts apoptosis. Caspase-3, -8 and 9 activity assay and cytochrome c release were measured. RESULTS: The size and number of ALP (+) CFU-Fs were also decreased by H2O2 treatment. When compared with the control group, H2O2 significantly decreased the total number of cells of each culture well during MTT assay. H2O2 significantly diminished expression of osteocalcin mRNA. N-acetylcystein (NAC) blocked the diminution of cell viability and the inhibition of osteocalcin mRNA expression by H2O2. H2O2 reduced matrix calcification. FACS analysis revealed H2O2 increased percentage of apoptotic cells. Addition of H2O2 resulted in the increase of caspase-9 and -3 activity but not caspase-8, and release of cytochrome c to the cytosol. CONCLUSION: These data suggest that, in primary human BMSCs, oxidative stress inhibits proliferation of stromal cells and inhibits the differentiation to osteoblastic lineage. In addition, oxidative stress induces apoptosis of human BMSC-derived osteoblasts and this may be mediated by mitochondrial pathway of apoptotic signal.

Citations

Citations to this article as recorded by

Antioxidaitve and Differentiation Effects of Artemisia capillaris T. Extract on Hydrogen Peroxide-induced Oxidative Damage of MC3T3-E1 Osteoblast Cells
Jee-Eun Seo, Eun-Sun Hwang, Gun-Hee Kim
Journal of the Korean Society of Food Science and Nutrition.2011; 40(11): 1532. CrossRef

The Changes in the Serum RANKL and OPG levels after Bone Marrow Transplantation: Association with Bone Mineral Metabolism.: Hyun Jung Tae, Ki Hyun Baek, Eun Sook Oh, Ki Won Oh, Won Young Lee, Hye Soo Kim, Je Ho Han, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Choon Choo Kim, Moo Il Kang; J Korean Endocr Soc. 2005;20(1):40-51. Published online February 1, 2005; DOI: https://doi.org/10.3803/jkes.2005.20.1.40

1,974 View
22 Download

Abstract PDF: BACKGROUND
The loss of bone mass is usually detected after bone marrow transplantation(BMT), particularly during the early post-transplant period. We recently reported that enhanced bone resorption following BMT was related to both the steroid dose and increase in IL-6. It was also suggested damage of the marrow microenvironment due to myeloablation and changes in bone growth factors contribute to post-BMT bone loss. Recently, the interactions of OPG and RANKL have been reported to be crucial in osteoclastogenesis and therefore in bone homeostasis. There are few data on the changes in RANKL/OPG status during the post-BMT period. This study investigated the changes in the levels of RANKL and OPG during the post-BMT period, and also assessed whether the changes in these cytokine levels actually influenced bone turnover and post-BMT bone loss. METHODS: We prospectively investigated 110 patients undergoing allogenic BMT and analyzed 36 (32.4+/-1.3 years, 17 men and 19 women) where DEXA was performed before and 1 year after the BMT. The serum bone turnover marker levels were measured before and 1, 2, 3, 4 and 12 wks, 6 Ms, and 1 yr after the BMT. The serum sRANKL and OPG levels were measured in all patients before and 1, 3 and 12 wks after the BMT. RESULTS: The mean bone losses in the lumbar spine and total proximal femur, which were calculated as the percent change from the baseline to 1 yr, were 5.2(P<0.01) and 11.6%(P<0.01), respectively. The mean serum ICTP, a bone resorption marker, increased progressively until 3 and 6 months after the BMT, but decreased gradually thereafter, reaching the basal values after 1 year. The serum osteocalcin levels decreased progressively until 3 wks after the BMT, then increased transiently at 3 and 6 Ms, but returned to the basal level by 1 yr. The serum sRANKL and OPG levels had increased significantly by weeks 1 and 3 compared with the baseline(P<0.01), but decreased at 3 months. The sRANKL/OPG ratio increased progressively until 3 weeks, but then decreased to the basal values. During the observation period, the percent changes from the baseline in the serum RANKL levels and RANKL/OPG ratio showed positive correlations with the percent changes from the baseline serum ICTP levels. Patients with higher RANKL levels and RANKL/OPG ratio during the early post-BMT period lost more bone mass at the lumbar spine. CONCLUSION: In conclusion, dynamic changes in the sRANKL and OPG levels were observed during the immediate post-BMT period, which were related to a decrease in bone formation and loss of L-spine BMD during the year following the BMT. Taken together, these results suggest that increased sRANKL levels and sRANKL/OPG ratios could be involved in a negative balance in bone metabolism following BMT.

The Changes of Serum Growth Factors after Hematopoietic Stem Cell Transplantation: Impact on Bone Mineral Metabolism.: Ki Hyun Baek, Eun Sook Oh, Ki Won Oh, Won Young Lee, Hye Soo Kim, Soon Yong Kwon, Je Ho Han, Moo Il Kang, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Choon Choo Kim; J Korean Endocr Soc. 2002;17(5):664-674. Published online October 1, 2002

1,342 View
20 Download

Abstract PDF: BACKGROUND
A loss of bone mass is usually detected after a bone marrow transplantation (BMT), especially during the early post-transplant period. We recently reported that enhanced bone resorption following a BMT was related to both the steroid dose and the increase in IL-6. We also suggested damage to the marrow stromal microenvironment, by myoablation, partly explains the impaired bone formation following a BMT. It is well known that some growth factors play important role in bone growth and osteogenesis. However, the pathogenetic role of bone growth factors in post-BMT bone loss is unknown and data on the changes in the growth factors, in accordance with bone turnover markers and bone mineral density (BMD) changes are scarce. We investigated changes in bone growth factors such as IGF-I (Insulin-like growth factor-I), fibroblast growth factor-2 (FGF-2) and Macrophage colony stimulating factor (M-CSF), during the post-BMT period, and assessed whether the growth factor changes influenced the bone turnover and post-BMT bone loss. The present study is the first prospective study to describe the changes in bone growth factors following a BMT. METHODS: We prospectively investigated 110 patients undergoing a BMT, and analyzed 36 patients (32.4+/-1.3 years, 17 men and 19 women) whose BMDs were measured before, and 1 year after, the BMT. The serum biochemical markers of bone turnover were measured before, 1, 2, 3 and 4 weeks, 3 and 6 months, and 1 year, after the BMT. The serum FGF-2, IGF-I and M-CSF levels were measured before and 1 and 3 weeks, and 3 months after the BMT. The correlation between the changes of growth factors and various bone parameters was analyzed. RESULTS: The mean bone losses in the lumbar spine and total proximal femur, calculated as the percentage change from the baseline to the level at 1 year, were 5.2 (p<0.05) and 11.6% (p<0.01), respectively. The serum type I carboxyterminal telopeptide (ICTP), a bone resorption marker, increased progressively until 6 months after the BMT, but thereafter decreased, to the base value after 1 year. Serum osteocalcin, a bone formation marker, decreased progressively, until 3 weeks after the BMT but then increased transiently, and finally returned to the base level at 1 year. The serum IGF-I and FGF-2 also decreased progressively until 3 weeks and 1 week after the BMT, respectively, then increased to the base values at 3 months. The serum M-CSF increased briskly at 1 week post-BMT, then decreased to the base level. There were positive correlations between the percentage changes from the baseline proximal femur BMD and the IGF-I levels 3 weeks and 3 months (r=0.52, p<0.01, r=0.41, p<0.05) post BMT. A Significant correlation was found between the IGF-I and osteocalcin levels pre-BMT, and 3 weeks after the BMT. Another positive correlation was found between the M-CSF and the ICTP levels at 3 weeks post BMT (r=0.54, p<0.05). CONCLUSION: In conclusion, there were significant changes in the serum IGF-I, FGF-2 and M-CSF levels in the immediate post-BMT period, which were related to a decrease in bone formation and loss in the proximal femoral BMD during the year following the BMT

The Effect of Hematopoietic Stem Cell Transplantation in the Origin and the Osteoblastic Differentiation of the Human Bone Marrow Stromal Cell.: Moo Il Kang, Seong Won Cho, Eun Sook Oh, Ki Hyun Baik, Won Young Lee, Ki Won Oh, Hye Soo Kim, Je Ho Han, Kun Ho Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Choon Choo Kim; J Korean Endocr Soc. 2000;15(4-5):571-581. Published online January 1, 2001

1,340 View
17 Download

Abstract PDF: BACKGROUND
Bone marrow transplantation is the treatment of choice for patients with certain- hematological malignancies, many of whom will survive many years thereafter. Bone disease is a potential longterm complication. But, little is known about the effects of bone marrow transplantation on bone. METHODS: In this study, bone marrow was obtained from healthy donor and transplant recipients. Then mononuclear cells including marrow stromal cells were isolated and cultured. At near confluence, bone marrow stromal cells were subcultured. Thereafter alkaline phosphatase activities of each group were measured by time course of secondary culture. We also analysed the origin of marrow stromal cells by the polymerase chain reaction using YNZ 22 minisatellite probe. RESULTS: l. Cells cultured in our system showed the characteristics of marrow stromal cells differentiated to osteoblasts. They were in fibroblast-like spindle shape and positive to alkaline pbosphatase histochemistry and Von Kossa histochemistry in secondary cultures. 2. The time required for the near confluence in the primary culture was 15 days and 22.9 days on the average in healthy donors and transplant recipients, respectively (p=0.003). 3. In secondary cultures, healthy donors and transplant recipients showed peak alkaline phosphatase activity at 10 days and 17 days, respectively (p=0.031). Alkaline phosphatase activity was lower in BMT recipients than in healthy donors during the whole period of secondary cultures. 4. In polymerase chain reaction analysis using YNZ 22 minisatellite probe, bone marrow stromal cells were of recipient origin. CONCLUSION: Recipient-derived bone marrow stromal cells may be damaged secondary to the effect of chemotherapy, glucocorticoid & total body irradiation which have given before bone marrow transplantation. So it may affect the differentiation of bone marrow stromal cells into the osteoblasts.

The Effect of Bone Marrow Transplantation on Bone Mineral Metabolism: 2 - Year Prospective Study.: Won Young Lee, Moo Il Kang, Eun Sook Oh, Ki Won Oh, Je Ho Han, Hyun Shik Son, Kun Ho Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Wan Sik Shin, Woo Sung Min, Choon Choo Kim; J Korean Endocr Soc. 2000;15(4-5):561-570. Published online January 1, 2001

1,349 View
18 Download

Abstract PDF: BACKGROUND
Loss of bone mass is usually detected after bone marrow transplantation (BMT), especially during the early post-transplant period. But little is known about the long-term effects of BMT on bone mineral metabolism. METHODS: We have investigated prospectively 12 patients undergoing BMT (4 autologous, 8 allogeneic) for hematologic diseases (8 leukemia, 3 SAA, 1 MDS). Serum concentrations of calcium, phosphorus, creatinine, gonadotropins, sex hormones and bone turnover markers (osteocalcin and ICTP) were measured. The samples were collected before BMT and 1, 2, 3, 4, and 12 weeks, 6 months and 1, 2 years thereafter. Bone mineral density (BMD) was measured with DEXA (Dual Energy X-ray Absorptiometry) before BMT, 1 year and 2 year after BMT. In patients with amenorrbea, hormone replacement therapy was started from around 1 year after BMT RESULTS: 1. The mean bone loss in the lumbar spine, calculated as the percent change from the baseline to the level at 1 year and 2 year was 7.3% and 1.9%, respectively. The mean bone loss in the total proximal femur from the baseline to the level at 1 year and 2 year was 8.0% and 8.3% respectively. 2. The serum ICTP increased progressively until four weeks after BMT. Thereafter, it decreased gradually to reach basal values after one year and thereafter no more change until 2 year. Serum osteocalcin decreased progressively until three weeks after BMT. After that, it increased and reached basal values after 3 months. Osteocalcin increased at 6 month transiently but thereafter, it decreased to the level of slightly above basal value at 2 year. 3. Patients who were treated with TBI or pateints with GVHD had a tendency of lower BMD at l year and 2 year after BMT than those of patients without TBI or GVHD. 4. Eight out of nine women went into a menopausal state immediately after BMT and remained amenorrhea, evidenced by high gonadotropins and low estradiol levels. In contrast to women, gonadotropins and testosterone levels were not changed significantly in men after BMT. CONCLUSION: The rapid impairment of bone formation and the increase in bone resorption, as shown by the biochemical markers in this study, might play a role in bone loss after BMT. The efficacy of HRT for the correction of hypogonadism and bone loss was evidenced by 2 year BMD which was much more increased compared to 1 year BMD, especially in vertebra.

The Changes of Cytokines and Bone Turnover Markers after Bone Marrow Transplantation.: Won Young Lee, Moo Il Kang, Ki Won Oh, Hye Soo Kim, Seong Dae Mun, Je Ho Han, Hyun Shik Son, Sung Koo Kang, Wan Sik Shin, Woo Sung Min, Choon Choo Kim; J Korean Endocr Soc. 2000;15(1):85-96. Published online January 1, 2001

1,185 View
18 Download

Abstract PDF: BACKGROUND
Loss of bone mass is usually detected after BMT. The causes of bone loss are related with gonadal dysfunction and immunosuppressants. Cytokines, especially IL-6, play an important role in the pathogenesis of postmenopausal osteoporosis. However, the pathogenetic role of cytokines in post-BMT bone loss is unknown and data on the changes of cytokines in accordance with bone turnover markers are scarce. The aim of this study is to assess the relationship of bone turnover markers and cytokines of peripheral blood and bone marrow before and after allogeneic BMT. METHODS: This prospective study included two analyses. The first was a study of 46 BMT recipients, examining the relationship between bone turnover markers and cytokines of serum which were measured before and 1, 2, 3, 4 week and 3 months after BMT. The second was a study of 14 BMT patients, measuring bone marrow plasma cytokines such as IL-6 and TNF-alpha at post-BMT 3 week and bone turnover marker at the same time to assess the relationship between two parameters. RESULTS: Serum ICTP, bone resorption marker, increased progressively until 4 weeks (peak) after BMT and then decreased thereafter. Serum osteocalcin, bone formation marker, decreased progressively until 3 weeks after BMT and then increased thereafter. There was positive correlation between serum ICTP and bone marrow IL-6 levels at the post-BMT 3 week with a statistical significance, but the correlation between bone turnover markers and bone marrow TNF-alpha or peripheral blood cytokines was not found. CONCLUSION: Our data suggest that the progressive increase of bone resorption after BMT is related with the increase of bone marrow IL-6, which is a potent stimulator of bone resorption in vivo.

Two Cases of Cryptococcosis in Patients with Cushing's Syndrome and Diabetes Mellitus.: Jong Kyu Lee, Hee Kyung Chun, Je Ho Han, Hyun Sik Son, Kun Ho Yoon, Moo Il Kang, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Ku Kang; J Korean Endocr Soc. 1995;10(1):58-64. Published online November 6, 2019

1,446 View
25 Download

Abstract PDF: Although cryptococcosis complicated with steroid therapy is well described, cryptococcosis has been rarely reported in the presence of Cushing's syndrome characterized by endogenous steroid excess. We experienced two cases of cryptococcosis in patients with Cushing's syndrome and diabetes mellitus. We describe a case of cryptococcal meningitis complicatiog Cushing's syndrome, secondary to pituitary adenoma. And another case of cryptococcal pneumonia complicatiog Cushing's syndrome, secondary to bilateral nodular adrenal hyperplasia. Before Cryptococcosis, two patients were suffered from diabetes mellitus, and they have got both adrenalectomy.

An Acromegalci Patient with Marked Tumor Shrinkoge after Continuous Infusion of Octreotide.: Je Ho Han, Hyun Sik Son, Kun Ho Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Ku Kang, Yoo Bae Ahn, Sang A Jang, Ki Ho Song, Soon Jip Yoo, Jong Min Lee; J Korean Endocr Soc. 1994;10(2):161-164. Published online November 6, 2019

1,064 View
18 Download

Abstract PDF: No abstract available.

A Case of Thyroid Hemiagenesis with Papillary Adenocarcinoma.: Je Ho Han, Bong Yun Cha, Ho Young Son, Yoo Bae Ahn, Kwang Woo Lee, Sung Koo Kang, Se Jeong Oh, Jong Soon Na, Sang Ah Jang, Moo Il Kang; J Korean Endocr Soc. 1994;9(4):385-389. Published online November 6, 2019

1,321 View
20 Download

Abstract PDF: Variation in the gross anatomy of the thyroid is relatively common. Although thyroid hemiagenesis is considered to be a rare congenital anomaly, its incidence is probably underestimated because the diagnosis is usually incidental.We present the case of a 26-year-old woman with right thyroid hemiagenesis associated with papillary adenocarcinoma. The diagnosis of hemiagenesis was established by isotope imaging, which showed hot nodule, thyroid ultrasonography and surgical exploration for proper management of a nodule in the left lobe of thyroid gland. As she was diagnosed to have papillary adenocarcinoma, total thyroidectomy was performed and at present she remains disease-free.

A Case of Primary Hyperparathyroidism Associated with Proximal Renal Tubular Acidosis and Postoperative Hungry Bone Syndrome.: Je Ho Han, Kun Ho Yoon, Bong Yun Cha, Ho Young Son, Kwang Woo Lee, Hae Ok Jung, Chang Sup Kim, Moo Il Kang, Chul Soo Cho, Ho Yun Kim, Sung Koo Kang; J Korean Endocr Soc. 1994;9(2):141-149. Published online November 6, 2019

1,579 View
39 Download

Abstract PDF: Primary hyperparathyroidism is a generalezed disorder of calcium, phosphorus and bone metabolism due to an increased secretion of parathyroid hormone. Single parathyroid adenoma is the most common cause of primary hyperparathyroidism. Because parathyroid hormone has been proposed as an important inhibitor of renal bicarbonate reabsorption of proximal tubule, proximal renal tubular acidosis is not rare in primary hyperparaphyroidism. After parathyroid resection, significant hypocalcemia and hypophosphatemia requiring prolonged medical management may develop, termed hungery bone syndrome. We experienced a case of primary hyperparathyroidism associated with proximal renal tubular acidosis, and severe hungry bone syndrome after resection of the adenoma of parathyroid gland.

Effect of cilostazol on diabetic peripheral vascular disease.: Kun Ho Yoon, Je Ho Han, Hyuk Ho Kwon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Ku Kang, Yong Seong Kim, Hyun Sang Oh, Soon Hyun Shinn; J Korean Endocr Soc. 1993;8(1):78-87. Published online January 1, 2001

1,169 View
19 Download

Abstract PDF: No abstract available.

Analysis of HLA-DQA1 genotype in Korea autoimmune thyroid disease and IDDM patients.: Moo Il Kang, Je Ho Han, Soon Jip Yoo, Jong Min Lee, Hyun Sik Son, Kun He Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Ku Kang, Choon Choo Kim, Dong Jip Kim; J Korean Endocr Soc. 1992;7(4):320-330. Published online January 1, 2001

1,077 View
16 Download

Abstract PDF: No abstract available.

Author index