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Volume 20(4); August 2005
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Review Articles
Endocrine Regeneration Therapy using Adenoviral vector.
Eun Jig Lee
J Korean Endocr Soc. 2005;20(4):301-305.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.301
  • 1,556 View
  • 16 Download
  • 1 Crossref
AbstractAbstract PDF
No Abstract available.

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  • Effects of Various Types of Distribution on Probabilistic Method and FAD
    Ouk Sub Lee, Dong Hyeok Kim
    Key Engineering Materials.2007; 353-358: 2561.     CrossRef
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Wnt Signal Transduction and Its Involvement in Human Diseases.
Eek Hoon Jho
J Korean Endocr Soc. 2005;20(4):306-318.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.306
  • 1,717 View
  • 17 Download
  • 1 Crossref
AbstractAbstract PDF
No Abstract available.

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  • Capsosiphon fulvescens glycoprotein inhibits AGS gastric cancer cell proliferation by downregulating Wnt-1 signaling
    YOUNG-MIN KIM, IN-HYE KIM, TAEK-JEONG NAM
    International Journal of Oncology.2013; 43(5): 1395.     CrossRef
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Editorial
Sequential and Combination Therapy using Parathyroid Hormone for Osteoporosis.
Ki Hyun Baek
J Korean Endocr Soc. 2005;20(4):319-322.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.319
  • 1,680 View
  • 17 Download
  • 1 Crossref
AbstractAbstract PDF
No Abstract available.

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  • Effects of the Pharmacopuncture in Animal Models for Treatment of Osteoporosis: A Review of Animal Study Reports Published in Korea
    Jung-min Kim, Soo-min Choi, Hee-Duk An
    Journal of Korean Medicine Rehabilitation.2016; 26(2): 75.     CrossRef
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Original Articles
Changes in Somatostatin Receptor mRNA Levels by G Protein Mutation in GH3 Cells Which Show Responsiveness to Growth Hormone-Releasing Hormone.
Eun Hee Kim, Sook Jin Sohn, Min A Lee, Sang Hee Seo, Sung Hee Ju, Dahm Lee, Hyun Ju Chung, Jee Chang Jung, Seung Joon Park
J Korean Endocr Soc. 2005;20(4):323-333.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.323
  • 1,755 View
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BACKGROUND
S: GH3 cells lack growth hormone(GH)-releasing hormone(GHRH) receptors. In this study, GH3 cells permanently transfected with human GHRH receptor cDNA(GH3-GHRHR cells), were established in order to examine the effects of GHRH and G protein mutation(gsp oncogene) on the levels of somatostatin receptor mRNA. METHODS: GH3 cells were permanently transfected with a plasmid expressing human GHRH receptor cDNA. The GHRH receptor mRNA was detected by RT-PCR. The responsiveness to GHRH was evaluated using a GHRH binding assay, Western blot analysis, Northern blot analysis, and measurements of the intracellular cAMP levels and GH release. Cells were transiently transfected with the gsp oncogene, and then treated with GHRH or octreotide for 4h. The sst1 and sst2 mRNA levels were measured using real-time RT-PCR analyses. RESULTS: GHRH receptor mRNA was detected in the GH3 cells permanently transfected with human GHRH receptor cDNA. The GHRH binding assay showed that GHRH was bound to the GH3-GHRHR cells. The GHRH treatment increased the intracellular cAMP levels, GH release, GH mRNA levels, and MAPK activity, as well as the levels of sst1 and sst2 mRNA. Transient expression of the gsp oncogene for 48h increased the cAMP, GH release, and levels of sst1 and sst2 mRNA. In the gsp-transfected GH3-GHRHR cells, GHRH stimulation resulted in decreases in the magnitude of the increase in the levels of sst1 and sst2 mRNA compared to those transfected with a control vector. Octreotide treatment did not alter the levels of sst1 and sst2 mRNA in either the control or gsp-transfected cells. CONCLUSION: These results suggest that GH3 cells permanently transfected with the GHRH receptor are useful in the in vitro studies on the actions of GHRH. The gsp oncogene was shown to increases the levels of sst1 and sst2 mRNA in GH3 cells, but these findings are unlikely to be the major mechanism by which gsp-positive pituitary tumors show a greater response to somatostatin. The discrepancy between the in vivo and these in vitro results should be examined further.
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Effect of Sequential Therapy with Incadronate after Withdrawal of Recombinant Human Parathyroid Hormone(1-84) on Bone Quantity and Quality in Ovariectomized Rats.
Yumie Rhee, Jong Chan Youn, Ye Yeon Won, Myong Hyun Baek, Sung Kil Lim
J Korean Endocr Soc. 2005;20(4):334-343.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.334
  • 1,511 View
  • 19 Download
AbstractAbstract PDF
BACKGROUND
Human parathyroid hormone(hPTH) is a promising anabolic agent. However, since hPTH (1-34) is available only via injection, and has a critical side effect of causing bone tumors during life-long administration in the rat, it would be practical to use PTH for the shortest possible duration to obtain the maximal effect. In addition, acquired bone mass due to hPTH tend to decrease after drug cessation. To determine the effectiveness of the osteoporosis-reversing concept of lose, restore, and maintain(LRM), recombinant human PTH(1-84)[rhPTH(1-84)] and the respective anti-resorptive agents were sequentially studied. METHODS: Thirty six, 20-week-old, Sprague-Dawley rats were used in this study. Treatment was started on the 25th week after an ovariectomy, which had been performed at 20weeks of age, with 5weeks of rhPTH (1-84) 100(microgram/kg/d), 5days/wk, followed by the respective sequential therapies for 5 weeks as follows: 1) Ovariectomized rats(OVX, n=6), 2) Sham operated rats(SHAM, n=6), 3) OVX rats with PTH maintenance(PTH-M, n=6), 4) OVX rats treated with PTH then withdrawn(PTH-W, n=6), 5) PTH-treated OVX rats then treated with 17beta-estradiol(PTH-E, 10microgram/d, SQ, 5days/wk, n=6), 6) PTH-treated OVX rats then treated with incadronate(PTH-I, 3mg/kg, per os 5 days/wk, n=6). The bone mineral density(BMD) of the right femurs was measured using dual X-ray absorptiometry(DXA). Microcomputed tomography(microCT) was used to measure the structural parameters of the 2nd lumbar vertebrae. A three-point bending test of the femur and compressive tests of vertebrae were also performed. RESULTS: Bone quantity data showed that the femoral BMD was significantly higher in the PTH-M and PTH-I groups than in the OVX and PTH-W groups(P<0.05). Measurement of the cortical thickness revealed that only the PTH-M group had a significant increase(P=0.001). The ultimate force(Fu) at the midshaft of the femur was stronger in the PTH-M group than in the OVX group(P<0.001). However, no significant difference was found among the treated groups. CONCLUSION: PTH withdrawal resulted in the loss of the acquired BMD, but sequential therapy with the anti-resorptive, incadronate, prevented further bone loss. The use of incadronate after rhPTH(1-84), as a sequential regimen, was significantly effective on the maintenance in the bone mass, but further clarification in the improvement in the bone quality is needed.
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Efficacy of Octreotide LAR in Acromegalic Patients.
Ji Youn Kim, Jae Hwan Jee, Chan Ho Yoon, Yun Jae Chung, Byung Wan Lee, Gun Yong Cho, Sang Young Kim, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
J Korean Endocr Soc. 2005;20(4):344-352.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.344
  • 2,317 View
  • 22 Download
  • 4 Crossref
AbstractAbstract PDF
BACKGROUND
Octreotide(OC)-LAR is a long-acting preparation of octreotide which has been effectively used to suppress GH/IGF-1 hypersecretion in acromegalic patients. The clinical response, biochemical outcomes, and safety of OC-LAR were evaluated in 27 active acromegalic patients. METHOD: 27patients with an active disease status (according to the clinical picture, GH >5microgram/L and elevated age-matched IGF-1), and previously treated with bromocriptine after surgery, comprised the study population. OC-LAR was given(20mg, i.m., every 4 week for 3 injections, then the doses were titrated individually) and the acromegalic symptoms and adverse reactions recorded. The serum levels of GH and IGF-1 were evaluated every 12 week. The acromegalic symptoms including headache, fatigue and arthralgia, improved in all patients. RESULTS: Gastrointestinal side effects were transient and mild. The levels of GH significantly decreased, from 8.9+/-3.5 to 2.9+/-2.2 microgram/L at 12 weeks(P<0.001, vs. baseline), to 2.9+/-2.1microgram/L after 24 weeks(P<0.001) and to 2.5 +/-1.3microgram/L at 48 weeks(P<0.001). The levels of IGF-1 significantly decreased, from 753.7+/-213.6 to 429.7+/-253.4 microgram/L at 12 weeks(P<0.001, vs. at baseline), to 405.7+/-213.3microgram/L at 24 weeks(P <0.001) and to 348.9+/-144.7microgram/L at 48 weeks(P<0.001). The safelevel of GH is less than 2.5microgram/L and normal age-matched IGF-1 levels were achieved in 63 and 52% of the patients, respectively. CONCLUSION: Octreotide-LAR was well tolerated and effective as an adjuvant treatment in lowering the levels of GH and IGF-1 in active acromegalic patients.

Citations

Citations to this article as recorded by  
  • Letter: Comparison of the Efficacy of Octreotide Long-acting Repeatable and Lanreotide Autogel in Acromegalic Patients (J Korean Endocr Soc 25:37-45, 2010)
    Yu-Bae Ahn
    Endocrinology and Metabolism.2010; 25(2): 157.     CrossRef
  • The Effect of Octreotide LAR on GH and TSH Co-Secreting Pituitary Adenoma
    Nam Keong Kim, Yu Jin Hah, Ho Young Lee, Sang Jin Kim, Mi Kyung Kim, Keun Gyu Park, Ealmaan Kim, Hyukwon Chang, Hye Soon Kim
    Endocrinology and Metabolism.2010; 25(4): 378.     CrossRef
  • Comparison of the Efficacy of Octreotide Long-acting Repeatable and Lanreotide Autogel in Acromegalic Patients
    Seul young Kim, Dohee Kim
    Journal of Korean Endocrine Society.2010; 25(1): 37.     CrossRef
  • Response: Comparison of the Efficacy of Octreotide Long-acting Repeatable and Lanreotide Autogel in Acromegalic Patients (J Korean Endocr Soc 25:37-45, 2010)
    Seul Young Kim, Dohee Kim
    Endocrinology and Metabolism.2010; 25(2): 159.     CrossRef
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Role of Protein kinase C in Desensitization of Somatostatin-induced Calcium Signalling in NG108-15 Cells.
Kyoung Mi Kim, Jong Ho Sung, Myung Jun Kim, Duck Joo Rhie, Yang Hyeok Jo, Sang June Hahn, Myung Suk Kim, Shin Hee Yoon, Bu Seung Kim
J Korean Endocr Soc. 2005;20(4):353-361.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.353
  • 1,644 View
  • 16 Download
AbstractAbstract PDF
BACKGROUND
Activation of G-protein coupled-somatostatin receptors induces the release of calcium from inositol 1, 4, 5-trisphosphate-sensitive intracelluar stores. G-protein-coupled receptor signaling decreases with prolonged exposure to an agonist. SEBJECTS and METHODS: Fura-2-based digital Ca2+ imaging was used to study the effects of prolonged exposure to an agonist on the somatostatin-induced intracellular Ca2+ concentration([Ca2+]i) increases in NG108-15 cells, which were differentiated with CO2-independent medium and 10micrometer forskolin. RESULTS: Exposure to somatostatin(1micrometer) for 30 min completely desensitized the NG108-15 cells to a second somatostatin-induced response. The cells recovered gradually over 20 min following washout of the somatostatin. The desensitization was not due to depletion of the intracellular Ca2+ stores, and pretreatment for 30 min with bradykinin(100nM), which activates phospholipase C, or DADLE(D-Ala2-D-Leu5 enkephalin, 1microM), which activates phospholipase C, failed to cross-desensitize the somatostatin-evoked [Ca2+]i increases. Treatment with 8-cpt-cAMP(0.1mM) for 30min did not influence the somatostatin-induced[Ca2+]i increases. Phorbol 12, 13-dibutyrate(PdBu, 1microM) blocked the response completely. Down-regulation of PKC due to 24 h exposure of PdBu (1microM) inhibited the somatostatin-induced desensitization. CONCLUSION: Prolonged exposure of somatostatin to NG108-15 cells desensitized the somatostatin-induced release of Ca2+ from the intracelluar store, with protein kinase C also involved in the desensitization.
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Chromosomal Analysis of Anaplastic Thyroid Carcinomas by Comparative Genomic Hybridization.
Mi Kyoung Kim, Chang Hun Lee, Jin Mi Song, Kyung Yub Gong, Yong Ki Kim
J Korean Endocr Soc. 2005;20(4):362-374.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.362
  • 1,540 View
  • 17 Download
AbstractAbstract PDF
BACKGROUND
Compared with common well-differentiated thyroid carcinomas, the genetic alterations underlying the development and progression of anaplastic thyroid carcinomas(ATC) are still uncharacterized. Comparative genomic hybridization(CGH) is a cytogenetic technique that can identify gains and losses in the DNA sequence copy number in tumors. METHODS: The authors studied the changes in the DNA copy number due to CGH in paraffin-embedded tissue blocks of 17 ATC cases, and tried to ascertain whether the genomic changes correlate with the clinicopathological parameters including patients' age, sex, primary tumor size, lymphovascular invasion, extrathyroid extension, regional node metastasis and immunohistochemical expression of cyclin D1. RESULTS: Fourteen of the 17 samples(82.4%) showed chromosomal changes, with a mean number of gains or losses per carcinoma of 3.6(range 2~6; 30 gains and 21 losses). The most frequently detected imbalance was the gain of chromosome 1q, which was seen in 35.7% of cases, particularly commonly in ATC associated with a papillary thyroid carcinoma. Other commonly occurring gains were present in 11q13 and 19(28.6%, respectively). Genomic amplification was detected in all four cases showing the 11q13 gain. Genomic losses were commonly noted in 3q, 6q, 18q andchi(21.4%, respectively). When numerical CGH alterations were compared to the clinicopathological parameters, there were no significant correlations(P>0.05). Cyclin D1 expression was noted in sixteen of the 17 cases(94.1%), but the extent of cyclin D1 expression was not correlated with the numerical CGH alterations(P>0.05). CONCLUSION: Taken together, the aberrations of 1q, 3q, 6q, 11q13 and 18q are relatively common in ATC, and may play an important role it developement. These findings should lead to the characterization of tumor suppressor genes and oncogenes that are potentially involved in the carcinogenesis of ATC. The amplification of 11q13 is characteristically found, but cyclin D1 in this region may be innocent of the aggressiveness of these carcinomas.
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Case Reports
A Case of Familial Medullary Thyroid Carcinoma with a E768D Mutation in RET Proto-Oncogene.
Yeon Kyeong Kim, Jin Woo Kim, Sang Mi Ahn, Kyoung Eun Song, Sun Hye Jung, Dae Jung Kim, Yoon Sok Chung, Kwan Woo Lee, Chul Ho Kim, Ji Hee Hong, Seon Yong Jeong, Hyon Ju Kim
J Korean Endocr Soc. 2005;20(4):375-380.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.375
  • 2,272 View
  • 26 Download
  • 2 Crossref
AbstractAbstract PDF
A medullary thyroid carcinoma, a neoplasm of parafollicular C cell origin, occurs as a sporadic or hereditary disease. A hereditary medullary thyroid carcinoma is an autosomal dominantly inherited disease, which is composed of multiple endocrine neoplasia 2A and 2B, with a familial medullary thyroid carcinoma. Germline mutations of the RET gene are the underlying cause of the majority of hereditary medullary carcinomas. Here, the case of a 42 years-old man with a familial medullary thyroid carcinoma, confirmed by the detection of a RET proto-oncogene mutation at exon 13 on codon 768 from a GAG(Glu) to a GAT(Asp), is described. The patient underwent a total thyroidectomy and modified radical neck dissection. His sister was found to have the same mutant gene.

Citations

Citations to this article as recorded by  
  • A Case of Medullary Thyroid Carcinoma with de novo V804M RET Germline Mutation
    Young Sik Choi, Hye Jung Kwon, Bu Kyung Kim, Su Kyoung Kwon, Yo Han Park, Jeong Hoon Kim, Sang Bong Jung, Chang Hoon Lee, Seong Keun Lee, Shinya Uchino
    Journal of Korean Medical Science.2013; 28(1): 156.     CrossRef
  • A Family of Multiple Endocrine Neoplasia Type 2A with a C634R Mutation and a G691S Polymorphism in RET Proto-oncogene
    Seoung Wook Yun, Won Sang Yoo, Koo Hyun Hong, Bae Hwan Kim, Min Ho Kang, Young Kwang Choo, Hee Yoon Park, Do Hee Kim, Hyun-Kyung Chung, Myung-Chul Chang, Mi Seon Kwon, Hee Jin Kim
    Journal of Korean Endocrine Society.2007; 22(6): 453.     CrossRef
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A Case of Thyrotoxicosis Presented as Rhabdomyolysis.
Yil Sik Hyun, Chang Beom Lee, Yong Soo Park, Dong Sun Kim, Woong Hwan Choi, Tae Wha Kim, You Hern Ahn
J Korean Endocr Soc. 2005;20(4):381-384.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.381
  • 2,194 View
  • 32 Download
  • 1 Crossref
AbstractAbstract PDF
There have been a few reports on rhabdomyolysis caused by thyroid storm, but no cases of thyrotoxicosis related rhabdomyolysis have been reported until now. Here, a rare case of rhabdomyolysis, accompanied by thyrotoxicosis, is reported. A 21-year-old man was admitted to our hospital with severe pain and weakness in both legs. The initial laboratory findings revealed a high muscle enzyme level and severe hypokalemia. In evaluation of the rhabdomyolysis, the thyroid function test was compatible with that of Graves' disease, with the rhabdomyolysis subsequently diagnosed, presenting as thyrotoxicosis. The possible mechanisms for this complaint were hypokalemia-induced muscle ischemia, a thyrotoxicosis-induced excessive hypermetabolic state and pressure-induced muscle ischemia. Therefore, the work up for the cause of rhabdomyolysis should include thyrotoxicosis. The management of rhabdomyolysis is hydration, prevention of acute renal failure, correction of aggravating factors and treatment of the underlying cause, for example, thyrotoxicosis.

Citations

Citations to this article as recorded by  
  • A Case of Thyrotoxic Periodic Paralysis with Rhabdomyolysis
    Seo Hee Lee, Seong Yeol Kim, Hae Ri Lee, Jun Goo Kang, Ohk Hyun Ryu, Chul Sik Kim, Byung Wan Lee, Seong Jin Lee, Eun-Gyoung Hong, Hyeon Kyu Kim, Doo-Man Kim, Jae Myung Yu, Sung-Hee Ihm, Moon Gi Choi, Hyung Joon Yoo
    Journal of Korean Endocrine Society.2008; 23(6): 425.     CrossRef
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A Case of Thyroid Abscess Associated with Lymphocytic Thyroidits.
Hyoun Jung Chin, Mi Kwang Kwon, Yeehuung Kim, Gwanpyo Koh, Keun Yong Park, Suk Chon, Seungjoon Oh, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Moon Ho Yang
J Korean Endocr Soc. 2005;20(4):385-389.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.385
  • 1,766 View
  • 17 Download
AbstractAbstract PDF
No Abstract available.
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A Case of Bilateral Macronodular Adrenocortical Hyperplasia Accompanied by Hyperresponsiveness to Vasopressin.
Deok In Kim, Seung Hee Lee, Eun A Kim, Hwi La Park, Gyeong Ug Lee, Seong Bin Hong, Moon Suk Nam, Seok Hwan Shin, Yong Seong Kim
J Korean Endocr Soc. 2005;20(4):390-394.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.390
  • 1,718 View
  • 17 Download
AbstractAbstract PDF
Cushing's syndrome associated with nodular adrenal hyperplasia glands is divided into 4 main categories: adrenal adenoma, adrenal carcinoma, primary pigmented nodular adrenal dysplasia and macronodular adrenal hyperplasia(MAH). The mechanism of bilateral MAH, when ACTH is suppressed, was previously unknown, and referred to as being "autonomous". Recently, several reports have shown MAH to be under the control of ectopic or eutopic membrane hormone. Here, a case of Cushing's syndrome, caused by bilateral MAH, is reported. A 62-year-old woman presented with Cushingoid features, hypertension and diabetes mellitus. In her case, abnormal adrenal stimulation of cortisol secretion in response to exogenous vasopression stimulation was shown. Her urine free cortisol was 726.0microgram/dL, which was not suppressed after administration of high-dose dexamethasone. Her plasma cortisol level was elevated, but without circadian rhythm. ACTH was undetectable. An abdomen CT scan demonstrated bilaterally enlarged multinodular adrenal glands. A Sella MRI revealed no alteration of the pituitary gland. The patient underwent a laparoscopic bilateral adrenalectomy. Histological examination revealed bilateral macronodular hyperplasia. After having recovered, the patient showed progressive regression of the Cushingoid status.
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A Case Report of von Hippel-Lindau Disease Manifested in a Monozygous Twin.
Jin Woo Kim, Sang Jo Choi, Yeon Kyeong Kim, Sang Mi Ahn, Kyoung Eun Song, Sun Hye Jung, Dae Jung Kim, Yoon Sok Chung, Kwan Woo Lee, Il Jin Kim, Hio Chung Kang, Jae Gahb Park
J Korean Endocr Soc. 2005;20(4):395-400.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.395
  • 2,027 View
  • 21 Download
  • 2 Crossref
AbstractAbstract PDF
Von Hippel-Lindau (VHL) disease is an autosomal dominant disease, which forms hypervascular tumors in multiple organs, such as hemangioblastomas in the retina and central nervous system, renal cell carcinomas, pheochromocytomas and cysts in various organs. Recent advances in gene testing have made it possible to screen family members for VHL disease. We experienced a 28 year-old male, who was diagnosed with bilateral pheochromocytomas through a family screening test when his elder monozygous twin brother was diagnosed with a pheochromocytoma. He received no treatment until December, 2004, when he visited the Emergency room due to a headache. A hemangioma of the cerebellum was seen in the brain MR study, leading to the diagnosis of type 2A VHL disease. An abdominal CT scan revealed no lesions of the pancreas or kidney. There was no evidence of a hemangioma in the retinal scan. The subsequent gene testing showed a germline mutation in exon 3 codon 167 of the VHL gene. The mother of the patient was revealed to have the same mutation of the VHL gene, but the elder brother of the patient did not.

Citations

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  • Germline mutation of Glu70Lys is highly frequent in Korean patients with von Hippel–Lindau (VHL) disease
    Sena Hwang, Cheol Ryong Ku, Ji In Lee, Kyu Yeon Hur, Myung-Shik Lee, Chul-Ho Lee, Kyo Yeon Koo, Jin-Sung Lee, Yumie Rhee
    Journal of Human Genetics.2014; 59(9): 488.     CrossRef
  • A Case of Type 1 von Hippel-Lindau (VHL) Disease associated with VHL Germline Mutation
    Jeong Hoon Seo, Jae Hong Yang, Pyoung Lak Choi, Yu Lee Kim, Young Sik Choi, Yo Han Park, Ji Ho Ko, Hio Chung Kang, IL Jin Kim, Jae Gahb Park
    Journal of Korean Endocrine Society.2006; 21(3): 239.     CrossRef
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A Case of Acromegaly with Gall Bladder Cancer.
Ji Sun Nam, Chul Sik Kim, Jee Hyun Kong, Hai Jin Kim, Jin A Park, Jong Suk Park, Chul Woo Ahn, Se Joon Lee, Bong Soo Cha, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee
J Korean Endocr Soc. 2005;20(4):401-406.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.401
  • 1,975 View
  • 24 Download
AbstractAbstract PDF
Acromegaly is a systemic endocrine disorder due to an excessive release of growth hormone, which increases the serum levels of insulin-like growth factor-1(IGF-1). Elevated levels of these hormones are assumed to increase the incidence of malignant tumors in patients with acromegaly, due to by stimulating the growth and maturation of cells. In particular, IGF-1 is considered to be closely related with the development of colon polyps and colon cancers. Studies suggest that various malignant tumors, including thyroid cancer, brain tumor and renal cell carcinomas, are also more common in patients with acromegaly. Here, a case of gall bladder cancer in a patient with acromegaly, and the possible relationships between these two disorders, is reported.
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A Case of Drug Induced Nephrogenic Diabetes Insipidus and Hyperprolactinemia in Schizophrenia Simultaneously.
Ho Yoel Ryu, Mi Young Lee, Yeon Lee, Jang Hyun Koh, Mi Jin Kim, Young Goo Shin, Choon Hee Chung
J Korean Endocr Soc. 2005;20(4):407-412.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.407
  • 2,366 View
  • 59 Download
AbstractAbstract PDF
In schizophrenia, when treatment using antipsychotics fails, lithium, which is known as an antimanic drug, can also be administered. It is reported that 12~20% of patients taking lithium develop nephrogenic diabetes lactotrophs. Hyperprolactinemia is induced by typical antipsychotics, as they block the dopamine-2 receptors of latotrophs in the pituitary gland. Therefore, atypical antipsychotics for decreasing the side effect, such as hyperprolactinemia, can be used. However, hyperprolactinemia can be induced by risperidone, one of the atypical antipsychotics. Here, a case of drug induced nephrogenic diabetes insipidus and simultaneous hyperprolactinemia, which occurred in a patient with schizophrenia, is reported.
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