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Volume 15(1); March 2000
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Review Articles
Oxidative Stress and Atherosclerosis.
Ha Young Kim, Joong Yeol Park
J Korean Endocr Soc. 2000;15(1):1-14.   Published online January 1, 2001
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No abstract available.
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Diagnosis and Differential Diagnosis of Endogenous Cushing's Syndrome.
Dong Sun Kim
J Korean Endocr Soc. 2000;15(1):26-30.   Published online January 1, 2001
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No abstract available.
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Original Articles
The Incidence and Clinical Characteristics of Cushing's Syndrome in Korea.
J Korean Endocr Soc. 2000;15(1):31-45.   Published online January 1, 2001
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BACKGROUND
Cushing's syndrome is a relatively well understood syndrome. In Korea, there was no large scaled epidemiological report for etiology, clinical manifestation and results of treatment for Cushing's syndrome so far. This study was undertaken to elucidate the clinical characteristics of Cushing's syndrome in Korea by the survey committee for endocrine disease in Korean society of endocrinology. METHODS: For the case collection, we developed the case analysis protocol and computer program. And then we sent those form and program to 51 hospitals lacated in all over the country except Jeju-Do. Finally we collected 180 cases of Cushing's syndrome newly diagnosed from Jan. 1st, 1988 to Dec. 31st, 1993 from 28 hospitals. In this study, we excluded the patients with iatrogenic Cushing's syndrome. RESULTS: 1. If we collected all the cases in Korea, 0.84 new cases/million was diagnosed annually. The incidence was 3.5 times greater in women than in men, and the most frequent age of onset was the fourth decade. 2. Pituitary microadenoma and adrenal adenoma were the major causes (43.3%, 41.7% respectively). The ectopic Cushing's syndrome had very low incidence (0.6%) then other western countries. 3. Liddle's low dose dexamethasone suppression test, 24hr urine free cortisol level and 1mg overnight dexamethasone suppression test as a screening tests showed good sensitivity (98.1%, 94.3%, 96.3% respectively). 4. Both of 8 mg overnight dexamethasone suppression test and basal plasma ACTH level as differential test of Cushing's disease from adrenal Cushing's syndromes showed good specificity (90.6%, 100% respectively) but relatively low sensitivity (60.7%, 26.3% respectively). 5. Combination of both 8 mg overnight dexamethasone suppression test and basal plasma ACTH level improved the sensitivity (75.0%) and specificity (94.7%) as differential tests. 6. Treatments depended on the etiology. Surgery was the best choice when it could be performed. Radiotherapy and medical treatments were performed as isolated or combined modality but results were poor. CONCLUSION: Cushing's syndrome in Korea were not significantly different from western cases except that adrenal adenomas were more frequent. Ectopic Cushing's syndrome and Cushing's disease must be attentioned for diagnosis and proper management. Early and exact diagnosis process will improve the morbidity, mortality and life quality of patients.
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Thyrotropin-releasing Hormone(TRH) Receptor Gene Expression in GH3 Cells Permanently Transfected with a Mutant Gs alpha Gene.
Seung Joon Park, In Myung Yang, Sung Vin Yim, Joo Ho Chung, Jee Chang Jung, Kye Chang Ko, Young Seol Kim, Young Kil Choi
J Korean Endocr Soc. 2000;15(1):46-54.   Published online January 1, 2001
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BACKGROUND
Gs alpha gene mutation, that constitutively increases intracellular cAMP, is found in some acromegalic patients. It was demonstrated that increased intracellular cAMP levels suppress the expression of rat TRH receptor (TRH-R) mRNA. We previously demonstrated that transient expression of a mutant Gs alpha gene suppress the rat TRH-R gene expression in the cultured rat growth hormone-secreting tumor cell line (GH3), whereas TRH-R gene expression in adenomas with Gs alpha gene mutation (gsp oncogene) did not differ from that in tumors without the mutation. The discrepancy suggests the possibilities that the effect of permanent expression of mutant Gs alpha gene on TRH-R gene expression is different from that of transient expression of the mutant gene and hypothalamic hormones including TRH regulate the gene expression. METHODS: We investigated whether permanent expression of the mutant-type Gs alpha does not suppress the TRH receptor gene expression in GH3 cells, and whether TRH suppresses the gene expression by using reverse transcription-polymerase chain reaction (RT-PCR) and in vitro transcription. RESULTS: Permanent expression of a mutant-type Gs alpha increased basal cAMP levels up to 1.7-fold relative to the controls, whereas the wild-type cell line did not show increased cAMP levels. Permanent expression of a mutant-type Gs alpha increased TRH receptor mRNA level up to 2.8 fold compared with the controls. Treatment of the permanently transfected GH3 cells with TRH suppressed TRH-R gene expression more prominently compared to the wild type GH3 cells. CONCLUSION: These results suggest that permanent expression of mutant Gs alpha enhances the expression of TRH-R in GH-secreting pituitary tumors with gsp oncogene, but the gene expression may also be regulated by other factors including TRH.
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Peroxiredoxin I and II are Involved in Hydrogen Peroxide Regulation in FRTL-5 Thyroid Cells.
Ho Kim, Tae Hoon Lee, Eun Shin Park, Jae Mi Suh, Soo Jung Park, Hyo Kyun Chung, Hyun Jin Kim, Soo Hong Chae, Do Hee Kim, O Yu Kwon, Young Kun Kim, Min Ho Shong, Heung Kyu Ro
J Korean Endocr Soc. 2000;15(1):55-69.   Published online January 1, 2001
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BACKGROUND
Peroxiredoxins (Prx) play an important role in regulating cellular differentiation and proliferation in several types of mammalian cells. One mechanism for this action involves modulation of hydrogen peroxide (H2O2)-mediated cellular responses. This report examines the expression of Prx I and Prx II in thyroid cells and their roles in eliminating H2O2 produced in response to TSH. METHODS: The expression of Prx-I and Prx-II were quantiated in FRTL-5 after stimulation with Thyroid stimulating hormone (TSH), Forskolin (FSK), Methimazole (MMI) and hydrogen peroxide (H2O2). Transient transfections were carried out with FRTL-5 cells at 80% confluency and 20microgram of pCRprx I and pCRprx II or equivalent molar amounts of the pCR3.1TM basic vector. Transient transfection used an electroporation technique. Intracellular H2O2 was assayed in FRTL-5 cells with a fluorescent dye, 2', 7'-dichlorofluoresceindiacetate (DCFH-DA). Apoptosis of cells were evaluated by using an detection kit (Promega, Inc., Madison, WI). RESULTS: Prx I and Prx II are constitutively expressed in FRTL-5 thyroid cells. Prx I expression, but not Prx II expression, is stimulated by exposure to TSH and H2O2. In addition, methimazole (MMI) induces a high level of Prx I mRNA and protein in these cells. Overexpression of Prx I and Prx II enhance the elimination of H2O2 produced by TSH in FRTL-5 cells. Treatment with 500microM H2O2 causes apoptosis in FRTL-5 cells as evidenced by standard assays of apoptosis (i.e., terminal deoxynucleotidyl transferase deoxyuridine triphosphate-biotin nick end-labeling (TUNEL), BAX expression and PARP cleavage. Overexpression of Prx I and Prx II reduces the amount of H2O2-induced apoptosis measured by these assays. CONCLUSION: These results suggest that Prx I and Prx II are involved in the removal of H2O2 in thyroid cells, and can protect these cells from undergoing apoptosis. These proteins are likely to be involved in the normal physiological response to TSH-induced production of H2O2 in thyroid cells.
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Routine Measurement of Serum Calcitonin Concentration is Useful in Early Detection of Medullary Thyroid Carcinoma Among Patients with Nodular Thyroid Disease.
Jong Ryeal Hahm, Jae Hoon Chung, Eun Young Oh, In Kyung Chung, Tae Young Yang, Dong Jun Kim, Byung Ju Kim, Sung Hoon Kim, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
J Korean Endocr Soc. 2000;15(1):70-84.   Published online January 1, 2001
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BACKGROUND
Serum calcitonin is a sensitive and specific marker for diagnosis of medullary thyroid carcinoma (MTC) and its determination leads to accurate preoperative diagnosis and gives chances of definite cure. However, since many non-MTC diseases are also associated with calcitonin elevation, its significance in patients with mild or moderately elevated basal serum calcitonin levels is not clear. Furthermore, the normal value of calcitonin using immunoradiometric assay (IRMA) kit has not so far been definitely ascertained. This study is aimed at assessing the clinical significance of routine measurement of serum basal calcitonin concentration in nodular thyroid disease patients and evaluating the pentagastrin stimulation test in case of mild or moderate elevation of basal calcitonin level. We also measured serum calcitonin value in 408 normal individuals. METHODS: The basal serum calcitonin concentrations using a commercial IRMA kit (Medgenix CT-U.S.-IRMA) were measured in 818 patients with nodular thyroid disease (average age 45 years with a range from 13 to 82 years; 125 males and 693 females) who visited thyroid clinics in Samsung Medical Center between June 1997 and December 1998. Serum concentrations of T3, T4, TSH and thyroid autoantibodies were measured and ultrasonography of thyroid and thyroid scan using 131I or 99mTc-pertechnetate were performed in all patients. We also studied 408 healthy subjects without any thyroid disease (average age 48 years with a range from 20 to 86 years; 224 females). RESULTS: The calcitonin value in normal subjects was found to range from 0 to 13 pg/mL, and it was shown that men had higher calcitonin level than women (p< 0.05). The rate of serum calcitonin elevation (> 10pg/mL) in nodular thyroid disease was 1.71% (14/818), and the incidence of MTC was 0.73% (6/818) in this study. MTC was found in all patients with basal serum calcitonin levels more than 100 pg/mL. Pentagastrin stimulation test was also required to diagnose MTC in patients with basal serum calcitonin levels between 30 and 100pg/mL. The calcitonin concentration stimulated by pentagastrin increased more than 400pg/mL or more than 3.8 times of basal concentration. It was possible to diagnose MTC with fine needle aspiration and cytology in only one case out of six patients with MTC. CONCLUSION: Fine needle aspiration and cytology in diagnosing MTC was not sensitive and not devoid of false positive results. We confirmed that serum calcitonin measurement was very useful means for the preoperative diagnosis of unsuspected MTC. Pentagastrin stimulation test may be a reliable means of evaluation in nodular thyroid disease patients with mild or moderate elevation of basal calcitonin level. We recommend routine measurement of serum calcitonin concentration in patients with nodular thyroid disease.
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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
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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.
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New Mutation Site in Vasopressin V2 Receptor Gene in a Family with Congenital Nephrogenic Diabetes Incipidus.
Soon Hee Lee, Chang Hoon Choi, See Hyung Park, Young Sun Choi, Jeong Gook Kim, Seung Woo Ha, Bo Wan Kim
J Korean Endocr Soc. 2000;15(1):97-106.   Published online January 1, 2001
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BACKGROUND
Congenital nephrogenic diabetes insipidus (NDI) is a rare inherited disorder, in which two different hereditary forms, X-linked and autosomal recessive traits, have been identified. The X-linked recessive form, mostly (>90%) congenital NDI, has been known to be caused by mutation of the arginine-vasopressin receptor 2 (AVPR2) gene. AVPR2 mutation sites are different in ethnic groups and recently 72 different mutation sites have been reported among AVPR2 gene. This study aimed to analyze AVPR2 gene in selected members in a Korean family with NDI and provided a report of the existence of a new mutation site in AVPR2 gene. METHODS: Three-generation maternal pedigree of the index patient (21-year old male, patient I) and his younger brother (19-year old male, patient II) with NDI was collected. Genomic DNA was obtained from patient I, II, III (index patient's male maternal cousin with NDI), index patient's mother, three maternal aunts, one female maternal cousin and, for control, one healthy male volunteer. Three coding exons of AVPR2 gene were amplified by PCR using 4 pairs of oligonucleotide primers. After direct sequencing of amplified PCR products, the sequence was compared with whole squence of normal AVPR2 gene and identification of a new site of mutation in this gene was done. RESULTS: 1) all three male patients had transversion of G to C at position 1033 of the AVPR2 gene, resulting in a subsequent change of amino acid from glycine to cysteine in codon 201. 2) Two small peaks of G and T, the result of direct sequencing in five female members in this family, would suggest that they are carriers of G to N transversion. CONCLUSION: These results can demonstrate the significant functional correlation of the mutation in AVPR2 gene sequence with clinical NDI, and suggest the clinical utility of direct mutation testing for congenital NDI in family.
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Case Report
Case of Sheehan's Syndrome Misdiagnosed as Pituitary Apoplexy due to Pituitary Adenoma.
Sun Hee Park, Do Joon Park, Kyoung Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee
J Korean Endocr Soc. 2000;15(1):107-112.   Published online January 1, 2001
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Postpartum ischemic necrosis of the pituitary gland, known as Sheehan's syndrome, is well-established clinical entity. The recent progress in radiological imaging allows an easy and noninvasive study of the pituitary area in the patients while still alive. An empty or partially empty sella is a constant feature of Sheehan's syndrome in the later phase. We report a case of nonhemorrhagic postpartum pituitary infarction documented in the acute phase with clinical, endocrine, and sequential magnetic resonance (MR) imaging studies.
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Original Article
Mutations in Thyroid Hormone Receptor-beta Associated with Patients with Generalized Resistance and Pituitary Resistance to Thyroid Hormone.
Yong Seok Yun, Sung Kkwan Hong, Chul Woo Ahn, Jae Hyun Nam, Seok Won Park, Bong Su Cha, Young Duk Song, Eun Jig Lee, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh
J Korean Endocr Soc. 2000;15(1):113-120.   Published online January 1, 2001
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We report a point mutation in the TRbeta gene in korean patients with generalized resistance and pituitary resistance to thyroid hormone. One mutation at TRbeta (P453S) were detected in patient with pituitary resistance to thyroid, which showed different phenotype, generalized resistance to thyroid hormone, in her mothers. But, the other (C31Y), did not show clear relations with the disease. Therefore, further study of molecular and cellular basis will be warranted to explain the clear mechanism of the resistance to thyroid hormone.
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Case Reports
Two Cases of Malignant Lymphoma Involving Bilateral Adrenal Glands as Huge Masses.
Seung Hyeok Han, Jin Seok Kim, Myung Soo Kim, Hye Won Chung, Jae Ho Jung, Young Suck Goo, Chul Woo Ahn, Jae Hyun Nam, Sang Soo Jung, Young Duk Song, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh, Jee Sook Hahn
J Korean Endocr Soc. 2000;15(1):121-127.   Published online January 1, 2001
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Adrenal gland is a common site of metastatic tumors such as breast cancer, lung cancer, and colon cancer. When adrenal mass is found incidentally, adenoma is the most common among single adrenal masses. But in the case of bilateral adrenal masses, infection, bilateral metastases and hemorrhage are common. Secondary involvement of the adrenal gland is found in 25% of autopsy cases of non-Hodgkin's lymphoma. However, adrenal insufficiency is rare because it becomes apparent only when approximately 90% of adrenal cortex is destructed. We exprienced two cases of malignant lymphoma which involved the adrenal glands bilaterally. One case in which adrenal insufficiency was suspicious, was accompanied by hypovolemic shock and sepsis at the initial presentation. He died of sepsis combined with DIC even though hydrocortisone, intravenous saline infusion, and antibiotics therapy were started immediately. The other one was found incidentally, in which adrenal infiltraion was confirmed by CT scan. Hormonal level was normal and adrenal masses disappeared after chemotherapy.
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A Case of Porphyria with Acute Pancreatitis.
Seok Won Chung, Jeong Hee Han, Young Min Ju, Kwang Hee Yoon, Won Seok Yang, Sung Koo Lee, Sung Kkwan Hong, Eun MEE hAN, Byung Sik Kim, Ki Up Lee
J Korean Endocr Soc. 2000;15(1):128-132.   Published online January 1, 2001
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The porphyrias are a group of disorders caused by deficiency in the enzymes of the heme biosynthetic pathway. Patients with porphyria may develop neurovisceral attacks which include severe abdominal pain, neuropsychiatric manifestations and potentially fatal respiratory paralysis. However, these patients may also have abdominal pain not due to porphyria itself, and in such case, careful evaluation is important. We report a case of acute pancreatitis with masquerading acute attack of porphyria, which made us difficult to make a correct diagnosis. A 29-year-old female, previously diagnosed to have hepatic porphyria, presented with acute abdominal pain, back pain and leg pain for 3 days. Serum amylase was normal and 24-hour urine -ALA and PBG showed increased levels. After intravenous infusion of glucose, symptoms were improved. From the 10th day of admission, she complained severe abdominal pain, and was found to have severe metabolic acidosis, shock, and signs of peritonitis on the 12th day of admission. Emergency exploration revealed edematous pancreas. Amylase and lipase levels in serum and ascites were found to be markedly elevated. After conservative management, her general condition gradually improved and serum amylase and lipase levels were normalized.
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Endocrinol Metab : Endocrinology and Metabolism