- A Case of Apical Hypertrohic Cardiomyopathy Associated with Pheochromocytoma.
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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
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J Korean Endocr Soc. 2004;19(5):522-527. Published online October 1, 2004
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- 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
- Korean Adult Growth Hormone Deficiency Treatment Registry.
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Sung Woon Kim, Seong Yeon Kim, Su Youn Nam, Yoon Sok Chung, Jae Hoon Chung, In Kyung Jung, Jong Ryeal Hahm, Minho Shong, Dong Sun Kim, Seong Keun Lee, Sung Dae Moon, Hyun Koo Yoon, Doo Man Kim, Sang Woo Kim, Hye Kyung Park
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J Korean Endocr Soc. 2002;17(1):43-47. Published online February 1, 2002
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- BACKGROUND
Adult growth hormone (GH) deficiency is related with decreased lean body mass, increased body fat, and poor quality of life. In western countries, adult GH deficiency treatment registriesy provide a database of the effects and safety of GH deficiency treatment. The Korean Adult Growth Hormone Study Group of the Korean Society of Endocrinology register adult GH deficiency since 1996. METHEODS: Subjects were aged over 15 years, had organic hypothalamo-pituitary disease, and GH deficiency as documented by GH stimulation test or serum insulin-like growth factor-I (IGF-I) level. The underlying etiology for GH deficiency, serum IGF-I level, starting and maintenance dose, and adult GH deficiency assessment (AGHDA) score were investigated. RESULTS: From January 1996 to May 2001. 115 patients were enrolled. Mean age was 43.7 13.8 years and 60% were female. Thirteen medical institutions were involved in the registry. The most common underlying diseases were Sheehan's syndrome and pituitary adenomas. GH starting dose was from 0.4 to 1.0 units. Maintenance dose was between 0.5 and 1.2 units. Serum IGF-I levels were increased after GH treatment (0-week, 93.7 69.7 ng/mL; 2-weeks, 184.9 89.0 ng/mL; 6-weeks, 188.4 94.8 ng/mL; 10-weeks, 207.6 111.1 ng/mL; 6 months, 281.9 95.5 ng/mL). AGHDA scores slightly improved from 10.25 6.70 to 8.58 5.47 after 6 months of GH deficiency treatment. CONCLUSION: The GH Treatment Registry will be beneficial in monitoring the effects of GH deficiency treatment on Korean adult GH deficient subjects
- The Diagnostic Value of a Low Dose (1ug) Rapid ACTH Stimulation Test to Assess the Adrenocortical Function.
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In Kyung Jung, Jae Seok Jeon, Young Joo Park, Chan Soo Shin, Kyoung Soo Park, Seong Yeon Kim, Hong Kyu Lee, Hee Jin Kim, Jae Hyeon Kim
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J Korean Endocr Soc. 1997;12(3):433-442. Published online January 1, 2001
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Abstract
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- BACKGROUND
Insulin induced hypoglycemia has been used to assess the adrenocortical function, but may be hazardous. The standard rapid ACTH stimulation test has been advocated as a substitute but is sometimes insensitive. In this study, low dose (1ug) rapid ACTH stimulation test was compared to insulin induced hypoglycemia and standard dose (250ug) rapid ACTH stimulation. METHODS: 27 patients (14 men and 13 women) with pituitary disease and definite adrenocortical dysfunction (14 patients were confirmed by insulin induced hypoglycemia) and 23 controls (pituitary control: 3 men and 7 women, confirmed by insulin induced hypoglycemia, normal control: 8 men and 5 women) were studied. All subjects underwent rapid ACTH stimulation test with 2 different level of stimulation (1 and 250ug). Serum cortisol levels were measured at 0, 30 and 60 min after each dose of ACTH injection. A normal response was defined as a peak cortisol value of 497nrnol/L (18ug/dL) or above, RESULTS: During rapid ACTH stimulation study in controls, the peak serum cortisol level was significantly lower (690+-25lnmol/L (25.0+-9.1ug/dL) vs. 933+-257nmol/L (33.8+-9.3ug/dL); p< 0.01) and the peak appeared earlier (30min. vs. 60min) after the administration of low dose ACTH than after standard dose. However, the serum cortisol level at 30min was not different. In patient group, each serum cortisol level at 30min and 60min had no difference between low and standard dose (p>0.1). None of these 27 patients showed normal response to low dose stimulation, but 2 of 27 did to standard dose. In controls, 19 of 23 showed normal response to low dose, and all of 23 did to standard dose (sensitivity 100% vs 92.5%, specificity 82.5% vs 100%). The results of low and high dose stimulation test agreed with those of insulin induced hypoglycemia (Kendalls g= 0.50 vs 0.92, p<0.01 vs 0.001). CONCLUSIONS: The results of a low dose (1ug) rapid ACTH stimulation test showed good correlation with those of the standard dose (250ug) rapid ACTH stimulation test and insulin induced hypoglycemia. Thus it may be used in screening for the diagnosis of adrenal insufficiency.
- A Study of Point Mutations of Human Insulin-like Growth Factor - 1 (IGF - 1) Promoter Gene in Familial Short Stature (FSS) Patients.
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In Myung Yang, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Hyun Ha Chang, In Kyung Jung, Tae Kwan Park
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J Korean Endocr Soc. 1996;11(4):500-509. Published online November 7, 2019
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- Background
FSS is a normal variants in Korea, but some of them had defect of noctumal GH pulse i.e. neurosecretory dysfunction. Although Korean children had strikingly got higher final height in the last decade. We are interested in what kinds of differences were existed in FSS group. Previous study showed theres no difference of GH related biochemical markers between normal and FSS group, like IGF-I, IGFBP-3 etc. We analyzed molecular difference in FSS group. Methods: We screened 23 FSS patients and 16 normal controls to IGF-I gene prornoter region with PCR-SSCP (single strand conformation polymorphisrn) method and sequenced 1 FSS patients who had abnormal SSCP band. Results: We found 1 out of 23 patients with abnormal SSCP band (none for 16 controls). Their IGF-I promoter gene were sequenced with modified Maxam-Gilbert method. One subject had 2 point mutations(+8 and +74). Conclusion: We found point mutations of IGF-I promoter in FSS group, This position was regarded as HNF(hepatic nuclear factor)-3 binding sites. We needed more study for the detection of its biological function according io linear growth with in vivo and in vitro study.
- Expression of Exon 1 and 6 of Indulin-like Growth Factor - 1 (IGF - 1) Gene in Thyroid Tissues.
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Sung Woon Kim, Hyun Ha Chang, In Kyung Jung, Jeong Taek Woo, In Myung Yang, Jin Woo Kim, Soung Seol Kim, Young Kil Choi
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J Korean Endocr Soc. 1996;11(4):409-417. Published online November 7, 2019
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Abstract
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- Background
Goiter has been a common problem in the thyroid disease. The exact mechanism of goiter had not been clarified yet, but some goiters were increased with TSH(thyrotropin releasing hormone) dependent manner. TSH might be a major influencing factor for increasing size of goiter(goitrogen) and theres many cofactors those influenced to goiter size. One of the rnost prominent growth factor as a goitrogen is a IGF-I(insulin-like growth factor-I). IGF-I play a great role as a cofactor of goitrogen with TSH. This study, therefore, is aimed to investigate intracellular activation of IGF-I gene promoter in the surgical specimens of thyroid tumor. Methods: We used surgical specimen of various thyroid tissues from normal to malignant along its cell nature. Actually we used normal liver tissue as a IGF-I control tissue, normal thyroid, benign adenoma, and papillary thyroid cancer tissue with its malignat nature. We checked Mrna expression of whole IGF-I and IGF-I exon 6 by Northern blot method, and IGF-I, promoter 1 expression by RT-PCR-transcription method. Autoradiographied signals were analysed with densitometer. Results: We found whole IGF-I mRNAs were expressed with alternate splicing in exon 1, 2 and exon 4, 5 respectively. Striking events of IGF-I transcription were multiple tranascription initiatian in Pl and P2, and 3 sites for polyadenylation in exon 6. Four or more Mrna bands in Northern blot analysis of IGF-I(0.8, 1.4, 4.2, and 7.8kb) were noted. In low molecular weight IGF-I Mrna did not change their signal intensity with tissues, but exan 6(7.8kb) signals were significantly increased to its hepatic expression levels in malignant tissue. IGF-I, exon 1 expression by RT-PCR-T7 transcription was strikingly increased in thyroid cancer tissue, but exon 6 expression was not a great expession. Conclusion: One possible guess for this expression discrepancy of each exon may be originated from different Mrna degradation of each IGF-I signals. We need more preeise experiment for Mrna degradation speed of IGF-I.
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