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Volume 12(3); September 1997
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Original Articles
Moleculan Genetics of Glucocorticoid Remediable Aldosteronism.
Jong Won Kim
J Korean Endocr Soc. 1997;12(3):341-345.   Published online January 1, 2001
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No abstract available.
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Androgens and Bone Mineral Density in Women.
In Kwon Han
J Korean Endocr Soc. 1997;12(3):346-348.   Published online January 1, 2001
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No abstract available.
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Expression of TRH Receptor Gene in GH-Secreting Piruitary Adenomas.
In Myung Yang, Seung Joon Park, Jeong Wha Ryu, Joo Ho Chung, Mee Sook Ryu, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi
J Korean Endocr Soc. 1997;12(3):349-356.   Published online January 1, 2001
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Background
To test the hypothesis that Galphas gene mutation may suppress the expression of TRH-R gene, we investigated whether hTRH-R gene expression is lower in human GH-secreting pituitary adenomas with Galphas mutation than in tumors without the mutation. Method: TRH-induced paradoxical response of GH was observed in 8 acromegalic patients. The mutation of gene was identified by direct sequencing of the genomic DNA prepared from GH-secreting pituitary adenomas. The expression of hTRHT mRNA was quantitated by RT-PCR. Results: The transcript of hTRH-R gene was detected in 6 of 8(75%) tumors. Three of these(50%) showed the paradoxical GH response to TRH and the other three patients did not show the response. The relative expression of hTRH-R mRNA in the tumors from patients with the paradoxical response of GH to TRH did not differ from that in the tumors from patients without the paradoxical response. Direct PCR sequencing of Galphas disclosed a mutant allele and a normal allele only at codon 201 in 4 of 8 tumors. The paradoxical response to TRH was observed in 2 of 4 patients without the mutation, and 2 of 4 patients with the mutation. The hTRH-R gene expression of pituitary adenomas did not differ between the tumors without the mutation and those with mutation. Conclusion: This study suggests that the expression of TRH-R gene is not likely to be a main determinant for the paradoxical response of GH to TRH, and that Galphas mutation does not seem to suppress the gene expression of TRH-R in GH secreting adenoma.
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Effect of Ga2 gene mutation on the Expression of Thyrotropin-Releasing Hormone ( TRH ) Receptor Gene in GH3 Cells.
Seung Joon Park, In Myung Yang, Jeong Hwa Ryu, Joo Ho Chung, Jee Chang Jung, Kye Chang Ko, Young Seol Kim, Young Kil Choi
J Korean Endocr Soc. 1997;12(3):357-363.   Published online January 1, 2001
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Insulin-Like Growth Factors and Their Bindign Proteins in Uterine Leiomyoma Pretreated with Gonadtropin Releasing Hormone Agonist.
Ki Chul Kim, Jung Gu Kim, Jin Yong Lee
J Korean Endocr Soc. 1997;12(3):364-375.   Published online January 1, 2001
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BACKGROUND
Uterine leiomyoma is the most common pelvic tumor, occurring in 20-25% of women in reproductive age. Gonadotropin releasing hormone agonist (GnRHa) has been reognized as a temporary medical management for this disorder. The etiology of these tumors is unknown but it has been shown that the insulin-like growth factors (IGF-I, IGF-II) are promoters of growth in nongynecologic tumors. Several recent studies have suggested the possible role of IGFs in human leiomyoma growth. The IGF binding proteins (IGFBPs) are believed to modulate actions of IGF and to have IGF-independent actions. The purpose of this study was to evaluate the type of IGF and IGFBP which may be involved in leiomyoma growth and to investigate a possible IGF related mechanism of action of GnRHa. METHOD: The IGFs and IGFBPs were measured by double antibody radioimmunoassay, western ligand blot and immunoprecipitation in the tissue cytosols of normal uterine myometria (n=15), nontumorous myometria adjacent to a leiomyoma and leiomyoma from patients nontreated (n=15) and treated (n=10) with GnRHa. RESULTS: The mean IGF-I and IGF-II level were significantly higher in leiomyoma from untreated patients than in the adjacent myometrium and normal myometrium but no significant differences in these IGF levels between normal myometrium and adjacent myometrium were noted. The IGFBP-2, IGFBP-3 and 26kDa IGFBP were detected variably but IGFBP-4 was consistently present in all tissues. There were no significant differences in the relative intensity for IGFBP-4 and the frequency of IGFBPs between leiomyoma, adjacent myometrium and normal myometrium from untreated patients. The IGF-I, IGF-II levels and the relative intensity of IGFBP-4 in leiomyoma from GnRHa-treated patients were significantly lower than those in untreated patients, but these levels in the adjacent myometrium were comparable. The frequency of each IGFBP in leiomyoma and the adjacent myornetrium from GnRHa-treated patients did not significantly differ from untreated patients. CONCLUSION: Both IGF-I and IGF-II are involved in the growth of leiomyoma and GnRHa may in part act to decrease size of leiomyoma by regulating the local levels of IGF-I, IGF-II and IGFBP-4.
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Characteristics of Serum Insulin-like Growth Factor ( IGF ) and IGF-Bindign Protein-3 during Pregnancy.
Dae Yeol Lee, Jung Soo Kim, Hong Ro Lee, Cheol Hee Rhee, Soo Chul Cho
J Korean Endocr Soc. 1997;12(3):376-385.   Published online January 1, 2001
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BACKGROUND
Pregnancy in human and rodents is associated with dramatic matemal metabolic changes. Insulin-like growth factors (IGFs) are mitogenic peptides that are essential for fetal and maternal tissue growth during pregnancy. They circulate complexed primarily with a serum IGF-binding protein (IGFBP-3) which regulates the availability of the IGFs to their specific target tissues. METHODS: To examine the changes of IGFs and IGFB-3 during pregnancy, we measured serum total IGF-I, free IGF-I, IGF-II and IGFBP-3 by using specific radioimmunoassay, immunoradio-metric assay, western ligand blot and western immunoblot. Blood samples were obtained from 88 pregnant women between 6-40 weeks gestation. RESULTS: While serum IGF-I levels increased up to 50% in late pregnancy, serum IGF-II levels remained unchanged. However, serum free IGF-I levels were significantly higher during pregnancy than in nonpregnancy. Western ligand blot analysis revealed that IGFBP-3 in pregnancy serum was significantly decreased at 6 weeks of gestation, continued decreased level until term, and returned to a nonpregnant level by postpartum 10 day. Serum IGFBP-3 profiles in Western immunoblot analysis revealed that 30 kDa fragments of IGFBP-3 were detectable in pregnancy serum but not in nonpregnancy serum. In contrast, serum IGFBP-3 levels using radioimmunoassay was significantly increased in late pregnancy. CONCLUSIONS: 1) serum IGF-I was significantly elevated in late pregnancy 2) serum IGF-II was not significantly changed 3) free IGF-I significantly elevated throughout gestation 4) intact IGFBP-3 was markedly reduced after 6 weeks of gestation.
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Primary empty sella syndrome.
Kyoung Rae Kim, Sung Kil Lim, Young Duk Song, Hyun Chul Lee, Kap Bum Huh, Eun Sook Kim, In Jai Kim, Yoon Jae Moon, Sang Kyu Na, Su Youn Nam, Eun Jig Lee
J Korean Endocr Soc. 1997;12(3):386-392.   Published online January 1, 2001
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BACKGROUND
Primary empty sella syndrome (PES) is thought to arise from an incompetent diaphragma allowing progressive herniation of arachnoid membrane with secondary compression and atrophy of the pituitary gland. As a consequence of the improvement and widespread use of neuroradiological techniques, such as computerized tomography (CT) and magnetic resonance imaging (MRI), empty sella is more frequently disclosed. The aim of this study is to assess the associated clinical characteristics and endocrinologic disturbance in empty sella syndrome. METHODS: From January 1986 to June 1996, 171 patients with empty sella syndrome have undergone analysis for clinical characteristics and associated disease. RESULT: In our study, PES was diagnosed in 131 of the 171 patients (77%). Primary empty sella syndrome was frequent in middle aged women (female:male 115:16, mean age: 50.6+12.6 years). The common clinical features were headache (80.2%), obesity (72.5%), and hypertension (27.5%). Most of patients with PES have normal pituitary function (75%). The frequent pituitary dysfunction was hyperprolactinemia in PES (21%). Partial and total emptiness of sella on sella CT or MRI were in 111 (84.7%) patients, and in 20 (15.4%) patients, respectively. The most common associated disease with empty sella syndrome was pituitary adenoma. CONCLUSION: PES should be considered as a possible cause in obese middle aged women with unexplained headache. The combined pituitary function test should be considered for evaluation of pituitary dysfunction when clinically suspected.
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Hormonal and Cytokine Regulation of ICAM-1 gene in FRTL-5 Thyroid Cells: Cloning and Analysis of 5-Regulatory Region of Rat ICAM-1 Gene.
Min Ho Song, Young Tae Shin, Young Kun Kim, Heung Kyu Ro
J Korean Endocr Soc. 1997;12(3):393-409.   Published online January 1, 2001
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BACKGROUND
We have found abnormal expression of ICAM-1 in thyroid follicular cells from patients with Graves disease and Hashimoto disease. In this report, we present the hormonal regulation of ICAM-1 mRNA expression and the primary structure of 5-regulatory region which is important for transcriptional regulation of ICAM-1 gene. A I.S kb fragment of the 5-regulatory sequences are identified and linked to luciferase as a reporter. METHOD: Those reporter constructs were used to evaluate the expression in response to cytokines and hormones. Deletion analysis of 1.8 kb fragment of ICAM-1 promoter in FRTL-5 cells provide the evidence for the existence of several regulatory elements of enhancer and silencer in ICAM-1 gene transcription in thyroid cells. RESULTS: ICAM-1 mRNA is easily detected by Northern analysis using total RNA from FRTL-5 cells regardless of culture conditions. The transcripts of rat ICAM-1 showed single band of 2.6 kb in length. The FRT cells which was come from early FRTL cell culture did not show ICAM-1 mRNA with usual Northern analysis, We found differential regulation of ICAM-1 RNA level in different culture condition in FRTL-5 cells, The cells maintained at 3H (no hydrocortisone, no insulin, no TSH) condition showed the highest expression level compared to 4H, 5H, or 6H medium. Hydrocortisone markedly decreased the ICAM-1 RNA and insulin partially recovered the hydrocortisone induced repression. TSH which is important in growth and function of FRTL-5 cells could independently downregulate the ICAM-1 RNA levels. Forskolin (10 mM) could mimic the action of TSH on ICAM-1 mRNA. TNF-a and interferon-y increase ICAM-1 expression in FRTL-5 thyroid cells. TSH/forskolin inhibited maximal expression of ICAM-1 by TNF-a and interferon-r. Promoter activity of the ICAM-1 gene was positively regulated by cytokines, TNF-a and IFN-r and negatively regulated by thyroid stimulating hormone. The addition of TSH and FSK caused a 50% decrease in ICAM-1 promoter activity within 24 hour. The TSH and FSK action was mapped at 175 bp and 97 bp of the start of translation. The mutant construct pCAM-175 delGAS which has no GAS sequence showed no TSH mediated suppression of promoter activity. CONCLUSION: These findings suggested that hormones and cytokines differentially regulated the ICAM-1 gene expression and TSH downregulated ICAM-1 gene transcription by inhibiting the activation of IFN-r induced transcription factors which can bind the GAS of ICAM-1 promoter.
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An Inhibitory Mechanism of Gastric Acid Secretion in Patients with Hyperthyroidism.
Hyeok Yil Kwon, Hyoung Jin Park
J Korean Endocr Soc. 1997;12(3):410-420.   Published online January 1, 2001
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BACKGROUND
Although hypochlorhydria, hypergastrinemia and antiparietal cell antibody have been well documented in the patients with hyperthyroidism, a cause of hypochlorhydria or hypergastrinemia is unknown at the present time. Therefore, in order to clarify an inhibitory mechansim of gastric acid secretion in the patients with hyperthyroidism, interrelationship among hypochlorhydria, hypergastrinemia and antiparietal cell antibody was investigated in this study. METHODS: The gastric secretory function, fasting and postprandial plasma concentrations of gastrin and titer of antiparietal cell antibody in the plasma were determined in the patients with hyperthyroidism and normal subjects. Immunoblot analysis was performed to identify the gastric membrane protein, a possible gastric antigen to antiparietal cell antibody. Using a immunocytochemical technique with electron microscopy, intracellular structure of the parietal cell reacted with antiparietal cell antibody was observed. RESULTS: The basal and pentagastrin-stimulated maximal acid output were reduced in the patients with hyperthyroidism. The fasting and postprandial plasma concentrations of gastrin were markedly elevated in the patients. The plasma gastrin concentration in the patients with the antiparietal cell antibody was higher than that of the norrnal subjects as well as the patients without the antibody not only in the fasting state but also in the postprandial state. However, the plasma gastrin concentration of the patients without the antiparietal cell antibody was elevated in the fasting state only. There was no difference in the gastrin content of the antral mucosa between the norrnal subjects and the patients. The antiparietal cell antibody was detected in 5 (38.5 %) out of 13 patients by using the indirect immunofluorescence method. Patient IgG dose-dependently inhibited rabbit gastric H (+),K (+)-ATPase activity. Among proteins of the rabbit gastric mucosa membrane, four high molecular weight proteins (91, 140, 170 and 210 K dalton) were reacted to the patient IgG. The patient IgG positive peroxidase-antiperoxidase (PAP) activity was electron microscopically detected on the intracellular cannalicular membrane of the parietal cell CONCLUSION: We conclude that hypochlorhydria and hypergastrinemia in the patients with hyperthyroidism are partially related to the antiparietal cell antibody and that the antigen to the antiparietal cell antibody may be H (+),K (+)-ATPase in the intracellular canalicular membrane of the parietal cell.
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Analysis of Prognostic Factors Determining the Recurrences in Patients with Papillary Thyroid Cancer After Surgical Treatment.
Jae Seok Jeon, Won Bae Kim, Hyun Kyung Chung, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Do Joon Park, Sun Wook Kim
J Korean Endocr Soc. 1997;12(3):421-432.   Published online January 1, 2001
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BACKGROUND
It is important to recognize the independent prognostic factors of papillary carcinoma of thyroid in therapeutic and follow up planning. However, its good prognosis and its low prevalence make it difficult to analyze prognostic factors determining patients survival in a relatively short period of time. We retrospectively investigated the independent prognostic factors for determining disease recurrence after surgery which, in adults, are known to be closely related to the prognosis of cancer. METHOD: We retrospectively reviewed the clinical records of 456 patients (male 70, female 381, unknown 5, mean age of 43.9+-12.9 years) who had visited the thyroid clinic in Seoul National University Hospital and analyzed the data with statistical software program. RESULTS: 1) At initial visit, chief complaint of the patients was abnormal neck mass in 90 percent. 2) In preoperative thyroid scan study, 82% showed cold area and 16% showed diffuse enlargement. 3) Of the 50 recurrent cases after surgery (11.5% of the total cases), 39 cases (78%) had recurred disease in neck area and 11 cases (22%) had recurrences at distant sites. (Lung 9 cases, Brain I case, Mediastinum 1case) 4) Statistically significant risk factors for recurrence after surgery were male sex, size of tumor (above 4.5cm in this study), extrathyroidal invasion of cancer, involvement of resection margin and no remnant ablation of thyroid tissue using radioiodine. CONCLUSION: Through retrospective study, we presented some clinical characteristics of papillary thyroid cancer in Korea and independent risk factors of cancer recurrences after surgery.
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The Diagnostic Value of a Low Dose (1ug) Rapid ACTH Stimulation Test to Assess the Adrenocortical Function.
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
J Korean Endocr Soc. 1997;12(3):433-442.   Published online January 1, 2001
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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.
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Clinical use of Urinary Androgen Metabolites in Hyperprolactinemia.
Kyoung Rae Kim, Sung Kil Lim, Young Duk Song, Hyun Chul Lee, Kap Bum Huh, Eun Sook Kim, Su Youn Nam, Eun Jig Lee, Bong Chul Jung, Byeong Kee Choi, Jae Ho Shin
J Korean Endocr Soc. 1997;12(3):443-449.   Published online January 1, 2001
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BACKGROUND
Hyperprolactinemia has been linked with hyperandrogenism and hirsutism in some women. High plasma Dihydroandrosterone and DHA-S levels were reported in patients with hyperprolactinemia and a dissociation of adrenal androgen and cortisol secretion occurs in normal subjects. The mechanism has not been elucidated, but it has been suggested that pituitary factors other than ACTH modulate adrenal androgen synthesis, One candidate hormone is prolactin. Adrenal tissue has been found to possess prolactin receptors and prolactin has been shown to act synergistically with ACTH and lowers the activity of the enzyme 5a-reductase or 3B-hydroxysteroid dehydrogenase (3B-HSD). The aim of this study was to investigate the secretion of adrenal androgen metabolites in patients with idiopathic hyperprolactinemia and prolactinoma and to deterrnine the relationship with prolactin and androgens. METHODS: We measured 24 hour-urinary DHEA, androstenedione, androsterone, pregnenolone, tetrahydrocorticoid and cortisol in 16 normal controls and 5 patients with idiopathic hyperprolac-tinemia (HP) and 12 patients with prolactonoma in the early follicular phase. RESULTS: Urinary DHEA, AD (androsteredione), and androsterone, the metabolites of adrenal androgen, were significantly higher in both patients with idiopathic HP and prolactinoma compared with those in normal controls (p<0.05), whereas they were not different in both disease groups. Urinary pregnenolone levels, early metabolite of adrenal steroid synthesis, were lower in patients. In contrast, urinary tetrahydorcortisol and cortisol were higher in patients compared to controls. There was no difference in DHEA:androsterone ratio between patients and controls. And there were no correlation between prolactin levels and the levels of androgenic metabolites or clinical symptoms. CONCLUSION: Prolactin has a tropic effct on the secretion of androgens and steroids by the adrenal cortex. But prolactin levels were not correlated with androgen levels or clinical symptoms (amenorrhea), and it might have little effect on lowering the activity of 3B-HSD.
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A Study About Correlation Between Urinary Androgen Metabolites and Bone Mineral Density in Psstmenopausal Women.
Kyoung Rae Kim, Ji Hyun Lee, Sung Kil Lim, Young Jun Won, Seok Ho Kwon, Bong Soo Cha, Young Duk Song, Hyun Chul Lee, Kap Bum Huh, Su Youn Nam, Bong Chul Jung
J Korean Endocr Soc. 1997;12(3):450-461.   Published online January 1, 2001
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BACKGROUND
Positive correlations between bone mass and androgen levels have been observed in premenopausal and postmenopausal women as well as in men. Androgen production was decreased in women with osteoporosis compared to that in age-matched controls. We hypothesized that androgen metabolism might be also deranged in osteoporosis. To clarify our hypothesis, we investigated the relationship between urinary metabolites of androgen and bone mineral density (BMD) in Korean postmenopausal osteoporotics. METHODS: We examined the anthropometry and bone turnover marker in 67 postmenopausal women. BMD was measured by dual energy X-ray absorptiometry (DEXA). Serurn levels of estrone, estradiol, free testosterone were measured by radioirnmunoassay and serum level of sex hormone binding globulin (SHBG) was measured by two site immunoradiometric assay. The urinary metabolites of androgen were determined by gas chromatography-mass spectrometry (GC-MS) at Korean Institute of Science and Technology Doping Control Center. RESULTS: 1. Spinal BMD had a positive correlation with height (r 0.3049, p<0.05), weight (r=0.4114, p<0.001) and body mass index (BMI, r=0.2638, p<0,05). 2. Spinal and femoral neck BMD had no correlation with serum levels of estrone, estradiol and ten major urinary metabolites of androgen, but serum free testosterone had positive correlation with spinal BMD (r=0.3622, p<0.01) and SHBG had negative correlation with femoral neck BMD (r=-0.2625, p< (0.05). 3. Serum free testosterone in osteoporotics was lower than non-osteoporotics with spinal BMD (p<0.05) and SHBG in patients with osteopenia was higher than non-osteopenic subjects with femoral neck BMD (p <0.05). 4. In multiple stepwise regression analysis, weight and serum free testosterone were statistically significant for spinal BMD (R =0.3072). As for femoral neck BMD, weight was the independent determinant (R 0.1307). 5. Serum level of osteo#ealcin and urinary deoxypyridinoline/creatinine had a positive correlation with urinary 11-ketoandrosterone (p<0.05). SHBG was positive correlation with osteocalcin (r=0.3190, p<0.05). 6. Serum free testosterone (r=-0.2740, p<0.05) decreased with aging. CONCLUSION: Our data suggest that androgen metabolism is not deranged in osteoporotics, but serum free testosterone is important than estrogen on postmenopausal osteoporosis after 5-10 years menopause.
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Case Reports
A Case of Isolated ACTH Deficiency Accompanied by hyperprolactinemia.
Young Seung Kim, Gwang Il Kim, Dae Su Kim, Jeon Ok An, Sang Jeong Yoon, Hee Cheol Jang, Kang Seo Park
J Korean Endocr Soc. 1997;12(3):462-467.   Published online January 1, 2001
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Isolated ACTH deficiency is a uncommon disorder causing secondary adrenocortical insufficiency. Less than 200 cases have been reported in the world. The major clinical manifestations are hypoglycemia, weight loss, hypotension, anemia, weakness, nausea, inability to excrete water load, and hyponatremia. A 56-year-old male was admitted because of weakness, fatigue, nausea and vomiting. He was pallor and not associated with hyperpigmentation. The basal plasma ACTH and cortisol levels were 8.30 pg/ml and 0.6 ug/dl. The serum cortisol did not response to rapid ACTH stimulation test. On combined pituitary stimulation test, the cortisol did not response to insulin-induced hypoglycemia. Other anterior pituitary hormones showed normal responses except elevated prolactin level. Six months after glucocorticoid replacement therapy, the elevated basal prolactin level returned to normal. Brain MRI did not show any anatomic abnormalities of the sellar and suprasella area. We report a case of isolated ACTH deficiency accompanied by hyperprolactineia, which respond to glucocorticoid replacement therapy.
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A Case of Thyroid Abscsess in Subacute Thyroiditis During Glucocorticoid Therapy.
Soon Jib Yoo, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Young Hwan Kim, Mi Ja Kang, Seung Hyeon Ko, Ki Uk Chang
J Korean Endocr Soc. 1997;12(3):468-472.   Published online January 1, 2001
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Subacute thyroiditis is a frequent benign thyroid disease associated with previous viral upper respiratory tract infection. Known complications of this disease are long-standing subclinical hypothyroidism, persistent anterior neck pain and rarely Graves disease. In general, thyroid abscess is an uncommon disease because of anatomic isolation of the gland and its rich system of drainage for blood and lymph. Especially, development of thyroid abscess in subacute thyroiditis is extremely rare phenomenan, but significant bad outcomes can be resulted. Its clinical BACKGROUND containes immune-suppressed state, anatomic defect, presence of underlying other thyroid disease and of non-thyroidal infectious foci. We experienced a case of subacute thyroiditis complicated with streptococcal thyroid abscess during glucocorticoid therapy. The patient was a 19-year-old female who was admitted due to anterior neck pain for 1 month. Typical subacute thyroiditis was suggested from initial laboratory findings including CBC, erythrocyte sedimentation rate, serum T3, T4, TSH levels, thyroid scan & thyroid uptake. But during oral prednisolone therapy, unexpected bacterial thyroid abscess was developed. We report this unusual case with review of literatures.
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