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Volume 14(4); December 1999
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Review Articles
Clinical Significance of Measuring Thyrotropin Recepter Antibody.
Young Kee Shong, Bo Youn Cho
J Korean Endocr Soc. 1999;14(4):609-619.   Published online January 1, 2001
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No abstract available.
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Transcription Factors.
Yong Joon Kim
J Korean Endocr Soc. 1999;14(4):620-626.   Published online January 1, 2001
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No abstract available.
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Radioactive Iodine Therapy in Differentiated Tyroid Carcinoma.
Jae Hoon Chung
J Korean Endocr Soc. 1999;14(4):627-635.   Published online January 1, 2001
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No abstract available.
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Original Articles
Changes of Glucose Tolerance in Acromegaly Patients with 24 Hour Continuous Subcutaneous Infusion of Octreotide.
Ki Hyun Baik, Kun Ho Yoon, Jeong Min Lee, Chang Wook Kim, Paek Sun Kim, Sang Aha Jang, Soon Jib Yoo, Hyun Sik Son, Moo II Kang, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang
J Korean Endocr Soc. 1999;14(4):636-644.   Published online January 1, 2001
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BACKGROUND
An important metabolic feature of acromegaly is a reduced action of insulin on hepatic gluconeogenesis and peripheral glucose disposal which mediated by growth hormone hypersecretion. Octreotide, a synthetic octapeptide somatostatin analogue exerts complex effects on hormonal and metabolic regulations affecting glucose homeostasis. This study was designed to ascertain the shorterm effect of octreotide on glucose tolerance in acromegaly. METHODS: 10 patients (five men and five women, age 47.9+/-11.8) were injected subcutaneously with octreotide, 100 micrograms for 24 hours. Patients were assessed with respect to growth hormone, glucose, and insulin response to a standard 100 g oral glucose tolerance test (OGTT) before and during the last 2 hour of octreotide infusion. RESULTS: During the therapy, there was significant decrease in mean blood glucose response to OGTT (678.4+/-51.9 vs 581.9+/-47.3 mg/dL/2hr: mean areas under the glucose curve, p=0.01) and mean serum insulin response to oral glucose load was significantly reduced in all patients (339.2+/-106.2 vs 256.7+/-111.3 U/mL/2hr: mean areas under the insulin curve, p=0.01). Using glucose tolerance test criteria three patients of 10 had normal glucose tolerance, four and three had impaired glucose tolerance and diabetes, respectively, at base line. While on octreotide these composition was changed to six patients of NGT, three of IGT and one diabetes. CONCLUSION: We conclude that insulin resistance mediated by GH hypersecretion was improved by shorterm octreotide treatment.
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KAL Gene and GnRH Receptor Gene Analysis in Patients with Kallmann's Syndrome.
Ki Hyun Park, Hyoung Jin Mo, Jin Young Kim, Jeong Yeon Kim, Sang Wook Bae, Byung Seok Lee, In Kyu Kim, Sei Kwang Kim, Kyung Ah Kim, Yong Ho Ahn
J Korean Endocr Soc. 1999;14(4):645-656.   Published online January 1, 2001
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BACKGROUND
Kallmann's syndrome is related to the defect in migration of olfactory neuron and GnRH neuron from the olfactory placode to the brain and it represents hypogonadism with anosmia or hyposmia. There are 3 modes of transmission in Kallmann's syndrome: X-linked, autosomal recessive and autosomal dominant. X-linked form is the most common. KAL gene is responsible for the X-linked form of Kallmann's syndrome and it had been localized to Xp22.3. The intron-exon organization had been determined and KAL gene mutation had also been identified in familial Kallmann's syndrome and it is very rare and shows heterogeneity. Furthermore, in the sporadic cases, KAL gene mutation is more rare. METHODS: In order to investigate the KAL gene mutation and the regulation of the gene expression in Kallmann's syndrome, we examined genomic DNA of 35 patients with sporadic Kallmann's syndrome. In the exon 3, 4, 5, 6, 7, 8, 9, 10, 11, 12 of KAL gene and 1, 2, 3 of GnRH receptor gene, the mutations were analyzed by PCR-based DNA sequencing. RESULTS: In our study, the mutation of KAL gene and GnRH receptor gene was not identified in the studied exons that were known as preferable sites of the mutation. CONCLUSION: The mutation of KAL gene and GnRH receptor gene is rare, and it might be needed to investigate mutations in other genes or in other part of the KAL gene such as intron or promoter region.
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Effect of Gs alpha Gene Mutation on the Expression of the Rat Somatostatin Receptor Gene.
I M Yang, S J Park, H G Jhang, G J Lee, S J Oh, S W Kim, J W Kim, Y S Kim, Y K Choi
J Korean Endocr Soc. 1999;14(4):657-666.   Published online January 1, 2001
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BACKGROUND
The growth hormone (GH)-secreting pituitary adenoma with mutation of Gs alpha gene (gsp oncogene) is known to show a higher response to somatostatin. The mechanism for the higher response is unclear. We previously demonstrated that transcription of the rat somatostatin receptor (SSTR) gene was increased by cAMP. Therefore, we investigated whether the mutation of Gs alpha gene can increase SSTR gene expression. METHODS: The mutant Gs alpha expressing plasmid of which arginine of codon 201was replaced with histidine was transfected transiently and permanently into GH3 cells. cAMP and rat GH were measured by radioimmunoassay. mRNA expression of the rat SSTR2 was determined by a semiquantitative RT-PCR. RESULTS: The intracellular cAMP production was increased by 1.8 folds in the transiently transfected cells and by 1.5 folds in permanently transfected cells compared to those in the cells transfected with the vehicle plasmid, plasmid expressing the wild type or the plasmid expressing the silent mutant of codon 226. The transcriptional activation by cAMP response element of somatostatin.gene was also increased by 2 folds 24 hours after transient transfection and by 3.5 folds in the permanently transfected cells. The transcriptional activation was not enhanced by forskolin in the transiently transfected cells, whereas it was more remarkably inhibited by somatostatin compared to that in the other transfected cells. The expression of SSTR2 was increased by 1.8 folds 24 hours after transfection in the transiently transfected cells and by 3 folds in the permanently transfected cells, and it was not enhanced by forskolin and isobutylmethylxanthine. The secretion of GH from the transiently transfected cells was not significantly higher than that from the wild type-expressing cells, but it was higher in the permanently transfected cells. The suppression of GH by somatostatin was more prominent in the permanently transfected cells compared to the other transfected cells. CONCLUSION: This study suggests that a higher expression of SSTR induced by the mutant Gs alpha may be a mechanism by which gsp-positive adenomas showed a higher response to somatostatin.
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Diagnostic Significance of Serum Thyroglobulin Measurement in the Follow - up of Patients with differentiated Thyroid Cancer.
Seon Hwa Lee, Byung Sool Moon, Sun Wook Kim, Jae Joon Koh, Do Joon Park, Won Bae Kim, Bo Youn Cho, Hong Kyu Lee
J Korean Endocr Soc. 1999;14(4):667-678.   Published online January 1, 2001
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BACKGROUND
Although serum thyroglobulin (Tg) has been proved to be a good tumor marker in the follow-up of the well differentiated thyroid cancer, some patients show low detectable Tg with negative 131I scan. In the present study, we tried to determine the lowest level of serum Tg which suggests requirement of aggressive work-up for the recurrent or metastatic thyroid cancer. METHODS: Serum Tg levels were measured in 102 patients with well differentiated thyroid cancer who had underwent thyroidectomy followed by 131I ablative therapy. Of 102 patients, 44 patients had no remnant thyroid tissue, while 58 patients had remnant thyroid. Serum Tg levels were measured while TSH-suppressive dose of T4 was administered (on T4 therapy) and then T4 was discontinued for 4 weeks to increase serum TSH level (off T4 therapy), then serum Tg levels were analyzed in relation to the presence or absence of recurrent or metastatic thyroid cancer, assessed by I scan and operation with reference to the physical examination, chest X-ray and thyroid ultrasonogram. RESULTS: Of 102 patients, 16 patients were found to have recurrent or matastatic thyroid cancer. Among them, 10 patients didnt have any remnant thyroid, while 6 patients had remnant thyroid. Serum Tg was undetectable on T4 therapy in 6 patients, but rose higher than 30 ng/mL off T4 therapy in 2 patients, while Tg remained undetectable in other 4 patients. In all 10 patients whoseTg levels were higher than 1 ng/mL. on T4 therapy, Tg rose higher than 30 ng/mL off T4 therapy. The best cut-off value of serum Tg which suggests recurrent or metastatic disease in patients without remnant thyroid was 3 ng/mL on T therapy (sensitivity 60%, specificity 91%, accuracy 84%) and 30 ng/mL off T4 therapy (sensitivity 80%, specificity 75%, accuracy 77%). In patients with remnant thyroid, cut-off value of serum Tg could not be determined because of the low sensitivity and specificity. CONCLUSION: In patients with well differentiated thyroid cancer who have no remnant thyroid, serum Tg level lower than 3 ng/mL on T4 therapy can warrant following-up of patients only with such clinical measures only such as physical examination and thyroid ultrasonogram. However, patients with Tg level of 3 ng/mL or more requires Tg measurements off T4 therapy and 131I scan to evaluate the possibility of recurrent or metastatic thyroid cancer.
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Therapeutic Response to Radioactive Iodine Treatment in Graves' Disease.
Hye Young Park, Hee Sang Kong, Yon Sil Jung, Sung Kwang Lee, Hong Kyu Kim, Moon Ho Kang
J Korean Endocr Soc. 1999;14(4):679-687.   Published online January 1, 2001
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BACKGROUND
Prediction of therapeutic response to radioactive iodine (RAI) in Graves disease is poorly understood. Although thyrotropin binding inhibitor immunoglobulin (TBII) level is a strong index for relapse after antithyroid drug treatment, conflicting results are described regarding its prognostic significance in Graves disease treated with RAI. This study is to evaluate possible prognostic factors including TBII wbich affect the outcome of RAI therapy in Graves disease. METHODS: Two hundred and one patients with Graves disease who were followed for over 12 months after RAI treatment were studied retrospectively. The subjects were divided into hypothyroid, euthyroid and hyperthyroid groups, based on the thyroid function evaluated at 12 months after RAI therapy. We evaluated the association of clinical parameters including patients age, goiter size, degree of hyperthyroidism and TBII index with outcome of RAI treatment. RESULTS: In Graves disease, response rate to RAI was 70.1% (hypothyroid 22.4% and euthyroid 47.7%) until 12th month. The mean age of hypothyroid group was 40+/-11 years, significantly older than that other groups (euthyroid: 33+/-12, hyperthyroid: 35+/-13, p<0.05). Initial level of thyroid function, duration of antithyroid drug treatment prior to RAI, goiter size and dosage of RAI were not significantly different between the groups. There were 61 patients who had both TBII tests before and after RAI. Twelve had negative TBII and 49 had positive TBII before RAI admini-stration. The rate of unremitted hyperthyroidism after RAI therapy was significantly lower in patients with negative TBII than in those with positive TBII prior to RAI treatment( 0% versus 46.9%, p<0.05). CONCLUSION: Graves patients with positive TBII prior to RAI therapy were associated with lower therapeutic response to RAI than those with negatve TBII. And old age was associated with the development of early hypothyroidism after RAI therapy. These results suggest these factors be also considered in the treatment of Graves disease with RAI.
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Bone Turnover and Bone Mineral Density in Acromegaly.
Sun Wook Kim, Hee Jin Kim, Seon Hwa Lee, Won Bae Kim, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee
J Korean Endocr Soc. 1999;14(4):688-697.   Published online January 1, 2001
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BACKGROUND
Abnormalities of calcium homeostasis and bone remodelling were known in acromegaly, but controversy concerning the influence of chronically elevated serum growth hormone (GH)/insulin like growth factor-I (IGF-I) concentrations on bone metabolism has been existed. In this study, we assess the effect of chronically elevated serum GH/IGF-I levels on bone metabolism and bone mineral density (BMD) in patients with acromegaly and compare the markers of bone metabolism and BMD of active acromegaly according to gonadal function. METHODS: We measured biochemical markers of bone turnover and BMD in 50 acromegalic patients (41 active disease, 9 inactive disease) and 41 control subjects. RESULTS: Active acromegalic patients had significantly higher serum oteocalcin levels (13.8+/-7.7 versus 6.8+/-4.7, 6.0+/--3.4 ng/mL, p<0.05) and urinary type I cross-linked N-telopeptide (101.7+/-64.2 versus 49.3+/-33.3, 56.1+/-39.4 nM BCM/mM Cr, p<0.05) compared with inactive acromegaly and control subjects. Serum IGF-I levels correlated positively with serum osteocalcin levels(r=0.69, p<0.05) and urinary type I cross-linked N-telopeptide (r=0.44, p<0.05). In the female patients with active acromegaly, BMD (T-score) was elevated in the femoral neck(1.00+/-0.14 versus 0.89+/-0.12,p<0.05) and trochanter (0.88+/-0.15 versus 0.77+/-0.11, p<0.05), whereas BMD of lumbar spine(1.13+/- 0.17 versus 1.17+/-0.17, p>0.05) and femoral Ward's triangle (0.78+/-0.16 versus 0.77+0.13, p>0.05) were not different from those of control subjects. In the patients with active acromegaly, serum osteocalcin levels (16.4+/-8.8 versus 14.9+/-10.1 ng/mL, p>0.05) as well as urinary type I cross-linked N-telopeptide (104.8+/-68.1 versus 122.0+/-80.3 nM BCM/mM Cr, p>0.05) were not different according to gonadal function. Also, femoral and spinal BMD were not different according to the gonadal function. CONCLUSION: GH/IGF-I excess increase bone turnover and might achieve a positive bone balance at each remodelling cycle. Markers of bone turnover and BMD of skeletal bone were not influenced by gonadal function in the patients with active acromegaly.
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Polymorphisms of the Interleukin - 6 Gene and Bone Mineral Density at Postmenopause in Korean Women.
Soo Young Yoon, Sung Kil Lim, Song Zae Li, Young Duk Song, Hyun Chul Lee, Kyung Rae Kim, Kap Bum Huh
J Korean Endocr Soc. 1999;14(4):698-705.   Published online January 1, 2001
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BACKGROUND
Interleukin-6 (IL-6) is one of the candidate cytokines to play an important role in bone loss followed by estrogen deficiency. Recently, the IL-6 VNTR (various number tandem repeats) genotype was reported to be associated with bone mineral density, raising the possibility that genotyping at this site might be of value in identifying women who are at risk for postmenopausal osteoporosis. To evaluate whether allelic variants in the gene encoding the polymorphism of VNTR located at the 3 flank of the IL-6 gene in Koreans were also the same as those of Caucasian, we analyzed the distribution pattern of the polymerase chain reaction product of the IL-6 gene. METHODS: The IL-6 VNTR were examined in 134 postmenopausal Korean women. Bone mineral densities were measured by DEXA (dual energy X-ray absorptiometry, Lunar Radiation, Madison, WI). RESULTS: The IL-6 VNTR polymorphism of Koreans was different from that of Caucasian, and four genotypes (KaKb, KbKb, KbKc and KbKd) were identified. The genotypes KaKb and KbKd were found only in one individual each and most Koreans had KbKb or KbKc genotypes. The overall prevalences of KbKb and KbKc genotypes were 76.9% Rlld 21.6%, respectively, and the distribution patterns of the genotypes were not different among normal, osteopenic and osteoporotic groups. The values of bone mineral density at the lumbar spine and femoral neck were not different between the frequent genotypes of KbKb and KbKc. Furthermore, the levels of alkaline phosphatase, osteocalcin and urinary deoxypyridinoline/creatinine were also not different between the two genotypes. CONCLUSION: There are ethnic differences in IL-6 VNTR polymorphism, and IL-6 VNTR polymorphism may not be associated with postmenopausal osteoporosis in Korean women. Our data suggest that the analysis of IL-6 VNTR polymorphism may not be helpful in detecting patients at risk of developing osteoporosis.
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Relation of beta 3-Adrenergic Receptor Gene Polymorphism to the Patterns of Body Fat Distribution and Insulin Sensitivity in Female Nondiabetic Offspring of Patients with NIDDM.
Jee Young Oh, Yeon Ah Sung, Nan Ho Kyung
J Korean Endocr Soc. 1999;14(4):706-718.   Published online January 1, 2001
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BACKGROUND
Obesity is an important metabolic abnormality as a pathogenesis of non-insulin dependent diabetes mellitus(NIDDM), and genetic factors have been suggested to be involved in the development of obesity and NIDDM. beta 3-adrenergic receptor gene polymorphism has been reported to be related to an earlier onset of NIDDM and increased capacity of weight gain in obesity. The purpose of this study was to investigate the relation of beta 3-adrenergic receptor gene polymorphism to body fat distribution pattern and insulin resistance in female nondiabetic offpsring of patients with NIDDM. METHODS: We assessed the patterns of body fat distribution by anthropometric measurement, bioelectric impedence analysis and computed tomogram; insulin sensitivity by using frequently sampled intravenous glucose tolerance test and the minimal model analysis. We inverstigated the beta 3 -adrenergic receptor gene polymorphism by PCR and RFLP. RESULTS: 1) The frequency of beta 3 adrenergic receptor gene polymorphism was as follows; wild type (Trp64Trp) 69.8%, Trp64Arg heterozygote 26.4%, Arg64Arg homozygote 3.8% in the offspring of patients with NIDDM. According to obesity, there was no significant difference of distribution of Arg64 allele between nonbese and obese subjects. 2) In the mutant subjects with Arg64 allele, the concentrations of total and LDL cholesterol were significantly increased (p<0.01), but fasting serum glucose and insulin, percent body fat, visceral fat area and visceral to subcutaneous fat area ratio were insignificantly increased, SI were insiginificantly decreased. 3) Multiple regression analysis showed that Arg64 allele did not significantly associated with visceral obesity and insulin resistance. CONCLUSION: The beta 3-adrenergic receptor gene polymorphism was related to dyslipidemia, but not related to visceral adiposity or insulin resistance in nondiabetic offspring women of patients with NIDDM. Further prospective studies in these subjects will be needed for the clarification of pathogenetic role of beta 3-adrenergic receptor gene polymorphism in the development of insulin resistance and NIDDM.
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Effect fo Nitric Oxide on Control of Insulin Secretion in Rat Pancreas.
Myung Jun Kim, Jong Ho Sung, Yang Hyeok Jo
J Korean Endocr Soc. 1999;14(4):719-728.   Published online January 1, 2001
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BACKGROUND
NO (nitric oxide), derived from L-arginine through the action of nitric oxide synthase (NOS), is a short-lived free radical transmitting cellular signals for vasodilation, neurotransmission, and cytotoxicity. Recently, this molecule has been reported to be involved in the various glandular secretion. Although the relationship between NO and the pancreatic endocrine secretion has been widely investigated, the role of NO on insulin secretion has not been elucidated. Therefore, the present study was designed to reveal the precise action of NO on the secretion and synthesis of insulin following administration of NAME (L-NG -nitroarginine methyl ester) or L-arginine using immunocytochemistry and in situ hybridization techniques. METHODS: NAME or L-arginine was administered into jugular vein of the male Sprague-Dawley rat (180~200 g, b,w.) exhibiting normoglycemia (80~120mg/dL). Blood glucose concentrations were measured at intervals of 30 minutes for 2 hours after drug treatment. The pancreatic tissues were taken out at 30 and 90 minutes following drugs administration for insulin immunocytochemistry and in situ hybridization. RESULTS: Both NAME and L-arginine treatments diminished blood glucose levels. The decrease of blood glucose level was more prominent in NAME-treated rats than that of L-arginine. Insulin immunoreactivity in drugs-treated rat pancreas decreased compared to that in normal control, while the expression of insulin mRNA was significantly increased. CONCLUSION: On the basis of present study, it is concluded that the transient changes of NO con-centration, regardless of increase or decrease, in Langerhans islet might act as a potent stimulant in insulin secretion and its synthesis.
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Cholesterol Lowering Effect of Cerivastatin in Korean Patients with Primary Hypercholesterolemia.
Sung Hoon Kim, Dong Jun Kim, Jong Rhulk Hahm, Byung Joon Kim, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
J Korean Endocr Soc. 1999;14(4):729-738.   Published online January 1, 2001
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BACKGROUND
Cerivastatin is a kind of statin, a synthetic HMG-CoA reductase inhibitor with high liver selectivity which lowers plasma cholesterol level by inhibiting endogenous cholesterol synthesis. This study evaluates the efficacy, safety, and tolerability of cerivastatin 0.1 mg and 0.3 mg in Korean patients with primary hypercholesterolemia. METHODS: A parallel group, randomized, placebo-controlled, double-blind study was conducted at Samsung Medical Center. The patients with primary hypercholesterolemia were placed on an American Heart Association Step 1 diet for whole study period. Single-blind placebo was administered for the final 4 weeks of period A, before randomization. Thirty two patients with low-density lipoprotein cholesterol (LDL-C) >160 mg/dL (if patients with a definite personal history of coronary heart disease (CHD) or with two or more cardiovascular risk factors, LDL-C >130 mg/dL) were randomized to 6 weeks treatment with one of the following regimens: cerivastatin 0.1 mg (n=11) or cerivastatin 0.3 mg (n=10) or placebo once daily at bedtime (n=11). RESULTS: Cerivastatin 0.1 mg and 0.3 mg treatment groups produced statistically significant (p<.05) changes at 6 weeks after treatment, compared to baseline and placebo in LDL-C (cerivastatin 0.1 mg 16.3%; cerivastatin 0.3 mg 35.2%; placebo 1.5%) and total cholesterol (cerivastatin 0.1 mg 10.3%; cerivastatin 0.3 mg 26.2%; placebo 1.3%). Cerivastatin 0.1 mg and 0.3 mg treatments were well tolerated and resulted in no significant increase in biochemical or clinical side effects compared to placebo. CONCLUSION: Cerivastatin at doses of 0.1 mg and 0.3 mg/day is a safe, well-tolerated, and highly effective HMG-CoA reductase inhibitor for the treatment of primary hypercholesterolemia.
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Case Reports
Two Cases of Extensive Pituitary Calcification.
Chul Woo Ahn, Shin Myung Kang, Do Young Kim, Jang Yel Shin, Seok Won Park, Jae Hyun Nam, Young Duk Song, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh
J Korean Endocr Soc. 1999;14(4):739-744.   Published online January 1, 2001
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Although calcification of such endocrine gland as adrenal or pineal gland is common, extensive calcification of the pituitary gland is unusual. Calcification is a well recognized but uncommon feature of prolactin-secreting, growth hormone-secreting and non-functioning pituitary tumours. The calcification varies in extent, but rarely exceeds a tiny amount histologically or radiologically. Recently, we had the opportunity to investigate two patients with radiologically demonstrated "pituitary stone" (severely calcified pituitary adenoma). The first Patient, a 51 year-old female, initially presented with general weakness, dizziness, visual disturbance, and loss of hair for 2 months. She was suspected to have a pituitary lesion. Decreased secretion of GH, TSH, LH, and FSH was demonstrated by dynamic tests. On CT scan, she was found to have multilobulated calcified sella mass. She was successfully managed by medical treatment. The second patient, a 65 year-old male, presented with general weakness, nausea, vomiting and polyuria for 2 months. Combined pituitary stimulation test showed subnormal response of GH and prolactine. Radiologic studies revealed pituitary stone which was managed with medical treatment of hormone replacement. We suggest that calcific changes in the pituitary adenoma might be common and occur to the extent of pituitary stone formation with the possible alteration of hormonal secretion.
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Brain Metastasis from Papillary Thyroid Carcinoma: Report of 2 Cases.
Jung Gu Lee, Ki Young Lee, Yon Sil Jung, Hong Kyu Kim, Hye Young Park, Jong Ho Kim, Moon Ho Kang
J Korean Endocr Soc. 1999;14(4):745-751.   Published online January 1, 2001
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Papillary carcinoma, the commonest thyroid malignancy, has an indolent clinical course and carries a good prognosis. Metastasis usually occurs to regional lymph nodes, including cervical and upper mediastinal nodes. Distant metastasis is uncommon, lung and bone being the commonest sites. Brain metastasis from papillary thyroid cancer is rare, with a frequency of less than 1% in several reported series and an extremely poor prognosis. The first case was a 74-year-old female patient with papillary cancer who took total thyroidectomy followed by 131I therapy 1 month later. Two days after 131I therapy, she developed headache, vomiting and left hemiplegia. Brain MRI and 131I whole body scan showed solitary brain metastasis in right parietal lobe. After a few weeks her condition improved enough to maintain her usual daily activity despite mild motor weakness. The second one, a 64-year-old female patient presented with headache and vomiting. Two years previously, she had taken total thyroidectomy and 131I ablation therapy after diagnosis of thyroid papillary cancer. Eight months before, she had undergone radical neck dissection because of relapse in cervical lymph nodes. Brain MRI revealed multple metastatic lesions including cerebellum. This patient did not report for follow-up after 2 months of discharge.
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