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Volume 16(1); February 2001
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Original Articles
Lanreotide Therapy in Graves' Ophthalmopathy.
Il Seong Nam-Goong, Eun Ju Lee, Jung Hwoon Kim, Jong Chul Won, Woo jae Lee, Jung Hee Han, sung Jin Lee, Sang Wook Kim, Moo Kon Son, Ho Hye Lee, Il Min Ahn
J Korean Endocr Soc. 2001;16(1):18-25.   Published online February 1, 2001
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BACKGROUND
Graves' ophthalmopathy (GO) is an autoimmune process that affects the orbital tissues. Patients with GO are usually treated with high doses of corticosteroids, retrobulbar irradiation, or by surgical decompression, however, those have some adverse effect. Recently, a synthetic somatostatin analogue has been reported for the treatment of GO. This study was performed prospectively to evaluate the therapeutic effects of lanreotide, a potent long acting synthetic somatostatin analogue, in patients that have GO. METHODS: Eight patients with moderate to severe GO (M:F=1:7, age 39.0+/-11.8 years) were included. Patients who had been treated with other modalities than GO, or had a systemic illness such as diabetes were excluded. Eight patients were given lanreotide, 40mg IM every 2 weeks over a period of 8 weeks. Their therapeutic responses were evaluated using an orbital CT or MRI and by ophthalmologic examinations. RESULTS: After 8 weeks' of lanreotide treatment, 4 patients showed decreased scores in the NOSPECS classification (p=0.059) as well as 5 patients in their clinical activity scores(p=0.109). All of the 8 patients showed improvements according to clinical evaluation criteria (p=0.008). Significant changes in the thickness of both the lateral rectus and superior rectus muscles were observed (p<0.05). No patient showed serious adverse effects related to lanreotide therapy during the follow-up periods. CONCLUSION: We conclude that lanreotide therapy has clinical benefits and show radiologic improvements in GO. Considering the minimal side-effects of lanreotide compared to those of corticosteroid, lanreotide therapy should be considered for use in selected patients that have Graves' ophthalmopathy
The Neuroprotective Effect of Growth Hormone on Neuronal Injury of Brain in Pilocarpine induced Status Epilepticus.
Ren Zhe An, Jae Hong Yu, Kyu Sang Song
J Korean Endocr Soc. 2001;16(1):26-38.   Published online February 1, 2001
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BACKGROUND
Several growth factors, including growth hormone (GH) and Insulin like growth factor-I, have been reported to have a neuroprotective effect in experimental models of hypoxic ischemia. This study is aimed at assessing the clinical significance of growth hormone for neuroprotection in status epilepticus induced neuronal cell deaths. METHODS: Pilocarpine induced status epilepticus (SE) was studied in rats (male, Sprague-Dawley). Rats were divided into pre- or post-treatment groups that had either a low (5 U/kg/day) or high (10 U/kg/day) dose of recombinant human GH (Eutropin, LGCI, Korea), and then subdivided into 24 hour, 72 hour and 1 week groups. This was done in the pretreatment groups for 5 days before SE and in the post-treatment groups for 5 days after 2 hrs of SE injection, after SE, the GH was daily injected via intraperitoneal route. Status epilepticus was induced by pilocarpine (360 mg/kg) with scoplamine (1 mg/kg) 30 minutes before pilocarpine injection using a stereotaxic instrument and EEG monitoring. Rats were killed at 24 and 72 hours after the SE in the pretreatment groups and at 1 week after the SE in the post-treatment groups for pathology studies. Neuronal injuries in the rat brain were studied by Hematoxylin & Eosin stain and the TUNEL method. RESULTS: Neuronal necrosis was found in the hippocampal CA1 and CA3 regions in all experimenatal groups after SE, and was more severe in the CA3 region. Apoptosis was found only in the pre-GH treated group and there were TUNEL-positive and morphologically necrotic cells in the hippocampal CA1 and CA3 regions at 72 hours after SE. Neuronal necrosis and apoptosis were significantly decreased in the high dose GH treated groups (p<0.05) compare to controlsd, but not in the low dose GH hormone treated groups (p>0.05). CONCLUSION: Growth hormone has a neuroprotective effect in neuronal cell death (necrosis and apoptosis) that is caused by pilocarpine induced status epilepticus in a dose dependent manner and prevents the activation of apoptosis by SE in neurons which eventually become necrotic.
The Combined Pituitary Stimulation Test in Patients Suffered from Massive Postpartum Hemorrhage.
Sang Hwa Kim, In Myung Yang, Cheol Young Park, Seung Joon Oh, Deog Yoon Kim, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Sun Woo Kim, Young Kil Choi
J Korean Endocr Soc. 2001;16(1):39-53.   Published online February 1, 2001
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BACKGROUND
ackground: Sheehan's syndrome secondary to severe postpartum hemorrhage is one of the major causes of pituitary insufficiency in Korea. Most of these patients do not manifest symptoms or signs of gross endocrinopathies. Earlier detection of pituitary insufficiency is of clinical importance. The combined pituitary stimulation test that uses the four hypothalamic releasing hormones is a rapid, safe, and effective way to evaluate anterior pituitary function. However, the criteria for a normal response has not been established in Korea. METHODS: Combined anterior pituitary stimulation tests were performed on fourteen healthy women who had no history of endocrine disease. Combined tests of anterior pituitary reserve were done no forty-five patients who suffered from massive postpartum hemorrhage which required transfusing, along with subsequent shock or changing consciousness and in thirty-nine patients who experienced mild postpartum hemorrhage. RESULTS: 1) In the severe hemorrhage group, thirty-three of forty-five women (73.3%) showed blunted responses in more than one of the anterior pituitary hormones in the combined pituitary stimulation tests. However, in the mild hemorrhage group, only eighteen of thirty-nine women (46.2%) demonstrated blunted responses of more than one of the anterior pituitary hormones. 2) In the severe hemorrhage group, the TSH response was blunted in twenty-five patients (55.6%), prolactin in eleven patients (24.4%), ACTH in ten patients (22.2%), LH in ten patients (22.2%), GH in nine patients (20%), and FSH in five patients (11.1%). 3) The results of combined pituitary stimulation tests in the normal control group were different from the results of other studies. CONCLUSION: It is recommended that the women who experienced a severe postpartum hemorrhage should be evaluated by using the combined pituitary stimulation test. Moreover, criteria for a normal response to the combined pituitary stimulation test should be established in Korea.
Early Detection of Medullary Thyroid Cancer by Screening of the RET Proto-oncogene Germ Line Point Mutation in Family Members Affected with Hereditary Medullary Thyroid Cancer .
Sun Wook Kim, Tae Yong Kim, Young Joo Park, Won Bae Kim, Chan Soo Shin, Do Joon Park, Kyoung Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee
J Korean Endocr Soc. 2001;16(1):54-64.   Published online February 1, 2001
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BACKGROUND
Conventional biochemical screening for family members with hereditary medullary thyroid cancer (MTC) is associated with problems of sensitivity and, specificity and it frequently detects gene carriers only after disease progression. Molecular genetic screening tests that detect germ-line point mutations of the RET proto-oncogene has changed our approach to hereditary MTC. In this study we screened members of a large Korean family that had a history of hereditary MTC by a molecular genetic method and propose a therapeutic approach in managing the disorder. METHODS: Using DNA acquired from peripheral blood leukocytes of the index patient, we performed PCR and direct sequencing of exon 10 of the RET proto-oncogene. PCR-RFLP using an Mbo II restriction enzyme was performed on family members who were at risk of MTC according to the family pedigree. Basal serum calcitonin level was determined in family members who had a point mutation of the RET proto-oncogene and a pentagastrin stimulation test was performed in 3 members. RESULTS: Genetic analysis in the index case revealed a mutation in exon 10, codon 618 of the RET proto-oncogene (TGC to AGC). Out of 28 members who were at risk of MTC, 24 members participated in the screening test. 9 members tested positive for a mutation in the same chromosomal location as the index patient by PCR-RFLP. Basal serum calcitonins were above 100 pg/mL in 2 members. 3 members who had a RET point muatation but a normal basal serum calcitonin level participated in the pentagastrin stimulation test and the results were negative in all members. We found a small medullary thyroid carcinoma that had a diameter of 0.2 cm in a 16 years old boy according to a negative pentagastrin stimulation test and who had received a prophylactic total thyroidectomy. He had no evidence of a lymph node metastasis. CONCLUSION: We detected a germ-line mutation of the RET proto-oncogene in codon 618 of Exon 10 by a molecular genetic method in a family with a hereditary MTC and found 9 members that had a negative history of MTC but had a RET point mutation. There was a very small MTC found in a 16 years old boy who had a normal pentagastrin stimulation test result. Therefore, It is recommended that a prophylactic total thyroidectomy be performed as well as in members that have a mutation of the RET proto-oncogene because MTC can metastasize early in its disease course.'
The Expression of c-met Oncogene in Thyroid Tumor.
Won Young Lee, Young Don lee, Young Jig Lee, Geun Sin Ryu
J Korean Endocr Soc. 2001;16(1):65-74.   Published online February 1, 2001
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BACKGROUND
The proto-oncogene c-met encodes the tyrosine kinase receptor for hepatocyte growth factor (HGF), which is a pleiotropic cytokine that controls growth, survival, motility, invasive migration, and differentiation of epithelial cells. Like several other epithelial neoplasms, thyroid carcinomas have been found to overexpress the c-met oncogene. We presently examine the expression of c-met protein in thyroid tumors and the correlation of c-met protein expression with prognostic factors in thyroid cancers. METHOD: We have examined the expression of the c-met oncogene in 62 paraffin-embedded thyroid cancer specimens (54 papillary carcinomas, 5 follicular carcinomas, 2 medullary carcinomas, and 1 anaplastic carcinoma), 20 benign tumors and 20 normal tissues using immunohistochemistry. We measured both the proportion and the intensity of stained cells and then calculated the staining index by multiplying the proportion and intensity scores. The staining index were categorized to be negative/low (staining index < or = 5) or high(staining index >5). The most important prognostic factors were age (over 45), tumor size (over 1.5 cm), lymph node metastasis, capsular invasion, vascular invasion and peripheral metastasis. RESULT: 1) The rate of expression of the c-met oncogene were 100%, 100% and 60% in thyroid cancer, benign tumors and normal thyroid tissue respectively. The expression of the c-met oncogene was restricted to the membrane. 2) The staining index of normal tissue, benign tumors and thyroid carcinomas was 1.8, 4.3 and 5.8 respectively. In malignancies, the staining index of papillary carcinoma was 5.7, follicular carcinoma 5.4, medullary carcinoma 7.5, and anaplastic cancer 9. 3) A high expression of c-met was not correlated with prognostic factors in papillary, follicular carcinomas or medullay carcinomas. CONCLUSION: The c-met oncogene might not play a role in the pathogenesis of thyroid neoplasia. There was no correlation between the high expression rate of the c-met oncogene and prognostic factors in papillary and follicular carcinomas.
Differential Diagnostic Value of TSH Receptor Antibody Measurements in Thyrotoxic Postpartum Patients with History of Graves' Disease.
Seong Jin Lee, Yun Ey Chung, Ha Young Kim, Jung Hee Han, Jong Chul Won, Ahm Kim, Jin Sook Ryu, Dae Hyuk Moon, Il Min Ahn
J Korean Endocr Soc. 2001;16(1):75-84.   Published online February 1, 2001
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BACKGROUND
It is known that pregnancy markedly influences the clinical course of autoimmune thyroid diseases. In the postpartum period, various kinds of autoimmune thyroid dysfunctions can be observed. Thyroid dysfunction is found in 5.5-7.1% of postpartum women in the general population. Among those who show thyroid dysfunction after delivery, some will develop Graves' disease and others will develop postpartum thyroiditis. It is also known that patients with Graves' disease may manifest thyrotoxicosis in the postpartum period because of postpartum thyroiditis or relapse of the Graves' disease itself. We evaluated the clinical features of postpartum thyrotoxicosis in Graves' disease patients to find diagnostic indices that could be used in differentiating between postpartum thyroiditis and relapse of Graves' disease. METHOD: We reviewed the cases with postpartum thyrotoxicosis in patients that had a history of Graves' disease between 1995 and 2000. The diagnosis of postpartum thyroiditis had been made by means of a 99mTc thyroid scan or by the observation of a typical triphasic thyroid function change, in cases where a 99mTc thyroid scan was not possible because of breast feeding. We measured the serum TSH, free T4, free T3, TSH binding inhibiting immunoglobulin (TBII), anti-thyroid peroxidase (TPO) antibody, and anti- thyroglobulin (Tg) antibody serially from the time of the diagnosis of Graves' disease to the time of postpartum thyroid dysfunction. RESULTS: Eleven patients, 5 patients in the postpartum thyroiditis (PPT group) and 6 patients with relapse of the Graves' disease (GD group), were identified. The mean values of TBII of two groups at the time of diagnosis of Graves' disease were 40.9+/-4.8 IU/mL (PPT group), 58.9+/-23.5 IU/mL (GD group) respectively, which were insignificant. The mean values of TBII of the two groups at early pregnancy were 3.2+/-1.9 IU/mL (PPT group), 41.6+/-22.6 IU/mL (GD group) and this difference was statistically significant (p=0.009). The mean values of TBII of the two groups at the time of postpartum thyrotoxicosis were 1.9+/-1.6 IU/mL (PPT group), 51.5+/-23.2 IU/mL (GD group) which were also statistically significant (p=0.003). The mean values of anti-TPO antibody, anti-Tg antibody, disease duration, and treatment duration between the two groups were not significantly different. The onsets of thyroid dysfunction after delivery in the two groups were 2.6+/-2.0 (PPT group), 4.0+/-3.9 (GD group) months which were statistically insignificant. CONCLUSION: These data suggest that the measurement of TBII at the time of the postpartum thyrotoxic period, could help to differentiate postpartum thyroiditis from a relapse of Graves' disease in those patients that have a history of Graves' disease especially when thyroid scan is not possible because of breast feeding.
Long-Term Effect of Glucocorticoid on Differentiation of Bone Marrow Stromal Cells .
Long Term Lee, Yong Soo Park, Dong Sun Kim, Woong Hwan Choi, Yon Hern Ahn, Tae Wha Kim
J Korean Endocr Soc. 2001;16(1):85-96.   Published online February 1, 2001
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BACKGROUND
Glucocorticoid-induced osteoporosis is characterized by decreased osteoblastic activity and replacement of bone marrow with adipocytes. Since osteoblast and adipocytes are derived from the same mesenchymal stem cell, one might speculate that there is an interaction between these two cells types. In fact, leptin that is secreted from adipocytes is known to stimulate differentiation of osteoblasts, while it inhibits the differentiation of adipocytes. Furthermore, it has been demonstrated that PPAR is present in osteoblasts and it is increased by leptin in adipocytes. However, the role of PPAR and leptin remains unknown in glucocorticoid-induced osteoporosis. The aims of this study are to investigate the effect of glucocorticoid on bone mineral density and gene expression in osteoblasts and adipocytes, and to study the role of PPAR and leptin in the mechanism of glucocorticoid-induced osteoporosis. METHODS: Methylprednisolone, 1 mg/200 g-weight, was injected into five rats (steroid group) and saline was given to five rats (control group) for eight weeks. The bone mineral density was determined by dual energy X-ray absoptiometry. Gene expression of osteocalcin, alkaline phosphatase, lipoptrotein lipase, and PPAR -2 was assessed by RT-PCR. Serum leptin level was measured using a commercial radioimmunoassay kit. RESULTS: 1) The body weight of the steroid group was significantly lower than that of the control group (451.4+/-12.9 g vs. 247.6+/-19.8 g, p<0.05). The bone mineral density of the steroid group tended to be lower than that of the control group (0.27+/-0.01 g/cm2 vs. 0.26+/-0.01 g/cm2, p>0.05). 2) In the steroid group, the gene expressions of osteocalcin (1.00+/-0.08 vs. 0.23+/-0.16, p<0.05) and alkaline phosphatase (0.47+/-0.07 vs. 0.33+/-0.18, p<0.05) were decreased significantly compared to those in controls. 3) In the steroid group, the gene expression of lipoprotein lipase (0.23+/-0.06 vs. 0.39+/-0.12, p>0.05) and+/-PAR 2 (0.17+/-0.08 vs. 0.22+/-0.12, p>0.05) tended to be increased compared to that in the contol group. 4) The serum leptin level of the steroid group tended to be lower than that of the control group (0.20+/-0.12 g/L vs. 0.10+/-0.09 g/L, p>0.05). CONCLUSION: These data suggest that long-term administration of a large dose of glucocorticoid suppresses differentiation of osteoblasts and enhances the differentiation of adipocytes, which may be mediated by increased expression of PPAR and decreased synthesis of leptin.
Association Between Peak Bone Mass and Genetic Polymorphisms of the Vitamin D Receptor, Estrogen Receptor, and Type I Collagen 1 Genes in Healthy Young Korean Women.
Hong Kyu Kim, Sang Wook Kim, Eun Sook Kim, Ghi Su Kim
J Korean Endocr Soc. 2001;16(1):97-114.   Published online February 1, 2001
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BACKGROUND
Genetic suggest that strongest effect is observed in the premenopausal peak bone mass, which become less with age. However, the evaluation of candidate genes polymorphisms has been most frequently done in postmenopausal women and the results have been controversial. Therefore, we studied the possible association of the peak bone mass and candidate for osteoporosis genes polymorphism in premenopausal women. METHODS: The associations between BMD and polymorphisms of the vitamin D receptor (3'-end region by BsmI restriction enzyme and start codon by FokI restriction enzyme), estrogen receptor (by PvuII and XbaI restriction enzyme), and type I collagen 1 (Sp1 binding site by MscI and BalI restriction enzyme) genes were examined in 100 healthy young Korean women who had a peak bone mass (age 20-35 years). Bone mineral densities were measured by dual energy X-ray absorptiometry (DEXA). Dietary calcium intake was also measured using a food frequency questionnaire. RESULTS: The frequencies of the B allele of the vitamin D receptor gene BsmI polymorphism and the X allele in the estrogen receptor gene, XbaI polymorphisms were lower in Koreans than those in Caucasians. The allelic frequencies of the vitamin vitamin D receptor gene FokI polymorphism and the estrogen receptor gene PvuII polymorphism were similar to those of Caucasians. No significant association was found between BMD and the vitamin D receptor genotype according to BsmI or FokI polymorphisms. There was also no significant relation between the PvuII or XbaI polymorphisms of the estrogen receptor gene and BMD. The associations between BMD and cross-genotypes combining the vitamin D receptor gene (BsmI and FokI) and estrogen receptor gene (PvuII and XbaI) polymorphisms were also analyzed. Among the subjects who lacked the Bf haplotype of the vitamin D receptor gene, the BMD of the femoral neck area was significantly higher in subjects lacking Px haplotypes of the estrogen receptor gene than in those having Px haplotype (p < 0.05). When dietary calcium intake was taken into consideration, there were significant differences in BMD according to the cross-genotype in the group having a low calcium intake (< 500 mg/day). The subjects that lacked the Bf and Px haplotypes had a significantly higher BMD in the femoral neck (p < 0.01), Ward's triangle (p < 0.05), and in the trochanteric area (p < 0.05) than those who lacked Bf but a Px haplotype. We did not find a polymorphism in the Sp1 binding site of the type I collagen 1 gene in our subjects. CONCLUSION: These data suggest that a complex interaction of vitamin D and the estrogen receptor gene with the dietary calcium intake, rather than a polymorphism of a single gene, may influence peak bone mass in healthy young Korean women.
Case Reports
2 Cases of Ectopic ACTH Syndrome due to Thymic Neuroendocrine Carcinoma Associated with Different Clinical Manifestations.
Yu Jeong Park, Moon Kyu Lee, Jong Ryeal Hahm, Jung Ho Do, Sang Taek Heo, Ju Sung Kim, Yong Ki Min, Myung Shik Lee, Kwang Won Kim, Joung Ho Han
J Korean Endocr Soc. 2001;16(1):115-122.   Published online February 1, 2001
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AbstractAbstract PDF
Primary neuroendocrine carcinoma of the thymus (formerly known as thymic carcinoids) are unusual tumors that account for 5% of all anterior mediastinal neoplasms. Thymic neuroendocrine carcinomas exhibit a much more aggressive behavior than those originating from other foregut locations and are associated with the ectopic ACTH syndrome in 38% of cases. Patients having a thymic neuroendocrine carcinoma usually present with symptoms such as chest tightness, dyspnea, a palpable neck mass and sometimes a weight gain. We report on 2 patients with thymic neuroendocrine carcinoma who showed different clinical manifestations each other. One presented with a typical. Cushingoid appearance and the other had symptoms of fatigue and weight loss which is a common symptom of malignant tumors.
Renin-responsive Adrenal Adenoma with a Suspicious Abberant Adrenal Vein.
Ji Hyeon Ju, Woo Lee Jung, Jung Min Lee, Kun Ho Yoon, Bong Yun Cha, Ho Young Son, Dong Gu Kim, Eung Kook Kim, Byung Ki Choi
J Korean Endocr Soc. 2001;16(1):123-129.   Published online February 1, 2001
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AbstractAbstract PDF
A renin- or angiotensin-II responsive aldosterone producing tumor is a rare cause of primary hyperaldosteronism. This tumor can be identified by tests that show that the aldosterone producing adrenal tumor is not fully autonomous. In other words partially it is responsible for the stimulation of aldosterone secretion that results aldosterone levels in an increase in serum in response to the upright posture and spironolactone treatment. Furthermore, the urinary 18-hydroxycortisol level is within the normal range. Because of different responses to surgical removal, the differential diagnosis of the causes of primary aldosteronism can't be overemphasized even for rare causes of primary aldosteronism such as unilateral nodular hyperplasia or a renin-responsible aldosterone producing tumor. We should consider renin or angiotensin-II responsive adrenal adenoma in the differential diagnosis of primary aldosteronism when biochemical data shows atypical results. Here we present the first case in Korea of a renin-responsive aldosterone producing adrenal adenoma which was fully accessible and was successfully treated by surgical removal. Also, sampling for aldosterone secretion just above the insertion site in the left renal vein before surgery showed a suspiciously abberant left adrenal vein drainage into the IVC, This was very helpful information during adrenal vein ligation in laparoscopic adrenalectomy.
A Case of Primary Amenorrhea due to 17 -Hydroxylase Deficiency.
Hong Seub Rim, Seon Hwa Lee, Jung Min Hong, Jae Hyun Nam, Hee Back Park, Chul Woo An, Do Min Ki, Sung Kil Lim, Young Duk Song, Hyun Chul Lee, Kap Bum Huh, Inn Soo Kang
J Korean Endocr Soc. 2001;16(1):130-133.   Published online February 1, 2001
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AbstractAbstract PDF
17 -Hydroxylase deficiency is a rare form of congenital adrenal hyperplasia that is characterized by primary amenorrhea, absence of secondary sex characteristics, hypertension, and a hypokalemic alkalosis that has resulted resulting from increased production of deoxycorticosterone and corticosterone by the adrenal. The diagnosis of this enzyme deficiency can be recognized by the increasing serum concentrations of steroid precursors, DOC and corticosterone and the decreasing concentrations of cortisol, and adrenal androgens. We diagnosed this in a 19 year old female who presented with primary amenorrhea. We report this case with a review of the literatures.
A Case of Adrenalectomy after Preterm Delivery in Cushing's Syndrome of Third Trimester Pregnant Woman.
Kwang Sik Song, Jae Kyung Hwang, Ki Tak Ju, Hang Jin Lee, Suk Ho Song, Ki Young Lee, Chan Jong Suh, Hong Kyu Kim, Hyu Young Park, Dal Mo Yang, Young Ha Oh, Moon Ho Kang
J Korean Endocr Soc. 2001;16(1):134-139.   Published online February 1, 2001
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AbstractAbstract PDF
A renin- or angiotensin-II responsive aldosterone producing tumor is a rare cause of primary hyperaldosteronism. This tumor can be identified by tests that show that the aldosterone producing adrenal tumor is not fully autonomous. In other words partially it is responsible for the stimulation of aldosterone secretion that results aldosterone levels in an increase in serum in response to the upright posture and spironolactone treatment. Furthermore, the urinary 18-hydroxycortisol level is within the normal range. Because of different responses to surgical removal, the differential diagnosis of the causes of primary aldosteronism can't be overemphasized even for rare causes of primary aldosteronism such as unilateral nodular hyperplasia or a renin-responsible aldosterone producing tumor. We should consider renin or angiotensin-II responsive adrenal adenoma in the differential diagnosis of primary aldosteronism when biochemical data shows atypical results. Here we present the first case in Korea of a renin-responsive aldosterone producing adrenal adenoma which was fully accessible and was successfully treated by surgical removal. Also, sampling for aldosterone secretion just above the insertion site in the left renal vein before surgery showed a suspiciously abberant left adrenal vein drainage into the IVC, This was very helpful information during adrenal vein ligation in laparoscopic adrenalectomy.
Clinical Features of Well Differentiated Thyroid Carcinomas in Pregnant Women.
Seong Jin Lee, Suk Joon Hong, Pyi Ryang Lee, Young Kee Shong
J Korean Endocr Soc. 2001;16(1):140-147.   Published online February 1, 2001
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AbstractAbstract PDF
BACKGROUND
In differentiated thyroid carcinomas (DTC), it has been reported that pregnancy may accelerate the course of the disease. But recent evidences suggested that the prognosis of DTC during pregnancy was similar to that of DTC in non-pregnant women of the same age. Also the optimal timing for the treatment is still controversial. We evaluated the clinical features of DTC in pregnant women. METHOD: We reviewed the histories of patients in whom the DTC was diagnosed before or during the pregnancy between 1994 and 1999. DTC were diagnosed by fine needle aspiration and the patients were treated by thyroid surgery. RESULTS: Six women who had a mean age of 30 years (27-34 years) were identified. The mean follow-up duration was 41 months (13-70 months). All patients had noticed a lump in their necks. In three patients, the nodules increased in size during pregnancy. A fine needle aspiration revealed a suspected malignancy in five patients and a postoperative biopsy confirmed the malignancy in one patient who had a preoperative cytologic diagnosis of nodular hyperplasia. All tumors were well differentiated and ranged in size from 1 to 6.5 cm. Radioactive iodine ablation and thyroid hormone suppression treatment were administered in five patients except in one case of papillary microcarcinoma. One patient had residual tumors in the right cervical lymph nodes and both lungs. She underwent repeated surgery and radioactive iodine therapy. CONCLUSION: This reports suggest that the DTC which is associated with pregnancy may have a similar prognosis to that of non-pregnant women and that the treatment of DTC in pregnant women may be safely delayed until after delivery in most patients. The treatment should not be delayed for more than a year.
A Case of 46 XX Male Syndrome.
Jae Myoung Lee, Myung Sook Shim, Young Uck Kim, Young Goo Shin, Choon Hee Chung
J Korean Endocr Soc. 2001;16(1):148-152.   Published online February 1, 2001
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AbstractAbstract PDF
The 46, XX male syndrome is rare disease that is characterized by a phenotypic male who has a 46, XX female karyotype. Since the first report by de la Chapelle and associates in 1964, several cases have been reported, but it is still a rare entity. Recently we examined a 20-year-old XX male who had the symptoms of gynecomastia, an infantile appearance of the external genitalia, scanty pubic hair, no Adams apple, and no axillary hair. We presently describe a patient with the 46, XX male syndrome who showed a 46, XX karyotype on chromosomal study and review the literatures.

Endocrinol Metab : Endocrinology and Metabolism