Endocrinology and Metabolism

Volume 19(4); August 2004

Original Articles

Metabolic Syndrome and Steroid: 11 -Hydroxysteroid Dehydrogenases (11 -HSDs).: Hong Woo Nam; J Korean Endocr Soc. 2004;19(4):289-299. Published online August 1, 2004

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Abstract PDF: No abstrat available.

Hypopituitarism and Cardiovascular Complications.: Nan Hee Kim; J Korean Endocr Soc. 2004;19(4):300-302. Published online August 1, 2004

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Abstract PDF: No abstract available.

The One Year Effects of Growth Hormone Replacement on the Body Composition in the Normal Adults.: Eui Hyun Kim, Suk Chon, Kwan Pyo Koh, Seong Joon Oh, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim; J Korean Endocr Soc. 2004;19(4):303-319. Published online August 1, 2004

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Abstract PDF: BACKGROUND
The secretion of growth hormone [GH] declines by 14.4% every decade, leading to the suggestion that the elderly are functionally GH deficient, which may increase adipose tissue and decrease the bone mass and density, as well as other negative changes in body composition. Recently, many studies have shown that GH replacement therapy may restore the changes that occur in the body composition with aging. AIM: The GH and insulin like growth factor-I[IGF-I] profiles were identified during GH replacement therapy in the elderly and compared with those of GH deficient[GHD] patients. The metabolic effects of GH replacement on the body composition of the elderly was also investigated, especially the body fat, muscle and bone parameters. Subjects and METHODS: 98 healthy normal out-patients and 13 GHD patients, who had peak GH concentrations less than 5 ng/mL after an insulin tolerance test [ITT] or growth hormone releasing hormone [GHRH] stimulation test, were the subjects of this study. All were receiving appropriate thyroid, adrenal and gonadal hormone replacements. The dose of recombinant human GH [rhGH] was 0.02~0.04 mg [0.06~0.12 IU]/kg of body weight.per week, given nightly by a subcutaneous injection, six times a week, over a 52 week period. The GH was measures after the ITT and GHRH stimulation tests, and the IGF-1, lipid parameters [total cholesterol, triglyceride, HDL-, and LDL cholesterol], visceral adipose tissue [VAT], subcutaneous adipose tissue [SAT], VAT/SAT ratio, quadriceps muscle area, total body fat, total bone mineral density [BMD], alkaline phosphatase [ALP], osteocalcin and urine deoxypyridinoline [DYP], as well as anthropometry, were also assessed. RESULTS: All the anthropometry features between the normal and GHD subjects were very similar. The hormonal profiles were checked; the GH peaks of the ITT and GHRH stimulation tests were significantly higher in the normal compared to the GHD patients, but the GHRH test showed lower GH peaks in than those of the ITT test in the normal subjects. The IGF-I levels after GH replacement were constantly maintained in the normal and GHD groups after 3 week and until the 52nd week. According to the lipid profiles, the GHD group showed significantly decreased total cholesterol and LDL-cholesterol after 12 weeks of GH replacement. The normal male group revealed constantly increased triglyceride levels during the entire 52 weeks of GH replacement, but thr other lipid parameters remained completely unchanged. The normal female group showed no change in any of their lipid parameters. Although the amounts of VAT at the baseline were the same in all groups, only the normal males showed effective visceral fat removal, with significantly reduced VAT after 52 weeks of GH treatment. In the normal female and GHD groups the bone mineral density had a V shaped curve after GH replacement, and the ALP and osteocalcin levels were significantly increased after 26 weeks of GH therapy in the GHD group. CONCLUSION: The body compositions in the normal male, female and GHD groups were similar before the GH replacement therapy, and the serum IGF-I levels were well maintained in all these groups during GH replacement. Although the majority of aging symptoms were improved, the body compositions tended to return to their original stati in the normal groups. GH replacement is recommended in the elderly for better health and well-being

Effect of Estrogen on H2O2 Induced Apoptosis of FRTL-5 Cells.: Won Bae Kim, Tae Yong Kim, Ja Young Song, Young Kee Shong; J Korean Endocr Soc. 2004;19(4):320-331. Published online August 1, 2004

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Abstract PDF: BACKGROUND
Understanding the pathways and controlling mechanisms of thyrocyte apoptosis is important for the elucidation of the pathogenesis of goiter or thyroid cancer. A system for evaluating apoptosis, in FRTL-5 cells, triggered by hydrogen peroxide (H2O2), a highly likely apoptogenic signal in physiologic condition, was be set up to see the effects of TSH and estrogen on H2O2-induced apoptosis. METHOD: DNA laddering was used in the optimization process or the conditions of the set-up of system for the evaluation of apoptosis in the FRTL-5 cells. To quantify the apoptosis under the optimized conditions, histone-bound DNA fragments in the cytoplasm were measured by ELISA. RESULTS: 1) The optimized conditions for induction of apoptosis in the FRTL-5 cells by H2O2 were; observation of DNA laddering 18~24 hrs after the addition of 0.3 mM H2O2 to cells maintained in TSH-free, low serum containing media (5H1 or 5H0 media) for 48 hrs. 2) Exposure of the FRTL-5 cells to TSH (1 mU/L) for more than 48 hrs (6H0 media). before the addition of H2O2 significantly decreased the degree of apoptosis, compared to cells maintained under TSH-free conditions (0.98+/-0.21 vs. 2.27 0.11 arbitrary unit, p<0.05), whereas exposure for 24 hrs. did not. 3) Exposure of the FRTL-5 cells to high dose 17- estradiol (1-100 M) significantly decreased the degree of H2O2-induced apoptosis in a dose dependent manner. The addition of serum (1%) blunted the effects of estrogen on H2O2-induced apoptosis, and TSH totally abrogated the estrogen effect.Physiologic doses of estrogen (10~100 nM) showed no suppressive effects on H2O2-induced apoptosis in FRTL-5 cells. CONCLUSION: A system for evaluating apoptosis in FRTL-5 cells triggered by hydrogen peroxide (H2O2), a highly likely apoptogenic signal in physiologic condition, was set up, and found for the first time that high dose estrogen suppressed the H2O2-induced apoptosis in FRTL-5 cells

Relationship between Serum Osteoprotegerin-Receptor Activator of NF-kappaB Ligand Levels and Bone Mineral Metabolism in Men.: Ki Won Oh, Eun Joo Yun, Eun Jung Rhee, Won Young Lee, Ki Hyun Baek, Moo Il Kang, Cheol Young Park, Sung Hee Ihm, Moon Gi Choi, Hyung Joon Yoo, Sung Woo Park; J Korean Endocr Soc. 2004;19(4):332-345. Published online August 1, 2004

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Abstract PDF: BACKGROUND
Osteoporosis is a growing health problem, not only in women, but in men also. Sex hormones and insulin-like growth factor-I (IGF-I) have been shown to be the major determinant in male bone metabolism. Osteoprotegerin (OPG) is a recently identified cytokine, which acts as a decoy receptor for the receptor activator of the NF- B ligand (RANKL). OPG and RANKL have been shown to be important regulators of osteoclastogenesis in animal models. The relationship between the OPG-RANKL system and male bone status in human populations is unclear. The aim of this study was to investigate the relationship between circulating the OPG-RANKL system and bone mineral metabolism in 80 Korean men. METHODS: The subjects of this study were 80 men aged between 42 and 70 (mean age, 54.5 yr). The serum concentrations of OPG and RANKL were measured by ELISA. The serum concentrations of estradiol, total testosterone, IGF-I and biochemical markers of bone turnover were measured by standard methods. The bone mineral densites (BMD) at the lumbar spine and femoral neck were measured by dual energy x-ray absorptiometry. RESULTS: A significant correlation was observed between the serum OPG/RANKL ratios and osteocalcin levels (r=-0.229, p<0.05). The serum OPG levels were significantly correlated to the femoral neck BMD (r=-0.227, p<0.05). The mean value of the serum OPG was found to be greater in patients with osteoporosis at the femoral neck (mean SD, 4.72.1 pmol/L) than in subjects with a normal BMD (3.30.9 pmol/L, p<0.05). The serum RANKL/OPG ratios were significantly positively correlated to the serum estradiol level (r=0.401, p<0.001). Also, there was a significant negative correlation between the serum OPG and estradiol levels (r=-0.288, p<0.05). In a multiple regression analysis, the BMI, serum OPG and RANKL levels, and the serum IGF-I level were identified as significant predictors of the femoral neck BMD. In another multiple regression analysis, only the serum estradiol level was identified as a significant predictor of the serum OPG level. CONCLUSION: In conclusion, our data show that the serum OPG and RANKL levels are partly associated with bone mineral metabolism, and are related to the endogenous estrogen levels in human male populations. Therefore, the possibility exists that the OPG-RANKL system may be a mediator of the estradiol in male bone metabolism. However, there have been few study published on the relation between the serum OPG and estradiol levels in men. Further studies are needed to clarify this relationship

Increased Activity of Insulin-like Growth Factor binding Protein-4 Protease in H-mole Patients.: Woo Seok Seo, Dong Won Byun, Ji Oh Mok, Ji Sung Yoon, Yeo Joo Kim, Hyung Kyu Park, Chul Hee Kim, Sang Jin Kim, Kyo Il Suh, Myung Hi Yoo, Hae Hyeog Lee, Soo Kyoon Rah; J Korean Endocr Soc. 2004;19(4):346-357. Published online August 1, 2004

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Abstract PDF: BACKGROUND
Hydatidiform mole (H-mole) is characterized by the neoplastic proliferation of trophoblasts. Only 1~10% of patients with partial H-mole will develop a trophoblastic tumor, but 18~29% of those with complete H-mole will develop a persistent trophoblastic tumor. Therefore, the early diagnosis and monitoring after operation of an H-mole disease are very important. Recently, the pregnancy associated plasma protein-A (PAPP-A) was proved to have a similar role as that of IGF binding protein-4 (IGFBP-4) protease, which has shown an increasing function in fetal growth and development by degradation of IGFBP-4 and an increase in IGF in the serum during pregnancy. Our hypothesis is "the H-mole, which shows placental hyperplasia will also have an IGFBP-4 protease activity, which may be used as in the early diagnosis and monitoring of H-mole disease". METHODS: Serum samples from 6 non-pregnant, 18 pregnant (5 in the 1st trimester, 10 in the 2nd, and 3 in the 3rd), 12 postpartum women and 3 H-mole patients(2 with complete H-mole and 1with partial H-mole) were collected and measured for the -HCG, IGF and PAPP-A levels and IGFBP-4 protease activities by a IGF-II ligand blot analysis and electrophoresis method. The IGFBP-4 protease activity of the serum during normal pregnancy was compared with that of H-mole disease. RESULTS: The results from the in vitro protease assays using recombinant IGFBP-4 determined that IGFBP-4 proteolysis was significantly increased during the first (56%) and second trimesters (90%), but reached a plateau by the third trimester (94%). In H-mole disease diagnosed 11 weeks after conception, the IGFBP-4 proteolytic activity was 97%, which was nearly the same as at terminal pregnancy. This activity gradually decreased to 75% at 1 week, 58.7% at 2 and 33% at 3 weeks after the operation. The -HCG was also decreased from 490,400 to 123,822.7, 1,352.3, and 128.5 mIU/mL at 1, 2 and 3 weeks after the operation, respectively. The PAPP-A level also gradually decreased from 34.87 to 25.5, 12.0 and 2.7 g/mL 1, 2 and 3 weeks after the operation, respectively. However, the IGF decreased from 238.3 to 172.9 ng/mL 1 week after the operation, but increased to 251.4 and 295 ng/mL at 2 and 3 weeks after the operation, respectively. CONCLUSION: These results demonstrated that the IGFBP-4 protease activity was significantly increased during pregnancy, and was extremely elevated durimg the early stages of H-mole disease, but gradually decreased after removal of molar tissue. Therefore, measuring the IGFBP-4 protease activity may play an important role in the early diagnosis and monitoring of H-mole disease

Insulin-dependent Stimulation of a Subtype of p38Map Kinases and Its Role in Insulin's Antiapoptotic Activity.: Shin Hae Kang, Ji Hoon Kang, Hee Kyoung Kang, Dae Ho Lee, Young Ki Lee, Deok Bae Park; J Korean Endocr Soc. 2004;19(4):358-368. Published online August 1, 2004

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Abstract PDF: BACKGROUND
The p38 mitogen-activated protein kinases (p38Map kinases) are a family of prolinedirected serine/threonine kinases. At least four isoforms of p38Map kinases have been identified; however, their physiological significances remain to be understood. Recently, the role of p38Map kinase in insulin-stimulated glucose uptake has been suggested. The present study aimed to investigate which isoform(s) were responsive to insulin stimulation. In addition, the activities of p38 Map kinase isoforms that may participate in the insulin's antiapoptotic function in CHO-IR cells were also determined. METHODS: Chinese hamster ovary cells, expressing wild- or mutated human insulin receptors (CHO-IR cells), were used to investigate whether insulin can stimulate any of the isoform(s) of the p38Map kinases. The p38Map kinase activity was determined by measuring the degree of 32P-labelling of ATF-2 protein, a specific substrate of p38Map kinase. A DNA laddering assay was performed to examine the degree of apoptosis and a RT-PCR analysis to determine which isoform(s) of the p38Map kinases were expressed in response to insulin. RESULTS: p38Map kinase activation by insulin was sharply suppressed in only the CHO-IR/A1018K cells, which lack the intrinsic tyrosine kinase activity of insulin receptors. Insulin stimulation of p38Map kinase was insensitive to SB203580, an inhibitor of the alpha(alpha)-and beta(beta)-isoforms of p38Map kinases. Moreover, orthovanadate, known as a specific stimulator of the gamma(gamma)-and delta(delta-) isoforms, stimulated the p38Map kinase activity in CHO-IR cells. Insulin increased the degree of mRNA expression of the delta-isoform, but not that of the alpha-isoform p38Map kinase. Interestingly, PD98059, an inhibitor of ERK, suppressed p38Map kinase stimulation, as well as the antiapoptotic protection of cells by insulin. As insulin was found to still protect ERK-lacking cells (CHO-IR/ SOS) from apoptosis, any substantial role(s) of ERK might be excluded. CONCLUSION: Our data suggest that insulin may stimulate the activity and expression of the-isoform of p38Map kinase in a MEK1/2-dependent manner. The involvement of the delta-isoform of p38Map kinase in insulin's antiapoptotic protection was also suggested, but remains to be investigated further to clarify the nature of its mechanism of action

Association of Serum Adiponectin Levels with Insulin Resistance in Women with Polycystic Ovary Syndrome.: Young Sun Hong, Jee Young Oh, Eun Kyung Byun, Yeon Ah Sung; J Korean Endocr Soc. 2004;19(4):369-378. Published online August 1, 2004

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Abstract PDF: BACKGROUND
Polycystic ovary syndrome (PCOS) is known to be associated with obesity and insulin resistance. The exact mechanism of insulin resistance in PCOS is not completely understood, but there are several pieces of evidence suggesting humoral mediator involvement. Adiponectin, an adipocyte-secreted protein, could be a possible link between adiposity and insulin resistance. This study was performed to see whether the serum adiponectin levels are suppressed in woman with PCOS and if this is associated with the characteristic hormonal and metabolic features of PCOS. METHODS: 20 women with PCOS and 8 normal controls with regular cycles were recruited. The serum adiponectin levels were measured by RIA, and the fasting glucose to insulin ratio (GIR) used as an insulin sensitivity index. RESULTS: The patients with PCOS were classified as lean (BMI < 23 kg/m2, n=9) and obese groups (BMI 25 kg/m2, n=11) based on the WPRO criteria. The GIR was significantly lower in the obese compared to the control group. The adiponectin level was lower in women with PCOS than the controls, but without statistical significance. In 5 of the 20 patients, the GIR was higher than 0.30, which was the lowest limit in the controls, and the adiponectin level was significantly higher than in those patients with a lower GIR. The adiponectin level was significantly correlated with the BMI, subcutaneous and visceral fat areas, post challenge 2 hr glucose, fasting insulin, GIR and SHBG. After adjustment for BMI, adiponectin was significantly correlated with the GIR in all subjects, including the controls. CONCLUSION: The serum adiponectin level was associated with and related to adiposity in women with PCOS; however, adiponectin might be associated with insulin resistance independently from adiposity

Relationship between Serum Leptin, Adiponectin, Resistin and Ghrelin Levels, and Bone Mineral Density in Men.: Ki Won Oh, Eun Joo Yun, Eun Jung Rhee, Won Young Lee, Ki Hyun Baek, Kun Ho Yoon, Moo Il Kang, Cheol Young Park, Sung Hee Ihm, Moon Gi Choi, Hyung Joon Yoo, Sung Woo Park; J Korean Endocr Soc. 2004;19(4):379-392. Published online August 1, 2004

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Abstract PDF: BACKGROUND
Fat mass is an important determinant of bone mineral density (BMD), but the mechanism involved in this relationship is uncertain. Several lines of evidence have suggested the effects of fat mass on BMD may be mediated by hormonal factors, with the principal candidates being serum sex hormones, insulin, leptin and adiponectin. Thus, the aim of this study was to investigate the relationship between the serum adipocytokine and ghrelin levels, and BMD in men. METHODS: Eighty men, aged 42~70 (mean age, 54.5 yr), were selected as the study subjects. The serum concentrations of leptin and ghrelin were measured with RIA, the adiponectin with ELISA and the resistin with EIA. The serum concentrations of estradiol, total testosterone and the biochemical markers of bone turnover were measured by standard methods. The BMD at the lumbar spine and femoral neck were measured by dual energy x-ray absorptiometry. RESULTS: The serum leptin level was found to correlate to the BMI, waist to hip ratio (WHR), blood pressure, fasting blood sugar, serum fasting insulin, total cholesterol, triglyceride and calcium levels. Although the serum leptin level was not significantly correlated to the serum estradiol level, it did show a weak trend. The serum adiponectin level were correlated to the BMI, WHR and serum fasting insulin level; and the resistin to serum total cholesterol and low density lipoprotein cholesterol levels; ghrelin to age, WHR and serum triglyceride levels. A significant negative correlation was observed between the serum resistin level and lumbar spine BMD. Also, there was a significant negative correlation between the serum leptin level and lumbar spine BMD. The above correlations were observed only when the BMI and the serum estradiol and insulin levels were included as independent variables in the regression analysis model. The serum adiponectin level was not significantly correlated with the BMD, either in the presence or absence of the BMI and serum insulin level. CONCLUSION: The serum adipocytokine level was observed to be partly associated with the BMD in men. Therefore, these data suggest that leptin and resistin may play roles in the bone mineral metabolism in men. Further studies are needed to larify this relationship

Case Reports

Diabetic Ketoacidosis in a Patient with Acromegaly.: Eun Hee Koh, Min Kyung Kim, Jin Tae Park, Il Seong Nam-Goong, Joong Yeol Park, Ki Up Lee, Min Seon Kim; J Korean Endocr Soc. 2004;19(4):393-398. Published online August 1, 2004

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Abstract PDF: Acromegaly is a chronic, debilitating condition caused by excessive secretion of growth hormone (GH). Impaired glucose tolerance is present in about 20-40% of acromegaly, with diabetes mellitus developing in about 10~15% of patients, but diabetic ketoacidosis is a rare association. Herein is reported a case of diabetic ketoacidosis in a 33 year-old female, with a 4 year history of typical acromegaly features. She presented with severe hyperglycemia and ketoacidosis, but with no other cause for this metabolic derangement. She had elevated plasma GH (50 ng/mL) and IGF-1 (1533 ng/mL) levels, and a pituitary macroadenoma. About 200 units of insulin per day were required for her glycemic control. However, the serum IGF-1 level and daily insulin requirement were significantly tapered after a transsphenoidal adenomectomy and long acting somatostatin analogue treatment. There was a good correlation with the daily insulin requirement and plasma IGF-1 level. This case demonstrates that severe GH excess can cause diabetic ketoacidosis, and that its successful treatment improves glucose metabolism.

A Case of Isolated Familial Somatotropinoma.: Hwi Ra Park, Eun A Kim, Mei Hua Jiang, Chang Soo Jang, Kyoung Wook Lee, Seong Bin Hong, Eun Young Kim, Myung Kwan Lim, Moon Suk Nam, Yong Seong Kim; J Korean Endocr Soc. 2004;19(4):398-405. Published online August 1, 2004

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Abstract PDF: The familial occurrence of a pituitary adenoma associated with multiple endocrine neoplasia (MEN) type 1 or Carney complex is a well-recognized entity. However, an isolated familial somatotropinoma is a rare inherited disease, which is characterized by clustering of a somatotrophic adenoma and acromegaly or gigantism in a family, but without other manifestations of MEN type 1, with only 68 cases, in 28 families, described in the literature. The mode of inheritance is autosomal dominant, with incomplete penetration, but the genetic background of these pituitary adenomas remains unknown. A family exists where both the father and son were affected. Endocrinological investigations confirmed hypersecretion of GH and IGF-1, and the pituitary adenomas were identified by magnetic resonance image in both cases. There was no symptom of MEN type 1 or other form of endocrine dysfunction. Herein is reported a case of an isolated familial somatotropinoma in Korea, with a review of the literature

A Case of Masked Hypoglycemia during Lactic Acidosis.: Hee Seon Kim, Ho Sung Yoon, Chang Ok Koh, Hyeon Kyu Kim, Choel Young Park, Seong Jin Lee, Gi Weon Oh, In Kyung Jeong, Eun Gyung Hong, Cheol Soo Choi, Doo Man Kim, Sung Hee Ihm, Jae Myung Yu, Moon Gi Choi, Hyung Joon Yoo, Sung Woo Park, Dong Jin Oh; J Korean Endocr Soc. 2004;19(4):406-410. Published online August 1, 2004

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Abstract PDF: Severe hypoglycemia induces neuroglycopenic symptoms, including mental alteration, as glucose is the exclusive fuel for the central nervous system. However, some reports have shown that non-glucose fuels, like lactates and ketones, could be utilized by the brain during severe hypoglycemia. Herein, a case of extreme hypoglycemia in a 44-year old woman, subsequently diagnosed as congestive heart failure accompanied by ischemic hepatitis and lactic acidosis, is presented. In two episodes of extreme hypoglycemia, she was fully alert without obvious neurological deficits. In this unusual case, an increased supply of lactate might have maintained the cerebral function and prevented cerebral injury during the hypoglycemia that was induced as a result of starvation and hepatic and cardiac dysfunctions

A Case of Follicular Thyroid Carcinoma Developed in Pendred Syndrome.: So Hun Kim, Ji Young Jung, Sung Jae Shin, So Young Park, Si Hoon Lee, Yoo Mee Kim, Yu Mie Rhee, Soon Won Hong, Bong Soo Cha, Chul Woo Ahn, Kyung Rae Kim, Sung Kil Lim, Hyun Chul Lee; J Korean Endocr Soc. 2004;19(4):411-418. Published online August 1, 2004

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Abstract PDF: Pendred syndrome is an autosomal recessive genetic disorder, which is characterized by sensorineural hearing loss, goiter and a positive perchlorate discharge test. It is caused by mutations of the PDS gene, and its clinical characteristics vary widely. The thyroid function in most cases is normal, or shows only mild hypothyroidism. In Pendred syndrome, there is an organification defect that leads to defective thyroid hormone synthesis, followed by chronic TSH stimulation. Herein is reported a case of a follicular thyroid carcinoma associated with Pendred syndrome. To our knowledge, this is the first case reported in Korea. The patient presented with a huge anterior neck mass, sensorineural hearing loss and a positive perchlorate discharge test. Fine needle aspiration cytology suggested malignancy of the thyroid, and a total thyroidectomy, with central compartment node dissection, was performed. The pathology from the thyroid mass showed a poorly differentiated follicular thyroid carcinoma

A Case of Thyrotoxic Paraplegia.: Gun Wha Lee, Jin Woo Park, Ji Sung Yoon, Ji O Mok, Yeo Joo Kim, Hyeong Kyu Park, Chul Hee Kim, Sang Jin Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo, Du Shin Jeong; J Korean Endocr Soc. 2004;19(4):419-425. Published online August 1, 2004

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Abstract PDF: Hyperthyroidism may be associated or present with a variety of neuromuscular disorders, including thyrotoxic myopathy, exophthalmic ophthalmoplegia, periodic paralysis and myasthenia gravis. In contrast to muscle, peripheral nerve involvement in hyperthyroidism is exceedingly rare, and has received little attention. Paraplegia-like weakness during severe hyperthyroidism was first described by Charcot in 1889, and called Basedow's paraplegia' by Joffory in 1894. However, there has been no reported case in Korea. A 38-year-old woman was admitted for evaluation of progressive weakness and a gait disturbance. Her endocrinological results were compatible with hyperthyroidism. The polyneuropathy was also confirmed with sequential electrophysiological studies of the nerves and muscles. Drug therapy for hyperthyroidism resulted in resolution of the clinical neurological symptoms and progressive improvement of electrophysiological findings. Hyperthyroidisms are common medical disorders, which are often accompanied by diverse types of neurological and neuromuscular dysfunctions. All of these neurological manifestations are important, as they can serve as important clues to the diagnosis of a thyroid disorder. Furthermore, they are often related to the patient's presenting complaint. Therefore, the physician must be alert to the diverse manifestations of thyroid dysfunction, as they can lead to the diagnosis of potentially serious but treatable disorders. Herein is reported a case of myopathy and neuropathy associated with hyperthyroidism (Basedow's paraplegia), with a review of the literature

A Case of Hashimoto's Thyroiditis Associated with Multiple Sclerosis.: Beom Ju Lee, Jong Chan Oh, Sang Yong Kim, Dong Hyun Choi, Jung In Kim, Gyung Nam Kim, Jin Hwa Kim, Hak Yeon Bae; J Korean Endocr Soc. 2004;19(4):426-432. Published online August 1, 2004

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Abstract PDF: Multiple sclerosis is an autoimmune disorder, which may be associated with other rheumatologic or endocrine diseases induced by autoantibodies. Hashimoto's thyroiditis is also an organ-specific autoimmune disorder, and its association with multiple sclerosis during interferon therapy has been reported. Cases of Hashimoto's thyroiditis with multiple sclerosis are very rare. Herein is reported our experience of a 27 year-old woman who presented with general weakness, cold intolerance and progressive muscle weakness. She had been treated with levothyroxine due to subclinical hypothyroidism, which rather aggravated the symptom. In a CSF analysis, the myelin basic protein level was above 10 ng/dL and that of the IgG and the IgG index were 135 mg/dL and 7.8, respectively. In a brain MRI, demyelinating lesions in the left middle pontocerebellar junction and right subcortex were shown. She was diagnosed with multiple sclerosis, and the symptom improved after glucocorticoid and levothyroxine therapy. Herein is reported the first Korean case of Hashimoto's thyroiditis associated with multiple sclerosis

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