Endocrinology and Metabolism

Special Article

Miscellaneous
Diagnosis and Treatment of Growth Hormone Deficiency: A Position Statement from Korean Endocrine Society and Korean Society of Pediatric Endocrinology: Jung Hee Kim, Hyun Wook Chae, Sang Ouk Chin, Cheol Ryong Ku, Kyeong Hye Park, Dong Jun Lim, Kwang Joon Kim, Jung Soo Lim, Gyuri Kim, Yun Mi Choi, Seong Hee Ahn, Min Ji Jeon, Yul Hwangbo, Ju Hee Lee, Bu Kyung Kim, Yong Jun Choi, Kyung Ae Lee, Seong-Su Moon, Hwa Young Ahn, Hoon Sung Choi, Sang Mo Hong, Dong Yeob Shin, Ji A Seo, Se Hwa Kim, Seungjoon Oh, Sung Hoon Yu, Byung Joon Kim, Choong Ho Shin, Sung-Woon Kim, Chong Hwa Kim, Eun Jig Lee; Endocrinol Metab. 2020;35(2):272-287. Published online June 24, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.2.272

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Growth hormone (GH) deficiency is caused by congenital or acquired causes and occurs in childhood or adulthood. GH replacement therapy brings benefits to body composition, exercise capacity, skeletal health, cardiovascular outcomes, and quality of life. Before initiating GH replacement, GH deficiency should be confirmed through proper stimulation tests, and in cases with proven genetic causes or structural lesions, repeated GH stimulation testing is not necessary. The dosing regimen of GH replacement therapy should be individualized, with the goal of minimizing side effects and maximizing clinical improvements. The Korean Endocrine Society and the Korean Society of Pediatric Endocrinology have developed a position statement on the diagnosis and treatment of GH deficiency. This position statement is based on a systematic review of evidence and expert opinions.

Citations

Citations to this article as recorded by

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Original Article

The Effect of Hormone Replacement Therapy on Carotid Intima-Media Thickness in Healthy Postmenopausal Women.: Jang Yel Shin, Bong Soo Cha, Choon Hee Chung, Won Heum Shim, Hyun Chul Lee; J Korean Endocr Soc. 2006;21(1):14-21. Published online February 1, 2006; DOI: https://doi.org/10.3803/jkes.2006.21.1.14

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Abstract PDF: BACKGROUND
Cardiovascular disease is the leading cause of death in postmenopausal women. The use of hormone replacement therapy (HRT) preventing for cardiovascular disease in postmenopausal women remains controversial. We investigated the effect of HRT on carotid intima-media thickness (IMT) according to the HRT duration in healthy postmenopausal women. METHODS: One hundred and twenty postmenopausal women (mean age: 55.4 +/- 3.3 years) were classified into never users, short-term, and long-term users according to the HRT duration. Carotid IMT was measured, and the clinical and biochemical cardiovascular risk factors were examined. RESULTS: The mean IMT was significantly thinner in the long-term users than that in the never users (0.62 +/- 0.11 vs. 0.71 +/- 0.14 mm, P < 0.01). Also, the maximal IMT was significantly thinner in the short-term and the long-term users. However, there is no significant difference in the mean and maximal IMTs between the estrogen alone and estrogen plus progestins used group. The period exposed to menopause was significantly shorter in the long-term users than that in the never users (1.8 +/- 2.3 vs. 4.3 +/- 3.3 years, P < 0.001). CONCLUSION: Our findings suggest that if HRT is initiated during early postmenopausal period before the onset of atherosclerosis, HRT may have a beneficial effect on the prevention of carotid atherosclerosis.

Case Report

A Case of Pancytopenia Caused by Sheehan's Syndorme Improved with Hormone Replacement Therapy.: Sung Ki Kim, Yoon Ju Oh, Park Young Joo, Young Whan Kim, Seong Bin Hong, Mi Rim Kim, Moon Suk Nam, Yong Seong Kim; J Korean Endocr Soc. 2000;15(4-5):595-599. Published online January 1, 2001

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Abstract PDF: Postpartum ischemic necrosis of the pituitary gland, known as Sheehan's syndrome, is well- established clinical entity. In anterior pituitary insufficiency, there is very often a normochromic or hypochromic anemia but pancytopenia secondary to the hypopituitarism is less common. We report a case of pancytopenia due to complete aplasia of the bone marrow associated with Sheehan's syndrome, in which hormone replacement therapy alone produced full hematological recovery.

Original Articles

Changes of Biochemical Bone Markers and Bone Mineral Density after Hormone Replacement Therapy in Korean Women.: Kyong Soo Park, Do Joon Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Jae Hyeon Kim, Jeong Goo Kim; J Korean Endocr Soc. 2000;15(2):226-236. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Biochemical bone markers have been suggested to reflect postmenopausal high bone turnover. These markers could be useful in following response to hormone replacement therapy (HRT). But we have few studies about the sequential changes of biochemical bone markers and bone mass after HRT in Korean women, and it is unclear whether women with early menopause have different response to HRT from women with normal menopause. The aims of the present study were to see the sequential changes of biochemical bone markers and bone mass after HRT in Korean women, to examine whether a single baseline biochemical bone marker or a change in biochemical bone marker could predict subsequent bone mass, and to determine the difference of response to HRT between women with early menopause and women with normal menopause. METHODS: Postmenopausal women (n=21) were divided with into three groups according to their age at menopause (AAM): the first group with AAM < or = 43 years (early menopause group, n=7), the second group with 43 years < or = AAM < or = 50 years (n=4), and the third group with AAM > or = 50 years (normal menopause group, n=10). For the HRT, conjugated estrogen (0.625mg per day) and continuous or cyclic medroxyprogesterone (2.5-10mg per day) were administered. Bone mineral density (BMD) was measured at baseline and 12 months and biochemical bone markers were measured at baseline and 3, 6, and 12 months during HRT. RESULTS: Deoxypyridinoline, type 1 collagen N-telopeptide, bone alkaline phosphatase, and osteocalcin were significantly decreased at 3 months, and mean percent changes from baseline of bone resorption markers were larger than those of bone formation markers. At 12 months, BMD was significantly increased at lumbar spine and Ward's triangle. But BMD was not significantly increased at femur neck and femur trochanter. Two baseline bone markers (bone alkaline phosphatase and type 1 collagen N-telopeptide) correlated with changes of BMD but any changes of bone markers at 3, 6 months didn't correlate with changes of BMD. In early menopause group, changes of bone markers and BMD were larger than those in normal menopause group, but the difference between the two groups was not significant. CONCLUSION: All four bone markers showed significant reduction at 3 months, but bone resorption markers were decreased more markedly and rapidly, and some baseline bone markers can predict the change of BMD after HRT. The difference of response to HRT between early menopause group and normal menopause group was not significant.

Association of Estrogen Receptor Genotypes with Serum Lipids and Responsiveness of Serum Lipids to Hormonal Replacement Therapy in Korean Postmenopausal Women.: So Ra Park, Jae Eun Park, Chung Kyu Hwang, Phil Ho Jung, Chang Hoon Yim, Ho Yeon Chung, Ki Ok Han, Hyun Ku Yoon, Hak Chul Jang, In Kwon Han; J Korean Endocr Soc. 1999;14(3):553-561. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Several biologically plausible mechanisms have been proposed for estrogen-mediated caridoprotection, including estrogen-assocaited changes in lipid metabolism and endothelial function of vessel walls. These effects are thought to be mediated via estrogen receptor (ER). Relationships between ER polymorphisms and serum lipid levels were not investigated enoughly. METHODS: Three restriction fragment length polymorphisms (RFLPs) at the ER gene locus, represented as B-variant, PvuII and XbaI, and their relationship to serum lipid levels were examined in 318 postmenopausal women. Their mean age was 54.5+/-6.5 years (mean+SD). An association between ER genotypes and changes in lipid levels after 1 year of estrogen replacement therapy was also investigated in follow-up 251 women. RESULTS: The B-variant was not found in Korean women. The distribution of the PvuII and XbaI polymorphisms was as follows: PP 109 (34%), Pp 166 (52%), pp 43 (14%), and XX 204 (64%), Xx 95 (30%), xx 19 (6%). Significant relationship was found between genotypes and changes in serum total cholesterol levels after lyr estrogen replacement therapy. There was no significant relationship between ER genotypes and changes in HDL cholesterol, LDL cholesterol and triglyceride levels after estrogen therapy. CONCLUSION: These data indicate that these polymorphisms are possible predictor on lipid response to estrogen replacement therapy.

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