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Endocrinol Metab : Endocrinology and Metabolism


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Goo Yeong Cho  (Cho GY) 2 Articles
The Changes in Atherosclerotic Markers and Adiopocytokines after Treatment with Growth Hormone for the Patients with Hypopituitarism and Growth Hormone Deficiency.
Hyun Won Shin, In Kyung Jeong, Goo Yeong Cho, Cheul Young Choi, Jong Yeop Kim, Yeong Je Chae, Min Ho Cho, Byung Wan Lee, Seong Jin Lee, Chul Young Park, Eun Gyoung Hong, Hyeon Kyu Kim, Doo Man Kim, Jae Myung Yu, Sung Hee Ihm, Moon Ki Choi, Hyung Joon Yoo, Sung Woo Park
J Korean Endocr Soc. 2006;21(6):515-525.   Published online December 1, 2006
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AbstractAbstract PDF
It is known that patients with hypopituitarism have a high mortality rate due to the presence of atherosclerosis, cardiovascular diseases and stroke. The aim of this study was the effect of growth hormone (GH) on the atherosclerotic markers and the adipocytokine levels. METHOD: The study was conducted on 13 adult patients with hypopituitarism and growth hormone deficiency (GHD), and they had been stabilized after receiving hormone replacement therapy for other insufficient pituitary hormones, other than GH, for more than one year. Before treatment with GH, we compared the lipid metabolism, glucose metabolism, cardiovascular risk factors and adipocytokine levels, including adiponectin, leptin, TNF-alpha and IL-6, between the GHD patients and 13 healthy adults who were of a similar age and gender distribution. Patients with GHD were treated with 1 U/day of GH for 6 months. We measured insulin-like growth factor-I (IGF-I), blood pressure, body composition, lipid metabolism, glucose metabolism and hs-CRP, cardiac function, adiponectin, leptin, TNF-alpha and IL-6 levels, flow mediated vasodilation (FMD) and nitroglycerin mediated vasodilation (NMD) before and after GH treatment. RESULTS: The patients with hypopituitarism and GHD showed significantly higher levels of total cholesterol (P = 0.002), low-density lipoprotein cholesterol (LDL-C) (P = 0.036), hs-CRP (P = 0.0087) and leptin (P < 0.001) than did the normal healthy adults. However, there was no difference between the normal adults and the patients with GHD for the systolic and diastolic BP, the levels of apoA, apoB, fasting blood glucose(FBG) and HOMA-IR. In the subjects with GHD after treatment with GH, the level of fat mass (P = 0.0017), total cholesterol (P = 0.004), LDL-C (P = 0.001), leptin (P = 0.013), TNF-alpha (P < 0.001) and hs-CRP (P = 0.0001) were significantly reduced, while lean body mass (P = 0.0161), FFA (P = 0.049) and FMD (P = 0.0051) showed a significant increase. However, there was no significant difference in the level of the systolic and diastolic BP, LDL-C, apoA, apoB, LP (a), HOMA-IR, ejection fraction, left ventricular posterior wall, E/A ratio, intraventricular septum, NMD, intima-media thickness, adiponectin, IL-6, FBG and fasting insulin before and after GH treatment. CONCLUSION: The subjects with GHD were vulnerable to cardiovascular disease. GH therapy for 6 months had a positive effect on their various cardiovascular risk factors.


Citations to this article as recorded by  
  • Molecular Biology of Atherosclerosis
    In-Kyung Jeong
    Endocrinology and Metabolism.2010; 25(3): 166.     CrossRef
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Sporadic Nonfamilial Hypophosphatemic Osteomalacia.
Young Kee Shong, Joong Yeol Park, Ghi Su Kim, You Sook Cho, Goo Yeong Cho, Sang Wook Kim, Jung Sik Park, Ki Up Lee
J Korean Endocr Soc. 1994;9(1):25-31.   Published online November 6, 2019
  • 1,128 View
  • 27 Download
AbstractAbstract PDF
Chronic hypophosphatemia caused by decreased intestinal absorption or increased renal clearance, may lead to rickets or osteomalacia independently of other predisposing abnormalities. The conditions commonly associated with increased renal clearance of phosphate are X-linked hypophosphatemic rickets, tumor associated rickets/osteomalacia, RTA and Fanconi syndrome. Recently we experienced 3 men with adult-onset, histologically proven osteomalacia associated with increased renal clearance of phosphate. None of them had a family history of bone disease, tumors or other tubular defects. All of these had remarkable biochemical and clinical improvement with medical treatment such as 1, 25-dihydroxyvitamin D and phosphate supplementation. Although we did not find tumors yet, we could not rule out the possibility of tumor-associated osteomalcia since it often takes several years to make a diagnosis because of small size, benign nature and unusual location of tumors. Thus, careful long-term follow up for tumor occurrence will be maintained in these patients with sporadic nonfamilial hypophosphatemic osteomalacia.
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