1.A concomitant decrease in cortical and trabecular bone mass in isolated hypogonadotropic hypogonadism and gonadal dysgenesis.
Ki Hyun PARK ; Sang Joon LEE ; Jin Young KIM ; Jeong Yeon KIM ; Sang Wook BAI ; Jae Wook KIM
Yonsei Medical Journal 1999;40(5):444-449
To assess the impact of hypogonadism on bone mineral density, we performed a cross-sectional study of 70 amenorrheic women, comprising 22 cases of gonadal dysgenesis and 48 cases of isolated hypogonadotropic hypogonadism (IHH). Bone mineral density was measured by DEXA at four sites: the femur neck, Ward's triangle, trochanter, and lumbar spine (L2-4). The results were compared to those of a control group consisting of 60 age-matched, normal-cycling women. Bone mineral densities around age 20 were already significantly lower at all four sites in patients with IHH and gonadal dysgenesis when compared with controls, suggesting that these patients failed to achieve peak bone mass during pubertal development. In patients with IHH, the initial BMD around age 18-20 were significantly lower at all four sites and the decrease in bone density continued rapidly during the early twenties up to age 25, and then it slowed markedly thereafter. Bone biochemical marker, ICTP and osteocalcin were significantly negatively correlated with age and remained increased until age 40, which was reminiscent of menopausal bone loss pattern such as high bone turn-over in the early twenties, followed by slow bone loss in the late twenties. In patients with gonadal dysgenesis, bone biochemical marker, ICTP and osteocalcin were also significantly negative correlated with age and remained increased until age 40, but no significant changes in BMD were noted as a function of age, which may be attributed to the small sample size and slow bone loss. These findings suggest that the initiation of prompt and timely therapeutic intervention as early as possible in the menarchal period and throughout the remainder of life, particularly during the period associated with rapid bone loss.
Adolescence
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Adult
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Bone Density*
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Collagen/analysis
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Female
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Gonadal Dysgenesis/therapy
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Gonadal Dysgenesis/metabolism*
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Human
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Hypogonadism/therapy
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Hypogonadism/metabolism*
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Osteocalcin/blood
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Peptides/analysis
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Puberty
2.Site-specific effect of testosterone on bone mineral density in male hypogonadism.
Hak Ryong CHOI ; Sung Kil LIM ; Moo Sang LEE
Journal of Korean Medical Science 1995;10(6):431-435
To assess the correlation between the remaining serum testosterone and bone mineral density(BMD), and to determine the effect of exogenous testosterone on BMD in subjects with male hypogonadism, we evaluated the serum testosterone levels and BMDs of the femur neck, Ward's triangle and the spine(L1-4) in 20 subjects with Klinefelter's syndrome and 7 with hypogonadotropic hypogonadism before and after testosterone replacement. BMDs of the femur neck, Ward's triangle and the spine were below the age-matched normal mean at 77.8%(21/20), 74.1%(20/27) and 88.9%(24/27), respectively. There were significant differences in serum testosterone levels and the spinal BMD between the two groups and the BMD of the spine closely correlated with the serum testosterone level (R = 0.63, p < 0.001). Following a mean 11.8 +/- 4.9 months of testosterone replacement, the BMD at all sites increased significantly and the pretreatment difference in spinal BMD between the two groups disappeared. We conclude that, although testosterone may increases the bone density, it has a site-specific effect of maintaining and increasing the bone mass especially at the spine in male hypogonadism.
Adult
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Bone Density/*drug effects/physiology
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Human
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Hypogonadism/blood/*metabolism
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Klinefelter Syndrome/blood/drug therapy/*metabolism
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Male
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Middle Age
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Testosterone/blood/metabolism/*pharmacology
3.Hypogonadism may cause insulin resistance in young males.
Jiang-feng MAO ; Xue-yan WU ; Nai-shi LI ; Yi-fan SHI
National Journal of Andrology 2006;12(7):612-614
OBJECTIVETo investigate the relationship between hypogonadism and insulin resistance in young male.
METHODSTwenty-one hypogonadism young males aged 15 to 30 years were included in the clinical trial group, and 11 healthy young males of similar age and BMI in the control. Height, weight, serum FSH, LH, total testosterone (TT), nuclear type and bone age were measured for all the subjects. Serum glucose and insulin levels were taken through 3 h OGTT at 0, 30, 60, 120 and 180 min. And comparisons were made of the levels of fast glucose and insulin, areas under the curve of glucose and insulin and HOMA insulin resistance indexes (HOMA-IR) between the two groups.
RESULTS(1) In the hypogonadism group the average value of TT was (0.9 +/- 0.6) nmol/L and 5 cases of Klinefelter syndrome had pubertal development with Tanner stage above P3, while the other 16 had no. (2) No significant differences were found in BMI, age, areas under the glucose and insulin secretory curve in OGTT between the two groups. (3) Three patients were diagnosed as IGT by OGTT in hypogonadism group, whose serum glucose levels at 120 min were 8.6, 7.9 and 8.2 mmol/L respectively. The maximal insulin excretion time was 30 min after glucose loading. No IGT or DM was found in the control group. (4) Significant difference was found in HOMA-IR and fast insulin level between the two groups.
CONCLUSION(1) IGT incidence was higher in the hypogonadism group than in the control. (2) HOMA-IR and fast insulin levels were significantly higher in the hypogonadism group than in the control, which suggests that lower serum testosterone may cause insulin resistance in young male patients.
Adolescent ; Adult ; Blood Glucose ; metabolism ; Case-Control Studies ; Glucose Tolerance Test ; Humans ; Hypogonadism ; physiopathology ; Insulin ; blood ; Insulin Resistance ; Male ; Testosterone ; blood
4.Effect and safety of testosterone undecanoate in the treatment of late-onset hypogonadism: a meta-analysis.
Yi ZHENG ; Xu-bo SHEN ; Yuan-zhong ZHOU ; Jia MA ; Xue-jun SHANG ; Yong-jun SHI
National Journal of Andrology 2015;21(3):263-271
OBJECTIVETo evaluate the efficacy and safety of testosterone undecanoate (TU) in the treatment of late-onset hypogonadism (LOH) by meta-analysis.
METHODSWe searched Pubmed (until April 1, 2014), Embase (until March 28, 2014), Cochrane Library (until April 17, 2014), CBM (from January 1, 2001 to February 2, 2014), CNKI (from January 1, 2001 to February 2, 2014), Wanfang Database (from January 1, 2000 to February 2, 2014), and VIP Database (from January 1, 2000 to Febru ary 2, 2014) for randomized controlled trials of TU for the treatment of LOH. We evaluated the quality of the identified literature and performed meta-analysis on the included studies using the Rveman5. 2 software.
RESULTSTotally, 14 studies were included after screening, which involved 1 686 cases. Compared with the placebo and blank control groups, TU treatment significantly increased the levels of serum total testosterone (SMD = 6.22, 95% CI 3.99 to 8.45, P < 0.05) and serum free testosterone (SMD = 4.35, 95% CI 1.86 to 6. 85, P < 0.05) but decreased the contents of luteinizing hormone (WMD = -2.23, 95% CI -4.03 to -0.42, P < 0.05), sex hormone binding globulin (WMD = 2.00, 95% CI 1.38 to 2.63, P < 0.05). TU also remarkably reduced the scores of Partial Androgen Deficiency of the Aging Males (WMD = -9.49, 95% CI -12.96 to -6.03, P < 0.05) and Aging Males Symptoms rating scale (WMD = -2.76, 95% CI -4.85 to -0.66, P <0.05) but increased the hemoglobin level (SMD = 2.35, 95% CI 0.29 to 4.41, P < 0.05) and packed-cell volume (SMD = 4.35, 95% CI 1.36 to 7.33, P < 0.05). However, no significant changes were shown in aspertate aminotransferase, alanine transaminase, prostate-specific antigen, or prostate volume after TU treatment (P > 0.05).
CONCLUSIONTU could significantly increase the serum testosterone level and improve the clinical symptoms of LOH patients without inducing serious adverse reactions. However, due to the limited number and relatively low quality of the included studies, the above conclusion could be cautiously applied to clinical practice.
Androgens ; therapeutic use ; Hemoglobin A ; metabolism ; Humans ; Hypogonadism ; blood ; drug therapy ; Luteinizing Hormone ; blood ; Male ; Prostate-Specific Antigen ; Randomized Controlled Trials as Topic ; Sex Hormone-Binding Globulin ; metabolism ; Testosterone ; adverse effects ; analogs & derivatives ; blood ; pharmacology
5.The method of tonifying kidneys and activating blood circulation increases testosterone secretion index in late-onset hypogonadism males with kidney deficiency.
Shao-Hu ZHOU ; Zhi-Wei WENG ; Tang-Lin LI
National Journal of Andrology 2013;19(7):647-651
OBJECTIVETo investigate the effect of the method of tonifying the kidney and activating blood circulation on the testosterone secretion index (TSI) in late-onset hypogonadism (LOH) male patients with kidney deficiency and its possible mechanisms.
METHODSWe screened 60 LOH male patients with kidney deficiency based on the scores on Partial Androgen Deficiency in Aging Males (PADAM), the levels of serum total testosterone (TT) and luteinizing hormone (LH), and TSI (TT/LH). We randomly divided the patients into a Nan Geng Ning (NGN) group (n = 40, aged 55.02 +/- 11.37 years) and a control group (n = 20, aged 54.56 +/- 12.12 years) to be treated orally with NGN decoction and testosterone undecanoate capsules, respectively, both for 12 consecutive weeks. We obtained the scores on psychological status, physical status and sexual function and observed the changes in serum TT, LH and TSI after 4, 8 and 12 weeks of treatment.
RESULTSCompared with the baseline, both the NGN and control groups showed a significant reduction after 12 weeks of medication in the LH level ([5.32 +/- 2.08] vs [4.89 +/- 1.46] IU/L and [5.36 +/- 2.07] vs [4.81 +/- 1.75] IU/L, P < 0.05), psychological status score (5.2 +/- 1.3 vs 2.7 +/- 1.4 and 4.8 +/- 2.2 vs 2.9 +/- 1.2, P < 0.05), physical status score (6.9 +/- 2.5 vs 2.9 +/- 1.6 and 7.1 +/- 2.7 vs 3.1 +/- 1.5, P < 0.05) and sexual function score (10.2 +/- 3.3 vs 4.5 +/- 2.9 and 9.8 +/- 3.1 vs 4.8 +/- 3.0, P < 0.05), but a remarkable increase in the TT level ([11.13 +/- 0.69] vs [14.55 +/- 0.75] nmol/L and [10.99 +/- 0.74] vs [14.74 +/- 0.83] nmol/L, P < 0.05) and TSI ([2.14 +/- 0.65] vs [2.99 +/- 0.72] nmol/IU and ([2.05 +/- 0.73] vs [3.11 +/- 0.65] nmol/IU, P < 0.05). However, no significant differences were found between the NGN and control groups at 12 weeks in LH ([4.89 +/- 1.46] vs [4.81 +/- 1.75] IU/L, P > 0.05), TT ([14.55 +/- 0.75] vs [14.74 +/- 0.83] nmol/L, P > 0.05), TSI ([2.99 +/- 0.72] vs [3.11 +/- 0.65] nmol/IU, P > 0.05), psychological status score (2.7 +/- 1.4 vs 2.9 +/- 1.2, P > 0.05), physi- cal status score (2.9 +/- 1.6 vs 3.1 +/- 1.5, P > 0.05) and sexual function score (4.5 +/- 2.9 vs 4.8 +/- 3.0, P > 0.05). There were no adverse events in either of the two groups throughout the whole experiment.
CONCLUSIONThe method of tonifying the kidney and activating blood circulation could significantly improve the clinical symptoms of LOH with kidney deficiency and increase the patient's serum TT level and TSI. NGN decoction works on LOH by acting on the hypothalamic-pituitary-gonad axis.
Adult ; Aged ; Humans ; Hypogonadism ; diagnosis ; drug therapy ; metabolism ; Luteinizing Hormone ; blood ; Male ; Medicine, Chinese Traditional ; methods ; Middle Aged ; Phytotherapy ; Testis ; secretion ; Testosterone ; analogs & derivatives ; blood ; therapeutic use ; Treatment Outcome
6.Growth Hormone Treatment in Prader-Willi Syndrome.
Ji Eun PARK ; Seung Won LEE ; Kyoung Eun SONG ; Hyoung Suk LEE ; Dae Jung KIM ; Yoon Sok CHUNG ; Kwan Woo LEE ; Hyon Joo KIM
Journal of Korean Society of Endocrinology 2006;21(1):40-46
BACKGROUND: Prader-Willi syndrome (PWS) is a congenital disorder, which is clinically characterized by a short stature, muscular hypotonia, hypogonadism, mental retardation and hyperphagia, leading to early childhood obesity. Impaired growth hormone (GH) secretion, hypogonadism, and obesity are common in patients with PWS. The purpose of this study was to find the effects of growth hormone treatment in patients with PWS. METHODS: Six patients with PWS confirmed by a genetic study were recruited, and treated with growth hormone(Eutropin(R))(0.8-1 IU/kg/week) divided into five or seven day doses per week for six months. The heights and weights of the subjects were evaluated. GH status were evaluated using the serum insulin-like growth factor (IGF)-I level, the L-dopa test, and insulin-induced hypoglycemia tess. Glucose metabolism was evaluated using the random serum glucose and HbA1c levels. RESULTS: GH was found to be deficient in 2 out of 6 subjects by the insulin test, in 3 out of 6 by the IGF-I level, and in 5 out of in 5 by the L-dopa test. After six months of GH treatment, the height percentile was increased and weight percentile decreased. The serum glucose and HbA1c levels remained unchanged. CONCLUSION: Six months of GH treatment in patients with PWS improved the height and degree of obesity. This study has shown the beneficial effects of GH treatment for patients with PWS, and without significant side effects.
Blood Glucose
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Congenital, Hereditary, and Neonatal Diseases and Abnormalities
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Glucose
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Growth Hormone*
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Humans
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Hyperphagia
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Hypoglycemia
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Hypogonadism
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Insulin
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Insulin-Like Growth Factor I
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Intellectual Disability
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Levodopa
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Metabolism
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Muscle Hypotonia
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Obesity
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Pediatric Obesity
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Prader-Willi Syndrome*
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Weights and Measures