A concomitant decrease in cortical and trabecular bone mass in isolated hypogonadotropic hypogonadism and gonadal dysgenesis.
10.3349/ymj.1999.40.5.444
- Author:
Ki Hyun PARK
1
;
Sang Joon LEE
;
Jin Young KIM
;
Jeong Yeon KIM
;
Sang Wook BAI
;
Jae Wook KIM
Author Information
1. Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea. jny6693@yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Bone;
density;
hypogonadism
- MeSH:
Adolescence;
Adult;
Bone Density*;
Collagen/analysis;
Female;
Gonadal Dysgenesis/therapy;
Gonadal Dysgenesis/metabolism*;
Human;
Hypogonadism/therapy;
Hypogonadism/metabolism*;
Osteocalcin/blood;
Peptides/analysis;
Puberty
- From:Yonsei Medical Journal
1999;40(5):444-449
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
