Follicle-stimulating hormone (FSH) was shown to have a direct impact on bone metabolism in experimental investigations, but the results of human studies, which were primarily done in females, were unreliable. For a study, researchers sought to compare primary and central hypogonadism for the first time in order to examine the potential impact of excess FSH on the health of male bones.
At the time of their first diagnosis of hypogonadism, 119 men were included in the cross-sectional observational research. All of the subjects had spontaneous pubertal development. In the case of hypergonadotropic hypogonadism (Hyper-H), patients with Klinefelter syndrome (KS) were separated from the other variants (non-KS-Hyper-H) based on the beginning of FSH increase. Bone mineral density (BMD) at the lumbar spine (LS) and femoral neck (FN), as well as the prevalence of morphometric vertebral fractures (VFx), were measured.
Higher LS and FN BMD were related to longer age at diagnosis and higher body mass index (BMI) across the whole population. After controlling for potential confounders (age at diagnosis, BMI, smoking habits, degree of hypogonadism defined by calculated free testosterone, and 25OH vitamin D levels), non-KS-Hyper-H patients had significantly lower LS BMD and tended to have lower FN BMD values than hypogonadotropic hypogonadism patients (Hypo-H). The LS BMD of KS males was substantially lower than that of non-KS-Hyper-H men. There were no significant variations in the prevalence of VFx across the groups.
The data pointed to a possible deleterious effect of high FSH on male bone mass, particularly near the spine. The findings may potentially be influenced by the duration of elevated FSH levels.
Reference: frontiersin.org/articles/10.3389/fendo.2022.939897/full
