Endocrine Abstracts

Bone health is increasingly recognized as a crucial factor for quality of life. Osteoporosis, defined as bone impairment leading to an increased risk of fracture, is an important source of morbidity and even mortality in later life. Both male and female achieve the peak bone mass at around the age of 25 years. This peak is significantly lower in case of puberty and/or growth disorders, thus increasing the risk of osteoporosis later in life.

Discussion: Our Reproductive Division of Endocrinology in Lausanne University Hospital specializes in Congenital Hypogonadotropic Hypogonadism (CHH), a disorder characterized by absent puberty and infertility due to complete or partial deficiency of GnRH, the hypothalamic hormone that initiates the reproductive cascade. When CHH is accompanied by anosmia, it is called Kallmann syndrome (KS). In our cohort of KS and CHH patients, there is an important decrease of bone density, which is more significant when the disease was diagnosed late in life, resulting in long periods without hormonal replacement. On the contrary, as our clinical cases illustrate, when diagnosis of these rare disorders is performed promptly and adequate treatment is followed, the patients maintain a near-normal bone density and avoid fractures later in life. In a different approach to the relation between bone and sexual hormones, using data from the OsteoLaus population-based study, a large cohort of post-menopausal women, we recently showed that menopausal hormone treatment (MHT) is associated with enhanced bone density and structure. Interestingly, the bone benefit seems to persist for at least 2 years after its withdrawal. These results corroborate other studies outlining that in young postmenopausal women aged 50 to 60 years old the ratio benefit/risk is clearly in favor of the benefits in terms of bone health, cardiovascular outcomes and even mortality. We should reconsider MHT for recently postmenopausal women with menopausal symptoms such as hot flushes and/or increased risk of fractures. In new unpublished data, we detected that MHT users have significantly lower visceral fat mass, an important element with potential bone and systemic implications.

Conclusion: Sexual hormone deficiency throughout lifespan severely impairs bone quantity and quality leading to bone fragility. Increased awareness of the link between bone and gonadal function is mandatory among endocrine physicians and nurses in order to promote early diagnosis and avoid lack of treatment. The risk of bone morbidity later in life can be an important argument to increase patient’s adherence to therapy.