Search

It is largely recognized that Growth Hormone (GH) plays an important role in linear growth during childhood and subsequent completion of appropriate height in early adulthood. It has also significant influence on a variety of metabolic activities, as well as the cardiovascular system and quality of life (QoL) in adults. GH is involved in the attainment of optimal Bone Mineral Density (BMD), the most important predictor of osteoporotic fractures, during the transition from paediatric to adult age. The time interval between paediatric and adult age is a critical period of life to clinically assess persistence of GHD in patients affected by childhood onset GHD (COGHD) and determine the need for continuing treatment with recombinant human Growth Hormone (rhGH) even in the face of closure of epiphyseal growth plates. It has been reported GHD is associated with higher fracture's risk in COGHD patients and GH therapy should minimize, if not prevent, osteoporosis in adulthood. We report the case of a COGHD young man, rhGH treated until final height completion, presenting a wrist fracture and precocious bone density loss.

Osteoporosis in men is less frequent than in women and is more often due to an underlying cause, such as nutritional deficiencies or lifestyle factors, endocrinological or systemic affections, long-term specific therapies. The growing attention on male osteoporosis is mainly explained by the increasing use of some drugs producing bone loss as frequent side effect, like gonadotropin-releasing hormone (GnRH) agonists for prostate cancer, immunosuppressive agents, or glucocorticoids. Glucocorticoids are largely used for the cure of lots of haematological, rheumatological, dermatological, pneumological, and other systemic diseases. It is well known glucocorticoid-induced osteoporosis (GIOP) develops rapidly at prednisone > 5mg/d or equivalent levels but recurrence is recently also observed in patients receiving low dose and intermittent therapy. However, the possible side effects of corticosteroids at low dose on bone are not completely understood and rightly prevented. We present the case of a young man with precocious bone loss. His improper and irregular use of corticosteroids at low dose was finally recognized as the underlying cause of his unexplainable bone demineralization. The following short review about effects of glucocorticoids on bone suggests fracture incidence and bone mineral density should be assessed even in young people and men perceiving glucocorticoids at undefined dose for long period.