Introduction: Osteoporosis in males is an underdiagnosed condition. It is considered to be of secondary pathogenesis in up to 60% of cases. In order to establish rational flow charts for the diagnosis and management of osteoporosis in men solid data seem to be necessary about the incidence of certain underlying diseases.
Methods: In a prospective screening for hormonal alterations we analysed 65 patients with male osteoporosis according to laboratory parameters which comprised routine laboratory profile and hormonal screening of Estradiol, Testosterone, SHBG, Prolactin, LH, FSH, IGF-1, GH; PTH, 25-OH-Cholecalciferol. Patients were included according to the German guidelines for postmenopausal osteoporosis. Patients already on antiresorptive therapy were also included.
Results: All patients had undergone a basal laboratory screen according to guidelines for female osteoporosis and no irregularities had been found. However we found abnormal serum hormone levels of at least one parameter in approx. two thirds of these patients. 28.6% of patients showed alterations in the vitamin D3/parathyroid hormone system, e.g. showed low levels of vitamin D3 and borderline or elevated PTH levels possibly indicating intestinal malabsorption even in those already on calcium/vitamin D3 therapy. 14.3% showed low testosterone levels with or without consecutive elevations of LH and/or FSH. Prolactin was not elevated in any of the cases. SHBG levels were elevated in 39.3% of patients as was the ratio between testosterone and SHBG. Basal IGF-1 was below normal in 4% possibly indicating growth hormone deficiency.
Conclusion: We conclude that in male osteoporosis the common screening procedure for secondary osteoporosis is insufficient and that dominant risk factors for osteoporosis can be found in a high percentage of patients. Further screening and consecutive stimulation tests of the somatotropic axis of the pituitary will foster these preliminary findings and will help to establish diagnostic algorithms. The diagnosis of growth hormone deficiency might allow the intervention by substituting GH.
01 - 05 Apr 2006
European Society of Endocrinology