[Diphosphonates: and alternative to estrogen therapy in postmenopausal osteoporosis. Experience with alendronate]

The post-menopausal osteoporosis represents an important complication during the climateric period; its clinical, economic and social weight is destined to increase with the aging of the population. The lack of oestrogens is the main etiopathogenetic element; this is the reason why the substitutive therapy during the menopause represents the most appropriate approach. However, the possibility of clinical contra-indications to the oestrogenic treatment, the compliance of the patient not always adequate, the possibility of side-effects, and the doubt about the real opportunity of this treatment in the advanced years, require therapeutic alternatives. Between these, the "inhibitors of the bone reuptake" are actually the more realistic and justified approach knowing the pathogenetic aspect of the disease. In this group of drugs, the biphosphonates are particularly useful because of their pharmacologic properties: a strong affinity for the bone, a specific action only in the area of the bone rearrangement, a strong and selective inhibition of the osteoclastic activity. Because of their long half-life in the bone tissue, it seemed interesting to evaluate mineral bone density and metabolic effects using the alendronate. A double blind controlled study was performed in order to evaluate the effect of this drug: two groups of 15 women in post-menopause with vertebral bone mineral density (BMD) > 2 S.D. behind the mean peak of the adult and without vertebral fractures, were randomized to receive a 20 mg/die dose of alendronate or a placebo for six months. The first treatment significantly reduced all the bone turnover indexes (idrossiprolin, collagen cross links, phosphatase alkalin activity) in three months; another slight reduction was observed in the next three months. After the interruption of the treatment all the indexes of the bone turn over were slowly increased and reached the pre-treatment values in six-nine months. The lumbar BMD is increased of 3.7% (+/- 1.7 SD) after six months of aleandronate treatment; there were no modifications 6 and 12 months after the interruption of the treatment (respectively +4.6 +/- 2.8 and +4.7 +/- 2.67 referred to the basal values). The control group presents a slow reduction of the lumbar BMD, but this was significative only at the 18 degrees month of the study. The femoral BMD was not modified in a relevant measure in the group treated with the drug, while a significative reduction of the neck value was observed in the control group. We conclude that a short treatment with the alendronate is able to increase the lumbar BMD and to prevent the femoral reduction in the woman affected by post-menopausal osteoporosis. Finally, in our experience the alendronate represents a promising alternative to the oestrogen treatment of the post-menopausal osteoporosis; this approach however should be verified in the reduction in the incidence of fractures with larger studies.