A risk-benefit assessment of alendronate in the treatment of involutional osteoporosis.
Osteoporosis is the most frequent metabolic condition experienced by elderly individuals. It is characterised by a low bone mass and microarchitectural deterioration of bone tissue leading to an increase in bone fragility and susceptibility to fracture. Osteoporosis constitutes a significant financial burden for health services as well as a source of pain and disability and a cause of a decrease in the quality of life for patients with the condition. Effective therapy for osteoporosis is, therefore, urgently needed. Currently, a number of different therapeutic approaches exist that have more or less proven positive effects on the incidence of fractures, for example estrogen replacement therapy, calcitonin, fluoride salts, calcium plus vitamin D supplementation and the first-generation bisphosphonate etidronate (etidronic acid). Alendronate (alendronic acid) is an alkylaminobisphosphonate with a very potent antiresorptive capability. In contrast to etidronate, alendronate possesses an excellent ratio between its potency for inhibiting bone resorption and its potency for impairing bone formation. In addition, no case of focal or generalised osteomalacia has so far been observed with alendronate. The bioavailability of oral alendronate is poor and the agent has to be taken in a fasting state, at least 30 minutes before breakfast, with a full glass of water. Alendronate has demonstrated its ability to increase bone mass significantly above the placebo values at any studied skeletal site in a wide variety of patient subgroups regardless of age, race, baseline rate of bone turnover or baseline bone mineral density. Alendronate is the only medication with a demonstrated positive effect on symptomatic and asymptomatic vertebral fracture rate, as well as on nonvertebral fracture rate. In clinical trials, alendronate was generally well tolerated and no significant clinical or biological adverse experiences were observed. However, postmarketing data have included reports of oesophageal lesions compatible with the diagnosis of alendronate-induced chemical oesophagitis, in around 1% of patients taking the agent. However, in the vast majority of cases alendronate tablets had been taken incorrectly. Therefore, with proper use, that is, use complying with the manufacturers administration recommendations, this potentially dangerous complication should be minimised and should not outweigh the overall positive benefit of alendronate in the prevention of fractures.
Department of Rheumatology, Saint-Luc University Hospital, Louvain University in Brussels, Belgium. Devogelaer@ruma.ucl.ac.be
J P
JP
Devogelaer
D000368:Aged; D019386:Alendronate / Q000009:adverse effects / Q000627:therapeutic use*; D015519:Bone Density / Q000187:drug effects; D001842:Bone and Bones / Q000187:drug effects; D005260:Female; D050723:Fractures, Bone / Q000517:prevention & control; D006801:Humans; D010024:Osteoporosis / Q000188:drug therapy*; D016103:Spinal Fractures / Q000517:prevention & control
D019386:Alendronate