Devogelaer J P
Department of Rheumatology, Saint-Luc University Hospital, Louvain University in Brussels, Belgium.
Drug Saf. 1998 Aug;19(2):141-54. doi: 10.2165/00002018-199819020-00005.
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.
骨质疏松症是老年人最常见的代谢性疾病。其特征是骨量低和骨组织微结构退化，导致骨脆性增加和骨折易感性增加。骨质疏松症给医疗服务带来了巨大的经济负担，也是疼痛和残疾的根源，并且会导致患者生活质量下降。因此，迫切需要有效的骨质疏松症治疗方法。目前，存在多种不同的治疗方法，这些方法或多或少已被证明对骨折发生率有积极影响，例如雌激素替代疗法、降钙素、氟化物盐、补充钙加维生素D以及第一代双膦酸盐依替膦酸（依替膦酸钠）。阿仑膦酸盐（阿仑膦酸钠）是一种具有非常强抗吸收能力的烷基氨基双膦酸盐。与依替膦酸不同，阿仑膦酸盐在抑制骨吸收的效力和损害骨形成的效力之间具有出色的比例。此外，迄今为止尚未观察到阿仑膦酸盐导致局灶性或全身性骨软化症的病例。口服阿仑膦酸盐的生物利用度较差，该药物必须在空腹状态下服用，至少在早餐前30分钟，用一整杯水送服。在各种患者亚组中，无论年龄、种族、骨转换基线率或基线骨矿物质密度如何，阿仑膦酸盐已证明其在任何研究的骨骼部位均能使骨量显著高于安慰剂值。阿仑膦酸盐是唯一一种对有症状和无症状椎体骨折率以及非椎体骨折率均有显著积极影响的药物。在临床试验中，阿仑膦酸盐总体耐受性良好，未观察到显著的临床或生物学不良事件。然而，上市后数据包括约1%服用该药物的患者出现与阿仑膦酸盐诱导的化学性食管炎诊断相符的食管病变报告。然而，在绝大多数情况下，阿仑膦酸盐片剂服用不当。因此，正确使用，即按照制造商的给药建议使用，这种潜在的危险并发症应降至最低，且不应超过阿仑膦酸盐在预防骨折方面的总体积极益处。
