Tóth M, Tulassay Z
II. Belgyógyászati Klinika, Semmelweis Orvostudományi Egyetem, Budapest.
Orv Hetil. 2000 Jan 30;141(5):219-23.
Chronic glucocorticoid treatment is the most frequent cause of secondary osteoporosis. The direct inhibitory effect of glucocorticoids on osteoblasts results in decreased bone formation. Increased osteoclastic bone resorption due to low concentrations of gonadal steroid hormones and glucocorticoid-induced direct suppression of intestinal calcium absorption also contribute to the decrease of bone mass in these patients. Bone loss is rapid, particularly in the first months of glucocorticoid therapy. Bone mineral density of the lumbar spine and proximal femur should be measured in patients who are starting chronic therapy with glucocorticoids. Although glucocorticoid-induced osteoporosis is a severe and nowadays partially preventable disorder, osteoporosis prophylaxis is only rarely prescribed to these patients. Recent randomized, controlled trials proved the therapeutic effects of hormone replacement therapy, as well as of bisphosphonates and active vitamin D analogs in primary and secondary prevention of glucocorticoid-induced osteoporosis.
长期糖皮质激素治疗是继发性骨质疏松最常见的原因。糖皮质激素对成骨细胞的直接抑制作用导致骨形成减少。性腺类固醇激素浓度降低以及糖皮质激素诱导的肠道钙吸收直接抑制导致破骨细胞骨吸收增加,这也促使这些患者骨量减少。骨丢失迅速,尤其是在糖皮质激素治疗的最初几个月。对于开始接受糖皮质激素长期治疗的患者,应测量其腰椎和股骨近端的骨密度。尽管糖皮质激素诱导的骨质疏松是一种严重且如今部分可预防的疾病,但这些患者很少接受骨质疏松预防治疗。近期的随机对照试验证明了激素替代疗法、双膦酸盐和活性维生素D类似物在糖皮质激素诱导的骨质疏松一级和二级预防中的治疗效果。