von Tirpitz C, Klaus J, Brückel J, Rieber A, Scholer A, Adler G, Böhm B O, Reinshagen M
Department of Medicine I, University of Ulm, Germany.
Eur J Gastroenterol Hepatol. 2000 Jan;12(1):19-24. doi: 10.1097/00042737-200012010-00005.
Low bone density with an increased risk of vertebral fractures is a frequent complication in inflammatory bowel disease. Since the aetiology of osteopathia in these patients is different compared to postmenopausal or steroid-induced osteoporosis, no treatment strategy is established. Supplementation of calcium and vitamin D has been shown to prevent further bone loss, but no data are available showing the anabolic effect of sodium fluoride in Crohn's disease.
We carried out a one-year prospective clinical trial in 33 patients with chronic active Crohn's disease who were randomly assigned to receive either calcium (500 mg b.i.d.) and 1000 IU vitamin D3 only, or retarded-release sodium fluoride (25 mg t.i.d.) additionally. The diagnosis of Crohn's disease had been made at least two years ago, and all patients had received systemic high-dose steroid therapy during the previous year. Eleven of 15 patients who received calcium/vitamin D and 15 of 18 patients who additionally received sodium fluoride completed the study. The primary endpoint of the study was the increase of bone mineral density, measured by dual energy X-ray absorptiometry (DXA) after one year of treatment. Bone-specific alkaline phosphatase and osteocalcin were used as markers for bone turnover.
In the calcium/vitamin D only group, bone density was not significantly changed after one year of treatment, whereas in the calcium/vitamin D/fluoride group, bone density of the lumbar spine increased from -1.39+/-0.3 (Z-score, mean +/- SEM) to -0.65+/-0.3 (P<0.05) after one year of treatment. Increase of bone density was positively correlated to the osteoblastic markers bone-specific alkaline phosphatase (r = 0.53) and osteocalcin (r = 0.43).
Sodium fluoride in combination with vitamin D and calcium is an effective, well-tolerated and inexpensive treatment to increase lumbar bone density in patients with chronic active Crohn's disease and osteoporosis.
骨密度降低且椎体骨折风险增加是炎症性肠病常见的并发症。由于这些患者骨病的病因与绝经后或类固醇诱导的骨质疏松症不同，尚未确立治疗策略。补充钙和维生素D已被证明可预防进一步的骨质流失，但尚无数据表明氟化钠对克罗恩病有合成代谢作用。
我们对33例慢性活动性克罗恩病患者进行了为期一年的前瞻性临床试验，这些患者被随机分配接受仅钙（每日两次，每次500毫克）和1000国际单位维生素D3，或额外接受缓释氟化钠（每日三次，每次25毫克）。克罗恩病的诊断至少在两年前做出，所有患者在前一年均接受了全身高剂量类固醇治疗。接受钙/维生素D的15例患者中有11例，额外接受氟化钠的18例患者中有15例完成了研究。该研究的主要终点是治疗一年后通过双能X线吸收法（DXA）测量的骨矿物质密度增加。骨特异性碱性磷酸酶和骨钙素用作骨转换的标志物。
仅钙/维生素D组在治疗一年后骨密度无显著变化，而在钙/维生素D/氟化物组中，治疗一年后腰椎骨密度从-1.39±0.3（Z评分，平均值±标准误）增加到-0.65±0.3（P<0.05）。骨密度增加与成骨标志物骨特异性碱性磷酸酶（r = 0.53）和骨钙素（r = 0.43）呈正相关。
氟化钠与维生素D和钙联合使用是一种有效、耐受性良好且廉价的治疗方法，可增加慢性活动性克罗恩病和骨质疏松症患者的腰椎骨密度。
