炎症性肠病患者维生素D缺乏症与低骨密度

G. Tapete, Veronica Almerigogna, A. Cozzi, M. Giannotta, S. Milani, M. Milla, S. Biagini
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引用次数: 1

摘要

背景:越来越多的证据表明,维生素D缺乏症在炎症性肠病(IBD)等免疫介导性疾病中起重要作用。维生素D缺乏症是骨质减少、骨质疏松和病理性骨折的危险因素。研究报道了维生素D缺乏症与克罗恩病(CD)和溃疡性结肠炎(UC)的病史和临床特征之间的相关性。本研究的目的是评估意大利IBD患者人群中维生素D血清水平和骨密度(BMD)改变的患病率,并将维生素D缺乏症的患病率与疾病史和临床特征联系起来。方法:在2013年10月至2014年11月期间,我们招募了本中心患有UC或CD的患者。排除标准为年龄在18岁以下,60岁以上,同时服用维生素D替代治疗,以及同时患有可能改变维生素D代谢的胃肠道或内分泌疾病。所有患者均行25- oh维生素D、ESR、c反应蛋白(CRP)、PTH、血清钙磷、β-CTX、碱性磷酸酶(骨同工酶)血浆测定和腰椎、股骨双能x线吸收仪(DXA)扫描评估骨密度(BMD)。这两项测量是在秋季和冬季同时进行的。根据2012年意大利骨质疏松协会指南,我们定义血浆维生素D值<30 ng/mL为维生素缺乏症,20 - 30 ng/mL为维生素D水平不足,<20 ng/mL为维生素D水平不足。我们收集了患者入组时的生活习惯、临床病史、病程和疾病临床活动等数据。在BMD评估中,计算每位患者腰椎(L1-L4)和股骨颈水平的t评分和/或z评分,并根据国际指南诊断骨质减少或骨质疏松。结果:我们纳入了88例患者(62例CD, 26例UC);入组时中位年龄为CD组42岁,UC组43岁。CD患者的平均身体质量指数(BMI)为22.6,UC患者为23.7。CD和UC的诊断年龄分别为29.8岁和33.5岁,CD和UC的平均病程分别为12.8年和9.1年。84.1%的患者出现维生素D缺乏症。其中,31.8%的人维生素D水平不足,而57.3%的人缺乏维生素D。平均维生素D水平为20.4 ng/mL,但在性别或疾病类型方面没有差异。事实上,维生素D缺乏症与病程或诊断时患者的年龄没有相关性。维生素D缺乏症与CD患者的类固醇依赖史(p=0.03)、抗TNF-α药物治疗需求(p=0.01)和吸烟习惯(p=0.01)有统计学意义的相关性。在CD患者中,我们也发现在有统计学意义的限度(p=0.05)下,维生素D缺乏症、高CRP值与入组时的HarveyBradshaw指数(HBI)之间存在相关性。70例患者行腰椎DXA分析,67例行股骨DXA分析。37.1%的患者发现腰椎骨密度低于正常范围,表明24.2%和12.9%的患者受到骨质减少或骨质疏松症的影响,与性别和疾病类型(CD或UC)无关。同样,43.3%的患者股骨骨密度低于正常年龄范围。这一数据与34.3%和9%的骨质减少或骨质疏松相一致,与性别和疾病类型无关,CD患者的股骨z评分明显低于UC患者(p=0.03)。结论:在我们的研究中,我们发现IBD人群中维生素D缺乏症的患病率很高,与患者的性别、类型和疾病持续时间无关。我们的数据显示,维生素D缺乏症与CD患者的类固醇依赖史、抗TNF-α药物治疗需求和吸烟习惯之间存在很强的相关性。维生素D缺乏症可能在引起IBD更严重的临床行为中起着至关重要的作用。骨代谢的改变是IBD患者关注的问题。我们观察到,无论IBD类型如何,受UC和CD影响的男性和女性,即使年轻且病程短,骨密度改变的患病率都很高。这类患者可开腰椎和股骨,特别是维生素D缺乏症和低BMI的病例。这将允许早期诊断骨密度改变,开始特定的治疗,并防止进一步的并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypovitaminosis D and Low Bone Mineral Density in Inflammatory Bowel Disease Patients
Background: Increasing evidences suggest that hypovitaminosis D can play an important role in immuno-mediated diseases, such as Inflammatory Bowel Diseases (IBD). The hypovitaminosis D is an established risk factor for the development of osteopenia, osteoporosis and pathological fractures. Studies have reported a correlation between hypovitaminosis D, disease history and clinical features in Crohn's Disease (CD) and Ulcerative Colitis (UC). The aim of this study is to evaluate the vitamin D serum levels and the prevalence of bone mineral density (BMD) alterations in a population of Italian IBD patients and to correlate the prevalence of hypovitaminosis D with disease history and clinical features. Method: Between October 2013 and November 2014 we enrolled patients from our center that were affected by UC or CD. Exclusion criteria were age below 18 and over 60, concomitant vitamin D replacement therapy and concomitant gastrointestinal or endocrinological diseases which may alter vitamin D metabolism. All patients underwent 25-OH-vitamin D, ESR, C-reactive protein (CRP), PTH, serum calcium and phosphorus, β-CTX, alkaline phosphatase (bone isoenzyme) plasma assay and bone mass density (BMD) evaluation by lumbar and femoral dual-energy X-ray absorptiometry (DXA) scan. Both measurements were made at the same time, during the autumn and winter months. Following 2012 Osteoporosis Italian Society Guidelines, we defined as hypovitaminosis D plasmatic values <30 ng/mL, vitamin D levels were considered as insufficient if between 20 and 30 ng/ mL and deficient if <20 ng/mL. We collected data regarding patients’ life habits and clinical history, disease course and disease clinical activity at enrollment. For BMD evaluation T-score and/or Z-score were calculated for each patient at lumbar (L1-L4) and femoral neck level, and the diagnosis of osteopenia or osteoporosis was made according to international guidelines. Results: We enrolled 88 patients (62 CD, 26 UC); median age at enrollment was 42 years for CD and 43 years for UC. Mean Body Mass Index (BMI) was 22.6 in CD and 23.7 in UC patients. Age at diagnosis was 29.8 years for CD and 33.5 years for UC, with mean disease duration of 12.8 years for CD and 9.1 years for UC.Hypovitaminosis D was observed in 84.1% of the patients. Of these, 31.8% had insufficient vitamin D levels, whereas 57.3% deficient. Mean vitamin D level was 20.4 ng/mL, but there was no difference with respect to sex or disease type. Indeed, there was no correlation between hypovitaminosis D and disease duration or patients age at diagnosis. A statistically significant correlation was found between hypovitaminosis D and history of steroid-dependancy (p=0.03), need of therapy with anti- TNF-α drugs (p=0.01) and cigarette smoke habit in CD patients (p=0.01). In CD patients we also found a correlation, at the limit of statistical significance (p=0.05), between hypovitaminosis D, high CRP values and HarveyBradshaw Index (HBI) at enrollment.70 patients underwent the lumbar DXA analysis, 67 the femoral DXA. Lumbar BMD was found to be below the normal range in 37.1% of the patients, suggesting that 24.2% and 12.9% were affected by osteopenia or osteoporosis, irrespective of sex and disease type (CD or UC). Similarly, femoral BMD was below the normal range for age in 43.3% of the patients. This figure is consistent with osteopenia or osteoporosis in 34.3% and 9%, irrespective of sex and disease type and femoral Z-score that was found significantly lower in CD than UC patients (p=0.03). Reduced BMD correlated with lower BMI and hypovitaminosis D. Conclusion: In our study we found a high prevalence of hypovitaminosis D in an IBD population irrespective of patients' sex, type and duration of disease. Our data show a strong correlation between hypovitaminosis D and a more aggressive disease course in terms of history of steroiddependancy, need of therapy with anti TNF-α drugs and smoke habit in CD patients. Hypovitaminosis D may play a crucial role in causing a more severe clinical behavior of IBD. Alteration of bone metabolism is a concern in IBD patients. We observed a high prevalence of BMD alterations in both men and women affected by UC and CD, even if of young age and with a short disease duration, irrespective of the type of IBD. Such patients may be prescribed lumbar and femoral, especially in cases of hypovitaminosis D and low BMI. This would allow an early diagnosis of BMD alterations, to start specific therapy and to prevent further complications.
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