炎症性肠病相关骨质疏松的若干研究

随着炎症性肠病（IBD）发病率和患病率的升高,骨质疏松作为IBD的并发症之一越来越受到重视。一般认为炎性因子、钙摄入量、维生素D水平、体重指数、年龄、性激素及使用糖皮质激素等与IBD并发骨质疏松相关。此文就IBD并发骨质疏松的危险因素的相关研究作一综述。     

炎症性肠病合并贫血的研究进展

贫血是炎症性肠病(IBD)患者常见的并发症之一,会导致生活质量下降,也可增加患者的住院频率。据报道IBD并发贫血的发病率为6～74[1]。IBD患者贫血的发病机制尚未完全明了,铁摄入与丢失的负平衡、慢性病所致贫血、VitB12和叶酸缺乏、药物介导、炎症因子、溶血等众多因素均可能参与贫血的发生。过去普遍认为贫血是IBD不可避免的伴随症状,往往重视度不够,但最近的观点强调,贫血是此类患者明确的治疗内容。     

益生菌治疗炎症性肠病的研究进展

炎症性肠病是难治性的肠道炎症性疾病 ,包括溃疡性结肠炎和克罗恩病 ,传统的药物治疗疗效不甚令人满意 ,且停药后易复发。随着微生态学的发展 ,对人体无害的益生菌治疗炎症性肠病取得了重要进展 ,此文就此作一综述     

炎症性肠病诊治进展

溃疡性结肠炎 (溃结 ,Ｕｌｃｅｒａｔｉｖｅｃｏｌｉｔｉｓ ,ＵＣ)与克鲁恩病(Ｃｒｏｈｎ’ｓｄｉｓｅａｓｅ ,ＣＤ)的发病在我国乃至亚洲地区呈明显增高趋势[1] 。这两种肠道炎症性疾病 ,以及另一种未确定型结肠炎(Ｉｎｄｅｔｅｒｍｉｎａｔｅｃｏｌｉｔｉｓ)的病因迄今均未明确。因此 ,临床上统称为特发性 (Ｉｄｉｏｐａｔｈｉｃ)炎症性肠病 (Ｉｎｆｌａｍｍａｔｏｒｙｂｏｗｅｌｄｉｓｅａｓｅ ,ＩＢＤ) [2 ] 。现就ＩＢＤ的诊断与治疗进展作一综述如下。1　诊　　断ＵＣ与ＣＤ ,无论其临床症状、内镜与放射学 ,以及组织学征象等方面 ,均…     

炎症性肠病动物模型的研究进展

炎症性肠病（IBD）包括溃疡性结肠炎（UC）和克罗恩病（Crohn病，CD），其病因和发病机制尚不清楚，目前关于IBD研究所取得的成果有相当一部分来源于对动物模型的研究，因而建立合适的动物模型显得至关重要。本文从IBD常用动物模型的主要机理，制备方法以及模型用途等方面作一综述。     

炎症性肠病与免疫学关系研究进展

炎症性肠病是一组病因未明的慢性肠道炎症性疾病,其临床症状以腹痛和腹泻为主,病因和发病机制错综复杂,包括多种因素,其中与机体免疫系统关系密切,目前研究发现免疫异常是炎症性肠病发病的重要因素,包括肠道内环境、免疫细胞、人类白细胞抗原、自身抗体、抗Laminaribioside糖抗体(ALCA)和抗Chitobioside lgA糖抗体(ACCA)、细胞因子、黏附分子、一氧化氮和核因子NF-kB等,他们在炎症的起始和持续发展中起重要的作用,本文就免疫因素在炎症性肠病中的作用作一综述.     

炎症性肠病的治疗进展

炎症性肠病（inflammatory bowel diseases，IBD）主要包括溃疡性结肠炎（ulcerative colitis，UC）和克罗恩病（crohn’s disease，CD），是一组慢性复发性疾病，病因未明，与肠道免疫机制有关，遗传和环境因素在IBD的发病中起重要作用。随着生活方式的改变，近年来IBD有增多趋势，对IBD发病机制的深入了解，发现分子和细胞介质在肠道免疫炎症过程中起重要作用，出现了环孢菌素、粘膜保护剂、抗肿瘤坏死因子抗体和白细胞去除术等新方法。本文就IBD的治疗进展作一综述。     

炎症性肠病中的血小板异常

ＩＢＤ存在着血小板形态和功能的异常，血小板的促炎和促血栓作用及其功能失调所致的血栓形成，血管炎和多灶微循环梗塞在ＩＢＤ粘膜损伤中起重要作用，血小板抑制剂治疗ＩＢＤ的临床意义尚有待证实。     

炎症性肠病的脑肠互动研究进展

随着各类生物制剂和新型小分子药物的研发,炎症性肠病(IBD)的治疗目标不断提高,不仅追求症状缓解,更致力于肠黏膜愈合、减少并发症发生以及维持患者长期良好的肠道和社会功能。在上述治疗理念的革新中,IBD患者的心理健康日益受到关注,临床医师逐渐认识到心理因素与肠道炎性反应之间存在双向关系。该文就心理因素对IBD发病的影响、以脑-肠轴(GBA)为介导的脑肠之间的交互机制和以GBA为靶点的IBD治疗策略作一综述。     

Clinical relevance of changes in bone metabolism in inflammatory bowel disease

Low bone mineral density is an established, frequent, but often neglected complication in patients with inflammatory bowel disease (IBD). Data regarding the diagnosis, therapy and follow-up of low bone mass in IBD has been partially extrapolated from postmenopausal osteoporosis; however, the pathophysiology of bone loss is altered in young patients with IBD. Fracture, a disabling complication, is the most important clinical outcome of low bone mass. Estimation of fracture risk in IBD is difficult. Numerous ...     

Basic and clinical aspects of osteoporosis in inflammatory bowel disease

Low bone mineral density and the increased risk of fracture in gastrointestinal diseases have a multifactorial pathogenesis. Inflammatory bowel disease （IBD） has been associated with an increased risk of osteoporosis and osteopenia and epidemiologic studies have reported an increased prevalence of low bone mass in patients with IBD. Certainly, genetics play an important role, along with other factors such as systemic inflammation, malnutrition, hypogonadism, glucocorticoid therapy in IBD and other lifestyle factors. At a molecular level the proinflammatory cytokines that contribute to the intestinal immune response in IBD are known to enhance bone resorption. There are genes influencing osteoblast function and it is likely that LRP5 may be involved in the skeletal development. Also the identification of vitamin D receptors （VDRs） and some of its polymorphisms have led to consider the possible relationships between them and some autoimmune diseases and may be involved in the pathogenesis through the exertion of its immunomodulatory effects during inflammation. Trying to explain the physiopathology we have found that there is increasing evidence for the integration between systemic inflammation and bone loss likely mediated via receptor for activated nuclear factor kappa-B （RANK）, RANK-ligand, and osteoprotegerin, proteins that can affect both osteoclastogenesis and T-cell activation. Although glucocorticoids can reduce mucosal and systemic inflammation, they have intrinsic qualities that negatively impact on bone mass. It is still controversial if all IBD patients should be screened, especially in patients with preexisting risk factors for bone disease. Available methods to measure BMD include single energy x-ray absorptiometry, DXA, quantitative computed tomography （QCT）, radiographic absorptiometry, and ultrasound.DXA is the establish method to determine BMD, and routinely is measured in the hip and the lumbar spine. There are several treatments options that have proven their effectiveness, whil     

炎症性肠病的诊治

近20年来，炎症性肠病（IBD），无论是溃疡性结肠炎（UC）还是克罗恩病（CD），在我国报告逐渐增多，以医院为基础的调查推测患病率，UC为11．6／10^5，CD为1．4／10^5，香港发病率UC为1．2／10^5，CD为1．0／10^5。由此带来纷繁复杂的临床问题，引起专业医生的高度重视。借鉴国外对疾病发病机制的研究直接用于临床的经验和不断更新的IBD处理指南，我国也在IBD的诊治方面进行了不懈的探索，并取得了一定的进展。     

炎症性肠病并发低骨量/骨质疏松的危险因素分析

目的 对炎症性肠病(IBD)患者的骨密度状况进行评估,探讨其下降的危险因素.方法 通过对IBD患者血液学指标、身高、体重及腰椎骨密度进行测量,并与健康志愿者比较,分析IBD患者骨质疏松的危险因素.结果 共收集克罗恩病(CD)77例,溃疡性结肠炎(UC)43例,37例健康志愿者作为对照组.CD组、UC组及对照组的腰椎骨质的T值分别为-1.72±1.20、-1.26±1.12和-0.62±0.87,CD组的T值低于UC组(P=0.045)和对照组(P=0.000),UC组T值低于对照组(P=0.014).CD组、UC组及对照组的腰椎骨质疏松的发生率分别为23.3%、14.0%和0;CD组的腰椎骨质疏松发生率高于对照组,差异有统计学意义(P=0.003);UC组的腰椎骨质疏松发生率有高于对照组的趋势,但差异无统计学意义(P=0.053).多元回归分析显示,低体重(BMI≤18.4kg/m~2)是CD(OR=11.25,95%CI 3.198～39.580,P=0.000)和UC(OR=14.50,95%CI 1.058～88.200,P=0.045)患者骨质疏松的危险因素.年龄、病程、病变部位、CD活动指数(CDAI)、服用糖皮质激素、服用免疫抑制剂、血清25-羟基维生素D浓度等因素与骨质疏松的发生无相关性.结论 骨密度下降的发生在IBD患者中较为普遍,低体重是IBD患者骨质丢失的危险因素.     

老年炎症性肠病患者的骨代谢和骨密度分析

目的 探讨老年炎症性肠病（inflammatory bowel disease,IBD）患者的骨代谢和骨密度情况与健康对照者的差异,为临床防治IBD引起的骨质疏松提供依据.方法 纳入复旦大学附属华东医院IBD患者20例为IBD组,同期健康体检者20例为对照组.记录并比较两组的年龄、病程、病变部位、糖皮质激素（Glucocorticoids,GCs）应用、骨代谢相关血清学指标检查结果以及髋关节和股骨颈骨密度T值.结果 溃疡性结肠炎组髋关节骨量减少的发生率高于对照组,差异有统计学意义（64.3％ vs 30.0％,P=0.048）.UC组的血清25-羟维生素D[25-hydroxyvitamin D,25-（OH） D]浓度低于对照组（t=0.036,P=-2.100）,IBD组的血清β-CTX浓度高于对照组（UC：=0.003,P=2.975; CD：t=0.024,P=2.253）.结论 老年UC患者髋关节骨量减少的发生率增加,25-（OH）D浓度降低;IBD患者血清β-CTX浓度升高.     

口服耐受与炎症性肠病

口服耐受是机体对口服抗原产生的特异性无应答或低应答状态.低剂量口服抗原主要通过调节性T细胞分泌抑制性细胞因子介导免疫抑制,高剂量口服抗原主要引起T细胞清除或T细胞失能.多次低剂量口服结肠炎提取蛋白或正常结肠提取蛋白均能缓解实验性结肠炎.目前,多次低剂量口服自体结肠提取蛋白已初步应用于临床试验,并证明是安全的治疗方案.充分发挥口服耐受对炎症性肠病的临床疗效仍需深入研究.     

肠道平滑肌动力与炎症性肠病研究进展

肠道平滑肌动力改变与炎症性肠病(IBD)的发病关系得到医学界的重视,并逐渐成为IBD发病机制研究的热点.肠道运动的异常和神经递质的失衡在IBD的发生和进展过程中起了重要作用;白细胞介素能在一定程度上反映肠道运动功能变化.因此,恢复神经递质的失衡并重建肠道动力平衡的策略在IBD治疗过程中有良好的应用前景.     

炎症性肠病患者骨密度降低的多因素分析

目的评估骨质疏松和(或)骨量减少在炎症性肠病(IBD)患者中的发生率,寻找IBD患者发生严重骨密度下降的主要因素,为临床尽早开展预防性治疗,及时诊断提供证据。方法选择66例IBD患者,其中克罗恩病(CD)38例,溃疡性结肠炎(UC)28例,测定患者骨密度,记录其主要症状,体征及实验室检查结果,制订治疗方案。根据CD活动指数(AI)和Truelove-Witts评分确定病情活动度。结果进行统计学分析。结果62例患者完成研究,平均年龄(40.9±15.4)岁。腰椎部出现骨质疏松和骨量减少者分别为21.0%和29.0%;股骨颈则分别为19.4%和6.5%,腰椎较股骨颈更易发生严重骨密度下降(P= 0.005)。CD患者较UC患者更易发生骨质疏松和(或)骨量减少(P=0.001)。激素用量、体重指数的变化、病变范围、女性绝经和患者T值变化均相关。结论骨量减少与骨质疏松在IBD患者中普遍存在。年龄、激素、体重指数、病变范围、女性绝经和患者T值变化均相关。疾病活动度与骨密度下降是否存在联系尚待明确。     

Update on inflammatory bowel disease in patients with primary sclerosing cholangitis

Patients with primary sclerosing cholangitis(PSC) complicated by inflammatory bowel disease(IBD) represent a distinct subset of patients with unique characteristics,which have serious clinical implications.The aim of this literature review was to shed light to the obscure clinical and molecular aspects of the two diseases combined utilizing current data available and putting issues of diagnosis and treatment into perspective.The prevalence of IBD,mainly ulcerative colitis in PSC patients is estimated to be 21%-80%,dependent on screening programs and nationality.PSC-associated colitis is likely to be extensive,characterized by rectal sparing,backwash ileitis,and generally mild symptoms.It is also more likely to progress to colorectal malignancy,making it imperative for clinicians to maintain a high level of suspicion when tackling PSC patients.There is no optimal surveillance strategy but current guidelines advocate that colonoscopy is necessary at the time of PSC diagnosis with annual endoscopic follow-up.Random biopsies have been criticized and a shift towards targeted biopsies using chromoendoscopy,laser endomicroscopy and narrow-band imaging has been noted.Techniques directed towards genetic mutations instead of histological abnormalities hold promise for easier,more accurate diagnosis of dysplastic lesions.Chemopreventive measures against colorectal cancer have been sought in these patients.Ursodeoxycholic acid seemed promising at first but subsequent studies yielded conflicting results showing anticarcinogenic effects in low doses(8-15 mg/kg per day) and carcinogenic properties in high doses(15-30 mg/kg per day).     

Osteoporosis in adult Sri Lankan inflammatory bowel disease patients

AIM： To determine if inflammatory bowel disease （IBD） is a risk factor for osteoporosis in adult Sri Lankans. METHODS： We identified eligible subjects from among consecutive patients diagnosed with IBD who attended our outpatient clinic. We included only patients aged between 20 and 70 years. Patients who were pregnant, had significant comorbidity, or were on calcium supplements or treatment for osteoporosis within the past 6 mo, were excluded. Healthy, ageand sex-matched controls were also recruited, in a control to patient ratio of 3：1. Both groups were screened for osteoporosis using peripheral dual energy X-ray absorptiometry scanning. RESULTS： The study population consisted of 111 IBD patients （male：female = 43：68; mean age 42.5 years） and 333 controls （male：female = 129：204; mean age 43.8 years）. The occurrence of osteoporosis among IBD patients （13.5%） was significantly higher than among controls （4.5%） （P = 0.001）. The frequency of osteoporosis was not significantly different between ulcerative colitis （14.45%） and Crohn＇s disease （10.7%）. However, on multivariate analysis, only age （P = 0.001）, menopause （P = 0.024） and use of systemic steroids （P 〈 0.001） were found to be associated independently with the occurrence of osteoporosis, while IBD, severity of disease, number of relapses, duration of illness or treatment other than systemic steroids were not. CONCLUSION： IBD does not appear to be an independent risk factor for the occurrence of osteoporosis in this population. However, the use of systemic steroids was a risk factor.