炎症性肠病858例临床分析

目的总结分析炎症性肠病（IBD）的临床特点,探讨诊治策略。方法对1998年1月至2009年7月354例炎症性肠病住院患者和2003年1月至2009年7月504例炎症性肠病门诊患者资料进行回顾性分析。结果本组资料显示我院近12年来IBD发病呈逐年上升趋势,溃疡性结肠炎（UC）明显多于克罗恩病（CD）。本组IBD患者中男女之比为1.28∶1。IBD平均发病年龄（41.07±16.07）岁。UC发病高峰年龄为30～49岁,CD发病高峰年龄为20～39岁。本组住院患者中UC和CD两组民族构成比较无统计学差异。肠镜检查中UC以直肠和乙状结肠病变为主,CD以回盲部及回肠末端病变为主。本组患者IBD病理组织学检出率为41.5%,UC误诊率为17.0%,CD误诊率为25.0%。治疗以氨基水杨酸类及类固醇激素为主。结论炎症性肠发病数呈逐年上升趋势;IBD诊断主要依靠内镜及病理。IBD呈慢性复发性发作过程,应长期维持治疗。     

伴有肛周疾病的炎症性肠病患者肛门功能及生活质量分析

目的分析肛周疾病对炎症性肠病（IBD）患者肛门直肠功能和生活质量的影响。 方法回顾性分析2018年6月至2020年6月淮安市第二人民医院收治的伴有肛门不适的53例IBD患者（IBD组）。其中CD43例，UC10例。包括肛瘘35例，大便失禁15例，肛门纤维化8例。选择同期来淮安市第二人民医院体检的健康人20名作为健康对照组。通过肛门直肠测压对IBD患者和健康对照组受试者肛门功能进行评估并进行比较。采用炎症性肠病患者生活质量量表（IBDQ）评分对IBD患者生活质量进行评估。 结果IBD患者与健康对照组最大肛门静息压、最大挤压压、直肠容量感觉阈值、最大耐受容量、肛管抑制反射阳性水平差异均无统计学意义（P均>0.05）。大便失禁的IBD患者最大肛门静息压、IBDQ评分均低于非大便失禁的IBD患者，且差异均有统计学意义（P<0.05）。CD与UC患者IBDQ评分差异无统计学意义（P>0.05）；大便失禁IBD患者IBDQ评分低于非大便失禁IBD患者，且差异有统计学意义（P<0.05）。 结论合并肛周疾病的IBD患者肛门直肠功能受损，大便失禁的患者生活质量差。     

乌司奴单抗治疗炎症性肠病的临床疗效和安全性分析

背景：乌司奴单抗（UST）对炎症性肠病（IBD）患者的疗效已在国外研究中得到证实,但在我国的使用时间较短,其疗效和安全性方面缺乏报道。目的：探讨UST治疗IBD患者的临床疗效和安全性。方法：纳入2020年11月—2022年6月于空军军医大学第一附属医院使用UST治疗的IBD患者,收集其临床资料并进行回顾性分析。结果：共筛选出46例使用UST治疗的IBD患者,其中克罗恩病（CD）患者41例,溃疡性结肠炎（UC）患者5例。治疗第8、16、24、56周时,CD患者的临床应答率分别为51.2%、75.6%、97.4%、100%,临床缓解率分别为2.4%、22.0%、59.0%、86.5%。治疗第24、56周时,CD患者内镜应答率分别为89.7%、97.3%,内镜缓解率分别为38.5%、70.3%。治疗第16周时,UST作为一线生物制剂治疗CD患者的临床缓解率为71.4%,明显高于UST作为非一线生物制剂治疗的临床缓解率（26.5%,P=0.035）,其余时间点UST作为一线和非一线生物制剂的临床应答率、内镜应答率、内镜缓解率均无明显差异（P>0.05）。治疗第56周时,5例UC患者均取得...     

糖皮质激素治疗炎症性肠病的随访研究

目的 回顾性分析糖皮质激素治疗炎症性肠病(IBD)1个月的疗效及1年后的转归.方法 1998年1月至2006年9年确诊为克罗恩病(CD)患者55例,溃疡性结肠炎(UC)患者154例,评估口服糖皮质激素治疗1个月和1年后的疗效.Logistic回归分析决定预后的影响因子.结果 共有21例(38.2%)CD患者和20例(13.0 %)UC患者口服糖皮质激素(2例UC患者失访).经1个月治疗后,21例CD患者中完全缓解15例(71.4%),部分缓解3例(14.3%),无效3例(14.3%);18例UC患者中,完全缓解15例(83.3%),部分缓解3例(16.7%).随访1年时,21例CD患者中,维持完全或部分缓解11例(52.4%),激素依赖6例(28.6%),被迫接受外科手术者4例(19.0%),18例UC患者中,维持完全或部分缓解11例(61.1%),激素依赖3例(16.7%),手术4例(22.2%).Logistic回归分析显示,发病时血清白蛋白水平与1年后的疗效有关(OR=1.320,95%CI:1. 032～1.690,P=0.027).结论 IBD患者对首次激素治疗有效,近期疗效良好.但无法长期维持缓解状态,亦无法降低手术风险.其预后与血清白蛋白水平相关.     

炎症性肠病的肠外表现

炎症性肠病（inflammatory bowel disease，IBD），包括溃疡性结肠炎（ulcerative colitis，UC）和克罗恩病（Crohn’s disease，CD），其肠外表现众多，可累及全身各器官。国内对IBD肠外表现的大规模统计资料较少。本研究对136例IBD患者进行回顾性分析，调查其肠外表现的发生情况。     

药物代谢遗传学检测在硫唑嘌呤治疗炎症性肠病中的应用

炎症性肠病（IBD）包括溃疡性结肠炎（UC）和克罗恩病（CD）.目前治疗该病的药物主要有氨基水杨酸、激素、免疫抑制剂及近年推出的生物制剂.其中的免疫抑制剂如硫唑嘌呤（AZA）和6-巯基嘌呤（6-MP）能够诱导和维持IBD缓解并减少激素依赖和耐药;但其疗效有明显的个体差异,约2/3患者有效,15%的患者无效,另有9%～25%的患者产生严重的骨髓抑制或肝毒性甚至危及生命.AZA治疗IBD在国外较普遍.近20年来,国人IBD患病率呈大幅增加,因此如何安全有效地用AZA治疗IBD具有重要的临床意义.     

ST2在炎症性肠病中的表达及其作用探讨

目的探讨血清中人基质裂解素（ST2）水平的变化在炎症性肠病（IBD）活动性评估中的意义。方法ELISA法（酶联免疫吸附测定）检测IBD患者45例，其中UC患者29例，CD患者16例，已排除IBD的其他胃肠疾病（包括主诉不明原因腹痛、腹泻、胃肠炎）的患者24例和15例健康人血清中ST2水平，20例IBD患者检测治疗前后ST2水平的改变。结果IBD活动期血清中ST2水平为（1884．72±338．38）pg／mL，显著高于缓解期（1292．27±347．73）pg／mL和健康对照组（1026．85±382．35）pg／mL，血清ST2水平在治疗前和治疗后（t=4．067，P〈0．01）、UC患者和CD患者（t=2．202，P=0．035）之间差异具有统计学意义。结论血清中ST2水平可作为炎症性肠病活动性评估和临床治疗效果的评价指标。     

合并肠外表现的炎症性肠病患者英夫利西单抗治疗效果分析

背景：炎症性肠病（IBD）发病率呈逐年升高的趋势,部分IBD患者合并肠外表现（EIM）,且EIM对IBD治疗产生一定的影响。目的：总结合并EIM的IBD患者临床特征,并评价英夫利西单抗（IFX）的治疗效果。方法：回顾性分析2010年1月—2020年12月于大连医科大学附属第一医院诊断为IBD且同时合并EIM患者的临床资料,探讨IFX的治疗效果。结果：811例IBD患者中,50例（6.17%）合并EIM。EIM以关节炎（78.00%）、结节性红斑（26.00%）最为常见。52.00%的IBD患者合并1种EIM。合并EIM的UC患者中病变范围累及以E3最常见（68.42%）,CD患者以L3最常见（50.00%）。共21例患者接受IFX治疗,用药后第2周HB、ALB明显上升,ESR、CRP、PLT明显下降;第22周83.33%的UC患者转为轻度,70.00%的CD患者进入缓解期。应用IFX后关节炎首次消失时间明显短于未应用IFX组（2.50 d对10.50 d,P<0.05）。CRP升高者关节炎首次消失中位时间亦明显短于CRP正常者（3.00 d对9.00 d,P<0.05）。结...     

235例炎症性肠病患者首次接受糖皮质激素治疗的临床疗效分析

目的探讨炎症性肠病(IBD)患者首次接受糖皮质激素(激素)治疗的疗效及疾病转归。方法收集2002年1月-2010年12月我院收治的首次使用激素治疗的IBD患者890例,对激素治疗30 d及随访1年的临床疗效进行回顾性分析。结果 890例IBD患者中,溃疡性结肠炎(UC)患者401例,克罗恩病(CD)患者489例,其中共有81例(81/401,20.2%)UC及154例(154/489,31.5%)CD患者使用口服或静脉滴注激素,激素治疗30 d时,UC患者完全缓解57例(57/81,70.4%),部分缓解22例(22/81,27.2%),无效2例(2/81,2.5%);CD患者完全缓解94例(94/154,61.0%),部分缓解45例(45/154,29.2%),无效15例(15/154,9.7%)。随访1年末,UC患者持续应答53例(53/79,67.1%),激素依赖26例(26/79,32.9%);CD患者持续应答102例(102/151,67.5%),激素依赖26例(26/15,17.2%),手术23例(23/15,15.2%)。激素短期及远期疗效的风险因素回归分析显示合用硫唑嘌呤/6-巯基嘌呤(AZA/6-MP)与CD患者激素治疗的远期疗效相关(P=0.03)。结论大部分IBD患者对激素治疗有效,UC患者激素治疗总有效率优于CD,随访1年32.9%UC及17.2%CD患者呈激素依赖,15.2%CD患者需手术切除病变肠段。     

炎症性肠病患者血清和肠黏膜组织中miR-31-3p的表达水平及临床意义

目的 观察炎症性肠病（IBD）患者血清和肠黏膜组织中miR-31-3p的表达情况,并分析其在疾病诊断和病情评估中的应用价值。方法 随机选取2019年6月至2021年6月成都大学附属医院消化内科收治住院的符合纳入及排除标准的95例IBD患者（设为IBD组）,其中克罗恩病（CD）有33例（设为CD组）,溃疡性结肠炎（UC）有62例（设为UC组）;同期招募67名健康志愿者作为对照组。收集受试对象的肠黏膜组织及血清样本,采用实时荧光定量PCR技术检测血清和肠黏膜组织中miR-31-3p的表达水平,并分析其在IBD组与对照组,以及不同活动度IBD患者间的差异。采用Pearson相关系数法分析血清和肠黏膜组织中miR-31-3p的表达水平与IBD患者疾病活动度的相关性;采用ROC曲线分析血清和肠黏膜组织中miR-31-3p对IBD的诊断及病情评估的价值。结果 CD组和UC组患者血清和肠黏膜组织中miR-31-3p的表达水平均显著高于对照组（P<0.05）。轻度活动期、中度活动期、重度活动期的CD和UC患者血清和肠黏膜组织中miR-31-3p的表达水平均依次升高,组间比较差异均有统计学意义（P...     

Oral iron therapy in inflammatory bowel disease: usage, tolerance, and efficacy

BACKGROUND: Iron deficiency is common in inflammatory bowel disease (IBD). Anecdotal evidence suggests that oral iron is poorly tolerated and may exacerbate disease activity in patients with IBD.AIM The aim of this study was to retrospectively compare usage, tolerance, and efficacy of oral iron therapy in patients with IBD and noninflammatory causes of iron deficiency. METHODS: Case records of 277 patients with IBD and 24 non-IBD iron-deficient control patients covering a 4-year period were retrospectively analyzed. RESULTS: Fifty-three of 277 (19%) of the patients with IBD studied had received oral iron. In only 40% of the patients who had IBD and 63% of the patients who did not (p = not significant) was iron deficiency formally confirmed before treatment. Intolerance to iron was reported in only 25% of the patients who had IBD and 17% of the patients who did not (p = not significant). In only two of eight adequately monitored iron-intolerant patients with IBD was iron therapy associated with an increase in inflammatory markers. When formally checked, iron repletion was successfully achieved as frequently in patients who had IBD (59%) as in patients who did not (45%). CONCLUSION: Iron therapy is often used without a formal diagnosis of iron deficiency having been made, at least in part because of the difficulty in making this diagnosis using ferritin, an acute-phase protein. Patients with IBD are no more intolerant of oral iron than other patients and have similar rates of repletion.     

Detection of Listeria monocytogenes by polymerase chain reaction in intestinal mucosal biopsies from patients with inflammatory bowel disease and controls

BACKGROUND AND AIMS: Components of the intestinal microflora are believed to play an important role in the pathogenesis of inflammatory bowel disease (IBD) in genetically susceptible hosts acting either as a non-specific antigenic stimulus or as a specific pathogen. Listeria monocytogenes has been suggested as an organism with the potential to cause IBD. The objective of the present study was to investigate the prevalence of L. monocytogenes DNA in intestinal biopsies from patients with IBD and from non-IBD controls by using nested polymerase chain reaction (PCR). METHODS: The DNA was extracted from 274 colonoscopic biopsies, which were obtained from 23 patients with Crohn's disease (CD), 28 with ulcerative colitis (UC) and 39 non-IBD control patients. Nested PCR amplification was used to detect the presence of the L. monocytogenes listeriolysin O (hly) gene. The sequences of positive PCR products were determined and compared with databases. RESULTS: The sensitivity of our nested PCR was 10 fg L. monocytogenes DNA. Overall, L. monocytogenes DNA was detected in 13.0% patients with CD, 17.9% patients with UC and 25.6% non-IBD control patients or in 29 of 274 (10.6%) endoscopic biopsies. Among them, L. monocytogenes DNA was detected in four of 67 (6%) biopsies from patients with CD, five of 94 (5.3%) biopsies from patients with UC and 20 of 113 biopsies (17.7%) from non-IBD control patients. Sequence analysis of positive PCR products demonstrated more than 95% similarity to the hly gene sequence of L. monocytogenes, confirming the authenticity of our PCR products. CONCLUSION: Listeria monocytogenes DNA was detected in the intestine of both patients with IBD and in non-IBD control patients, probably reflecting the widespread presence of this organism in the environment. The low yield of positive biopsies in our IBD patients (5-6%) and the fact that the detection rate of L. monocytogenes DNA was similar in endoscopic biopsies from IBD patients and non-IBD controls does not support a direct role for L. monocytogenes in the pathogenesis of IBD, at least in New Zealand patients.     

Detection of Chlamydia pneumoniae by polymerase chain reaction-enzyme immunoassay in intestinal mucosal biopsies from patients with inflammatory bowel disease and controls

BACKGROUND AND AIM: It has been suggested that Chlamydia is an organism that may have the potential to cause inflammatory bowel disease (IBD) in susceptible individuals. Chlamydia pneumoniae has emerged as an important human pathogen in the last decade. The objective of the present study was to investigate the frequency of the presence of C. pneumoniae DNA in intestinal biopsies from patients with IBD and from non-IBD controls. METHODS: The DNA was extracted from 222 colonoscopic biopsies, which were obtained from 11 patients with Crohn's disease (CD), 18 patients with ulcerative colitis (UC) and from 37 non-IBD control patients. The presence of the C. pneumoniae omp1 gene and C. trachomatis 16S rRNA gene was determined using a rapid and sensitive polymerase chain reaction-enzyme immunoassay (PCR-EIA). RESULTS: The C. pneumoniae-specific DNA was detected in 32 (14.4%) of 222 endoscopic biopsies. Among them, C. pneumoniae DNA were found in nine of 42 (21.4%) biopsies from patients with CD, nine of 59 (15.3%) biopsies from patients with UC, and 14 out of 122 (11.4%) biopsies from non-IBD control patients, respectively. Moreover, the percentage of patients with at least one biopsy positive for C. pneumoniae was higher, although not statistically significant, in CD (36.4%) and UC patients (38.9%) compared to non-IBD controls (16.2%). In contrast, C. trachomatis DNA was detected in only two of 222 (0.9%) biopsy samples. CONCLUSION: The C. pneumoniae DNA was detected in the intestine of both patients with IBD and in non-IBD control patients, probably reflecting the high prevalence of this organism in the environment. The moderate yield of positive biopsies in our IBD patients and the fact that the detection rate of C. pneumoniae DNA was similar in endoscopic biopsies from IBD patients and non-IBD controls does not support a direct role for this organism in the pathogenesis of IBD.     

Change of diagnosis during the first five years after onset of inflammatory bowel disease: Results of a prospective follow-up study (the IBSEN Study)

Objective. An exact diagnosis of inflammatory bowel disease (IBD) and further subclassification may be difficult even after clinical, radiological and histological examinations. A correct subclassification is important for the success of both medical and surgical therapeutic strategies, but there is a dearth of information available on the frequency of changes in diagnosis in population-based studies. The objective of this work was prospectively to re-evaluate the diagnosis in an unselected cohort of IBD patients during the first five years after the initial diagnosis. Material and methods. Patients classified as IBD or possible IBD in the period 1990–94 (the IBSEN cohort) had their diagnosis re-evaluated after 1 and 5 years. Initially, the patients were classified as ulcerative colitis (UC), Crohn's disease (CD), indeterminate colitis (IC) or possible IBD. At the 5-year visit, patients were classified as UC, CD or non-IBD. Results. A total of 843 patients (518 UC, 221 CD, 40 IC and 64 possible IBD) were identified. Clinical information was available for 94% of the patients who survived after 5 years. A change in diagnosis was found in 9% of the patients initially classified as UC or CD. A change to non-IBD was more frequent than a change between UC and CD. A large proportion of patients initially classified as IC or possible IBD were diagnosed as non-IBD after 5 years (22.5% versus 50%). When IBD was confirmed in these groups, UC was more frequent than CD. Two changes in diagnosis during follow-up were observed in 2.8% of the patients; this was more frequent in patients initially classified as IC or possible IBD. Conclusions. There are obvious diagnostic problems in a minority of patients with IBD; a systematic follow-up is therefore important in these patients.     

Current practice in the diagnosis and management of IBD-associated anaemia and iron deficiency in Germany: The German AnaemIBD Study

Background/aimAnaemia is a common complication in inflammatory bowel disease (IBD), frequently resulting from iron deficiency. IBD guidelines advocate intravenous iron administration although some patients respond to oral supplementation. This non-interventional study investigates the current status of anaemia management in German IBD patients.MethodsBaseline data on pre-study treatment for anaemia were retrospectively analysed in IBD patients with anaemia participating in a prospective trial of the efficacy and safety of ferric carboxymaltose. Data were collected from 55 German gastroenterological centres up to August 2010. Subjects had received care at their centre for at least 12 months prior to baseline.Results193 cases of IBD-associated anaemia (115 Crohn's disease, 77 ulcerative colitis) were analysed (mean age: 39 years (18–83), 79 (41%) males). Anaemia and iron status were usually assessed by haemoglobin (100%), serum ferritin (97%), and transferrin saturation (82%). In the previous 6 months, only 84 patients (43.5%) had been treated for anaemia: 47 (56%) with oral iron, 13 (15%) parenteral iron, 16 (19%) oral plus parenteral iron and 8 (10%) transfusions. No patients received erythropoietin stimulating agents.ConclusionAlthough intravenous iron supplementation is recommended in IBD patients, current German practice still relies on oral therapy, even in severe anaemia. The high incidence of severe anaemia in this cohort reflects inadequate iron replacement and status monitoring. While the proportion of IBD patients with inadequately treated anaemia/iron deficiency is unknown, greater awareness of existing guidelines for iron deficiency management in IBD patients appears necessary.     

Pancreatic Autoantibodies in Greek Patients with Inflammatory Bowel Disease

Pancreatic autoantibodies (PAbs) have been suggested as a specific but not sensitive marker for Crohn's disease (CD). The aim of this study was to assess the value of detecting PAbs in Greek patients with ulcerative colitis (UC) and CD. Sera were collected from 150 patients with IBD (73 with UC and 77 with CD), 31 cases with non-IBD intestinal inflammation, 16 cases with other autoimmune diseases, and 104 healthy controls. Determination of PAbs was performed by a standard indirect immunofluorescence technique. PAbs were detected in 18 of 73 (24.7%) samples from UC patients and in 32 of 77 (41.6%) samples from CD patients. The prevalence of positive PAbs was significantly higher in CD than in UC (P= 0.04). None of the 104 samples from healthy controls and the 31 cases with non-IBD intestinal inflammation had detectable PAbs. One patient with Sjogren's syndrome was PAbs positive. No association of PAbs with IBD activity, IBD localization, or medical treatment was found. Patients with stenotic CD had a significantly higher prevalence of PAbs positivity (60%) compared with patients with inflammatory (28.6%) and fistulizing (41.2%) disease (P= 0.02). The prevalence of PAbs in Greek CD patients was found to be similar to that in previous reports. In contrast to these studies we found also increased prevalence of PAbs in UC patients. These findings suggest that PAbs should be considered as a specific marker for IBD rather than for CD.     

High Prevalence of Mycoplasma pneumoniae in Intestinal Mucosal Biopsies from Patients with Inflammatory Bowel Disease and Controls

Intestinal microflora are believed to play an important role in the pathogenesis of inflammatory bowel disease (IBD). Mycoplasma have been suggested previously as organisms of ubiquitous distribution with the potential to cause inflammatory diseases, including IBD in susceptible individuals. The aim of this study was to determine the frequency of the presence of M. pneumoniae DNA in intestinal biopsies from patients with IBD and non-IBD controls using a microplate polymerase chain reaction–hybridization assay (PCR-ELISA). A total of 260 endoscopic biopsies (49 from 19 patients with Crohn's disease, 76 from 27 patients with ulcerative colitis, and 135 from 43 non-IBD controls) were used in this study. Overall, M. pneumoniae-specific DNA was detected in 100 endoscopic biopsy samples (38.5%). Among them, the detection rate of M. pneumoniae DNA was significantly higher in biopsies from patients with CD (59.2%) than in those from patients with UC (26.3%) or non-IBD controls (37.7%) (² = 13.65, P 0.001). The high prevalence of M. pneumoniae in both IBD patients and controls suggest this organism is ubiquitous and may persist in the intestinal mucosa. Epidemiological studies in IBD suggest acquisition of some agents early in life probably during epidemics in temperate latitudes. M. pneumoniae could be one of the ubiquitous agents implicated in the pathogenesis of IBD.     

Spatial distribution and histogenesis of colorectal Paneth cell metaplasia in idiopathic inflammatory bowel disease

BACKGROUND AND AIM: Colorectal Paneth cell metaplasia (PCM) is known to be a sign of idiopathic inflammatory bowel disease (IBD), although its distribution and histogenesis are not fully understood. Objectives of this research were to investigate the spatial distribution of PCM in IBD and other forms of colitis (non-IBD), and to find stimuli causing PCM. METHODS: We studied multiple biopsy specimens from 181 patients with ulcerative colitis (UC), 159 with Crohn's disease (CD), 448 with non-IBD, and 78 normal controls. Paneth cell metaplasia frequency, at each colorectal site, was evaluated to find possible differences among diseases, phases of activity, and extents of disease. RESULTS: In non-IBD and controls, PCM was rarely (0-1.9%) seen at distal sites, but frequently (up to 48.7%) found at the ascending colon and cecum (P < 0.001). Paneth cell metaplasia frequency was significantly higher in IBD than in non-IBD patients and controls at distal sites (P < 0.001), but did not differ significantly between UC and CD, or among active, resolving, and quiescent phases. In UC, proctitis and left-sided colitis rarely displayed PCM at unaffected sites. Multiple logistic regression analysis revealed that PCM was positively associated with crypt distortion and mononuclear cell infiltration (P < 0.005), but negatively or not significantly associated with crypt atrophy, mucin depletion, acute inflammation, or phase of activity. CONCLUSIONS: Paneth cell metaplasia is a non-specific phenomenon in the proximal colon, but distal PCM, which occurs exclusively in affected mucosa, is a useful marker indicating IBD, even in the inactive phase. Regression analysis suggests that repair and regeneration may be the most potent stimuli causing PCM.     

Inflammatory Bowel Disease Promotes Venous Thrombosis Earlier in Life

Background: Patients with inflammatory bowel disease (IBD) may be at increased risk of having venous thromboembolism. Methods: Medical records from 1253 IBD patients attending hospital care during the years 1987-97 were studied. These patients were recruited from a population of 340,000 inhabitants. Patients with verified venous thrombosis were characterized clinically, and blood samples were examined for coagulopathy including analyses of antithrombin, plasminogen, protein C, protein S, factor V, and prothrombin mutations. As control groups we used 99 patients with verified venous thrombosis and no history of IBD and 288 volunteers with no history of thrombosis. Results: The incidence of venous thrombosis was 1.5/1000 IBD patients per year, which is comparable to the background population. The mean age was significantly lower in IBD patients than in non-IBD patients (53 versus 64 years, P = 0.0225). We found one patient with antithrombin deficiency but none with protein C, protein S, or plasminogen deficiency. Factor V mutation was as prevalent in IBD patients with thrombosis as in thrombotic non-IBD patients (27% versus 28%) and 3.0 times (95% confidence interval, 0.8-11.9) more frequent in IBD patients with thrombosis than in healthy controls. Prothrombin mutation was not detected in IBD patients with venous thrombosis. Conclusion: We found no increased incidence of venous thrombosis in IBD patients compared with a background population. However, IBD patients had venous thrombosis earlier in life than non-IBD patients. Although factor V mutation may contribute to thrombosis, IBD acts as a trigger through mechanisms that still remain unexplained.