强直性脊柱炎患者外周血CD4^＋CD25^＋CD127^low/-T细胞检测及其意义△

目的检测CD4^＋CD25^＋CD127^low/-T细胞在强直性脊柱炎（ankylosing spondylitis，AS）患者外周血的表达，并分析其与CD4^＋CD25^＋FOXP3^＋T细胞的相关性。方法 以21例AS患者外周血为研究组，20例类风湿关节炎（rheumatoid arthritis，RA）患者和24名正常人外周血作为对照组，采用三色直接荧光素标记法和多参数流式细胞仪检测外周血CD4^＋CD25^＋CD127^low/-T细胞、CD4^＋CD25^high细胞及CD4^＋CD25^＋FOXP3^＋T细胞的比例，同时检测外周血C反应蛋白（C-reactive protein，CRP）、血沉（ESR）、免疫球蛋白、补体等水平以及HLA—B27并进行相关性分析。结果与正常对照组相比，AS患者外周血CD4^＋CD25^＋CD127^low/-T及CD4^＋CD25^＋FOXP3＋T细胞百分率降低（均P〈0．05）。CD4^＋CD25^＋细胞百分率升高（P〈0．05）；CD4^＋CD25^＋CD127^low/-T细胞与CD4^＋CD25^＋FOXP3^＋T细胞呈正相关（r=0．589，P=0．021），与CRP、ESR、血小板及免疫球蛋白（IgG、IgA、IgM）和补体（C3、C4）、BASDAI、HLA-B27等均无明显相关性（均P〉0．05）。AS患者外周血CD4^＋CD25^＋CD127^low/-T细胞、CD4^＋CD25^＋FOXP3^＋T细胞和CD4＋CD25^highT细胞的百分率与RA患者外周血比较差异均无统计学意义（P〉0．05）。结论AS患者外周血CD4^＋CD25^＋CD127^low/-T细胞降低，且与CD4^＋CD25^＋FOXP3^＋T细胞呈正相关，提示在调节性T细胞研究中CD127具有替代FOXP3的可能性。     

间日疟患者外周血NK γδ T Treg细胞含量的变化

目的 分析间日疟原虫现症感染者外周血中NK、γδ T细胞、CD4^＋CD25^＋T淋巴细胞及其FOXP3的表达情况，以初步了解患者的一些细胞免疫特性。方法用流式细胞仪检测25例间日疟原虫现症感染者（AC）、13例免疫对照者（IC）及14例正常对照者（NC）外周血中NK、γδT细胞和CD4^＋CD25^＋T淋巴细胞的百分含量，同时观察CD4^＋CD25^＋T细胞中表达FOXP3群体的百分含量。结果AC组外周血NK细胞百分含量为8．48％，与NC组（15．53％）及IC组（17．69％）比较，明显降低（P均〈0．05）,AC组外周血γδT细胞、CD4^＋CD25^＋T细胞百分含量分别为4．32％和5．42％，较NC组（2．55％和3．94％）及IC组（2．70％和3．44％）明显升高（P均〈0．05）；AC组外周血CD4^＋CD25^＋T淋巴细胞中表达FOXP3的细胞数量为8．14％，低于NC组的11．09％及IC组的11．32％，但差异无统计学意义（P〉0．05）。结论间日疟原虫急性感染期患者外周血NK细胞数量减少，但γδT淋巴细胞增加；CD4^＋CD25^＋T淋巴细胞中表达FOXP3群体的细胞稍有降低。     

肺结核病患者外周血淋巴细胞亚群的绝对数分析及临床意义

目的检测分析肺结核病患者外周血CD3^＋细胞,CD3^＋CD4^＋细胞,CD3^＋CD8^＋细胞,NK细胞（CD3^-/（CDr（16＋56^＋）,B细胞（CD19）数量及CD_3^＋CD_4^＋／CD3^_CD_8^＋比值的变化,并探讨其临床意义。方法采用多参数流式细胞术（FCM）检测21例肺结核患者外周血淋巴细胞亚群水平与15例健康者比较研究。结果肺结核病患者外周血CD3^＋细胞,CD3^＋CD4^＋细胞,CD3^＋CDR^＋细胞,NK细胞数量均比正常人明显减少（P〈0．01）,而B细胞数量没明显改变,CD3^＋CD4^＋／CD_3^＋CD_8^＋比值明显下降（P〈0．01）。结论肺结核病患者细胞免疫功能紊乱,监测结核病患者淋巴细胞亚群水平,对评价患者的细胞免疫功能及对疾病的免疫治疗均有重要的指导意义。     

抗病毒治疗对慢性丙型肝炎CD4^＋CD25^＋调节性T细胞频率和功能的影响

目的研究抗病毒治疗前后慢性丙型肝炎患者CD4^＋CD25^＋调节性T细胞（Treg）频率和功能的变化。方法筛选HLA—A2阳性慢性丙型肝炎患者31例，给予聚乙二醇化干扰素α-2a（相对分子质量为40000）180μg每周1次皮下注射，联合口服利巴韦林。分别在治疗前和治疗结束随访24周时应用流式细胞仪检测患者CD4^＋CD25^＋ Treg细胞占外周血CD4^＋T细胞的频率，应用液闪计数仪检测其对HCV特异性CD8^＋T细胞增殖的抑制作用，ELISA法检测细胞培养上清γ干扰素（IFN-γ）水平的变化情况。结果治疗结束随访24周，患者外周血CD4^＋CD25^＋ Treg细胞频率为（9．6±3．0）％，明显低于治疗前的（11．0±2．3）％（t=2．028，P〈0．05）；持续病毒学应答（SVR）组CD4^＋CD25^＋ Treg细胞频率为（8．9±2．7）％，明显低于未获得SVR患者组的（10．4±2．3）％（t=3．324，P〈0．01）。抗病毒治疗后CD4^＋CD25^＋ Treg细胞抑制HCV特异性CD8^＋T细胞增殖的作用减弱。治疗后患者IFN-γ水平为（3959±577）pg／ml，明显高于治疗前的（1965±326）pg／ml（t=16．1，P〈0．01）；获得SVR患者组IFN-γ（6824±568）pg／ml，明显高于未获得SVR患者组的（2219±286）pg／ml（t=29．853，P〈0．001）。结论慢性丙型肝炎患者随着HCV RNA水平的下降，CD4^＋CD25^＋Treg细胞频率降低，抑制HCV特异性CD8^＋T细胞增殖的作用减弱。     

重型再生障碍性贫血CD4+ CD25+调节性T细胞的变化

应用流式细胞术检测重型再生障碍性贫血（SAA）患者外周血CD4^＋CD25^＋T细胞、CD4^＋CD25kighT细胞的数量。结果10例初治SAA患者外周血CD4^＋CD25^＋T细胞占CD4＋T细胞的（6．23±1．82）％,明显低于正常对照组（9.20＋2．95）％（P〈0．01）,CD4^＋CD25^highT细胞比例为（1．02±0．11）％,亦明显低于正常对照组（1．43±0．41）％;10例造血恢复SAA患者CD4^＋CD25^＋T细胞和CD4^＋CD25^hishT细胞比例分别为（8．92±1．22）％和（1．41±0．64）％,与正常对照组无明显差异（P〉0．01）。认为CD4^＋CD25^＋、CD4^＋CD25^highT细胞水平与SAA密切相关。     

131I治疗后分化型甲状腺癌患者外周血淋巴细胞亚群的变化

目的 评价分化型甲状腺癌^131I治疗后外周血B细胞（CD19）、T细胞（CD3）、NK细胞和CD4^＋、CD8^＋亚群的变化。方法 分化型甲状腺癌患者102例，分为A（8例）、B（43例）、C（51例）3组。A组为甲状腺癌术后首次用^131I清除残余甲状腺者，用50mCi^131I治疗。B组为颈部淋巴结转移者，用100mCi^131I治疗。C组为远端转移者，用200mCi^131治疗。分别于患者口服^131I治疗前1天和治疗后第7天、1个月、3个月取外周血，用流式细胞仪检测外周血B细胞、T细胞、NK细胞，CD4^＋、CD8^＋亚群的百分比。同时检测10名正常人的外周血淋巴细胞亚群水平，作为正常对照组。结果 A组中，仅治疗后7dNK细胞（P〈0．05）和B细胞（P〈0．05）百分比显著降低。B组中，治疗后7d（P〈0．01）和1个月（P〈0．05）NK细胞百分比显著下降，而B细胞百分比仅在治疗后7d显著下降（P〈0．05）；对于T细胞，仅治疗后1个月CD4^＋／CD8^＋的比值下降（P〈0．05）。C组中，NK细胞和B细胞百分比在治疗后7d（P〈0．05）和1个月（P〈0．05）均显著下降；治疗后1个月，CD4^＋／CD8^＋的比值显著下降（P〈0．05）。^131I治疗后3个月，3组中所有患者外周血淋巴细胞亚群百分比与治疗前相比，均无显著变化。结论 分化型甲状腺癌^131I治疗时，外周血淋巴细胞对^131I内照射的辐射敏感性主要取决于淋巴细胞的类型和^131I的剂量。NK细胞和B细胞对^131I的辐射可能最为敏感。大剂量^131治疗时，B细胞、T细胞、NK细胞，CD4、CD8亚群都将受到不同程度的影响，但这种影响是可恢复的。因此，^131I内照射治疗的免疫抑制作用是暂时的和可逆的。     

温下法与温涩法对溃疡性结肠炎外周血T淋巴细胞亚群的影响

[目的]探讨温下法与温涩法在溃疡性结肠炎（UC）细胞免疫调节方面的不同作用机制。[方法]采用流式细胞仪三色标记法检测治疗前后温下组、温涩组和对照组的外周血T淋巴细胞亚群的水平，比较3组治疗前后的变化。[结果]治疗前，温下组、温涩组和对照组外周血CD8^＋细胞绝对计数均显著高于正常参考值（P〈0．05），CD4^＋／CD8^＋比值均显著低于正常参考值（P〈0．05）；温下组与对照组外周血CD3^＋、CD4^＋细胞绝对计数亦显著高于正常参考值（P〈0．05）。治疗后，温下组外周血CD3^＋、CD4^＋与CD8^＋细胞绝对计数变化差值均显著高于温涩组与对照组（P〈0．01）；温涩组外周血CD3^＋与CD8^＋细胞绝对计数变化差值均显著高于对照组（P〈0．01），CD4^＋／CD8^＋比值变化差值高于温下组与对照组（P〈0．05）。[结论]①UC患者外周血T淋巴细胞亚群的变化总体以CD8^＋细胞水平升高及CD4^＋／CD8^＋比值下降为主，而CD4^＋细胞绝对数增多与其活动性有关。②温涩法不但能显著降低CD3^＋细胞计数和CD8^＋细胞计数，还能提高CD4^＋／CD8^＋比值；温下法能显著降低CD3^＋、CD4^＋与CD8^＋细胞计数，但不能提高CD4^＋／CD8^＋比值。     

支气管哮喘大鼠CD4^＋CD25^＋T细胞的变化及地塞米松干预作用的研究

目的研究支气管哮喘（简称哮喘）大鼠模型支气管肺泡灌洗液（BALF）、血液、脾脏CD4^＋CD25^＋T细胞的变化,及地塞米松对CD4^＋CD25^＋T细胞的影响。方法50只SD大鼠随机分为5组,空白对照（A）组,哮喘（B）组,地塞米松1（C）组、地塞米松2（D）组,地塞米松3（E）组。A组第1天给予腹腔注射生理盐水1ml,第15～21天每天给予生理盐水雾化。B、C、D、E组用卵蛋白建立哮喘大鼠模型,第1天,每只大鼠腹腔注射抗原1ml（卵蛋白1mg＋灭活百日咳杆菌9×10。个＋氢氧化铝干粉100mg）混悬液,第15～21天给予1％的卵蛋白雾化30min,C、D、E组于雾化后分别给予腹腔注射地塞米松0．2mg／kg、1mg／kg、2mg／kg。采用流式细胞仪检测的方法,观察大鼠体内BALF、外周血、脾脏CD4^＋CD25^＋T细胞的变化及使用不同剂量地塞米松后对其的影响。结果B组BALF、外周血、脾脏CD4^＋CD25^＋T细胞表达占CD4^＋T细胞的百分比分别是（42．21±5．62）％、（12．69±2．70）％、（11．15±1．05）％,A组结果分别是（18．76±5．85）％、（6．21±1．73）％、（7．85±2．13）％。B组与A组比较,差异均具有统计学意义（P〈0．01,P〈0．01,P〈0．05）;C组、D组、E组BALF中CD4^＋CD25^＋T细胞占CD4^＋T细胞的百分比表达分别是（10．49±4．03）oA、（13．28±5．12）％、（7．51±5．39）％,显著低于A组和B组,（P〈0．05,P〈0．01）;外周血中,C组（6．03±1．43）％、D组（4．88±0．95）％与A组（6．21±1．73）％比较,差异无统计学意义,E组（3．49士0．62）％与C组、A组比较,差异有统计学意义（P〈0．05）。脾脏中,c组（7．25±1．82）%、D组（8．63±3．18）％与A组（7．85±2．13）％比较,差异无统计学意义,E组（3．38±1．37）％与C组、D组、A组比较,差异有统计学意义（P〈0．05）。结论CD4^＋CD25^＋T细胞在哮喘大鼠体内有明显的优势表达,可能是哮喘发病的机制之一。地塞米松可以抑制CD4^＋CD25^＋T细胞的表达。BALF内CD4^＋CD25^＋T细胞的变化与外周血和脾脏的变化具有一致性,监测外周血或脾脏CD4^＋CD25^＋T细胞变化可了解肺部情况。     

白细胞介素-2穴位注射对晚期恶性肿瘤患者免疫功能的影响

目的探讨提高晚期恶性肿瘤患者免疫功能的有效方法。方法将30例晚期恶性肿瘤患者随机分为A、B、C组各10例，A组予0．9％氯化钠注射液2ml足三里穴位注射，B组和C组分别予白细胞介素-2（IL-2）100万U＋0．9％氯化钠注射液稀释至2ml肌注、足三里穴位注射，1次／d，10d为一疗程。治疗前、后检测外周静脉血CD3^＋、CD4^＋、CD2^＋、CD4／CD8^＋。结果与治疗前比较，治疗后B组和C组外周血CD4^＋、CO4^＋/CD8^＋均明显升高（P〈0．05、0．01），C组显著高于B组（P〈0．05）；C组不良反应发生率显著低于B组（P〈0．05）。结论足三里穴位注射IL-2能明显增强晚期恶性肿瘤患者的细胞免疫功能。     

系统性红斑狼疮患者外周血CD4+CD25+FOXP3+调节性T细胞的检测和意义

目的检测系统性红斑狼疮（SEE）患者外周血CD4^＋CD25^＋FOXP3^＋调节性T细胞（Treg）的百分比，并分析其与疾病活动的相关性。方法采用流式细胞仪检测28例SLE患者（其中活动组18例）及22名正常对照组的外周血CD4^＋CD25^＋FOXP3^＋Treg的百分比，同时评估SLE疾病活动指数（SLEDAI）及检测血抗dsDNA水平，分析相关性。结果SLE患者外周血CD4^＋CD25^＋FOXP3^＋Treg占CD4^＋T细胞的百分比较对照组降低（P〈0．05），以活动组尤为明显，CD4^＋CD25^＋FOXP3^＋Treg的百分比与SLEDAI呈明显的负相关（P〈0．01），同时显示血抗dsDNA阳性组较阴性组患者外周血CD4^＋CD25^＋FOXP3^＋Treg的百分比显著下降（P〈0．01）。结论SLE患者外周血CD4^＋CD25^＋FOXP3^＋Treg的百分比在活动期下降为明显，其在SLE的发病机制中可能起到重要的作用。     

Lung disease in Niemann-Pick disease

BACKGROUND: Lung involvement in children with Niemann-Pick disease has rarely been studied systematically. OBJECTIVE: To assess the involvement of the lung and the value of bronchoalveolar lavage in children with Niemann-Pick diseases. DESIGN: Retrospective analysis of patient records. PATIENTS: Thirteen patients, with type A (n = 1), type B (n = 10), and type C (n = 2) Niemann-Pick disease, aged 2 months to 9 years at diagnosis, were included in the study. INTERVENTIONS: Lung involvement was assessed by clinical evaluation, chest radiograph, lung computed tomography (CT) scan, pulmonary function tests, and bronchoalveolar lavage fluid analysis. RESULTS: Respiratory symptoms were present at diagnosis in 10 patients and developed during follow up in the three other patients. All patients showed signs of interstitial lung disease on chest X-ray and lung CT scan. Bronchoalveolar lavage fluid analysis (n = 7) revealed a marked accumulation of foamy macrophages (Niemann-Pick cells) in all patients. At follow up, one patient died of respiratory failure, five patients required long term oxygen therapy and seven other patients presented a chronic obstructive pulmonary disease (n = 6) or chronic cough (n = 1). CONCLUSION: Lung disease was observed in all the patients included in the present study. Bronchoalveolar lavage may be useful in Niemann-Pick diseases by showing the presence of characteristic Niemann-Pick cells.     

Hepatobiliary disease in inflammatory bowel disease

Many hepatobiliary diseases are seen in IBD. PSC is the most common, occurring in 7.5% of patients with UC. The cause of PSC is not well understood, but PSC seems to be associated with genetic susceptibility, sharing some immunologic abnormalities with UC. A characteristic cholangiogram in a patient with abnormal liver function tests usually establishes the diagnosis. Liver biopsy is not essential but can help make the diagnosis of small duct PSC in patients with a normal cholangiogram. There are no medications that treat PSC effectively. Endoscopic dilation of dominant strictures reduces the frequency of cholangitis and may improve survival. OLT remains the only proven treatment of advanced PSC. Cholangiocarcinoma is a feared complication of PSC that is difficult to diagnose. Cholelithiasis, PBC, portal vein thrombosis, and hepatic abscess are hepatobiliary disorders that occur less frequently in IBD patients.     

Joint disease in inflammatory bowel disease

The joint disorders taxonomically included in the group of seronegative spondyloarthropathies under the generic name of enteropathic arthropathy represent the most frequent extra-intestinal manifestation of inflammatory bowel disease (IBD), affecting 33% of patients. Their frequency is similar to that of ulcerative colitis and Crohn's disease. Enteropathic arthropathy consists of two main joint alterations, peripheral and axial arthritis, as well as a variable group of other peri-articular disorders. Type 1, or pauciarticular, peripheral arthritis generally coincides with IBD exacerbations, while type 2, or polyarticular, peripheral arthritis follows an independent course from IBD. Axial involvement precedes and follows an independent course from IBD and can behave as ankylosing spondylitis or asymptomatic sacroiliitis. The treatment of these rheumatologic disorders is based on the application of general measures and the use of nonsteroidal anti-inflammatory agents; intraarticular corticosteroid administration may eventually become necessary. Sulphasalazine and/or infliximab, which are indicated when the previously mentioned measures fail, can be used to treat both the articular and intestinal diseases simultaneously.     

Metabolic bone disease in inflammatory bowel disease

Osteoporosis is associated with a high morbidity rate and is a risk factor for fractures. Patients with inflammatory bowel disease are at increased risk of developing osteopenia and osteoporosis. Corticosteroid use, malnutrition, and proinflammatory cytokines are unique risk factors for bone loss in ulcerative colitis and Crohn disease. Bone mineral density is assessed by dual-energy X-ray absorptiometry and reported as a T score or number of standard deviations away from the mean. A T score < 1 SD below the mean is normal, 1 to 2.5 SD below the mean is consistent with osteopenia, and greater than 2.5 SD below the mean is defined as osteoporosis. Treatment includes a combination of basic preventative measures, for example, weight-bearing exercise, calcium, vitamin D, and pharmacologic agents, (e.g., bisphosphonates).     

Cardiac disease in diabetic end-stage renal disease

Summary Little is known about the epidemiology of cardiac disease in diabetic end-stage renal disease. We therefore prospectively followed a cohort of 433 patients who survived 6 months after the inception of dialysis therapy for an average of 41 months. Clinical and echocardiographic data were collected yearly. At baseline, diabetic patients (n = 116) had more echocardiographic concentric left ventricular hypertrophy (50 vs 38 %, p = 0.04), clinically diagnosed ischaemic heart disease (32 vs 18 %, p = 0.003) and cardiac failure (48 vs 24 %, p < 0.00 001) than non-diabetic patients (n = 317). After adjusting for age and sex, diabetic patients had similar rates of progression of echocardiographic disorders, and de novo cardiac failure, but higher rates of de novo clinically diagnosed ischaemic heart disease (RR 3.2, p = 0.0002), overall mortality (RR 2.3, p < 0.0001) and cardiovascular mortality (RR 2.6, p < 0.0001) than non-diabetic patients. Mortality was higher in diabetic patients following admission for clinically diagnosed ischaemic heart disease (RR 1.7, p = 0.05) and cardiac failure (RR 2.2, p = 0.0003). Among diabetic patients older age, left ventricular hypertrophy, smoking, clinically diagnosed ischaemic heart disease, cardiac failure and hypoalbuminaemia were independently associated with mortality. The excessive cardiac morbidity and mortality of diabetic patients seem to be mediated via ischaemic disease, rather than progression of cardiomyopathy while on dialysis therapy. Potentially remediable risk factors include smoking, left ventricular hypertrophy, and hypoalbuminaemia. [Diabetologia (1997) 40: 1307–1312] Received: 25 March 1997 and in final revised form: 23 June 1997     

Cardiac disease in chronic obstructive pulmonary disease

The cardiac manifestations of chronic obstructive pulmonary disease (COPD) are numerous. Impairments of right ventricular dysfunction and pulmonary vascular disease are well known to complicate the clinical course of COPD and correlate inversely with survival. The pathogenesis of pulmonary vascular disease in COPD is likely multifactorial and related to alterations in gas exchange and vascular biology, as well as structural changes of the pulmonary vasculature and mechanical factors. Several modalities currently exist for the assessment of pulmonary vascular disease in COPD, but right heart catheterization remains the gold standard. Although no specific therapy other than oxygen has been generally accepted for the treatment of pulmonary hypertension in this population, there has been renewed interest in specific pulmonary vasodilators. The coexistence of COPD and coronary artery disease occurs frequently. This association is likely related to shared risk factors as well as similar pathogenic mechanisms, such as systemic inflammation. Management strategies for the care of patients with COPD and coronary artery disease are similar to those without COPD, but care must be given to address their respiratory limitations. Arrhythmias occur frequently in patients with COPD, but are rarely fatal and can generally be treated medically. Use of beta-blockers in the management of cardiac disease, while a theoretical concern in patients with increased airway resistance, is generally safe with the use of cardioselective agents.     

Cardiovascular disease in chronic obstructive pulmonary disease

Smoking is a major cause of chronic obstructive pulmonary disease (COPD) and cardiovascular disorders, including coronary heart disease (CHD) and peripheral arterial disease. Smoking-induced inflammation and other risk factors like dyslipidemia cause vascular endothelial damage via oxidative stress, and a vicious cycle with the characteristics of atherosclerosis ensues. Inflammatory cytokines stimulate hepatic acute-phase protein production, and C-reactive protein is now used widely to assess inflammation in the arterial wall. Smoking is associated with many alterations in lipids and lipoproteins, and is also prothrombotic. Global risk assessment, which determines the absolute risk for developing CHD in 10 years, is used widely to determine who should receive lipid-lowering therapy. Major CHD risk factors include age, sex, smoking, blood pressure, lipoproteins, and cholesterol, but COPD is not among them. Future studies should determine the absolute risk for developing CHD in patients with COPD. The 3-hydroxy-3-methylglutaryl coenzyme-A reductase inhibitors (statins) are used widely to treat and prevent cardiovascular disease. The statins may also produce other beneficial pleiotropic effects, including increased nitric oxide and prostacyclin, antithrombosis, and decreased inflammation, perhaps indicating utility in the therapy for COPD. Efforts are currently underway to determine if such antiinflammatory effects are independent of or in addition to simply lowering low-density lipoprotein cholesterol.     

Determining disease activity in inflammatory bowel disease

To provide a stronger relationship between clinical assessment of disease activity and laboratory measurements, we studied hemoglobin concentrations, sedimentation rates, and the serum levels of albumin and of seromucoids in 86 patients; first when seriously ill with either ulcerative colitis or Crohn's disease, and then again when they were well. Only albumin and seromucoids were separated clearly in the two states: hemoglobin and sedimentation rates showed significant overlap. Paired correlation tests between 10 laboratory variables in 149 patients with Crohn's disease of varying severity revealed a highly significant correlation between seromucoids and albumin (r = 0.71). Both variables correlated with six others, but at lower levels. Processing the correlation matrix by factor analysis suggested that the serum levels of albumin and seromucoid are indicators of the same effect--disease activity. A simple index using only hemoglobin, albumin, and seromucoid values, was derived from this analysis, positive values indicating health and negative ill health. Serum levels of albumin and seromucoids provide the essential data to determine disease activity at routine follow-up of inflammatory bowel disease or to indicate the success or failure of therapeutic regimens, overriding any arbitrary clinical assessment.