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| 1 | 2010年世界胃肠病学组织关于炎症性肠病诊断和治疗的实践指南显示文摘炎症性肠病(IBD)是一组特发性、慢性、炎症性肠道疾病状态,包括两种主要类型:克罗恩病(CD)和溃疡性结肠炎(UC),两者的临床和病理特征既有重叠又有区别。IBD过去常见于发达国家,近几十年,发展中国家的患病率逐步上升。本指南就IBD诊断和治疗方面提出的独特议题在当前的文献和指南中几乎从未被提及。由于各地区的IBD临床特点差异较大,因此根据患者的主诉诊断IBD或评估疾病活动度需随地区的变化而变化。同样,治疗亦应根据疾病的分类和当地医疗资源进行调整。世界胃肠病学组织根据世界各国医疗资源的差异,采用级联方法制订了IBD的诊疗指南。 | Charles N.Bernstein Michael Fried J.H.Krabshuis Henry Cohen R.Eliakim Suleiman Fedail Richard Gearry K.L.Goh Saheed Hamid Aamir Ghafor Khan A.W.LeMair Malfertheiner Qin Ouyang J.F.Rey Ajit Sood Flavio Steinwurz Ole O.Thomsen Alan Thomson Gillian Watermeyer 杨钊斌 杨川华 钱本余 | 2010 | 胃肠病学2010，15，9： | 101 |
| 2 | Probiotic effects on intestinal fermentation patterns in patients with irritable bowel syndrome显示文摘AIM: To determine whether Lactobacillus casei strain Shirota (Yakult ) can alter small intestinal bacterial overgrowth (SIBO), as tested by the lactulose breath test, and whether this is associated with changes in symptoms in irritable bowel syndrome (IBS). METHODS: 18 patients with IBS (Rome Ⅱ criteria), who showed an early rise in breath hydrogen with lactulose (ERBHAL), consumed 65 mL of Yakult daily for 6 wk. Lactulose breath test was repeated at the end of the treatment period. Symptoms were recorded daily using a 10 cm visual analogue scale. RESULTS: 14 patients completed the study, 9 (64%) had reversal of ERBHAL, with the median time of f irst rise in breath hydrogen increasing from 45 to 75 min (P = 0.03). There was no signifi cant improvement in the symptom score with probiotic therapy, except for wind (P=0.04). Patients commencing with at least moderate symptoms and who no longer had ERBHAL at the end of treatment, showed improvement in the overall symptoms scores [median fi nal score 5.3 (IQR3.9-5.9), 55% reduction; n=6] to a greater extent than those who had had persisting ERBHAL [final score 6.9 (5.0-7.0), 12% reduction; n = 5; P = 0.18]. CONCLUSION: Yakult is effective in altering fermentation patterns in the small bowel, consistent with reducing SIBO. The loss of ERBHAL was associated with reduced symptoms. The true interpretation of these fi ndings awaits a randomised, controlled trial. | Jacqueline S Barrett Kim EK Canale Richard B Gearry Peter M Irving Peter R Gibson | 2008 | World Journal of Gastroenterology2008，14，32： | 16 |
| 3 | Use of exclusive enteral nutrition in adults with Crohn's disease: A review显示文摘Exclusive enteral nutrition(EEN)is well-established as a first line therapy instead of corticosteroid(CS)therapy to treat active Crohn’s disease(CD)in children.It also has been shown to have benefits over and above induction of disease remission in paediatric populations.However,other than in Japanese populations,this intervention is not routinely utilised in adults.To investigate potential reasons for variation in response between adult studies of EEN and CS therapy.The Ovid database was searched over a 6-mo period.Articles directly comparing EEN and CS therapy in adults were included.Eleven articles were identified.EEN therapy remission rates varied considerably.Poor compliance with EEN therapy due to unpalatable formula was an issue in half of the studies.Remission rates of studies that only included patients with previously untreated/new CD were higher than studies including patients with both existing and new disease.There was limited evidence to determine if disease location,duration of disease or age of diagnosis affected EEN therapy outcomes.There is some evidence to support the use of EEN as a treatment option for a select group of adults,namely those motivated to adhere to an EEN regimen and possibly those newly diagnosed with CD.In addition,the use of more palatable formulas could improve treatment compliance. | Catherine L Wall Andrew S Day Richard B Gearry | 2013 | World Journal of Gastroenterology2013，19，43： | 15 |
| 4 | Macrophage migration inhibitory factor gene polymorphisms in inflammatory bowel disease: An association study in New Zealand Caucasians and meta-analysis显示文摘AIM:To investigate the association of macrophage migration inhibitory factor(MIF)promoter polymorphisms with inflammatory bowel disease(IBD)risk.METHODS:One thousand and six New Zealand Caucasian cases and 540 Caucasian controls were genotyped for the MIF SNP-173G>C(rs755622)and the repeat polymorphism CATT5-8(rs5844572)using a predesigned TaqMan SNP assay and capillary electrophoresis,respectively.Data were analysed for single site and haplotype association with IBD risk and phenotype.Meta-analysis was employed,to assess cumulative evidence of association of MIF-173G>C with IBD.All published genotype data for MIF-173G>C in IBD were identified using PubMed and subsequently searching the references of all PubMed-identified studies.Imputed genotypes for MIF-173G>C were generated from the Wellcome Trust Case Control Consortium(and National Institute of Diabetes and Digestive and Kidney Diseases).Separate meta-analyses were performed on Caucasian Crohn’s disease(CD)(3863 patients,6031controls),Caucasian ulcerative colitis(UC)(1260 patients,1987 controls),and East Asian UC(416 patients and 789 controls)datasets using the Mantel-Haenszel method.The New Zealand dataset had 93%power,and the meta-analyses had 100%power to detect an effect size of OR=1.40 atα=0.05,respectively.RESULTS:In our New Zealand dataset,single-site analysis found no evidence of association of MIF polymorphisms with overall risk of CD,UC,and IBD or disease phenotype(all P values>0.05).Haplotype analysis found the CATT5/-173C haplotype occurred at a higher frequency in New Zealand controls compared to IBD patients(0.6 vs 0.01;P=0.03,OR=0.22;95%CI:0.05-0.99),but this association did not survive bonferroni correction.Meta-analysis of our New Zealand MIF-173G>C data with data from seven additional Caucasian datasets using a random effects model found no association of MIF polymorphisms with CD,UC,or overall IBD.Similarly,meta-analysis of all published MIF-173G>C data from East Asian datasets(416UC patients,789 controls)found no association of this promoter polymorphism with UC. | James D Falvey Robert W Bentley Tony R Merriman Mark B Hampton Murray L Barclay Richard B Gearry Rebecca L Roberts | 2013 | World Journal of Gastroenterology2013，19，39： | 9 |
| 5 | The low FODMAP diet improves gastrointestinal symptoms in patients with irritable bowel syndrome: a prospective study显示文摘 | R. H. Roest B. R. Dobbs B. A. Chapman B. Batman L. A. O’Brien J. A. Leeper C. R. Hebblethwaite R. B. Gearry | 2013 | Int J Clin Pract2013，，9： | 7 |
| 6 | Single nucleotide polymorphism in the tumor necrosis factor-alpha gene affects inflammatory bowel diseases risk显示文摘AIM: To investigate the role that single nucleotide polymorphisms (SNPs) in the promoter of the tumour necrosis factor-alpha (TNF-α) gene play in the risk of inflammatory bowel diseases (IBDs) in a New Zealand population, in the context of international studies. METHODS: DNA samples from 388 patients with Crohn's disease (CD), 405 ulcerative colitis (UC), 27 indeterminate colitis (IC) and 201 randomly selected controls, from Canterbury, New Zealand were screened for 3 common polymorphisms in the TNF-α receptor: -238 G→A, -308 G→A and -857C→T, using a TaqmanR assay. A meta-analysis was performed on the data obtained on these polymorphisms combined with that from other published studies. RESULTS: Individuals carrying the -308 G/A allele had a significantly (OR = 1.91, χ2 = 17.36, P < 0.0001) increased risk of pancolitis, and a 1.57-fold increased risk (OR = 1.57, χ2 = 4.34, P = 0.037) of requiring a bowel resection in UC. Carrying the -857 C/T variant decreased the risk of ileocolonic CD (OR = 0.56, χ2 =4.32, P = 0.037), and the need for a bowel resection (OR = 0.59, χ2 = 4.85, P = 0.028). The risk of UC was reduced in individuals who were smokers at diagnosis, (OR = 0.48, χ2 = 4.86, P = 0.028). CONCLUSION: TNF-α is a key cytokine known to play a role in inflammatory response, and the locus for the gene is found in the IBD3 region on chromosome 6p21, known to be associated with an increased risk for IBD. The -308 G/A SNP in the TNF-α promoter is functional, and may account in part for the increased UC risk associated with the IBD3 genomic region. The -857 C/T SNP may decrease IBD risk in certain groups. Pharmaco- or nutrigenomic approaches may be desir- able for individuals with such affected genotypes. | Lynnette R Ferguson Claudia Huebner Ivonne Petermann Richard B Gearry Murray L Barclay Pieter Demmers Alan McCulloch Dug Yeo Han | 2008 | World Journal of Gastroenterology2008，14，29： | 7 |
| 7 | Are faecal markers good indicators of mucosal healing in inflammatory bowel disease?显示文摘AIM: To review the published literature concerning the accuracy of faecal inflammatory markers for identifying mucosal healing. METHODS: Bibliographical searches were performed in MEDLINE electronic database up to February 2015,using the following terms: 'inflammatory bowel disease','Crohn′s disease','ulcerative colitis','faecal markers','calprotectin','lactoferrin','S100A12','endoscop*','mucosal healing','remission'. In addition,relevant references from these studies were also included. Data were extracted from the published papers including odds ratios with 95%CI,P values and correlation coefficients. Data were grouped together according to each faecal marker,Crohn's disease or ulcerative colitis,and paediatric compared with adult study populations. Studies included in this review assessed mucosal inflammation by endoscopic and/or histological means and compared these findings to faecal marker concentrations in inflammatory bowel diseases(IBD) patient cohorts. Articles had to be published between 1990 and February 2015 and written in English. Papers excluded from the review were those where the faecal biomarker concentration was compared between patients with IBD and controls or other disease groups,those where serum biomarkers were used,those with a heterogeneous study population and those only assessing post-operative disease. RESULTS: The available studies show that faecal markers,such as calprotectin and lactoferrin,are promising non-invasive indicators of mucosal healing. However,due to wide variability in study design,especially with regard to the definition of mucosal healing and evaluation of marker cut offs,the available data do not yet indicate the optimal roles of these markers. Thirty-six studies published between 1990 and 2014 were included. Studies comprised variable numbers of study participants,considered CD(15-164 participants) or UC(12-152 participants) separately or as a combined group(11-252 participants). Eight reports included paediatric patients. Several indices were used to document mucosal inflammation,encompassing elevenendoscopic and eight histologic grading systems. The majority of the available reports focused on faecal calprotectin(33 studies),whilst others assessed faecal lactoferrin(13 studies) and one study assessed S100A12. Across all of the biomarkers,there is a wide range of correlation describing the association between faecal markers and endoscopic disease activity(r values ranging from 0.32 to 0.87,P values ranging from < 0.0001 to 0.7815). Correlation coefficients are described in almost all studies and are used more commonly than outcome measures such as sensitivity,specificity,PPV and/or NPV. Overall,the studies that have evaluated faecal calprotectin and/or faecal lactoferrin and their relationship with endoscopic disease activity show inconsistent results. CONCLUSION: Future studies should report the results of faecal inflammatory markers in the context of mucosal healing with clear validated cut offs. | Gudula JAM Boon Andrew S Day Chris J Mulder Richard B Gearry | 2015 | World Journal of Gastroenterology2015，21，40： | 4 |
| 8 | NOD2 and ATG16L1 polymorphisms affect monocyte responses in Crohn's disease显示文摘AIM:To assess whether polymorphisms in NOD2 and ATG16L1 affect cytokine responses and mycobacterium avium subspecies paratuberculosis (MAP) survival in monocytes from Crohn's disease (CD) patients.METHODS:Monocytes were isolated from peripheral blood of CD patients of known genotype for common single nucleotide polymorphisms of NOD2 and ATG16L1.Monocytes were challenged with MAP and bacterial persistence assessed at subsequent time-points.Cytokine responses were assayed using a Milliplex multi-analyte profiling assay for 13 cytokines.RESULTS:Monocytes heterozygous for a NOD2 polymorphism (R702W,P268S,or 1007fs) were more permissive for growth of MAP (P=0.045) than those without.There was no effect of NOD2 genotype on subsequent cytokine expression.The T300A polymorphism ofATG16L1 did not affect growth of MAP in our model (P=0.175),but did increase expression of cytokines interleukin (IL)-10 (P=0.047) and IL-6 (P=0.019).CONCLUSION:CD-associated polymorphisms affected the elimination of MAP fromex vivo monocytes (NOD2),or expression of certain cytokines (ATG16L1),implying independent but contributory roles in the pathogenesis of CD. | Dylan M Glubb Richard B Gearry Murray L Barclay Rebecca L Roberts John Pearson Jacqui I Keenan Judy McKenzie Robert W Bentley | 2011 | World Journal of Gastroenterology2011，17，23： | 2 |
| 9 | Inter-observer agreement for Crohn’s disease sub-phenotypes using the Montreal Classification: How good are we? A multi-centre Australasian study显示文摘 | Krupa Krishnaprasad Jane M. Andrews Ian C. Lawrance Timothy Florin Richard B. Gearry Rupert W.L. Leong Gillian Mahy Peter Bampton Ruth Prosser Peta Leach Laurie Chitti Charles Cock Rachel Grafton Anthony R. Croft Sharon Cooke James D. Doecke Graham L. Rad | 2011 | Journal of Crohn’s and Colitis2011，，3： | 2 |
| 10 | Psychotherapy for inflamma- tory bowel disease: a review and update 显示文摘 | McCombie AM Mulder RT Gearry RB | 2013 | J Crohns Colitis2013，7，12： | 1 |
| 11 | Predictors of poor outcome in patients w ith autoimmune hepatitis: A population‐based study显示文摘 | Jing Hieng Ngu Richard Blair Gearry Chris Miles Frampton Catherine A.M. Stedman | 2013 | Hepatology2013，，： | 1 |
| 12 | Review of fecal biomarkers in inflammatory bowel disease显示文摘 | Sutherland AD Gearry RB Frizelle FA | 2008 | Dis Colon Rectum2008，51，8： | 1 |
| 13 | Lack of association between the ITPA 94C>A polymorphism and adverse effects from azathioprine显示文摘 | Roberts RL Barclay ML | 2004 | Pharmacogenetics2004，14，11： | 1 |
| 14 | IMPDH1 promoter mu- tations in a patient exhibiting azathioprine resistance 显示文摘 | Roberts RL Gearry RB Barclay ML | 2007 | Pharmacog- enomics J2007，7，5： | 1 |
| 15 | Azathioprine and 6-mercaptopurine pharmacogenetics and metabolite monitoring in inflammatory bowel disease显示文摘 | Gearry RB Barclay ML | 2005 | J Gastroenterol Hepatol2005，20，8： | 1 |
| 16 | Azathioprine and 6-mercaptopurine pharmacogenetics and metabolite monitoring in inflammatory bowel disease显示文摘 | Gearry RB Barclay ML | 2005 | J Gastroenterol Hepatol2005，20，8： | 1 |
| 17 | The role of S100A12 as a systemic marker of inflammation显示文摘 | Meijer B Gearry RB Day AS | | 0，，： | 1 |
| 18 | The role of S100A12 as a systemic marker of inflammation 显示文摘 | MEIJER B GEARRY R B DAY A S | 2012 | Int J Inflam2012，3，： | 1 |
| 19 | 925j Optimising post-operative Crohn’s disease management: best drug therapy alone versus colonoscopic monitoring with treatment step-up. The POCER study.显示文摘 | Peter De Cruz Michael A. Kamm Amy L. Hamilton Kathryn J. Ritchie Soula Krejany Alexandra Gorelik Danny Liew Lani Prideaux Ian C. Lawrance Jane M. Andrews Peter A. Bampton Miles Sparrow Timothy H. Florin Peter R. Gibson Henry Debinski Richard B. Gearry Fin | 2013 | Gastroenterology2013，，5： | 1 |
| 20 | Psychotherapy for inflammatory bowel disease: A review and update显示文摘 | Andrew M. McCombie Roger T. Mulder Richard B. Gearry | 2013 | Journal of Crohn’s and Colitis2013，，： | 1 |
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