Pub Date : 2017-02-01DOI: 10.1097/MIB.0000000000001006
B. Korelitz, S. Shamah
{"title":"The Ileitis of Ulcerative Colitis. Why Is It Not Crohn's Disease?","authors":"B. Korelitz, S. Shamah","doi":"10.1097/MIB.0000000000001006","DOIUrl":"https://doi.org/10.1097/MIB.0000000000001006","url":null,"abstract":"","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"39 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125649145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.1097/01.MIB.0000512619.42520.76
Mario Peralta Mateo, J. Goméz, Tomas Cortés Espinosa, H. Velázquez, J. Terrazas
{"title":"P-099 Impact of Inflammatory Bowel Disease on Sexual Function of Patients in a Mexican Population","authors":"Mario Peralta Mateo, J. Goméz, Tomas Cortés Espinosa, H. Velázquez, J. Terrazas","doi":"10.1097/01.MIB.0000512619.42520.76","DOIUrl":"https://doi.org/10.1097/01.MIB.0000512619.42520.76","url":null,"abstract":"","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"46 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120958658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.1097/MIB.0000000000001010
X. Qin
{"title":"Damage of the Mucus Layer: The Possible Shared Critical Common Cause for Both Inflammatory Bowel Disease (IBD) and Irritable Bowel Syndrome (IBS).","authors":"X. Qin","doi":"10.1097/MIB.0000000000001010","DOIUrl":"https://doi.org/10.1097/MIB.0000000000001010","url":null,"abstract":"","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123375572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.1097/01.MIB.0000512747.92245.32
Hilarious De Jesus
encouragement. A child will likely encounter many different staff over the course of their pediatric care. This tool provides continuity in the IBD education and expectations and a means of assessing progress towards self care This is best done in age appropriate stages with consistent reinforcement enabling the patient, family and health care team to feel confident that independence has been achieved.
{"title":"P-232 YI A Grounded Theory Exploration of Self-management in Paediatric IBD","authors":"Hilarious De Jesus","doi":"10.1097/01.MIB.0000512747.92245.32","DOIUrl":"https://doi.org/10.1097/01.MIB.0000512747.92245.32","url":null,"abstract":"encouragement. A child will likely encounter many different staff over the course of their pediatric care. This tool provides continuity in the IBD education and expectations and a means of assessing progress towards self care This is best done in age appropriate stages with consistent reinforcement enabling the patient, family and health care team to feel confident that independence has been achieved.","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"20 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134495764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.1097/MIB.0000000000001015
X. Qin
To the Editor: I read with great interest the article by Ward et al published recently in this journal regarding the effect of antibiotics on dextran sulfate sodium–induced colitis.1 It is found that treatment with broadspectrum antibiotics protected mice against colitis by changes in gut microbiota. However, as discussed in the article,1 this is in contrast to multiple studies demonstrating antibiotics increased the risk of inflammatory bowel disease in human and colitis in animals in a variety of models. The mechanism behind this remains elusive. At present, the mainstream of research including this article still mainly focused on immune response of the body or the production of some bioactive agents such as short chain fatty acids by gut bacteria. Here I suggest that inactivation of digestive proteases within gut lumen and degradation of the mucus at gut surface may be actually the primary determinant factors for the observed effects of antibiotics. The evidence that I collected during the last 15 years made me to believe that impaired inactivation of digestive proteases due to reduction in gut bacteria in modern society may have played a causative role in the pathogenesis of inflammatory bowel disease.2,3 Studies showed that under conventional conditions, pancreatic digestive proteases are hardly detectable in the lower gut, whereas a large amount of them appeared in the large intestine of animals raised under germ-free conditions, suggesting the critical role of gut bacteria in inactivation of these digestive proteases in the lower intestine. Different kinds and doses of antibiotics may have different effects on digestive proteases inactivation. Nevertheless, mucin, the structural molecule of the protective mucus layer, is composed of 15% of a central core peptide and 85% of side carbohydrate branches that can only be effectively degraded in the existence of both digestive proteases from the pancreas and glycosidases from gut bacteria.4 Thus, as discussed in my articles,3,4 certain extent of reduction of gut bacteria by antibiotics may exacerbate the injury of gut as the result of accelerated degradation of the protective mucus layer by the synergic action of poorly inactivated digestive proteases and glycosides in the remaining gut bacteria, while further extensive reduction in gut bacteria may become less detrimental or even protective because of the striking decrease in bacterial glycosides and retarded degradation of the mucus layer as well as decreased infiltration of bacterial toxicant due to the decrease in bacterial load in gut lumen. This may have contributed explain the less gut damage in both poor hygiene and germ-free conditions,4 as well as the different effects of antibiotics on the gut. Therefore, I recommend conducting more research in this regard.
{"title":"Inactivation of Digestive Proteases and Degradation of Mucus: The Possible Key Factors That Determined the Different Effects on the Gut by Antibiotics.","authors":"X. Qin","doi":"10.1097/MIB.0000000000001015","DOIUrl":"https://doi.org/10.1097/MIB.0000000000001015","url":null,"abstract":"To the Editor: I read with great interest the article by Ward et al published recently in this journal regarding the effect of antibiotics on dextran sulfate sodium–induced colitis.1 It is found that treatment with broadspectrum antibiotics protected mice against colitis by changes in gut microbiota. However, as discussed in the article,1 this is in contrast to multiple studies demonstrating antibiotics increased the risk of inflammatory bowel disease in human and colitis in animals in a variety of models. The mechanism behind this remains elusive. At present, the mainstream of research including this article still mainly focused on immune response of the body or the production of some bioactive agents such as short chain fatty acids by gut bacteria. Here I suggest that inactivation of digestive proteases within gut lumen and degradation of the mucus at gut surface may be actually the primary determinant factors for the observed effects of antibiotics. The evidence that I collected during the last 15 years made me to believe that impaired inactivation of digestive proteases due to reduction in gut bacteria in modern society may have played a causative role in the pathogenesis of inflammatory bowel disease.2,3 Studies showed that under conventional conditions, pancreatic digestive proteases are hardly detectable in the lower gut, whereas a large amount of them appeared in the large intestine of animals raised under germ-free conditions, suggesting the critical role of gut bacteria in inactivation of these digestive proteases in the lower intestine. Different kinds and doses of antibiotics may have different effects on digestive proteases inactivation. Nevertheless, mucin, the structural molecule of the protective mucus layer, is composed of 15% of a central core peptide and 85% of side carbohydrate branches that can only be effectively degraded in the existence of both digestive proteases from the pancreas and glycosidases from gut bacteria.4 Thus, as discussed in my articles,3,4 certain extent of reduction of gut bacteria by antibiotics may exacerbate the injury of gut as the result of accelerated degradation of the protective mucus layer by the synergic action of poorly inactivated digestive proteases and glycosides in the remaining gut bacteria, while further extensive reduction in gut bacteria may become less detrimental or even protective because of the striking decrease in bacterial glycosides and retarded degradation of the mucus layer as well as decreased infiltration of bacterial toxicant due to the decrease in bacterial load in gut lumen. This may have contributed explain the less gut damage in both poor hygiene and germ-free conditions,4 as well as the different effects of antibiotics on the gut. Therefore, I recommend conducting more research in this regard.","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"28 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114797149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.1097/01.MIB.0000512623.88262.5c
J. L. Hyun, Jun Park Jae
{"title":"P-104 Association Between pANCA Status and Clinical Characteristics and Outcomes of Ulcerative Colitis: A Meta-analysis","authors":"J. L. Hyun, Jun Park Jae","doi":"10.1097/01.MIB.0000512623.88262.5c","DOIUrl":"https://doi.org/10.1097/01.MIB.0000512623.88262.5c","url":null,"abstract":"","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"56 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124647085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-12-01DOI: 10.1097/MIB.0000000000000976
R. Burakoff, R. Macdermott
{"title":"Passing the Torch: Thank You from the Coeditors in Chief.","authors":"R. Burakoff, R. Macdermott","doi":"10.1097/MIB.0000000000000976","DOIUrl":"https://doi.org/10.1097/MIB.0000000000000976","url":null,"abstract":"","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126994164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-01DOI: 10.1097/MIB.0000000000000942
F. Caldera, M. Hayney
REFERENCES 1. Bouma G, Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol. 2003;3:521–533. 2. Stoll M, Corneliussen B, Costello CM, et al. Genetic variation in DLG5 is associated with inflammatory bowel disease. Nat Genet. 2004;36: 476–480. 3. Nakamura H, Sudo T, Tsuiki H, et al. Identification of a novel human homolog of the Drosophila dlg, P-dlg, specifically expressed in the gland tissues and interacting with p55. FEBS Lett. 1998;433:63–67. 4. Tepass U, Tanentzapf G, Ward R, et al. Epithelial cell polarity and cell junctions in Drosophila. Annu Rev Genet. 2001;35:747–784. 5. Coradini D, Casarsa C, Oriana S. Epithelial cell polarity and tumorigenesis: new perspectives for cancer detection and treatment. Acta Pharmacol Sin 2011;32:552–564.
{"title":"Barriers to Administration of Herpes Zoster Immunization in Patients with Inflammatory Bowel Disease.","authors":"F. Caldera, M. Hayney","doi":"10.1097/MIB.0000000000000942","DOIUrl":"https://doi.org/10.1097/MIB.0000000000000942","url":null,"abstract":"REFERENCES 1. Bouma G, Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol. 2003;3:521–533. 2. Stoll M, Corneliussen B, Costello CM, et al. Genetic variation in DLG5 is associated with inflammatory bowel disease. Nat Genet. 2004;36: 476–480. 3. Nakamura H, Sudo T, Tsuiki H, et al. Identification of a novel human homolog of the Drosophila dlg, P-dlg, specifically expressed in the gland tissues and interacting with p55. FEBS Lett. 1998;433:63–67. 4. Tepass U, Tanentzapf G, Ward R, et al. Epithelial cell polarity and cell junctions in Drosophila. Annu Rev Genet. 2001;35:747–784. 5. Coradini D, Casarsa C, Oriana S. Epithelial cell polarity and tumorigenesis: new perspectives for cancer detection and treatment. Acta Pharmacol Sin 2011;32:552–564.","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"16 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124160749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-01DOI: 10.1097/MIB.0000000000000927
X. Qin
{"title":"Perinuclear Antineutrophil Cytoplasmic Antibody with a Large Portion Being Anti-β-Glucuronidase, May Have Played a Causative Role in the Pathogenesis of Inflammatory Bowel Disease.","authors":"X. Qin","doi":"10.1097/MIB.0000000000000927","DOIUrl":"https://doi.org/10.1097/MIB.0000000000000927","url":null,"abstract":"","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"244 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116796216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-06-01DOI: 10.1097/MIB.0000000000000774
X. Qin
IBD. NHE3 knockout mice, which display congenital mild diarrhea and reduced body weight develop spontaneous colitis when housed in a conventional facility, and lethal colitis when exposed to low concentrations of dextran sulfate sodium. However, housing these mice in an ultraclean facility improved colitis symptoms emphasizing the importance of the gut microbiome in the development of colitis, as well as an immunomodulatory effect of NHE3 downregulation in IBD. Along these lines, we would like to point to our recent identification of germline mutations in NHE3 and in a regulator of NHE3, guanylate cyclase C in patients with congenital sodium diarrhea. Congenital sodium diarrhea refers to an intractable diarrhea of intrauterine onset with high fecal sodium loss. Recessive NHE3 mutations resulted in absent or nonfunctional protein in a subset of patients, and NHE3 was downregulated in another subset of congenital sodium diarrhea patients harboring constitutively activating and hyper-stimulating mutations in guanylate cyclase C. Interestingly, several patients with germline guanylate cyclase C and NHE3 mutations developed IBD, with varying ages of onset implicating reduced NHE3 activity as a predisposition for IBD. Taken together, NHE3 might be considered to play a role in the composition of the gut microbiota, and its deficiency may thus contribute to dysbiosis observed in patients with IBD.
{"title":"How Sugar and Soft Drinks Are Related to Inflammatory Bowel Disease?","authors":"X. Qin","doi":"10.1097/MIB.0000000000000774","DOIUrl":"https://doi.org/10.1097/MIB.0000000000000774","url":null,"abstract":"IBD. NHE3 knockout mice, which display congenital mild diarrhea and reduced body weight develop spontaneous colitis when housed in a conventional facility, and lethal colitis when exposed to low concentrations of dextran sulfate sodium. However, housing these mice in an ultraclean facility improved colitis symptoms emphasizing the importance of the gut microbiome in the development of colitis, as well as an immunomodulatory effect of NHE3 downregulation in IBD. Along these lines, we would like to point to our recent identification of germline mutations in NHE3 and in a regulator of NHE3, guanylate cyclase C in patients with congenital sodium diarrhea. Congenital sodium diarrhea refers to an intractable diarrhea of intrauterine onset with high fecal sodium loss. Recessive NHE3 mutations resulted in absent or nonfunctional protein in a subset of patients, and NHE3 was downregulated in another subset of congenital sodium diarrhea patients harboring constitutively activating and hyper-stimulating mutations in guanylate cyclase C. Interestingly, several patients with germline guanylate cyclase C and NHE3 mutations developed IBD, with varying ages of onset implicating reduced NHE3 activity as a predisposition for IBD. Taken together, NHE3 might be considered to play a role in the composition of the gut microbiota, and its deficiency may thus contribute to dysbiosis observed in patients with IBD.","PeriodicalId":339644,"journal":{"name":"Inflammatory Bowel Disease","volume":"145 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121872934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：