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Eosinophil granule major basic protein 1 deposition in eosinophilic esophagitis correlates with symptoms independent of eosinophil counts.

Recent Articles on Eosinophilic Oesophagitis (External) -

Eosinophil granule major basic protein 1 deposition in eosinophilic esophagitis correlates with symptoms independent of eosinophil counts.

Dis Esophagus. 2019 Jul 16;:

Authors: Peterson KA, Gleich GJ, Limaye NS, Crispin H, Robson J, Fang J, Saffari H, Clayton F, Leiferman KM

Abstract
In patients with eosinophilic esophagitis (EoE), symptoms often do not correlate with peak eosinophil counts (PEC) determined on histopathological examination of biopsy specimens. This may be because eosinophils degranulate during active disease and lose their morphological identity as intact cells and, therefore, are not enumerated on microscopic examination. Eosinophil granule proteins that are released into tissues with degranulation, including major basic protein 1 (eMBP1), likely contribute to disease pathogenesis and, therefore, may correlate with symptoms better than PEC. We sought to determine whether symptoms in patients with EoE more closely relate to eosinophil granule protein deposition than to eosinophil enumeration, especially in patients with fewer than 15 eosinophils per high power field (HPF). Esophageal biopsy specimens from 34 patients diagnosed with EoE were obtained for histopathological examination and for evaluation of eMBP1 staining by indirect immunofluorescence. PEC by histopathology were compared to extracellular eMBP1 grades by immunostaining. PEC and eMBP1 grades also were analyzed for their relationship to symptoms and clinical course. Biopsy specimens from 19 of the 34 patients had fewer than 15 PEC on histopathological examination, and the other 15 patients had 15 or greater PEC. Positive eMBP1 immunostaining was found in all symptomatic patients. EoE symptoms were related to eMBP1 immunostaining grades (p = 0.0001), but not PEC (P = 0.14). Eosinophil granule protein deposition, specifically eMBP1, is increased in esophageal biopsy specimens from symptomatic patients with EoE and may be a marker of disease activity, including patients with EoE who have 'resolved' disease.

PMID: 31310661 [PubMed - as supplied by publisher]

Changes in the rate of and trends in colectomy for ulcerative colitis during the era of biologics and calcineurin inhibitors based on a Japanese nationwide cohort study.

IBD on PubMed -

Changes in the rate of and trends in colectomy for ulcerative colitis during the era of biologics and calcineurin inhibitors based on a Japanese nationwide cohort study.

Surg Today. 2019 Jul 15;:

Authors: Uchino M, Ikeuchi H, Hata K, Okada S, Ishihara S, Morimoto K, Sahara R, Watanabe K, Fukushima K, Takahashi K, Kimura H, Hirata K, Mizushima T, Araki T, Kusunoki M, Nezu R, Nakao S, Itabashi M, Hirata A, Ozawa H, Ishida T, Okabayashi K, Yamamoto T, Noake T, Arakaki J, Watadani Y, Ohge H, Futatsuki R, Koganei K, Sugita A, Higashi D, Futami K

Abstract
PURPOSE: We evaluated the recent incidence of surgery and the changing surgery trends for ulcerative colitis (UC) in Japan due to the increasing use of anti-tumor necrosis factor (TNF) agents.
METHODS: A questionnaire survey was performed to assess the number of surgeries, surgical indications, surgical timing, and immunosuppressive treatments before surgery between 2007 and 2017.
RESULTS: A total of 3801 surgical cases were reported over 11 years. The prevalence of UC surgery decreased over the period studied. The rate of prednisolone (PSL) use did not change. The prevalence of both calcineurin inhibitors (CNIs) and anti-TNF agents increased during the period studied (p < 0.01). The prevalence of urgent/emergent surgery did not change. The most distinctive change in surgical indications was the increase in cancer/dysplasia (CAC), the prevalence of which increased from 20.2% in 2007 to 34.8%.
CONCLUSION: The prevalence of UC surgery seems to be decreasing according to the increasing rate of anti-TNF agent and CNI administration. However, the indication of CAC significantly increased. Further research should evaluate whether or not long-term remission maintained with several agents can lead to increasing CAC.

PMID: 31309329 [PubMed - as supplied by publisher]

Estimated prevalence of ulcerative colitis and Crohn's disease in Japan in 2014: an analysis of a nationwide survey.

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Estimated prevalence of ulcerative colitis and Crohn's disease in Japan in 2014: an analysis of a nationwide survey.

J Gastroenterol. 2019 Jul 15;:

Authors: Murakami Y, Nishiwaki Y, Oba MS, Asakura K, Ohfuji S, Fukushima W, Suzuki Y, Nakamura Y

Abstract
BACKGROUND: Almost a quarter century has passed since the first nationwide survey on ulcerative colitis (UC) and Crohn's disease (CD) was conducted in Japan. In this study, we used a nationwide survey to estimate the number of patients and prevalence of these diseases in Japan in 2014.
METHODS: We conducted a mail-based survey targeting hospitals to estimate the annual numbers of patients with UC and CD in 2014. Respondents were asked to report the numbers of patients who met specific diagnostic criteria for these two conditions. A stratified random sampling method was used, and a total of 3712 departments (internal medicine, surgery, pediatrics, and pediatric surgery) were selected for analysis. The overall and sex-specific annual numbers of UC and CD patients were estimated. The corresponding prevalence rates per 100,000 population were calculated by dividing the number of patients with each disease by the mid-year population of Japan in 2014.
RESULTS: The overall survey response rate was 56.7% (2016 departments). The estimated numbers of patients with UC and CD were 219,685 (95% confidence interval: 183,968-255,403) and 70,700 (56,702-84,699), respectively. The annual prevalence rates of UC and CD per 100,000 population were 172.9 (men: 192.3; women: 154.5) and 55.6 (men: 79.5; women: 33.1), respectively. These numbers are almost tenfold increase in comparing the previous survey (22,300 in UC and 7,400 in CD). The male-to-female ratios were 1.24 for UC and 2.40 for CD, and the UC-to-CD ratio was 3.11.
CONCLUSIONS: The prevalence of UC and CD in Japan has risen substantially over the past two decades, and their disease burden requires further examination.

PMID: 31309327 [PubMed - as supplied by publisher]

Current concepts in pediatric inflammatory bowel disease; IL10/IL10R colitis as a model disease.

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Current concepts in pediatric inflammatory bowel disease; IL10/IL10R colitis as a model disease.

Int J Pediatr Adolesc Med. 2019 Mar;6(1):1-5

Authors: Almana Y, Mohammed R

Abstract
Inflammatory bowel disease (IBD) is a heterogeneous group of disorders composed mainly of ulcerative colitis (UC) and Crohn's disease (CD) and undetermined IBD. The peak incidence of occurrence is mainly beyond the pediatric age group. Recent knowledge about genetic factors had been strongly linked to pediatric IBD (PIBD). Recent advances in genomic technologies have prompted the identification of genetic defects underlying rare, very early-onset IBD (VEO-IBD) as a disease subgroup noted especially in populations with higher consanguinity rates. A better understanding of key players in the complex homeostasis of the immune system in the gut and illustrating the relationships between intestinal microbiome, systemic immune dysregulation and primary immunodeficiency have received growing recognition over the years. In this article, we provide a review of the key players of the immunity of the gut, compare between adult and pediatric IBD as an interesting module to investigate the relationship between monogenic and multifactorial/polygenic diseases, list genetic mutations confirmed to be linked to VEO IBD and summarize the scientific work that led to the discovery of one of the monogenic mutations related to infantile colitis, namely IL10 and IL10 receptor defects.

PMID: 31304220 [PubMed]

Dynamic gut microbiome changes following regional intestinal lymphatic obstruction in primates.

IBD on PubMed -

Dynamic gut microbiome changes following regional intestinal lymphatic obstruction in primates.

Pathophysiology. 2019 Jun 28;:

Authors: Becker F, Gavins FNE, Fontenot J, Jordan P, Yun JY, Scott R, Polk PR, Friday RE, Boktor M, Musso M, Romero E, Boudreaux S, Simmons J, Hasselschwert DL, Goetzmann JE, Vanchiere J, Cvek U, Trutschl M, Kilgore P, Alexander JS

Abstract
The pathogenesis of inflammatory bowel disease (IBD) has been linked with lymphostasis, but whether and how lymphatic obstruction might disturb the intestinal microbiome in the setting of Crohn's Disease (CD) is currently unknown. We employed a new model of CD in African Green monkeys, termed 'ATLAS' (African green monkey truncation of lymphatics with obstruction and sclerosis), to evaluate how gut lymphatic obstruction alters the intestinal microbiome at 7, 21 and 61 days. Remarkable changes in several microbial sub- groupings within the gut microbiome were observed at 7 days post-ATLAS compared to controls including increased abundance of Prevotellaceae and Bacteroidetes-Prevotella-Porphyromonas (BPP), which may contribute to disease activity in this model of gut injury. To the best of our knowledge, these findings represent the first report linking lymphatic structural/gut functional changes with alterations in the gut microbiome as they may relate to the pathophysiology of CD.

PMID: 31301989 [PubMed - as supplied by publisher]

Tumor necrosis factor stimulates fibroblast growth factor 23 levels in chronic kidney disease and non-renal inflammation.

IBD on PubMed -

Tumor necrosis factor stimulates fibroblast growth factor 23 levels in chronic kidney disease and non-renal inflammation.

Kidney Int. 2019 May 14;:

Authors: Egli-Spichtig D, Imenez Silva PH, Glaudemans B, Gehring N, Bettoni C, Zhang MYH, Pastor-Arroyo EM, Schönenberger D, Rajski M, Hoogewijs D, Knauf F, Misselwitz B, Frey-Wagner I, Rogler G, Ackermann D, Ponte B, Pruijm M, Leichtle A, Fiedler GM, Bochud M, Ballotta V, Hofmann S, Perwad F, Föller M, Lang F, Wenger RH, Frew I, Wagner CA

Abstract
Fibroblast growth factor 23 (FGF23) regulates phosphate homeostasis, and its early rise in patients with chronic kidney disease (CKD) is independently associated with all-cause mortality. Since inflammation is characteristic of CKD and associates with increased plasma FGF23 we examined whether inflammation directly stimulates FGF23. In a population-based cohort, plasma tumor necrosis factor (TNF) was the only inflammatory cytokine that independently and positively correlated with plasma FGF23. Mouse models of CKD showed signs of renal inflammation, renal FGF23 expression and elevated systemic FGF23 levels. Renal FGF23 expression coincided with expression of the orphan nuclear receptor Nurr1 regulating FGF23 in other organs. Antibody-mediated neutralization of TNF normalized plasma FGF23 and suppressed ectopic renal Fgf23 expression. Conversely, TNF administration to control mice increased plasma FGF23 without altering plasma phosphate. Moreover, in Il10-deficient mice with inflammatory bowel disease and normal kidney function, plasma FGF23 was elevated and normalized upon TNF neutralization. Thus, the inflammatory cytokine TNF contributes to elevated systemic FGF23 levels and also triggers ectopic renal Fgf23 expression in animal models of CKD.

PMID: 31301888 [PubMed - as supplied by publisher]

Hematopoiesis and the bacterial microbiome.

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Hematopoiesis and the bacterial microbiome.

Blood. 2018 08 09;132(6):559-564

Authors: Yan H, Baldridge MT, King KY

Abstract
Recent studies have revealed that the intestinal bacterial microbiome plays an important role in the regulation of hematopoiesis. A correlation between adverse hematologic effects and imbalance of the intestinal microbiome, or dysbiosis, is evident in several human conditions, such as inflammatory bowel disease, obesity, and, critically, in the setting of antibiotic exposure. Here we review the effects of gut dysbiosis on the hematological compartment and our current understanding of the mechanisms through which changes in the bacterial microbiome affect hematopoiesis.

PMID: 29853538 [PubMed - indexed for MEDLINE]

Neuronal Nitric Oxide Mediates the Anti-Inflammatory Effects of Intestinal Ischemic Preconditioning.

Recent PubMed Articles on Gut Motility -

Neuronal Nitric Oxide Mediates the Anti-Inflammatory Effects of Intestinal Ischemic Preconditioning.

J Surg Res. 2019 Jul 10;244:241-250

Authors: Varga S, Juhász L, Gál P, Bogáts G, Boros M, Palásthy Z, Szabó A, Kaszaki J

Abstract
BACKGROUND: Ischemic preconditioning (IPC) can provide a defense against ischemia-reperfusion (IR)-induced acute inflammation and barrier dysfunction in many organs. Because nitric oxide (NO) has been implicated as a trigger or mediator in the IPC mechanism and because neuronal NO synthase (nNOS) is a dominant isoform of NOS in the gastrointestinal tract, our aim was to investigate the role of nNOS in IPC-induced protection after mesenteric IR.
MATERIALS AND METHODS: Intestinal IR was induced in sodium pentobarbital-anesthetized dogs by clamping the superior mesenteric artery for 60 min followed by 2 h of reperfusion (IR group; n = 7). In further groups, IPC was used (three cycles of 5-min ischemia/5-min reperfusion periods) before IR in the presence or absence of selective inhibition of nNOS with 7-nitroindazole (5 mg/kg, intravenously, in a bolus 15 min before IPC, n = 6 each). Changes in mesenteric vascular resistance, intramucosal pH (pHi), and small bowel motility were monitored. Plasma nitrite/nitrate levels, intestinal NO synthase activity, leukocyte accumulation, mast cell degranulation, and histologic injury were also determined.
RESULTS: Ischemia significantly decreased mesenteric vascular resistance and pHi, whereas IR induced a temporary bowel hypermotility and acute inflammatory reaction. IPC facilitated pHi recovery, attenuated motility dysfunction, elevated NOS-dependent NO production, and reduced leukocyte accumulation, mast cell degranulation, and mucosal injury. Pretreatment with 7-nitroindazole halted the IPC-induced increase in NO availability, pHi recovery, and the anti-inflammatory and morphologic effects.
CONCLUSIONS: Our data demonstrate that NO generated by intestinal nNOS plays a pivotal role in IPC-linked tissue protection by inhibiting an IR-related acute inflammatory response.

PMID: 31301480 [PubMed - as supplied by publisher]

IBD prevalence in Lothian, Scotland, derived by capture-recapture methodology.

IBD on PubMed -

IBD prevalence in Lothian, Scotland, derived by capture-recapture methodology.

Gut. 2019 Jul 11;:

Authors: Jones GR, Lyons M, Plevris N, Jenkinson PW, Bisset C, Burgess C, Din S, Fulforth J, Henderson P, Ho GT, Kirkwood K, Noble C, Shand AG, Wilson DC, Arnott ID, Lees CW

Abstract
OBJECTIVE: IBD prevalence is estimated to be rising, but no detailed, recent UK data are available. The last reported prevalence estimate in the UK was 0.40% in 2003. We aimed to establish the current, and project future, prevalence in Lothian, Scotland.
DESIGN: We conducted an all-age multiparameter search strategy using inpatient IBD international classification of disease (ICD-10) coding (K50/51)(1997-2018), IBD pathology coding (1990-2018), primary and secondary care prescribing data (2009-2018) and a paediatric registry, (1997-2018) to identify 'possible' IBD cases up to 31/08/2018. Diagnoses were manually confirmed through electronic health record review as per Lennard-Jones/Porto criteria. Autoregressive integrated moving average (ARIMA) regression was applied to forecast prevalence to 01/08/2028.
RESULTS: In total, 24 601 possible IBD cases were identified of which 10 499 were true positives. The point prevalence for IBD in Lothian on 31/08/2018 was 784/100 000 (UC 432/100 000, Crohn's disease 284/100 000 and IBD unclassified (IBDU) 68/100 000). Capture-recapture methods identified an additional 427 'missed' cases (95% CI 383 to 477) resulting in a 'true' prevalence of 832/100 000 (95% CI 827 to 837).Prevalence increased by 4.3% per year between 2008 and 2018 (95% CI +3.7 to +4.9%, p<0.0001). ARIMA modelling projected a point prevalence on 01/08/2028 of 1.02% (95% CI 0.97% to 1.07%) that will affect an estimated 1.53% (95% CI 1.37% to 1.69%) of those >80 years of age.
CONCLUSIONS: We report a rigorously validated IBD cohort with all-age point prevalence on 31/08/2018 of 1 in 125, one of the highest worldwide.

PMID: 31300515 [PubMed - as supplied by publisher]

Slowed gastric emptying and improved oral glucose tolerance produced by a nanomolar-potency inhibitor of calcium-activated chloride channel TMEM16A.

Recent PubMed Articles on Gut Motility -

Slowed gastric emptying and improved oral glucose tolerance produced by a nanomolar-potency inhibitor of calcium-activated chloride channel TMEM16A.

FASEB J. 2019 Jul 12;:fj201900858R

Authors: Cil O, Anderson MO, Yen R, Kelleher B, Huynh TL, Seo Y, Nilsen SP, Turner JR, Verkman AS

Abstract
Interstitial cells of Cajal, which express the calcium-activated chloride channel transmembrane member 16A (TMEM16A), are an important determinant of gastrointestinal (GI) motility. We previously identified the acylaminocycloalkylthiophene class of TMEM16A inhibitors, which, following medicinal chemistry, gave analog 2-bromodifluoroacetylamino-5,6,7,8-tetrahydro-4H-cyclohepta[b]thiophene-3-carboxylic acid o-tolylamide (TMinh-23) with 30 nM half-maximal inhibitory concentration. Here, we tested the efficacy of TMinh-23 for inhibition of GI motility in mice. In isolated murine gastric antrum, TMinh-23 strongly inhibited spontaneous and carbachol-stimulated rhythmic contractions. Pharmacokinetic analysis showed predicted therapeutic concentrations of TMinh-23 for at least 4 h following a single oral or intraperitoneal dose at 10 mg/kg. Gastric emptying, as assessed following an oral bolus of phenol red or independently by [99mTc]-diethylenetriamine pentaacetic acid scintigraphy, was reduced by TMinh-23 by ∼60% at 20 min. Interestingly, there was little effect of TMinh-23 on baseline whole-gut transit time or time to diarrhea induced by castor oil. Consequent to the delay in gastric emptying, TMinh-23 administration significantly reduced the elevation in blood sugar in mice following an oral but not intraperitoneal glucose load. These results provide pharmacological evidence for involvement of TMEM16A in gastric emptying and suggest the utility of TMEM16A inhibition in disorders of accelerated gastric emptying, such as dumping syndrome, and potentially for improving glucose tolerance in diabetes mellitus/metabolic syndrome and enhancing satiety in obesity.-Cil, O., Anderson, M. O., Yen, R., Kelleher, B., Huynh, T. L., Seo, Y., Nilsen, S. P., Turner, J. R., Verkman, A. S. Slowed gastric emptying and improved oral glucose tolerance produced by a nanomolar-potency inhibitor of calcium-activated chloride channel TMEM16A.

PMID: 31299174 [PubMed - as supplied by publisher]

First translational consensus on terminology and definitions of colonic motility in animals and humans studied by manometric and other techniques.

Recent PubMed Articles on Gut Motility -

First translational consensus on terminology and definitions of colonic motility in animals and humans studied by manometric and other techniques.

Nat Rev Gastroenterol Hepatol. 2019 Jul 11;:

Authors: Corsetti M, Costa M, Bassotti G, Bharucha AE, Borrelli O, Dinning P, Di Lorenzo C, Huizinga JD, Jimenez M, Rao S, Spiller R, Spencer NJ, Lentle R, Pannemans J, Thys A, Benninga M, Tack J

Abstract
Alterations in colonic motility are implicated in the pathophysiology of bowel disorders, but high-resolution manometry of human colonic motor function has revealed that our knowledge of normal motor patterns is limited. Furthermore, various terminologies and definitions have been used to describe colonic motor patterns in children, adults and animals. An example is the distinction between the high-amplitude propagating contractions in humans and giant contractions in animals. Harmonized terminology and definitions are required that are applicable to the study of colonic motility performed by basic scientists and clinicians, as well as adult and paediatric gastroenterologists. As clinical studies increasingly require adequate animal models to develop and test new therapies, there is a need for rational use of terminology to describe those motor patterns that are equivalent between animals and humans. This Consensus Statement provides the first harmonized interpretation of commonly used terminology to describe colonic motor function and delineates possible similarities between motor patterns observed in animal models and humans in vitro (ex vivo) and in vivo. The consolidated terminology can be an impetus for new research that will considerably improve our understanding of colonic motor function and will facilitate the development and testing of new therapies for colonic motility disorders.

PMID: 31296967 [PubMed - as supplied by publisher]

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Klin Lab Diagn. 2018;63(1):44-50

Authors: Gurina OP, Stepanova AA, Dementieva EA, Blinov AE, Varlamova ON, Blinov GA

Abstract
The purpose of study is to establish features of autoimmune reaction of children with Crohn's disease. The sampling included 62 patients aged from 2 to 17 years with diagnosis of Crohn's disease. The evaluation was carried out concerning concentration in blood serum of immunoglobulins IgA, IgM, IgG, IgЕ, antibodies to Saccharomyces cerevisiae (ASCA) classes IgA, IgG и IgЕ, antibodies to Candida albicans classes IgA, IgM, IgG и IgЕ, anti-neutrophilic cytoplasmic antibodies (ANCA) to myeloperoxidase (MPO), to proteinase 3 (PR3), anti-nuclear antibodies (ANA), antibodies to DNAds, DNAss (to double-helical and single-stranded DNA), antibodies to antigens of small and large intestines, pancreas, circulating immune complexes. The hyperimmunoglobulinemia was diagnosed in 47 (75.8%) out of 62 patients with Crohn's disease. The increased level of IgM in blood was detected in 29 patients (46.8%). The hyperimmunoglobulinemia У was established in 19 (30.6%) out of 62 children. The hypoimmunoglobulinemia was detected in 22 (35.5%) of patients and in 17 (77.3%) out of them the disimmunoglobulinemia type IV (isolated decreasing of concentration of IgA). The evaluation of rate of occurrence of specifc antibodies in blood serum demonstrated that in patients most frequently was detected presence of specifc IgE to Saccharomyces cerevisiae (70.9%). The increased level of ASCA (IgA, IgG) was detected in 22 (35.5%) patients. The concentration of antibodies to DNAds, DNAss in blood exceeded standard value in 4.8% and 16.1% patients correspondingly. The increased level of circulating immune complex was established in 20 (32.3%) patients. The concentration of ANA corresponded to standard values in all 62 (100%) patients. The evaluation of results of correlation analysis established a strong positive correlation of concentration in blood of antibodies to antigens of small and large intestines; average positive correlation of level of antibodies to antigens of small intestine and IgM, ANCA PR3, ASCA IgE, antibodies to Candida albicans classes IgM, IgG, IgE, antibodies to antigens of pancreas; average degree of positive correlation between concentration of antibodies to antigens of large intestine and IgA, IgM, circulating immune complex, ANCA PR3, DNAss, ASCA IgE, antibodies to antigens of pancreas; strong positive correlation between concentrations of IgA to Candida albicans and ANA. The detection of auto-to antibodies Saccharomyces cerevisiae, Candida albicans, ANCA, antigens of small and large intestines, pancreas and expressed degree of correlation of many indices of autoimmune reaction indicate to intensity of immune pathological process under Crohn's disease. Under Crohn's disease, the formation of antibodies to ASCA is a prognostically unfavorable sign. The immune diagnostic under Crohn's disease is necessary for evaluating severity of course of disease, differential diagnostic, establishment of prognosis and selection of individual immune correcting therapy.

PMID: 30550091 [PubMed - indexed for MEDLINE]

Liberalized Versus Strict Cow's Milk Elimination for the Treatment of Children with Eosinophilic Esophagitis.

Recent Articles on Eosinophilic Oesophagitis (External) -

Liberalized Versus Strict Cow's Milk Elimination for the Treatment of Children with Eosinophilic Esophagitis.

J Can Assoc Gastroenterol. 2019 May;2(2):81-85

Authors: Teoh T, Mill C, Chan E, Zimmer P, Avinashi V

Abstract
Objectives: Cow's milk is a commonly implicated trigger in eosinophilic esophagitis (EoE). Exclusive cow's milk avoidance has been reported previously, but the degree of elimination required for remission is unclear. Strict food avoidance may confer a risk of developing immunoglobulin E (IgE)-mediated allergy. The goal of this study was to evaluate the effectiveness of cow's milk elimination (CME) in children with EoE and compare responses of strict and liberalized CME diets.
Methods: Children (≤16 years) diagnosed with EoE who were treated with exclusive CME diets were evaluated clinically and histologically. Strict diets eliminated all milk products, including 'may-contain' and baked milk goods. Liberalized diets eliminated obvious sources including milk, cheese, yogurt, cream-based products but permitted foods with traces of milk and baked goods.
Results: Cow's milk elimination induced histological remission of <15 eosinophils per high-powered field in 18 of 31 children (58%) and complete remission in 23%. Overall, 77% had decreased eosinophils with this single intervention. Symptoms were improved in 90% of patients, regardless of histologic response. A liberalized (n=7) CME diet was associated with a nonsignificantly lower response compared with strict (n=24) elimination (29% versus 67%, P=0.099). Eight responders to strict elimination were transitioned to a liberalized diet; 63% maintained remission.
Conclusion: Cow's milk elimination induced clinicopathological remission in a majority of patients with EoE, supporting its use as a first-line intervention. Liberalized CME allows dietary freedom and may prevent subsequent development of anaphylactic milk allergy but may be inferior to strict CME for improving EoE.

PMID: 31294369 [PubMed]

Patient Decision-Making in Severe Inflammatory Bowel Disease: The Need for Improved Communication of Treatment Options and Preferences.

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Patient Decision-Making in Severe Inflammatory Bowel Disease: The Need for Improved Communication of Treatment Options and Preferences.

Colorectal Dis. 2019 Jul 11;:

Authors: Lai C, Sceats L, Qiu W, Park KT, Morris AM, Kin C

Abstract
AIM: Patients with inflammatory bowel disease and their physicians must navigate ever-increasing options for treatment. The aim of this study was to elucidate the key drivers of treatment decision-making in inflammatory bowel disease.
METHODS: We conducted qualitative semi-structured in-person interviews of 20 adult patients undergoing treatment for inflammatory bowel disease at an academic medical centre who either recently initiated biologic therapy or underwent an operation or surgical evaluation. Interviews were audio-recorded, transcribed verbatim, iteratively coded, and discussed to consensus by five researchers. We used thematic analysis to explore factors influencing decision-making.
RESULTS: Four major themes emerged as key drivers of treatment decision-making: perceived clinical state and disease severity, the patient-physician relationship, knowledge, attitudes, and beliefs about treatment options, and social isolation and stigma. Patients described experiencing a clinical turning point as the impetus for proceeding with a previously undesired treatment such as infusion medication or surgery. Patients reported delays in care or diagnosis, inadequate communication with their physicians, and lack of control over their disease management. Patients often stated that they considered surgery to be the treatment of last resort, which further compounded the complexity of making treatment decisions.
CONCLUSION: Patients described multiple barriers to making informed and collaborative decisions about treatment, especially when considering surgical options. Our study reveals a need for more comprehensive communication between the patient and their physician about the range of medical and surgical treatment options. We recommend a patient-centred approach toward the decision-making process that accounts for patient decision-making preferences, causes of social stress, and clinical status. This article is protected by copyright. All rights reserved.

PMID: 31295766 [PubMed - as supplied by publisher]

Childhood growth and risk of inflammatory bowel disease: a population-based study of 317,030 children.

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Childhood growth and risk of inflammatory bowel disease: a population-based study of 317,030 children.

Scand J Gastroenterol. 2019 Jul 11;:1-6

Authors: Mendall M, Jensen CB, Ängquist LH, Baker JL, Jess T

Abstract
Background: Growth in childhood is associated with later development of autoimmune diseases and cancer, but the impact of growth on risk of inflammatory bowel disease (IBD) remains unknown. We conducted a population-based cohort study to examine whether birth weight, childhood height, or changes in height associated with later risk of IBD. Methods: Our cohort consisted of 317,030 children from the Copenhagen School Health Records Register (born 1930-1989) with height repeatedly measured from age 7 to 13 and with data on birth weight on a subset. Through linkage to the Danish National Patients Register, cases of IBD were identified. Cox proportional hazard regression was used to examine associations between measures of childhood growth and risk of IBD. Results: During more than 9 million years of follow-up, 1612 individuals were diagnosed with Crohn's disease (CD) and 2,640 with ulcerative colitis (UC). Birth weight and childhood heights were not associated with subsequent risk of CD or UC (HRs close to 1.00). Childhood growth from 7 to 10 years (CD: HR, 1.00; 95% CI, 0.85-1.18; UC: HR, 0.92; 95% CI, 0.81-1.05) and 10 to 13 years (CD: HR, 1.02; 95% CI, 0.89-1.17; UC: HR, 0.95; 0.85-1.05) did not associate with risk of IBD either. Conclusion: In this large population-based cohort study, birth weight and childhood growth did not influence risk of IBD, which contrasts with observations in other chronic diseases. Thereby, the study also suggests that pre-clinical effects of adult IBD are not measurable in childhood and that childhood risk factors for IBD do not influence growth.

PMID: 31294613 [PubMed - as supplied by publisher]

The Impact of Inflammatory Bowel Disease in Canada 2018: IBD Research Landscape in Canada.

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The Impact of Inflammatory Bowel Disease in Canada 2018: IBD Research Landscape in Canada.

J Can Assoc Gastroenterol. 2019 Feb;2(Suppl 1):S81-S91

Authors: Rose KL, Sherman PM, Cooke-Lauder J, Mawani M, Benchimol EI, Kaplan GG, Bernstein CN, Bitton A, Murthy SK, Nguyen GC, Lee K

Abstract
Background: Health research in Canada is funded by government, health charities, foundations and industry. We investigated levels of IBD research funding and the scientific impact of this research in Canada between 2013 and 2017.
Methods: An analysis of global and Canadian funding in IBD research was conducted using the Canadian Institutes of Health Research (CIHR) Funded Research Database and UberResearch's Dimensions platform. Examples of priority-driven and investigator-initiated IBD research in Canada are provided. Bibliometric analysis was used to assess the quality of IBD research output in Canada.
Results: Total funding for IBD research Canada between 2013 and 2017 was over $119 million Canadian dollars (CAD), with CIHR, the largest funder, contributing almost $66 million CAD, and Crohn's and Colitis Canada, investing more than $32 million CAD. This ranks Canada fourth internationally. A comparative analysis indicates that publications by Canadian IBD researchers have a greater impact than other Canadian and international comparators. When productivity and impact in IBD research are combined, Canada is among the top three in the world.
Conclusions: Investment in IBD research in Canada has resulted in the development of a strong collaborative group of researchers producing impactful, world-class research. On all measures of academic productivity and influence, Canada ranks in the top two or three internationally. The challenges ahead are to continue to fund innovative IBD research and grow the next generation of IBD researchers while moving research findings into changes in health policy and practice in order to benefit affected patients and their families-and ultimately, to find the cause(s) and identify the cure(s).

PMID: 31294388 [PubMed]

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