IBD on PubMed

CD99 refers to the activity of inflammatory bowel disease.

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CD99 refers to the activity of inflammatory bowel disease.

Scand J Gastroenterol. 2016 Nov 21;:1-6

Authors: Zhou G, Yang W, Yu L, Yu T, Liu Z

Abstract
BACKGROUND: Inflammatory bowel disease (IBD), composed of Crohn's disease (CD) and ulcerative colitis (UC), is an inflammatory autoimmune disease. CD99 has been reported to participate in migration of leukocytes and T cell activation. However, the roles of CD99 in IBD are obscure.
MATERIALS AND METHODS: CD99 expression was examined in peripheral blood mononuclear cells (PBMCs) and inflamed mucosa from IBD patients by qRT-PCR. Serum TNF-α and IL-17A levels were detected by ELISA. Correlations of CD99 expression with TNF-α, IL-17A, Crohn's disease activity index (CDAI), simple endoscopic score for CD (SES-CD), Mayo index, and Truelove grading were performed by Pearson's correlation.
RESULTS: CD99 expression was increased in PBMCs and inflamed mucosa from active CD and UC patients, and CD99 expression was also increased in the inflamed mucosa compared with unaffected control from the same patients. Serum TNF-α and IL-17A levels were increased in active CD or UC patients, and positively correlated with CD99 expression in PBMCs (CD: r = .402, p = .009; r = .350, p = .025. UC: r = .289, p = .028; r = .322, p = .014). Moreover, CD99 expression in inflamed mucosa was correlated with CDAI, SES-CD, Mayo index, and Truelove grading (r = .410, p = .012; r = .341, p = .005; r = .366, p = .002; r = .312, p = .011).
CONCLUSION: CD99 expression is increased in patients with active IBD, and positively correlated with disease activity. Therefore, CD99 expression can be used as an index to evaluate the activity of IBD.

PMID: 27866429 [PubMed - as supplied by publisher]

Elevated systemic interleukin-7 in patients with colorectal cancer and individuals at high risk of cancer: association with lymph node involvement and tumor location in the right colon.

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Elevated systemic interleukin-7 in patients with colorectal cancer and individuals at high risk of cancer: association with lymph node involvement and tumor location in the right colon.

Cancer Immunol Immunother. 2016 Nov 19;

Authors: Krzystek-Korpacka M, Zawadzki M, Neubauer K, Bednarz-Misa I, Górska S, Wiśniewski J, Witkiewicz W, Gamian A

Abstract
Interleukin (IL)-7 is a cytokine essential for protective immunity, and it is considered as a promising agent for cancer immunotherapy. Recent studies, however, appear to associate IL-7 with aggressiveness of solid tumors. The IL-7 has been less studied in colorectal cancer (CRC) and conditions associated with increased risk of CRC development. To explore IL-7 status in bowel diseases, it was measured immunofluorometrically in 431 individuals (110 with CRC) by using Luminex platform. A level of IL-7 in CRC patients was significantly higher than in controls, did not differ from those with adenomas, but was lower than in both active and inactive inflammatory bowel disease (IBD) cases. In CRC, IL-7 was higher in patients with lymph node and distant metastases and with tumors located in right colon. In adenomas, IL-7 elevation was associated exclusively with villous growth pattern, while in IBD, circulating IL-7 reflected clinical activity of Crohn's disease and ulcerative colitis. Systemic TNFα, IL-10, and PDGF-BB were independent predictors of circulating IL-7. In summary, our study is the first to demonstrate IL-7 elevation in CRC in association with metastatic disease and tumor location. Both associations should be considered when designing IL-7-based immunotherapies for CRC. Further studies on IL-7 functionality in CRC are necessary.

PMID: 27866242 [PubMed - as supplied by publisher]

Evaluation of Serum Trace Element Levels and Superoxide Dismutase Activity in Patients with Inflammatory Bowel Disease: Translating Basic Research into Clinical Application.

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Evaluation of Serum Trace Element Levels and Superoxide Dismutase Activity in Patients with Inflammatory Bowel Disease: Translating Basic Research into Clinical Application.

Biol Trace Elem Res. 2016 Nov 18;

Authors: Mohammadi E, Qujeq D, Taheri H, Hajian-Tilaki K

Abstract
The relationship of minerals and trace elements with inflammatory bowel disease (IBD) is complex. Alterations in their metabolism can be induced by the diseases and their complications. To study the role of trace elements in IBD patients' serum zinc and copper and their related enzymes, including superoxide dismutase (SOD), activity were measured in patients with IBD patients as well as in healthy subjects. In addition, the correlation between serum trace element levels, albumin, total protein, urea level, copper/zinc ratio, and disease activity (DA) was determined in these subjects. Serum samples were obtained from 35 patients (19 ulcerative colitis (UC) and 16 Crohn's disease (CD)) in the active phase of the disease and 30 healthy control subjects. Serum levels of zinc, copper, SOD activity, albumin, total protein, and urea were measured. The results were compared between the two groups using independent Student's t test in statistical analysis. Serum levels of zinc, SOD activity, albumin, and total protein were significantly lower (P < 0.05) in patients than controls, while serum urea level was significantly higher in patients compared to controls. Copper concentrations did not differ between patients with IBD (mean ± SD, 58.8 ± 20.7 μg/d) and controls (55.57 ± 12.6 μg/d). Decreased levels of zinc and SOD activity are associated with increased inflammatory processes indicating inappropriate antioxidant system in patients with IBD. Additionally, lower levels of albumin and total protein with higher level of urea reflect metabolic problems in liver system.

PMID: 27864666 [PubMed - as supplied by publisher]

Erratum to: Vedolizumab Therapy Is Associated with an Improvement in Sleep Quality and Mood in Inflammatory Bowel Diseases.

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Erratum to: Vedolizumab Therapy Is Associated with an Improvement in Sleep Quality and Mood in Inflammatory Bowel Diseases.

Dig Dis Sci. 2016 Nov 18;

Authors: Stevens BW, Borren NZ, Velonias G, Conway G, Cleland T, Andrews E, Khalili H, Garber JJ, Xavier RJ, Yajnik V, Ananthakrishnan AN

PMID: 27864657 [PubMed - as supplied by publisher]

Endovascular Treatment of Common Iliac Artery Aneurysms With an Iliac Branch Device: Multicenter Experience of 140 Patients.

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Endovascular Treatment of Common Iliac Artery Aneurysms With an Iliac Branch Device: Multicenter Experience of 140 Patients.

J Endovasc Ther. 2016 Nov 17;:

Authors: Jongsma H, Bekken JA, Bekkers WJ, Zeebregts CJ, van Herwaarden J, Hoksbergen A, Cuypers P, de Vries JP, Verhagen HJ, Fioole B

Abstract
PURPOSE: To evaluate the efficacy, feasibility, and long-term outcomes of the Zenith ZBIS iliac branch device (IBD) to preserve internal iliac artery (IIA) perfusion in a large Dutch multicenter cohort.
METHODS: Between September 2004 and August 2015, 140 patients (mean age 70.9±7.4 years; 130 men) with 162 IBD implantations were identified in 7 vascular centers. The indication for IBD implantation was an abdominal aortic aneurysm >55 mm with a concomitant common iliac artery (CIA) aneurysm >20 mm (n=40), a CIA aneurysm with a diameter >30 mm (n=89), or revision of a type Ib endoleak after endovascular aneurysm repair (n=11).
RESULTS: Technical success (aneurysm exclusion, no type I or III endoleak, and a patent IIA) was obtained in 157 (96.9%) of 162 IBD implantations. Six (4.3%) patients developed major complications; 2 (1.4%) died. Mean follow-up was 26.6±24.1 months, during which 17 (12.1%) IBD-associated secondary interventions were performed. Including technical failures and intentional IIA embolizations, 15 (9.3%) IIA branch occlusions were identified; buttock claudication developed in 6 of these patients. The freedom from secondary intervention estimate was 75.9% (95% confidence interval 59.7 to 86.3) at 5 years.
CONCLUSION: CIA aneurysms can be treated safely and effectively by IBDs with preservation of antegrade flow to the IIA. Secondary interventions are indicated in >10% of patients during follow-up but can be performed endovascularly in most.

PMID: 27864456 [PubMed - as supplied by publisher]

Acute colitis chronically alters immune infiltration mechanisms and sensory neuro-immune interactions.

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Acute colitis chronically alters immune infiltration mechanisms and sensory neuro-immune interactions.

Brain Behav Immun. 2016 Nov 15;:

Authors: Campaniello MA, Mavrangelos C, Eade S, Harrington AM, Ashley Blackshaw L, Brierley SM, Smid SD, Hughes PA

Abstract
[OBJECTIVE]: Little is understood regarding how disease progression alters immune and sensory nerve function in colitis. We investigated how acute colitis chronically alters immune recruitment and the impact this has on re-activated colitis. To understand the impact of disease progress on sensory systems we investigated the mechanisms underlying altered colonic neuro-immune interactions after acute colitis. [DESIGN]: Inflammation was compared in mouse models of Health, Acute tri-nitrobenzenesulphonic acid (TNBS) colitis, Remission and Reactivated colitis. Cytokine concentrations were compared by ELISA in-situ and in explanted colon tissue. Colonic infiltration by CD11b/F4-80 macrophage, CD4 THELPER (TH) and CD8 TCYTOTOXIC (TC) and α4β7 expression on mesenteric lymph node (MLN) TH and TC was determined by flow cytometry. Cytokine and effector receptor mRNA expression was determined on colo-rectal afferent neurons and the mechanisms underlying cytokinergic effects on high-threshold colo-rectal afferent function were investigated using electrophysiology. [RESULTS]: Colonic damage, MPO activity, macrophage infiltration, IL-1β and IL-6 concentrations were lower in Reactivated compared to Acute colitis. TH infiltration and α4β7 expression on TH MLN was increased in Remission but not Acute colitis. IFN-γ concentrations, TH infiltration and α4β7 expression on TH and TC MLN increased in Reactivated compared to Acute colitis. Reactivated explants secreted more IL-1β and IL-6 than Acute explants. IL-6 and TNF-α inhibited colo-rectal afferent mechanosensitivity in Remission mice via a BKCa dependent mechanism. [CONCLUSIONS]: Acute colitis persistently alters immune responses and afferent nerve signalling pathways to successive episodes of colitis. These findings highlight the complexity of viscero-sensory neuro-immune interactions in painful remitting and relapsing diseases.

PMID: 27864046 [PubMed - as supplied by publisher]

Anti-TNF therapy is able to stabilize bowel damage progression in patients with Crohn's disease. A study performed using the Lémann Index.

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Anti-TNF therapy is able to stabilize bowel damage progression in patients with Crohn's disease. A study performed using the Lémann Index.

Dig Liver Dis. 2016 Nov 2;:

Authors: Bodini G, Giannini EG, De Maria C, Dulbecco P, Furnari M, Marabotto E, Savarino V, Savarino E

Abstract
AIMS: The Lémann Index (LI) was developed to assess the cumulative structural damage of the intestinal tract in patients with Crohn's Disease (CD) independently of clinical and biochemical activity. Recently, the goal of CD focused on obtaining mucosal healing and deep remission rather than simple symptom control. These new therapeutic aims emphasize the need to prevent progression of bowel damage. In this study we aimed to evaluate the influence of different treatments on structural damage progression, assessed by means of LI in a series of CD patients consistently treated with various drugs.
METHODS: The LI was calculated at inclusion and at the end of follow-up in 104 CD patients subdivided according to treatments received: biological drugs (n=40, 38.4%), azathioprine (n=19, 18.3%), and mesalazine (n=45, 43.3%).
RESULTS: The median follow-up was 29 months, with no difference among groups. During follow-up, the median LI was stable in the biological group [from 6.3 (range, 0.6-37.3) to 6.4 (range, 0.6-37.6), P=0.543], whereas it significantly increased from 4.1 (range, 0.6-30) to 8.3 (range, 0.6-31.8) in the azathioprine group (P=0.0006), and from 2.4 (range, 0.6-25.8) to 4.1 (range, 0.6-28.8) in the mesalazine group (P<0.0001). Also during follow-up the LI increased significantly (P=0.004) in the azathioprine (68.4%) and mesalazine (60.0%) groups as compared with the biological therapy group (30.0%).
CONCLUSIONS: In CD patients the LI tends to increase over time, although the use of biological drugs rather than azathioprine or mesalazine seems to be able to reduce the progressive bowel damage.

PMID: 27864028 [PubMed - as supplied by publisher]

The Multibiome: The Intestinal Ecosystem's Influence on Immune Homeostasis, Health, and Disease.

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The Multibiome: The Intestinal Ecosystem's Influence on Immune Homeostasis, Health, and Disease.

EBioMedicine. 2016 Oct 6;:

Authors: Filyk HA, Osborne LC

Abstract
Mammalian evolution has occurred in the presence of mutualistic, commensal, and pathogenic micro- and macro-organisms for millennia. The presence of these organisms during mammalian evolution has allowed for intimate crosstalk between these colonizing species and the host immune system. In this review, we introduce the concept of the 'multibiome' to holistically refer to the biodiverse collection of bacteria, viruses, fungi and multicellular helminthic worms colonizing the mammalian intestine. Furthermore, we discuss new insights into multibiome-host interactions in the context of host-protective immunity and immune-mediated diseases, including inflammatory bowel disease and multiple sclerosis. Finally, we provide reasons to account for the multibiome in experimental design, analysis and in therapeutic applications.

PMID: 27863931 [PubMed - as supplied by publisher]

Single nucleotide polymorphisms in major histocompatibility class II haplotypes are associated with potential resistance to inflammatory bowel disease in German shepherd dogs.

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Single nucleotide polymorphisms in major histocompatibility class II haplotypes are associated with potential resistance to inflammatory bowel disease in German shepherd dogs.

Vet Immunol Immunopathol. 2016 Dec;182:101-105

Authors: Peiravan A, Allenspach K, Boag AM, Soutter F, Holder A, Catchpole B, Kennedy LJ, Werling D, Procoli F

Abstract
German shepherd dogs (GSD) in the UK are at increased risk of developing the Inflammatory Bowel Disaese (IBD). IBD is believed to be a multifactorial immune mediated disease affecting genetically predisposed dogs. The aim of the current study was to investigate whether susceptibility to IBD in GSD is associated with the major histocompatibility complex (MHC) class II locus (Dog Leukocyte Antigen, DLA). Sequence-based genotyping of the three polymorphic DLA genes DLA-DRB1, -DQA1 and -DQB1 was performed in 56 GSDs affected by IBD and in 50 breed-matched controls without any history of gastrointestinal signs. The haplotype DLA-DRB1*015:02-DQA1*006:01-DQB1*023:01 was found to be present only in the control population and was associated with a reduced risk of IBD (P<0.001). In contrast, the haplotype DLA-DRB1*015:01-DQA1*006:01-DQB1*003:01 was associated with IBD (Odds ratio [OR]=1.93, confidence interval [CI]=1.02-3.67, P=0.05). This study has identified an association between DLA-type and canine IBD, supporting the immunogenetic aetiology and immunopathogenesis of this disease.

PMID: 27863539 [PubMed - in process]

Preventive effects of Goji berry on dextran-sulfate-sodium-induced colitis in mice.

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Preventive effects of Goji berry on dextran-sulfate-sodium-induced colitis in mice.

J Nutr Biochem. 2016 Oct 27;40:70-76

Authors: Kang Y, Xue Y, Du M, Zhu MJ

Abstract
Goji berry (Lycium barbarum) exerts immune modulation and suppresses inflammation in vitro and in vivo. We hypothesized that Goji berry had beneficial effects on dextran sulfate sodium (DSS)-induced colitis in C57BL/6 mice through suppressing inflammation. Six-week-old male C57BL/6 mice were supplemented with a standard AIN-93G diet with or without 1% (w/w) Goji berry for 4 weeks. Then, colitis was induced by supplementing 3% DSS in drinking water for 7 days, followed by 7 days of remission period to mimic ulcerative colitis symptoms. Goji berry supplementation ameliorated DSS-induced body weight loss, diminished diarrhea and gross bleeding, and resulted in a significantly decreased disease activity index, as well as DSS-associated colon shortening. Moreover, 30% mortality rate caused by DSS-induced colitis was avoided because of Goji berry supplementation. Histologically, Goji berry ameliorated colonic edema, mucosal damage and neutrophil infiltration into colonic intestinal tissue in response to DSS challenge, which was associated with decreased expression of chemokine (C-X-C motif) ligand 1 and monocyte chemoattractant protein-1, as well as inflammatory mediators interleukin-6 and cyclooxygenase-2. In conclusion, Goji supplementation confers protective effects against DSS-induced colitis, which is associated with decreased neutrophil infiltration and suppressed inflammation. Thus, dietary Goji is likely beneficial to inflammatory bowel disease patients as a complementary therapeutic strategy.

PMID: 27863347 [PubMed - as supplied by publisher]

Study on the physicochemical properties and anti-inflammatory effects of paeonol in rats with TNBS-induced ulcerative colitis.

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Study on the physicochemical properties and anti-inflammatory effects of paeonol in rats with TNBS-induced ulcerative colitis.

Int Immunopharmacol. 2016 Nov 15;42:32-38

Authors: Zong SY, Pu YQ, Xu BL, Zhang T, Wang B

Abstract
Paeonol, an active component from Paeonia suffruticosa Andr., has a variety of biological activities, such as vascular endothelial cell protection, anti-oxidation, and anti-inflammation. The aim of this study was to investigate the basic physicochemical properties of paeonol, including solubility, oil-water partition coefficient, and permeability. Then evaluated the anti-inflammatory effects of paeonol were evaluated on 2,4,6-trinitrobenzenesulfonic acid-induced ulcerative colitis in rats. The rats were divided randomly into 6 groups, namely, normal, model, paeonol-treated (100, 200, and 400mg/kg), and positive. Each group had 10 rats. Inhibition effects were evaluated by the disease activity index (DAI), colon weight/length ratio, as well as macroscopical and histological evaluations. Serum interleukin (IL)-17, IL-6 and transforming growth factor beta 1 (TGF-β1) levels were determined by enzyme-linked immunosorbent assay. The solubility and oil-water partition coefficient of paeonol in different phosphate buffer solutions were 284.06-598.23 and 461.97-981.17μg/mL, respectively. The effective passive permeability value Pe was 23.49×10(-6)cm/s. In terms of anti-inflammatory results, compared with the model group, treatment with 200 and 400mg/kg doses of paeonol had significantly decreased DAI, colon weight/length ratio, and macroscopic and histopathological scores. Furthermore, the serum levels of IL-17 and IL-6 were significantly reduced, whereas the TGF-β1 level was increased in the two paeonol-treated groups (medium- and high-dose group). Therefore, paeonol had poor water solubility, but oral absorption was good. In addition, paeonol had therapeutic effects on ulcerative colitis, and the therapeutic efficacy was dose dependent. The results presented in this study provide evidence for the development of a novel therapeutic agent in the treatment of UC. However, whether this agent could have therapeutic benefit or adverse effects in human IBD remains to be fully explored.

PMID: 27863299 [PubMed - as supplied by publisher]

De novo inflammatory bowel disease after pediatric kidney or liver transplant.

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De novo inflammatory bowel disease after pediatric kidney or liver transplant.

Pediatr Transplant. 2016 Nov 11;:

Authors: Fernandes MA, Braun HJ, Evason K, Rhee S, Perito ER

Abstract
A subset of children who receive a liver and/or kidney transplant develop de novo inflammatory bowel disease-like chronic intestinal inflammation, not explained by infection or medications, following transplant. We have conducted a single-center, retrospective case series describing the unique clinical and histologic features of this IBD-like chronic intestinal inflammation following solid organ transplant. At our center, nine of 327 kidney or liver recipients developed de novo IBD following transplant (six liver, two kidney, one liver-kidney). Most children presented with prolonged hematochezia and diarrhea and were treated with aminosalicylates. At time of diagnosis, five were not currently using mycophenolate mofetil for transplant immunosuppression. Histologic and endoscopic findings at IBD diagnosis included inflammation, ulcerations, granulomas, and chronic colitis. Since diagnosis, no patients have required surgical intervention, or escalation to biologic therapy, nor developed stricturing or perianal disease. In this case series, de novo post-transplant IBD developed in 4% of pediatric liver and/or kidney recipients; however, it often does not fit the classic patterns of Crohn's disease or ulcerative colitis.

PMID: 27862714 [PubMed - as supplied by publisher]

Lymphogranuloma venereum with only proximal rectal involvement mimicking inflammatory bowel disease: a potential diagnostic pitfall.

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Lymphogranuloma venereum with only proximal rectal involvement mimicking inflammatory bowel disease: a potential diagnostic pitfall.

J Eur Acad Dermatol Venereol. 2016 Nov 15;:

Authors: Rob F, Kašpírková J, Jůzlová K, Pešta M, Hercogová J

Abstract
Lymphogranuloma venereum (LGV) is a sexually transmitted infection (STI) caused by the invasive serovars L1, L2 and L3 of Chlamydia trachomatis (C. trachomatis). [1] The incidence of LGV is rising in many Western countries. [2] The most common symptoms of LGV are proctitis and inguinal lymphadenopathy. LGV mimicking inflammatory bowel disease (IBD) is not a rare condition and has already been described in several reports. [3,4] LGV can affect even more proximal parts of the bowel. [5] Diagnosis of LGV is usually done by positive NAAT for C. trachomatis with subsequent specifying of LGV serovars. [1] This article is protected by copyright. All rights reserved.

PMID: 27862349 [PubMed - as supplied by publisher]

CDX2 expression induced by leukocytapheresis might be associated with mucosal healing in ulcerative colitis.

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CDX2 expression induced by leukocytapheresis might be associated with mucosal healing in ulcerative colitis.

J Gastroenterol Hepatol. 2016 Nov 11;:

Authors: Tsuchiya K, Hayashi R, Fukushima K, Hibiya S, Horita N, Negi M, Itoh E, Akashi T, Eishi Y, Motoya S, Takeuchi Y, Kunisaki R, Fukunaga K, Nakamura S, Yoshimura N, Takazoe M, Iizuka B, Suzuki Y, Nagahori M, Watanabe M

Abstract
BACKGROUND AND AIMS: Ulcerative colitis (UC) is a chronic inflammatory disease of the colon with an intractable, recurrent course. Although the goal of UC therapy has recently been to target mucosal healing, the molecular mechanism of mucosal healing remains unknown. In this study, we aimed to elucidate the molecular dynamics related to the proliferation and differentiation of intestinal epithelial cells (IECs) during cytapheresis therapy in a short duration.
METHODS: Endoscopy was performed in 26 patients with UC in multicentre hospitals, and biopsy specimens were collected from the rectum before and within two weeks after leukocytapheresis (LCAP). The expression of representative proteins in IECs and pathological findings were compared before and after LCAP.
RESULTS: The expression of caudal type homeobox 2 (CDX2) and a hairy-related protein 1 (HES1) markedly increased after LCAP. Patients with endoscopic improvement after LCAP showed the expression of CDX2 before LCAP. Moreover, the number of goblet cells significantly increased after LCAP. Patients without endoscopic improvement after LCAP did not show the expression of CDX2 before LCAP. However, the expression of CDX2 markedly increased after LCAP.
CONCLUSION: This study suggests that cytapheresis might induce CDX2 expression without affecting the cell proliferation; thus, resulting in mucosal healing with goblet cell restoration.

PMID: 27862316 [PubMed - as supplied by publisher]

Irritable bowel syndrome and active inflammatory bowel disease diagnosed by faecal gas analysis.

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Irritable bowel syndrome and active inflammatory bowel disease diagnosed by faecal gas analysis.

Aliment Pharmacol Ther. 2016 Nov 10;:

Authors: Aggio RB, White P, Jayasena H, de Lacy Costello B, Ratcliffe NM, Probert CS

Abstract
BACKGROUND: Inflammatory bowel disease and irritable bowel syndrome may present in a similar manner. Measuring faecal calprotectin concentration is often recommended to rule out inflammatory bowel disease, however, there are no tests to positively diagnose irritable bowel syndrome and invasive tests are still used to rule out other pathologies.
AIM: To investigate a platform technology for diagnosing inflammatory bowel disease and irritable bowel syndrome based on faecal gas.
METHODS: The platform technology is composed of a gas chromatography column coupled to a metal oxide gas sensor (OdoReader) and a computer algorithm. The OdoReader separates the volatile compounds from faecal gas and the computer algorithm identifies resistance patterns associated with specific medical conditions and builds classification models. This platform was applied to faecal samples from 152 patients: 33 patients with active inflammatory bowel disease; 50 patients with inactive inflammatory bowel disease; 28 patients with irritable bowel syndrome and 41 healthy donors (Control).
RESULTS: The platform classified samples with accuracies from 75% to 100% using rigorous validation schemes: namely leave-one-out cross-validation, 10-fold cross-validation, double cross-validation and their Monte Carlo variations. The most clinically important findings, after double cross-validation, were the accuracy of active Crohn's disease vs. irritable bowel syndrome (87%; CI 84-89%) and irritable bowel syndrome vs. controls (78%; CI 76-80%). These schemes provide an estimate of out-of-sample predictive accuracy for similar populations.
CONCLUSIONS: This is the first description of an investigation for the positive diagnosis of irritable bowel syndrome, and for diagnosing inflammatory bowel disease.

PMID: 27862117 [PubMed - as supplied by publisher]

Systematic review with meta-analysis: comparative efficacy of immunosuppressants and biologics for reducing hospitalisation and surgery in Crohn's disease and ulcerative colitis.

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Systematic review with meta-analysis: comparative efficacy of immunosuppressants and biologics for reducing hospitalisation and surgery in Crohn's disease and ulcerative colitis.

Aliment Pharmacol Ther. 2016 Nov 10;:

Authors: Mao EJ, Hazlewood GS, Kaplan GG, Peyrin-Biroulet L, Ananthakrishnan AN

Abstract
INTRODUCTION: Crohn's disease (CD) and ulcerative colitis (UC) have a progressive course leading to hospitalisation and surgery. The ability of existing therapies to alter disease course is not clearly defined.
AIM: To investigate the comparative efficacy of currently available inflammatory bowel disease (IBD) therapies to reduce hospitalisation and surgery.
METHODS: We conducted a systematic review in MEDLINE/PubMed for randomised controlled trials (RCT) published between January 1980 and May 2016 examining efficacy of biological or immunomodulator therapy in IBD. We performed direct comparisons of pooled proportions of hospitalisation and surgery. Pair-wise comparisons using a random-effects Bayesian network meta-analysis were performed to assess comparative efficacy of different treatments.
RESULTS: We identified seven randomised controlled trials (5 CD; 2 UC) comparing three biologics and one immunomodulator with placebo. In CD, anti-TNF biologics significantly reduced hospitalisation [Odds ratio (OR) 0.46, 95% confidence interval (CI) 0.36-0.60] and surgery (OR 0.23, 95% CI 0.13-0.42) compared to placebo. No statistically significant reduction was noted with azathioprine or vedolizumab. Azathioprine was inferior to both infliximab and adalimumab in preventing CD-related hospitalisation (>97.5% probability). Anti-TNF biologics significantly reduced hospitalisation (OR 0.48, 95% CI 0.29-0.80) and surgery (OR 0.67, 95% CI 0.46-0.97) in UC. There were no statistically significant differences in the pair-wise comparisons between active treatments.
CONCLUSIONS: In CD and UC, anti-TNF biologics are efficacious in reducing the odds of hospitalisation by half and surgery by 33-77%. Azathioprine and vedolizumab were not associated with a similar improvement, but robust conclusions may be limited due to paucity of RCTs.

PMID: 27862107 [PubMed - as supplied by publisher]

Addition of an immunomodulator can reverse antibody formation and loss of response in patients treated with adalimumab.

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Addition of an immunomodulator can reverse antibody formation and loss of response in patients treated with adalimumab.

Aliment Pharmacol Ther. 2016 Nov 16;:

Authors: Ungar B, Kopylov U, Engel T, Yavzori M, Fudim E, Picard O, Lang A, Williet N, Paul S, Chowers Y, Bar-Gil Shitrit A, Eliakim R, Ben-Horin S, Roblin X

Abstract
BACKGROUND: Anti-adalimumab antibodies (AAA) are associated with loss of clinical response (LOR). Addition of an immunomodulator has been shown to reverse immunogenicity and regain response with infliximab monotherapy. Similar data on adalimumab are lacking.
AIM: To study the impact of immunomodulator addition on the emergence of AAA and LOR among adalimumab therapy patients.
METHODS: The databases of three tertiary medical centres were reviewed to identify patients who developed AAA during adalimumab monotherapy with resultant LOR, and received an immunomodulator as a salvage combination therapy. All sera were prospectively analysed using previously described ELISA assays. Clinical response was determined using appropriate clinical scores. Elimination of AAA, designated as 'sero-reversal', elevation of drug levels and regained clinical response were the sought outcomes.
RESULTS: Twenty-three patients (21 Crohn's disease, and 2 ulcerative colitis) developed AAA with subsequent LOR and were thereafter prescribed an immunomodulator as salvage therapy (thiopurine n = 14, methotrexate n = 9). Eleven patients (48%) underwent sero-reversal with gradual elimination of AAA, increase in drug trough levels and restoration of clinical response (median time to sero-reversal 5 months). In 12 patients (52%), immunogenicity and loss of response could not be reversed. There was no difference between responders and nonresponders in the type of immunomodulators used or baseline clinical characteristics.
CONCLUSIONS: In almost half of inflammatory bowel disease patients developing anti-adalimumab antibodies and loss of response, established immunogenicity of adalimumab can be gradually reversed by the addition of immunomodulator therapy with restoration of a clinico-biological response. However, these observations need to be confirmed with larger studies.

PMID: 27862102 [PubMed - as supplied by publisher]

Sibship Analysis Based on Parental Genotype Reconstruction from Any Number of Reference Siblings.

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Sibship Analysis Based on Parental Genotype Reconstruction from Any Number of Reference Siblings.

J Forensic Sci. 2016 Nov 11;:

Authors: Huang J, Huang Y

Abstract
Previous analyses of alleged siblings have calculated the conditional probability of a test sibling's genotype given a reference sibling's genotype; however, more genetic information is available when two or more reference siblings are tested. Based on the root concept of identity by descent (IBD), we present a sibship method of parental genotype reconstruction (PGR) that can use any number of reference sibs. Nine PGR patterns, along with their respective IBD proportions of full-sibs and half-sibs, were identified and used to calculate joint sibship probabilities and likelihood ratio formulas. In addition, a correction PGR was developed for situations involving the same genotype repeating in the reference sibs. The method is simple and can be applied to any number of alleged full or half-siblings.

PMID: 27861876 [PubMed - as supplied by publisher]

Genetic Risk for Inflammatory Bowel Disease Is a Determinant of Crohn's Disease Development in Chronic Granulomatous Disease.

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Genetic Risk for Inflammatory Bowel Disease Is a Determinant of Crohn's Disease Development in Chronic Granulomatous Disease.

Inflamm Bowel Dis. 2016 Dec;22(12):2794-2801

Authors: Huang C, De Ravin SS, Paul AR, Heller T, Ho N, Wu Datta L, Zerbe CS, Marciano BE, Kuhns DB, Kader HA, Holland SM, Malech HL, Brant SR, NIDDK IBD Genetics Consortium,

Abstract
BACKGROUND: Approximately, one-third to one-half of children with chronic granulomatous disease (CGD) develop gastrointestinal inflammation characteristic of idiopathic inflammatory bowel disease (IBD), usually Crohn's disease. We hypothesized that the overall IBD genetic risk, determined by IBD genetic risk score (GRS), might in part determine IBD development in CGD.
METHODS: We reviewed medical records to establish IBD diagnoses in CGD subjects seen at NIAID. IBD risk single nucleotide polymorphism genotypes were determined using the Immunochip, and GRS were estimated by Mangrove.
RESULTS: Among 157 white patients with CGD, 55 were confirmed, 78 excluded, and 24 were uncertain for IBD. Two hundred one established, independent European IBD risk single nucleotide polymorphisms passed quality control. After sample quality control and removing non-IBD CGD patients with perianal disease, mean GRS for 40 unrelated patients with CGD-IBD was higher than 53 CGD non-IBD patients (in log2-scale 0.08 ± 1.62 versus -0.67 ± 1.64, P = 0.026) but lower than 239 IBD Genetics Consortium (IBDGC) young-onset Crohn's disease cases (0.76 ± 1.60, P = 0.025). GRS for non-IBD CGD was similar to 609 IBDGC controls (-0.69 ± 1.60, P = 0.95). Seven established IBD single nucleotide polymorphisms were nominally significant among CGD-IBD versus CGD non-IBD, including those near LACC1 (P = 0.005), CXCL14 (P = 0.007), and TNFSF15 (P = 0.016).
CONCLUSIONS: The weight of the common IBD risk alleles are significant determinants of IBD in CGD. However, IBD risk gene burden among CGD children with IBD is significantly lower than that in nonsyndromic pediatric Crohn's disease, congruent with the concept that defective superoxide production in CGD is also a major IBD risk factor. Individual IBD genes might interact with the CGD defect to cause IBD in CGD.

PMID: 27861181 [PubMed - in process]

Epithelial derived-matrix metalloproteinase (MMP9) exhibits a novel defensive role of tumor suppressor in colitis associated cancer by activating MMP9-Notch1-ARF-p53 axis.

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Epithelial derived-matrix metalloproteinase (MMP9) exhibits a novel defensive role of tumor suppressor in colitis associated cancer by activating MMP9-Notch1-ARF-p53 axis.

Oncotarget. 2016 Nov 16;:

Authors: Walter L, Pujada A, Bhatnagar N, Bialkowska AB, Yang VW, Laroui H, Garg P

Abstract
Colitis associated cancer (CAC) is chronic inflammation driven colon cancer, prevalent among individuals with Inflammatory Bowel Disease. Matrix-metalloproteinase (MMP9) is one of the essential regulators of extra cellular matrix components. We have shown that MMP9 is protective in CAC contrary to its inflammatory role in acute-colitis. Aim of our study is to identify the mechanism of the protective role of epithelial derived-MMP9 in CAC. We used homozygous transgenic mice constitutively-expressing MMP9 in colonic-epithelium (TgM9) and wild-type (WT) littermates for in vivo experiments. Stably-transfected HCT116 with/without MMP9, and mouse embryonic-fibroblasts (WT and MMP9-/-, MEFs) were used for in vitro experiments. TgM9 mice exhibited less tumor burden, increased apoptosis, and increased expressions of active-Notch1, p53, p21WAF1/Cip1, caspase-3 and cyclin E in CAC compared to WTs. These results were supported by MEFs data. HCT116-cells overexpressing MMP9 indicated decreased cell proliferation, S-phase cell-cycle arrest and less DNA damage compared to vector. MMP9-/- mice showed attenuation of MMP9 was directly associated with p19ARF. Our study identifies the tumor suppressor role of epithelial derived-MMP9 in CAC via novel mechanistic pathway "MMP9-Notch1-ARF-p53 axis" regulating apoptosis, cell-cycle arrest and DNA damage implying, that MMP9 expression might be a natural/biological way to suppress colonic ulceration due to chronic inflammation.

PMID: 27861153 [PubMed - as supplied by publisher]

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