Introduction Anxiety and depression are common in patients with celiac disease (CD), and many psychosocial explanations have been considered. However, as the gut-brain axis is becoming increasingly understood, biological mechanisms have been proposed, including vitamin or mineral deficiencies and gut inflammation. Aim To investigate associations between anxiety/depression and symptom severity, vitamin status, and gut inflammation in untreated adult patients presenting with a serologic indication of celiac disease. Methods The Hospital Anxiety and Depression Scale (HADS), Celiac Symptom Index (CSI), and Perceived Stress Scale (PSS) questionnaires were administered to 17 patients over a 14-month period. Duodenal biopsies were obtained to determine histological Marsh scores. Iron, B12, folate, vitamin D, and thyroid function tests were reviewed. Results HADS-Anxiety (HADS-A) scores correlated with symptom severity (rs = 0.62, P = 0.008), but not with any hematological investigations or degree of intestinal inflammation. No patients scored highly for depression. Iron deficiency was the most common deficiency observed (n= 6). Greater symptomatology was associated with female sex (females versus males: average CSI scores, 32.1 versus 23.6; t17 = 2.1, P < 0.05), younger age at presentation (rs = -0.55, P = 0.02), and lower Marsh score (Marsh 0 versus Marsh 3C: mean scores, 36 versus 24.5; t5= 6.2, P= 0.009). Conclusions The anxiety experienced by patients with CD at presentation is likely a reactive form due to gastrointestinal symptoms rather than a biological process specific to CD. Older patients tend to present less symptomatically, highlighting the need for screening of at-risk individuals. The degree of villous atrophy does not correlate well with clinical presentation. Highly symptomatic patients should be screened for anxiety at presentation.

Studies of inflammatory bowel disease (IBD) have been inconclusive in relating microbiota with distribution of inflammation. We report microbiota, host transcriptomics, epigenomics and genetics from matched inflamed and non-inflamed colonic mucosa [50 Crohn’s disease (CD); 80 ulcerative colitis (UC); 31 controls]. Changes in community-wide and within-patient microbiota are linked with inflammation, but we find no evidence for a distinct microbial diagnostic signature, probably due to heterogeneous host-microbe interactions, and show only marginal microbiota associations with habitual diet. Epithelial DNA methylation improves disease classification and is associated with both inflammation and microbiota composition. Microbiota sub-groups are driven by dominant Enterbacteriaceae and Bacteroides species, representative strains of which are pro-inflammatory in vitro, are also associated with immune-related epigenetic markers. In conclusion, inflamed and non-inflamed colonic segments in both CD and UC differ in microbiota composition and epigenetic profiles.

Background H. pylori eradication rates for 7 day triple therapy regimens have decreased in many countries in recent years. Recent European guidelines recommend that standard triple therapy should not be used where local H. pylori resistance rates are greater than 15%. Aim Aim of study was to compare H. pylori eradication rates of one week, metronidazole vs Chlarithromycin based, triple therapy regimens in a south of Ireland patient cohort. Method From January 2015 to September 2016 undergoing upper GI endoscopy by two gastroenterologists at the Bon Secours Hospital Cork had H. pylori status determined by CLO test (BioHIT). All Clo positive patients received one of two seven day H. pylori treatment regimens; PPI, Amoxycillin, Clarithromycin (PAC) or PPI, Amoxycillin, Metronidazole (PAM). All treated patients were offered urea breath test (Diabact UBT)3- 4 months following treatment. Results Of 2595 patients having upper endosocpy 188 (7.2%) had positive CLO tests.45% (106/188) were females and mean age 56 (17 to 84 years).Of the 188 Clo positive patients,118 (63%) received PAC treatment and 70 (37%) received PAM treatment. Of the 118 PAC patients 83 (69%) attended for UBT and 24 (29%) were positive. Of the 70 patients treated with PAM 50 (71%) returned for UBT and 14 (28%) were positive. Conclusions In a patient cohort with relatively low H.pylori infection rates, one week based Clarithromycin and Metronidazole based triple therapy regimens achieved equivalent eradication of H.pylori (71% PAC,72% PAM). H. pylori eradication rates are somewhat higher than recently reported in Ireland, they are well short of current European guidelines and add further weight to the recommendation that one week triple therapy regimen should not be used in this country for first line H. pylori eradication.

Acute pancreatitis remains one of the most feared complications from endoscopic retrograde cholangiopancreatography (ERCP). Evidence in high‐risk cases suggests that a combination of Non steroidal anti inflammatory drugs (NSAID) and selective pancreatic stenting reduces the risk of post ERCP pancreatitis (PEP). However, few studies have investigated whether this is beneficial for normal risk ERCP.

Introduction Lupus like syndrome is a rarely reported adverse event for Anti TNF therapies (1) We noted a significant number of adverse events in particular drug induced SLE like syndrome (DILE) amongst our IBD patients receiving infliximab. Aims/Background The aim of this study was to quantify the real life prevalence of significant side effects and in particular lupus like syndrome to infliximab therapy. Method We reviewed retrospectively notes of all patients receiving infliximab therapy between Sep 2009 and Sep 2012 in GI unit. Results 327 no of infusions was given to 39 patients (16 Crohns /23 UC, M:F ratio 21:18) over study period. 24/37 (64.8%) patients stopped therapy in that period after a median of 4(1–12) infusions. 30.4% (7/23) patients stopped therapy in setting of clinical remission. 17.4% ( 4/23) patients stopped therapy because of treatment failure. (11/37 (29.7%) patients stopped treatment because of significant side effects. (3/37 8.1%) experienced acute infusion reaction, 1/37 (2.7%) MS. 5/37 (13.5%) patients manifested lupus like syndrome, 2/37 (5.4%) hilar adenopathy on CXR with strongly pos. ANA and antidsDNA. Older age at diagnosis (47 vs. 32) yrs. predicted increased risk of developing lupus like syndrome (p<0.05) as did history of previous azathioprine intolerance (100 vs. 43) % (p<0.05). Conclusion We report a higher than previously reported prevalence of DILE with anti-TNF therapy in an Irish cohort of IBD patients. Future studies are required to determine if this represents a cluster or predicts a real life higher prevalence in Irish population.

Introduction Best practise guidelines recommend that all patients starting Anti-TNF therapies should be pre-screened and vaccinated to reduce risk of opportunistic infections (ECCO guidelines 2009) and should be counselled re potential risks and benefits of treatments. Aims/Background To review documentation of anti-TNF therapy information provision and compliance with ECCO guidelines in prevention of opportunistic infections. Method We reviewed retrospectively the notes of all patients receiving infliximab therapy between Sep 2009 and Sep 2012 in BSH GI unit, Cork. Results 327 no of infusions was given to 39 patients (16 crohns/23 UC, M:F ratio 21:18) over study period. Discussion re treatment risks was clearly documented in 32/37(86%) patients, in 84% cases by IBD specialist nurse. Screening for opportunistic infections was incomplete. TB screening was undertaken in 100% (37/37) of cases but HIV testing was not routinely undertaken. 65%(24/37) patients had Hep B immunity status assessed but none were referred for vaccination programme. Varicella immunity was checked in 46% (17/37) patients, 2/17 (11.8%) patients non-immune! New tick-box proforma designed. Conclusion Rolling out of new guidelines which encorporate new practise is challenging and difficult to coordinate. In an effort to standardise approach we have designed a tick box proforma to use as part of our initial assessment of IBD patients. Our aim is to screen all patients at point of diagnosis of illness rather than at point of prescribing therapy so that vaccination can be coordinated when necessary in anticipation of requirement of therapies. Further studies will be required to look at success of this measure.

Introduction Best practise guidelines recommend that all patients starting Anti-TNF therapies should be pre-screened and vaccinated to reduce risk of opportunistic infections (ECCO guidelines 2009) and should be counselled re potential risks and benefits of treatments. Aims/Background To review documentation of anti-TNF therapy information provision and compliance with ECCO guidelines in prevention of opportunistic infections. Method We reviewed retrospectively the notes of all patients receiving infliximab therapy between Sep 2009 and Sep 2012 in BSH GI unit, Cork. Results 327 no of infusions was given to 39 patients (16 crohns/23 UC, M:F ratio 21:18) over study period. Discussion re treatment risks was clearly documented in 32/37(86%) patients, in 84% cases by IBD specialist nurse. Screening for opportunistic infections was incomplete. TB screening was undertaken in 100% (37/37) of cases but HIV testing was not routinely undertaken. 65%(24/37) patients had Hep B immunity status assessed but none were referred for vaccination programme. Varicella immunity was checked in 46% (17/37) patients, 2/17 (11.8%) patients non-immune! New tick-box proforma designed. Conclusion Rolling out of new guidelines which encorporate new practise is challenging and difficult to coordinate. In an effort to standardise approach we have designed a tick box proforma to use as part of our initial assessment of IBD patients. Our aim is to screen all patients at point of diagnosis of illness rather than at point of prescribing therapy so that vaccination can be coordinated when necessary in anticipation of requirement of therapies. Further studies will be required to look at success of this measure.

Introduction Best practise guidelines recommend that all patients starting Anti-TNF therapies should be pre-screened and vaccinated to reduce risk of opportunistic infections (ECCO guidelines 2009) and should be counselled re potential risks and benefits of treatments. Aims/Background To review documentation of anti-TNF therapy information provision and compliance with ECCO guidelines in prevention of opportunistic infections. Method We reviewed retrospectively the notes of all patients receiving infliximab therapy between Sep 2009 and Sep 2012 in BSH GI unit, Cork. Results 327 no of infusions was given to 39 patients (16 crohns/23 UC, M:F ratio 21:18) over study period. Discussion re treatment risks was clearly documented in 32/37(86%) patients, in 84% cases by IBD specialist nurse. Screening for opportunistic infections was incomplete. TB screening was undertaken in 100% (37/37) of cases but HIV testing was not routinely undertaken. 65%(24/37) patients had Hep B immunity status assessed but none were referred for vaccination programme. Varicella immunity was checked in 46% (17/37) patients, 2/17 (11.8%) patients non-immune! New tick-box proforma designed. Conclusion Rolling out of new guidelines which encorporate new practise is challenging and difficult to coordinate. In an effort to standardise approach we have designed a tick box proforma to use as part of our initial assessment of IBD patients. Our aim is to screen all patients at point of diagnosis of illness rather than at point of prescribing therapy so that vaccination can be coordinated when necessary in anticipation of requirement of therapies. Further studies will be required to look at success of this measure.

Proton pump inhibitors (PPIs) are drugs which irreversibly inhibit proton pump (H+/K+ ATPase) function and are the most potent gastric acid-suppressing agents in clinical use. There is now a substantial body of evidence showing improved efficacy of PPIs over the histamine H 2 receptor antagonists and other drugs in acid-related disorders. Omeprazole 20 mg/day, lansoprazole 30 mg/day, pantoprazole 40 mg/day or rabeprazole 20 mg/day for 2 to 4 weeks are more effective than standard doses of H 2 -receptor antagonists in healing duodenal and gastric ulcers. Patients with gastric ulcers should receive standard doses of PPIs as for duodenal ulcers but for a longer time period (4 to 8 weeks). There is no conclusive evidence to support the use of a particular PPI over another for either duodenal or gastric ulcer healing. For Helicobacter pylori- positive duodenal ulceration, a combination of a PPI and 2 antibacterialswill eradicate H. pylori in over 90% of cases and significantly reduce ulcer recurrence. Patients with H. pylori- positive gastric ulcers should be managed similarly. PPIs also have efficacy advantages over ranitidine and misoprostol and are better tolerated than misoprostol in patients taking nonsteroidal anti-inflammatory drugs (NSAIDs). In endoscopically proven gastro-oesophageal reflux disease, standard daily doses of the PPIs are more effective than H 2 -receptor antagonists for healing, and patients should receive a 4 to 8 week course of treatment. For severe reflux, with ulceration and/or stricture formation, a higher dose regimen (omeprazole 40mg, lansoprazole 60mg, pantoprazole 80mg or rabeprazole 40mg daily) appears to yield better healing rates. There is little evidence that PPIs lead to resolution of Barrett's oesophagus or a reduction of subsequent adenocarcinoma development, but PPIs are indicated in healing of any associated ulceration. In Zollinger-Ellison syndrome, PPIs have become the treatment of choice for the management of gastric acid hypersecretion.

AIM:To study the mechanisms by which Campylobacter jejuni (C. jejuni) causes inflammation and diarrhea. In particular, direct interactions with intestinal epithelial cells and effects on barrier function are poorly under-stood.METHODS:To model the initial pathogenic effects of C. jejuni on intestinal epithelium, polarized human colonic HCA-7 monolayers were grown on permeabilized filters and infected apically with clinical isolates of C. jejuni. Integrity of the monolayer was monitored by changes in monolayer resistance, release of lactate dehydrogenase, mannitol fluxes and electron microscopy. Invasion of HCA-7 cells was assessed by a modified gentamicin protection assay, translocation by counting colony forming units in the basal chamber, stimulation of mediator release by immunoassays and secretory responses in monolayers stimulated by bradykinin in an Ussing chamber.RESULTS:All strains translocated across monolayers but only a minority invaded HCA-7 cells. Strains that invaded HCA-7 cells destroyed monolayer resistance over 6 h, accompanied by increased release of lactate dehydrogenase, a four-fold increase in permeability to [(3)H] mannitol, and ultrastructural disruption of tight junctions, with rounding and lifting of cells off the filter membrane. Synthesis of interleukin (IL)-8 and prostaglandin E(2) was increased with strains that invaded the monolayer but not with those that did not.CONCLUSION:These data demonstrate two distinct effects of C. jejuni on colonic epithelial cells and provide an informative model for further investigation of initial host cell responses to C. jejuni.

Over 400 000 cases of tuberculosis existed in Europe in 2002, 1% of which were intestinal tuberculosis. With population migrations on the increase, physicians may have to face an increase in intestinal tuberculosis. One of the attributes of intestinal tuberculosis is its ability to present in nonspecific ways and to mimic other disorders, in particular inflammatory bowel disease. We present a case series of intestinal tuberculosis presenting as inflammatory bowel disease and referred for management to a specialized clinic in inflammatory bowel disease, followed by a discussion of the difficulties encountered with this condition. We highlight the consequences that misdiagnosis can have, in an era where population demographics are changing in Europe and where immunomodulators and biological agents have the potential to do more harm than good.

AIMS:Selective cyclooxygenase (COX)-2 inhibitors have recently been implicated as enhancing risk of myocardial infarction (MI). Nonselective nonsteroidal anti-inflammatory drugs (NSAIDs) are also effective COX-2 inhibitors, so we investigated the hypothesis that they too increase risk of MI. METHODS:We conducted a case-control study with direct structured interview of cases and controls. Cases were all subjects (N = 205) with a first nonfatal MI who had no previously recognized cardiovascular disease. Community controls (N = 258) were randomly selected from the same practice as the index case. Hospital controls (N = 205) were those admitted at the same time as index cases for nonmyocardial conditions not influenced by NSAID use. The effects of aspirin, NSAIDs and previously recognized influences on MI were investigated by unconditional logistic regression analysis. RESULTS:NSAID use was associated with an increase risk of MI with an odds ratio of 1.77 (1.03, 3.03) vs. community controls and 2.61 (1.38, 4.95) vs. hospital controls. These values were 5.00 (1.18, 21.28) and 7.66 (0.87, 67.48), respectively, in aspirin users. Results were similar when naproxen was grouped with aspirin. Odds ratios for smoking and for use of antidiabetic medication were 3.91 (2.52, 6.04) and 3.92 (1.25, 12,33), respectively, vs. community controls. CONCLUSIONS:Like selective COX-2 inhibitors, non-selective NSAIDs [corrected] are associated with an increased risk of MI. The extent to which this reflects interference with aspirin warrants further investigation.

Ulcerative colitis (UC) and Crohn’s disease (CD), collectively termed inflammatory bowel disease (IBD), are chronic spontaneously relapsing enteropathies of unknown aetiology. Pharmacotherapy for IBD has essentially been unchanged for over twenty years, with therapy based around 5-aminosalicylic acid (5-ASA) preparations, corticosteroids, antibiotics and immunosuppression. Much of the controversy surrounding optimal use of these drugs in IBD arises as a consequence of methodological deficiencies in many of the early trials combined with the difficulty in consistent patient selection due to the heterogeneous nature of both UC and CD. More recently, well-designed clinical trials have attempted to provide an ‘evidence based’ approach to managing IBD which, in time, will allow optimisation of current therapies and accurate evaluation of novel agents. Over the past two decades, improved research methodology has considerably increased our molecular understanding of the aetiopathogenesis of IBD which has ultimately lead to the development of specific mediator directed or ‘designer’ drug therapy for IBD. This review evaluates the literature on current IBD therapy, summarises the important recent studies which have made an impact on clinical practice, and examines the risks and benefits of the novel agents which are currently under investigation in clinical trials of IBD therapy.

Background : The role of immunosuppressive therapy in ulcerative colitis remains controversial. There is little information available on how frequently immunosuppressives are used, the circumstances, dose and duration of use and perceived benefit. Methods : A postal survey was sent to consultant gastroenterologist members of the British Society of Gastroenterology. Results : Questionnaires were returned by 81% of the 496 UK consultants approached. Azathioprine use was frequent, with 93% reporting previous use and 86% use within the past year. Although 95% usually prescribed a ≤ 2 mg/kg dose, only 39% were prepared to prescribe higher doses. There was marked variation in duration of use, with 46% using azathioprine for < 2 years and 17% continuing it for 4 years or longer. Consultants with more experience of azathioprine in ulcerative colitis used it at higher maintenance doses for longer periods, and in patients with less extensive disease. Cyclosporin use was reported by 47% of those caring for ulcerative colitis patients, with 36% having used it at least once in the past year. However, 65% of users estimated that fewer than 50% of patients subsequently avoided colectomy. On stopping cyclosporin only 21% always introduced an alternative immunosuppressive, while 23% never did so. Potentially serious side‐effects attributable to azathioprine and cyclosporin were reported by 36% and 45% of users of each drug, respectively. Conclusions : This survey reveals considerable variation in the amount and pattern of immunosuppressive use in ulcerative colitis, with serious side‐effects commonly seen. There is a pressing need for further randomized controlled trials to provide reliable evidence as to how immunosuppressive therapy should be used in ulcerative colitis.

Proton pump inhibitors (PPIs) are drugs which irreversibly inhibit proton pump (H+/K+ ATPase) function and are the most potent gastric acid-suppressing agents in clinical use. There is now a substantial body of evidence showing improved efficacy of PPIs over the histamine H-2 receptor antagonists and other drugs in acid-related disorders, Omeprazole 20 mg/day, lansoprazole 30 mg/day, pantoprazole 40 mg/day or rabeprazole 20 mg/day for 2 to 4 weeks are more effective than standard doses of H-2-receptor antagonists in healing duodenal and gastric ulcers. Patients with gastric ulcers should receive standard doses of PPIs as for duodenal ulcers but for a longer time period (4 to 8 weeks). There is no conclusive evidence to support the use of a particular PPI over another for either duodenal or gastric ulcer healing.For Helicobacter pylori-positive duodenal ulceration, a combination of a PPI and 2 antibacterials will eradicate H. pylori in over 90% of cases and significantly reduce ulcer recurrence. Patients with H. pylori-positive gastric ulcers should be managed similarly. PPIs also have efficacy advantages over ranitidine and misoprostol and are better tolerated than misoprostol in patients taking nonsteroidal anti-inflammatory drugs (NSAIDs).In endoscopically proven gastro-oesophageal reflux disease, standard daily doses of the PPIs are more effective than H-2-receptor antagonists for healing, and patients should receive a 4 to 8 week course of treatment. For severe reflux, with ulceration and/or stricture formation, a higher dose regimen (omeprazole 40 mg, lansoprazole 60 mg, pantoprazole 80 mg or rabeprazole 40 mg daily) appears to yield better healing rates. There is little evidence that PPIs lead to resolution of Barrett's oesophagus or a reduction of subsequent adenocarcinoma development, but PPIs are indicated in healing of any associated ulceration. In Zollinger-Ellison syndrome, PPIs have become the treatment of choice for the management of gastric acid hypersecretion.

Proton pump inhibitors (PPIs) are drugs which irreversibly inhibit proton pump (H+/K+ ATPase) function and are the most potent gastric acid-suppressing agents in clinical use. There is now a substantial body of evidence showing improved efficacy of PPIs over the histamine H2 receptor antagonists and other drugs in acid-related disorders.

Ulcerative colitis and Crohn's disease, collectively known as inflammatory bowel disease (IBD), are chronic, spontaneously relapsing disorders of unknown cause. These diseases appear to be immunologically mediated and have genetic and environmental influences. Although the cause of these diseases remains obscure, the pathogenesis of chronic intestinal inflammation is becoming clearer, due to improved animal models of enterocolitis and important advances in immunological techniques. Traditional therapy for IBD, although helping to induce and maintain disease remission, does little to alter the underlying fundamental disease process. New IBD therapy has not developed significantly over the past twenty years and includes 5-aminosalicylic acid preparations, corticosteroids and immunomodulatory agents, such as azathioprine, 6-mercaptopurine and methotrexate. There is, therefore, a need for new, specific disease-modifying therapy and the development of such therapy has been hastened by a greater understanding of the pathophysiology of IBD. This review examines the most recent novel therapies for IBD, with specific emphasis on immunomodulatory and novel anti-inflammatory therapies. Recent clinical trials are reviewed, and the potential advances and clinical impact that these novel agents may provide are discussed.