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Background Sportspeople are more prone to binge drink than their peers. Aims We aimed to assess alcohol consumption, harms and behaviours in an elite Irish sporting population (Gaelic footballers and hurlers). Methods An anonymous web-based questionnaire (demographics, alcohol consumption, culture and related harms) was administered to all elite players. The AUDIT-C questionnaire (frequency, quantity of alcohol consumption and frequency of binge drinking) was used to assess for adverse alcohol use. Univariate and multivariate analyses assessed for predictors of adverse alcohol use. Results 717 players (mean age 24 years) were analysed. The majority of patients were male (75%), unmarried (93%) and had completed university (67%). 96% were current drinkers. Players consumed more alcohol during the off-season (median 20 versus 8 standard drinks in 28 days) compared to the elite season. Amongst current drinkers, 73% exhibit adverse alcohol use, 93% reported binge drinking and 65% an alcohol related harm in the past year. Most players would turn to family (36%) or friends (21%) for help. There were significant associations between monthly bingeing (OR 18.4), smoking (OR 3.3), generally drinking in public (OR 3.2), current gambling (OR 2.3), male gender (OR 2.1), an alcohol harm in the past year (OR 1.9) and adverse alcohol use. In contrast, co-habiting with a partner (OR 0.5) was protective. Conclusions Excess alcohol consumption, alcohol related harms and binge drinking are prevalent in an elite sporting population, particularly during the off-season. Specific strategies are required to reduce alcohol related harms, particularly amongst high-risk groups during the off-season.

This study reviews the safety and efficacy of treatment with vedolizumab for patients with inflammatory bowel disease across 9 Irish hospitals. It generates valuable and timely real-world data on treatment outcomes to add to the existing evidence base. Our population represents a refractory cohort with most patients previously exposed to at least one anti-TNFa agent and expressing an inflammatory phenotype. Results are reassuringly similar to larger international studies with additional insights into potential predictors of treatment response. This study further supports the safety and efficacy of vedolizumab in the treatment of inflammatory bowel disease. Key SummaryVedolizumab has growing real world data on its safety and efficacy in the treatment of IBD. Data on predictors of response are lacking. Studies such as VARSITY require new real-world data to help identify the place VDZ will occupy in the treatment algorithm for IBDThis study provides national Irish data on the safety and efficacy of VDZ in the treatment of IBD. It gives insight into various predictors of response for both UC and CD. It strengthens the available body of evidence on the use of VDZ and helps us determine its position on the treatment algorithm.

Background & Aim In the mid-1990s, a group of Rh negative women was diagnosed with hepatitis C virus (HCV) genotype 1b infection, following administration of contaminated anti-D immunoglobulin in 1977–79. We aimed to describe their disease history and estimate the effect of selected host and treatment factors on disease progression. Methods We conducted a cohort study on the women infected with HCV. Information was collected from records at seven HCV treatment centres on demographics, treatment and health outcomes up to the 31st December 2013. We calculated cumulative incidence, case fatality, and sub hazard ratios (SHR) for disease progression using competing risks regression. Results Six hundred and eighty-two patients were included in the study. Among the chronically infected patients (n=374), 35% completed interferon-based antiviral treatment; 42% of whom had a sustained virological response. At the end of 2013, 19%, 1.9%, and 4.9% of chronically infected patients had developed cirrhosis, hepatocellular carcinoma, and liver-related death, respectively, compared with 10%, 0.8%, and 2.4% at the end of 2008. At the end of 2013, 321 (86%) of the chronically infected patients remained alive, 247 (77%) of whom were still chronically infected. Factors associated with increased cirrhosis rates included high alcohol intake (aSHR=4.9 [2.5–9.5]) and diabetes mellitus (aSHR=5.0 [2.9–8.8]). Conclusions Development of liver-related outcomes accelerated with time, with the risk of cirrhosis, hepatocellular carcinoma, and liver-related death doubling in the last five years of follow-up, particularly in women with high alcohol consumption and diabetes mellitus. We recommend that patients with chronic HCV infection be advised of the additive harmful effect of alcohol, and that data be collected on this cohort after a further five years to analyse the effect of subsequent antiviral treatment during this rapidly evolving period in HCV treatment history. Lay summary In the mid-1990s, a group of women were diagnosed with chronic hepatitis C virus (HCV) infection following receipt of contaminated anti-D immunoglobulin between 1977 and 1979 in Ireland. Seventy-two (19%) developed cirrhosis and 18 had died from liver-related causes (5%) after 36years of infection. Disease progression accelerated in the last five years of follow-up, particularly in women with diabetes mellitus and high alcohol consumption. We recommend that patients with chronic HCV infection be advised of the additive harmful effect of high alcohol consumption.

We investigated the real-world effectiveness of interferon-free regimens for the treatment of patients with compensated cirrhosis infected with hepatitis C virus (HCV).Using the Irish national HCV treatment registry, the effectiveness and safety of interferon-free regimens for HCV-infected patients treated between April 2015 and August 2016, was determined.A SVR12 was achieved in 86% of subjects treated with sofosbuvir/ledipasvir ± ribavirin (SOF/LDV±RBV), 93% treated with paritaprevir, ombitasvir and ritonavir combined with dasabuvir ± ribavirin (3D±RBV) and 89% treated with sofosbuvir/daclatasvir ± ribavirin (SOF/DCV±RBV). The discontinuation rate was 5% and the on-treatment mortality rate was 1%.The availability of interferon-free regimens represents a significant breakthrough for the treatment of HCV infection. Treatments options, with high SVR12 rates, are now available for patients with compensated cirrhosis who were unsuitable for treatment with interferon-based regimens. Data obtained from studies conducted in real world practice provide robust information fundamental for input into future economic evaluations for agents used for the treatment of HCV infection.

Deregulation of the ubiquitin-proteasome pathway has been frequently observed in a number of malignancies. Using quantitative Western blotting of normal and matched tumour tissue, we here identified a significant increase in the 19S proteasome subunit Rpt4 in response to chemoradiation in locally advanced rectal cancer patients with unfavourable outcome. We therefore explored the potential of Rpt4 reduction as a therapeutic strategy in colorectal cancer (CRC). Utilizing siRNA to down regulate Rpt4 expression, we show that silencing of Rpt4 reduced proteasomal activity and induced endoplasmic reticulum stress. Gene silencing of Rpt4 also inhibited cell proliferation, reduced clonogenic survival and induced apoptosis in HCT-116 colon cancer cells. We next developed a cell penetrating peptide-based nanoparticle delivery system to achieve in vivo gene silencing of Rpt4. Administration of Rpt4 siRNA nanoparticles reduced tumour growth and improved survival in a HCT-116 colon cancer xenograft tumour model in vivo. Collectively, our data suggest that inhibition of Rpt4 represents a novel strategy for the treatment of CRC.

Golimumab (GLB) is an antitumour necrosis factor-α (anti-TNF) therapy that has shown efficacy as induction and maintenance therapy for ulcerative colitis (UC). We aimed to describe the outcome of GLB therapy for UC in a real-world clinical practice.Consecutive patients receiving GLB for UC in six Irish Academic Medical Centres were identified. The primary study endpoint was the 6-month corticosteroid-free remission rate. The secondary endpoints included the 3-month clinical response, time free of GLB discontinuation and adverse events.Seventy-two patients were identified [57% men; median (range) age of 41.4 years (20.3-76.8); disease duration 6.6 years (0-29.9); follow-up 8.7 months (0.4-39.2)]. Sixty-four percent of patients were anti-TNF naive. The 3-month clinical response and the 6-month corticosteroid-free remission rates were 55 and 39%, respectively. Forty-four percent of patients discontinued GLB during the follow-up, median (95% confidence interval) time to GLB discontinuation 18.7 months (9.2-28.1). A C-reactive protein more than 5 mg/l at baseline was associated with failure to achieve 6-month corticosteroid-free remission and a shorter time to GLB discontinuation, odds ratio 0.2 (0.1-0.7), P=0.008, and hazard ratio (95% confidence interval) 2.8 (1.3-5.7), P=0.007, respectively. Adverse events occurred in 7% of patients (n=5), all of which were minor and self-limiting.These real-world clinical data suggest that GLB is an effective and safe therapy for a UC cohort with significant previous anti-TNF exposure. An elevated baseline C-reactive protein, likely reflective of increased inflammatory burden, is associated with a reduced likelihood of a successful outcome of GLB therapy.

Introduction As finite healthcare resources come under pressure, the value of physician activity is assuming increasing importance. The value in healthcare can be defined as patient health outcomes achieved per monetary unit spent. Even though some attempts have been made to quantify the value of clinician activity, there is little in the medical literature describing the importance of endoscopists' activity. This study aimed to characterize the value of endoscopic retrograde cholangiopancreatography (ERCP) performance of five gastroenterologists. Patients and methods We carried out a retrospective-prospective cohort study using the databases of patients undergoing ERCP between September 2014 and March 2017. We collected data from 1070 patients who underwent ERCP comparing value among the ERCPists at index ERCP. Procedure value was calculated using the formula Q/(T/C), where Q is the quality of procedure, T is the duration of procedure and C is the adjusted for complexity level. Quality and complexity were derived on a 1-4 Likert scale on the basis of American Society for Gastrointestinal Endoscopy criteria; time was recorded (in min) from intubation to extubation. Endoscopist time calculated from procedure time was considered a surrogate marker of cost as individual components of procedure cost were not itemized. Results In total, 590 procedures were analysed: 465 retrospectively over 24 months and 125 prospectively over 6 months. There was a 32% variation in the value of endoscopist activity in a more substantial retrospective cohort, with an even more considerable 73% variation in a smaller prospective arm. Conclusion In an analysis of greater than 1000 ERCPs by a small cohort of experienced ERCPists, there was a wide variation in the value of endoscopist activity. Although the precision of estimating procedural costs needs further refinement, these findings show the ability to stratify ERCPists on the basis of the value their activity. As healthcare costs are scrutinized more closely, such value measurements are likely to become more relevant.

Dihydroxy bile acids, such as chenodeoxycholic acid (CDCA), are well known to promote colonic fluid and electrolyte secretion, thereby causing diarrhoea associated with bile acid malabsorption. However, CDCA is rapidly metabolised by colonic bacteria to ursodeoxycholic acid (UDCA), the effects of which on epithelial transport are poorly characterised. Here, we investigated the role of UDCA in the regulation of colonic epithelial secretion. Cl(-) secretion was measured across voltage-clamped monolayers of T84 cells and muscle-stripped sections of mouse or human colon. Cell surface biotinylation was used to assess abundance/surface expression of transport proteins. Acute (15 min) treatment of T84 cells with bilateral UDCA attenuated Cl(-) secretory responses to the Ca(2+) and cAMP-dependent secretagogues carbachol (CCh) and forskolin (FSK) to 14.0 ± 3.8 and 40.2 ± 7.4% of controls, respectively (n = 18, P < 0.001). Investigation of the molecular targets involved revealed that UDCA acts by inhibiting Na(+)/K(+)-ATPase activity and basolateral K(+) channel currents, without altering their cell surface expression. In contrast, intraperitoneal administration of UDCA (25 mg kg(-1)) to mice enhanced agonist-induced colonic secretory responses, an effect we hypothesised to be due to bacterial metabolism of UDCA to lithocholic acid (LCA). Accordingly, LCA (50-200 μm) enhanced agonist-induced secretory responses in vitro and a metabolically stable UDCA analogue, 6α-methyl-UDCA, exerted anti-secretory actions in vitro and in vivo. In conclusion, UDCA exerts direct anti-secretory actions on colonic epithelial cells and metabolically stable derivatives of the bile acid may offer a new approach for treating intestinal diseases associated with diarrhoea.

Increasing attention is being focused on reigning in escalating costs of healthcare, i.e. trying to 'bend the cost curve'. In gastroenterology (GI), inpatient hospital care represents a major component of overall costs. This study aimed to characterize the trend in cost of care for GI-related hospitalizations in recent years and to identify the most costly diagnostic groups.All hospital inpatients admitted between January 2008 and December 2009 with a primary diagnosis of one of the six most common GI-related Diagnosis Related Groups (DRGs) in this hospital system were identified; all DRGs contained at least 40 patients during the study period. Patient Level Costing (PLC) was used to express the total cost of hospital care for each patient; PLC comprised a weighted daily bed cost plus cost of all medical services provided (e.g., radiology, pathology tests) calculated according to an activity-based costing approach; cost of medications were excluded. All costs were discounted to 2009 values. Mean length of stay (LOS) was also calculated for each DRG.Over 2 years, 470 patients were admitted with one of the six most common GI DRGs. Mean cost of care increased from 2008 to 2009 for all six DRGs with the steepest increases seen in 'GI hemorrhage (non-complex)' (31 % increase) and 'Cirrhosis/Alcoholic hepatitis (non-complex)' (45 % increase). No differences in readmission rates were observed over time. There was a strong correlation between year-to-year change in costs and change in mean LOS, r = 0.93.The cost of GI-related inpatient care appears to be increasing in recent years with the steepest increases observed in non-complex GI hemorrhage and non-complex Cirrhosis/Alcoholic hepatitis. Efforts to control the increasing costs should focus on these diagnostic categories.

Apoptotic desensitization is a hallmark of cancer cells, but present knowledge of molecular systems controlling apoptosis has yet to provide significant prognostic insights. Here, we report findings from a systems study of the intrinsic pathway of apoptosis by BCL2 family proteins and clinical translation of its findings into a model with applications in colorectal cancer (CRC). By determining absolute protein quantifications in CRC cells and patient tumor samples, we found that BAK and BAX were expressed more highly than their antiapoptotic inhibitors. This counterintuitive finding suggested that sole inhibition of effector BAX and BAK could not be sufficient for systems stability in nonstressed cells. Assuming a model of direct effector activation by BH3-only proteins, we calculated that the amount of stress-induced BH3-only proteins required to activate mitochondrial apoptosis could predict individual death responses of CRC cells to 5-fluorouracil/oxaliplatin. Applying this model predictor to protein profiles in tumor and matched normal tissue samples from 26 patients with CRCs, we found that differences in protein quantities were sufficient to model the increased tumor sensitivity to chemotherapy compared with normal tissue. In addition, these differences were sufficient to differentiate clinical responders from nonresponders with high confidence. Applications of our model, termed DR_MOMP, were used to assess the impact of apoptosis-sensitizing drugs in lowering the necessary dose of state-of-the-art chemotherapy in individual patients. Together, our findings offer a ready clinical tool with the potential to tailor chemotherapy to individual patients. ispartof: Cancer Research vol:73 issue:2 pages:519-528 ispartof: location:United States status: published

We report the case of a 45-year-old haemodialysis patient who achieved a sustained virological response (SVR) following pegylated interferon therapy for hepatitis C virus (HCV) genotype 2 infection. He was subsequently cohorted with other HCV-infected dialysis patients and became re-infected with HCV genotype 3a. Epidemiological and molecular investigations identified a highly viraemic HCV genotype 3a-infected dialysis patient as the likely source of this infection. This critical incident informed a revision to local and national infection control policy regarding the dialysis management of patients who achieve an SVR following anti-viral treatment.

Objective To assess how interpretation of abnormalities at the oesophago-gastric junction (OGJ) when making a diagnosis of Barrett9s oesophagus (BO) varies between endoscopists and to examine the impact of the endoscopy experience on these decisions. Design/setting Members of the Irish Society of Gastroenterology who regularly perform gastroscopy were invited to participate in a web based image assessment study. Interventions Questions were posed to ascertain level of endoscopy experience, and participants were asked to indicate the presence or absence of BO in 12 endoscopic images of the OGJ. Outcome measures Primary outcome was overall level of agreement in responses and relationship to endoscopy experience. Results The responses of 65 clinicians regularly performing gastroscopy were analysed. In 3/12 images, showing typical long segment BO, there was a strong consensus on the endoscopic diagnosis (>95% agreement). However, agreement was fair to poor (κ for multiple raters, 0.31) on the presence or absence of short BO segments at endoscopy. Minimal differences were observed between experienced endoscopists (individuals with >10 years9 endoscopy experience) and less experienced counterparts in the threshold for BO diagnosis. Inter-endoscopist agreement overall was not significantly better within the more experienced group. Conclusion The study demonstrates low interobserver agreement in endoscopic diagnosis of (short segment) BO, even among experienced endoscopists. Given the costs associated with endoscopic surveillance of BO, prompt efforts to promote consensus diagnosis and improve agreement are required as an important quality improvement measure in this area.

Optimizing endoscopy efficiency is becoming increasingly important. This study profiled ERCP availability and assessed resource leveling as a strategy to enhance efficiency. All ERCPs performed at an academic teaching hospital between January 2007 and December 2008 were reviewed. Procedure timeliness (time between admission and ERCP) and demand were analyzed to assess resource utilization. Data were recorded for 393 ERCPs. Profiling identified an unequal distribution of waiting times from admission to procedure due to restricted ERCP availability. Use of resource leveling methodology demonstrated that a small increase in procedure availability (one additional half day per week) would significantly reduce the hospital stay of ERCP patients. Resource leveling can be applied to balance procedure provision with demand to cope with fluctuations in demand. The impact of resource leveling can be truly measured only by implementing these changes and prospectively studying the effect.

Proton pump inhibitors (PPIs) reduce the risk of upper gastrointestinal hemorrhage (UGIH) associated with the use of many medications.To examine how clinicians perceive such risk and whether PPI co-prescribing is based on an accurate assessment.Clinicians in a single teaching hospital were asked to estimate risk of UGIH and comment on PPI co-prescription in hypothetical patients. Records of 160 hospital in-patients (median age; 74 y) were then reviewed to examine PPI prescribing and risk factors for UGIH.In general, clinicians estimated UGIH risk accurately and reported low thresholds for PPI co-prescription. Prescribing records showed regular PPI use increased between admission and discharge of patients from 61/160 (38%) to 93/160 (58%). Ten percent had a prior history of peptic ulcer disease. Proton pump inhibitor prescription was significantly associated with the use of aspirin and clopidogrel. Half of the patients with multiple risk factors for UGIH on admission and almost a third at discharge were not co-prescribed a PPI.Clinicians generally estimate correctly the risk of UGIH and report a low threshold for prescribing gastro-protection. Despite this, prescribing practice does not consistently take account of relative risk of UGIH. Targeted PPI co-prescribing on the basis of risk factors would lead to more rational PPI use.

Neuroimmune agonists induce epithelial Cl−secretion through elevations in intracellular Ca2+or cAMP. Previously, we demonstrated that epidermal growth factor receptor (EGFR) transactivation and subsequent ERK MAPK activation limits secretory responses to Ca2+-dependent, but not cAMP-dependent, agonists. Although JNK MAPKs are also expressed in epithelial cells, their role in regulating transport function is unknown. Here, we investigated the potential role for JNK in regulating Cl−secretion in T84colonic epithelial cells. Western blot analysis revealed that a prototypical Ca2+-dependent secretagogue, carbachol (CCh; 100 μM), induced phosphorylation of both the 46-kDa and 54-kDa isoforms of JNK. This effect was mimicked by thapsigargin (TG), which specifically elevates intracellular Ca2+, but not by forskolin (FSK; 10 μM), which elevates cAMP. CCh-induced JNK phosphorylation was attenuated by the EGFR inhibitor, tyrphostin-AG1478 (1 μM). Pretreatment of voltage-clamped T84cells with SP600125 (2 μM), a specific JNK inhibitor, potentiated secretory responses to both CCh and TG but not to FSK. The effects of SP600125 on CCh-induced secretion were not additive with those of the ERK inhibitor, PD98059. Finally, in apically permeabilized T84cell monolayers, SP600125 potentiated CCh-induced K+conductances but not Na+/K+ATPase activity. These data demonstrate a novel role for JNK MAPK in regulating Ca2+but not cAMP-dependent epithelial Cl−secretion. JNK activation is mediated by EGFR transactivation and exerts its antisecretory effects through inhibition of basolateral K+channels. These data further our understanding of mechanisms regulating epithelial secretion and underscore the potential for exploitation of MAPK-dependent signaling in treatment of intestinal transport disorders.

The Bcl-2 homology 3-only protein Bid is an important mediator of death receptor-induced apoptosis. Recent reports and this study suggest that Bid may also mediate genotoxic drug-induced apoptosis of various human cancer cells. Here, we characterized the role of Bid and the mechanism of Bid activation during oxaliplatin-induced apoptosis of HeLa cervical cancer cells. Small hairpin RNA-mediated silencing of Bid protected HeLa cells against both death receptor- and oxaliplatin-induced apoptosis. Expression of a Bid mutant in which caspase-8 cleavage site was mutated (D59A) reactivated oxaliplatin-induced apoptosis in Bid-deficient cells but failed to reactivate death receptor-induced apoptosis, suggesting that caspase-8-mediated Bid cleavage did not contribute to oxaliplatin-induced apoptosis. Overexpression of bcl-2 or treatment with the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-dl-Asp-fluoromethylketone abolished caspase-2, -8, -9, and -3 activation as well as Bid cleavage in response to oxaliplatin, suggesting that Bid cleavage occurred downstream of mitochondrial permeabilization and was predominantly mediated by caspases. We also detected an early activation of calpains in response to oxaliplatin. Calpain inhibition reduced Bid cleavage, mitochondrial depolarization, and activation of caspase-9, -3, -2, and -8 in response to oxaliplatin. Further experiments, however, suggested that Bid cleavage by calpains was not a prerequisite for oxaliplatin-induced apoptosis: single-cell imaging experiments using a yellow fluorescent protein-Bid-cyan fluorescent protein probe demonstrated translocation of full-length Bid to mitochondria that was insensitive to calpain or caspase inhibition. Moreover, calpain inhibition showed a potent protective effect in Bid-silenced cells. In conclusion, our data suggest that calpains and Bid act in a cooperative, but mutually independent, manner to mediate oxaliplatin-induced apoptosis of HeLa cells.

Background: Cyclooxygenase-2 (COX-2) is over-expressed in colorectal cancer (CRC), rendering tumour cells resistant to apoptosis. Selective COX-2 inhibition is effective in CRC prevention, although having adverse cardiovascular effects, thus focus has shifted to downstream pathways. Methods: Microarray experiments identified genes regulated by COX-2 in HCA7 CRC cells. In vitro and in vivo regulation of DRAK2 (DAP kinase-related apoptosis-inducing kinase 2 or STK17β, an apoptosis-inducing kinase) by COX-2 was validated by qRT-PCR. Results: Inhibition of COX-2 induced apoptosis and enhanced DRAK2 expression in HCA7 cells (4.4-fold increase at 4 h by qRT-PCR, P=0.001), an effect prevented by co-administration of PGE2. DRAK2 levels were suppressed in a panel of human colorectal tumours (n=10) compared to normal mucosa, and showed inverse correlation with COX-2 expression (R=−0.68, R2=0.46, P=0.03). Administration of the selective COX-2 inhibitor rofecoxib to patients with CRC (n=5) induced DRAK2 expression in tumours (2.5-fold increase, P=0.01). In vitro silencing of DRAK2 by RNAi enhanced CRC cell survival following COX-2 inhibitor treatment. Conclusion: DRAK2 is a serine–threonine kinase implicated in the regulation of apoptosis and is negatively regulated by COX-2 in vitro and in vivo, suggesting a novel mechanism for the effect of COX-2 on cancer cell survival.

With the growing demand on endoscopy services, optimising practice efficiency has assumed increasing importance. Prior research has identified practice changes, which increase the efficiency in endoscopy. In this study, the potential impact of these practice changes on the current and projected future endoscopy waiting times at our institution was assessed.The annual volume of endoscopic procedures performed at a major teaching hospital and the annual procedure demand from 2000 to 2007 were reviewed. Procedure demand and waiting times were projected until 2012. The impact of three practice changes, which have been shown to increase efficiency was assessed: 1. routinely obtaining i.v. access and consent in patients prior to endoscopy (approach 1); 2. routinely obtaining i.v. access and consent, and sedating the patient prior to endoscopy (approach 2); 3. utilizing a two-room per endoscopist model (approach 3).There has been a significant increase in annual procedure volume (36%) and annual procedure demand (69%) from 2000 to 2007. Annual waiting times for routine procedures have lengthened, from 6 weeks (2000) to 22 weeks (2007). Assuming continued linear growth in demand up to 2012, the projected waiting times will continue to rise reaching 40 weeks in 2012. Routinely obtaining i.v. access/consent prior to procedure (approach 1) would shorten the average routine waiting times so that 8 weeks (recommended HSE maximum) would not be exceeded until early 2006; routinely obtaining i.v. access/consent and sedating patient prior to procedure (approach 2) would shorten the average routine waiting time so that 8 weeks would not be exceeded until 2008; utilising two rooms per endoscopist (approach 3) would shorten the average routine waiting time so that 8 weeks would not be exceeded until early 2012.Maintaining timely access to endoscopic services is becoming more challenging in the face of growing demand. Modifications in routine clinical practice can significantly impact procedure waiting times. In an era where economic aspects of medical care are becoming increasingly important and where there is growing focus on waiting times as a measure of clinical performance, these findings underscore the importance of providing clinical care in the most efficient manner possible.

COX-2 is upregulated at an early stage in colorectal carcinogenesis and generates prostaglandins, which promote cancer cell proliferation, impair apoptosis and enhance angiogenesis, promoting tumour growth and metastasis. There are ample data from animal models and human studies to demonstrate enhanced tumour progression associated with COX-2 activity in cancer cells. Conversely, NSAIDs including aspirin inhibit COX-2 and, therefore, have anti-neoplastic properties. There has been sustained interest in COX-2 as a chemopreventive target in colorectal cancer (CRC) and although both aspirin and COX-2 selective NSAIDs have demonstrated efficacy, adverse effects have limited their widespread adoption. In particular, evidence of the cardiovascular effects of COX-2 selective inhibitors has led to questioning of the suitability of COX-2 as a target for chemoprevention. This review examines the basis for targeting COX-2 in CRC chemoprevention, evaluates the efficacy and safety of the approach and examines future strategies in this area.

The medical literature describes disparity in colonoscopy performance. This randomised, controlled study aimed to characterise the impact of feedback on colonoscopy performance among gastroenterology (GI) trainees. Gastroenterology trainees of similar experience levels who independently performed 581 colonoscopies over the study period were randomised to receive feedback/no feedback on their colonoscopy performance. Baseline colonoscopy performance was similar in both groups. Following feedback, caecal intubation improved by 10.5% (from 72.9 to 83.4%, p = 0.04) in the feedback group and declined by 6.1% (from 78 to 71.9%, p = 0.2) in the control group; polyp detection improved by 5.1% (from 12.9 to 18.0%, p = 0.2) in the feedback group and by 2.9% (from 16.7 to 19.6%, p = 0.5) in the control group. Systematic feedback appears to enhance colonoscopy performance among GI trainees.

The level of awareness among the Irish public regarding colorectal cancer (CRC) remains uncertain. This study aimed to characterise CRC knowledge levels among a cohort of Irish patients.A survey evaluating CRC knowledge levels was distributed among outpatients at a gastroenterology clinic in a Dublin teaching hospital.In total, 472 surveys were distributed of which 465 (98.5%) were returned. Twenty-nine percent of respondents correctly judged CRC to be the commonest cause of cancer death among the options provided while 26% correctly judged the lifetime risk of CRC; 59% underestimated and 15% overestimated the risk. Most patients (91%) were willing to pay 300 euros for a prompt colonoscopy if recommended by their physician while 7% opted to wait 6 months for a free colonoscopy.There is a willingness to embrace CRC screening and to shoulder some of the financial burden that this entails.

This study assessed implications for well-being of iatrogenic Hepatitis C Virus (HCV) infection compared with women at similar risk for HCV who were HCV negative, women not at similar risk (Rhesus positive), and individuals with non-iatrogenic HCV (ex-injecting drug users). Measures used: identity subscale of the Illness Perception Questionnaire; Hospital Anxiety and Depression Scale; and Schedule for the Evaluation of Individual Quality of Life-Direct Weighting. Symptom reporting was significantly higher in the iatrogenic group than the HCV negative, Rhesus positive, and non-iatrogenic groups, as was symptom severity. Anxiety and depression levels were also significantly higher in the iatrogenic group than the HCV negative, Rhesus positive, and non-iatrogenic groups. Well-being was not influenced by disease status in those with iatrogenic HCV infection. Quality of life score comparisons yielded no significant findings. Iatrogenic transmission of HCV infection has significant negative implications for phy...

Background and Aims Little medical literature exists for the use of fully covered self-expanding metal stents (CSEMSs) in the management of retained common bile duct (CBD) stones. Our aim was to assess the safety and efficacy of CSEMSs for the indication of retained "difficult" CBD stones. Methods This retrospective cases series included 44 patients (30 women; median age, 69 years [range, 24-88]) who underwent CSEMS insertion for the indication of retained "difficult" CBD stones in 2 tertiary referral centers. Patients underwent temporary placement of CSEMSs after incomplete stone clearance at ERCP. Follow-up ERCP was arranged for stent removal and subsequent attempt at duct clearance. Procedure-related adverse events were also recorded. Results Successful biliary drainage was achieved in all cases after CSEMS placement. Forty-two stents were removed with successful duct clearance achieved in 36 cases (82%) after a median in-stent duration of 8 weeks. There were 10 cases (22.7%) of stent migration, all noted incidentally during follow-up. One patient died of nonbiliary causes before attempted removal. Conclusion This is the largest published retrospective case series for use of CSEMSs for management of retained CBD stone disease to date. We have shown high success rates for this indication. A well-designed, multicenter, randomized controlled trial might address the uncertainty of cost-to-benefit ratio and appropriate duration for CSEMSs to be left in situ. Specific stent modification for this indication, including wider distal flare and retrieval purse string loop, may also be useful.

Background and Aim: Cyclooxygenase-2 (COX-2), a target of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs), is upregulated in chronic hepatitis B and may have a role in hepatocellular carcinoma. Little is known about the expression of COX-2 in chronic hepatitis C (HCV) infection. The aim the present study was to evaluate the extent of COX-2 expression in liver biopsies in patients with HCV infection and to determine the effect of treatment with interferon α (IFN). Methods: Percutaneous liver biopsy specimens were retrieved. Following formalin fixation and paraffin embedding, the biopsies were histologically evaluated for inflammation and fibrosis. The extent of COX-2 expression was measured by the avidin biotin immunohistochemical technique using a monoclonal COX-2 antibody. The extent of COX-2 expression was graded according to the number of hepatocytes expressing COX-2. Data were analyzed using Student's t-test. Results: Liver biopsies from 10 patients before and after treatment with IFN were obtained and compared with nine normal liver biopsies. All of the liver biopsies showed some COX-2 expression. COX-2 expression was confined to hepatocytes and bile duct epithelium and was not detected in vascular endothelium or inflammatory cells. The extent of COX-2 expression was greater in hepatitis C infected liver biopsies than in normal biopsies. Following treatment with IFN, there was a greater than threefold reduction in COX-2 expression (P

Dihydroxy bile acids, such as chenodeoxycholic acid (CDCA), are well known to promote colonic fluid and electrolyte secretion, thereby causing diarrhoea associated with bile acid malabsorption. However, CDCA is rapidly metabolised by colonic bacteria to ursodeoxycholic acid (UDCA), the effects of which on epithelial transport are poorly characterised. Here, we investigated the role of UDCA in the regulation of colonic epithelial secretion. Cl(-) secretion was measured across voltage-clamped monolayers of T84 cells and muscle-stripped sections of mouse or human colon. Cell surface biotinylation was used to assess abundance/surface expression of transport proteins. Acute (15 min) treatment of T84 cells with bilateral UDCA attenuated Cl(-) secretory responses to the Ca(2+) and cAMP-dependent secretagogues carbachol (CCh) and forskolin (FSK) to 14.0 ± 3.8 and 40.2 ± 7.4% of controls, respectively (n = 18, P0.001). Investigation of the molecular targets involved revealed that UDCA acts by inhibiting Na(+)/K(+)-ATPase activity and basolateral K(+) channel currents, without altering their cell surface expression. In contrast, intraperitoneal administration of UDCA (25 mg kg(-1)) to mice enhanced agonist-induced colonic secretory responses, an effect we hypothesised to be due to bacterial metabolism of UDCA to lithocholic acid (LCA). Accordingly, LCA (50-200 μm) enhanced agonist-induced secretory responses in vitro and a metabolically stable UDCA analogue, 6α-methyl-UDCA, exerted anti-secretory actions in vitro and in vivo. In conclusion, UDCA exerts direct anti-secretory actions on colonic epithelial cells and metabolically stable derivatives of the bile acid may offer a new approach for treating intestinal diseases associated with diarrhoea.

In 1996 we initiated a retrospective-prospective study in 184 untreated women infected in 1977 with chronic hepatitis C virus (HCV). To provide insight into the natural history of HCV, we determined liver fibrosis outcomes and any predictors of such.Baseline 1994 biopsy specimens (size,or=15 mm; portal areas,or=5) and sequential biopsy specimens were assessed by Ishak score for grade change (increase or decrease ofor=2 points) and stage progression or regression (increase or reduction ofor=1 point), the latter correlated with digital quantification of fibrosis percentage.No baseline biopsy specimens had cirrhosis, therefore all could potentially progress. Grade and stage scores decreased or increased significantly in 28% and 18% and 24% and 27% of patients, respectively. There was a positive correlation between baseline and sequential grade/stage scores (r = .39, P.001), and between semiquantitative Ishak scores and fibrosis percentage (Spearman rho = .85; P.01). Baseline alanine transaminase values (mean, 49 U/L; range, 23-363 U/L) correlated positively with changes in grade (r = .41, P.01) and stage (r = .39, P.01), and regression analyses indicated that baseline alanine transaminase value was a good predictor of such changes. Confounding variables (alcohol, smoking, and herbal and paracetamol [acetaminophen] use) did not correlate with histologic outcomes.In a follow-up study, 49% of patients showed no change in fibrosis, 24% showed regression, and only 27% showed progression, including 4 patients (2.1%) who developed stage 6 cirrhosis. Unidirectional sequential grade/stage concordance attested to biopsy sample reliability. Given the current age of these women in their fifth decade, some still may have a risk for more advanced liver disease, but for most of these patients it appears unlikely.

Aims Adverse drug reactions (ADRs) account for 3.2–7% of acute hospital admissions. The aim of this study was to assess prospectively knowledge of ADRs in patients admitted through the emergency department of a teaching hospital. Methods Three hundred and ninety-nine patients were admitted on acute medical call during study periods in September 2002 and May 2003. One hundred gave their perception of the risk of ADRs using visual analogue scales, where 0 indicates minimum and 10 maximum risk. The medications studied were warfarin, proton pump inhibitors (PPIs), corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin. Responses are compared against a medical control group. Results Corticosteroids were ranked most dangerous by patients (median score, 25th–75th centiles: 5.4, 2.9–8.7). Medical staff ranked NSAIDs as highest risk (6.2, 4.0–7.5). Patients identified NSAIDs as low risk (2.1, 0.7–4.9), perceiving the risk of cardiac arrhythmias and disturbance in liver biochemistry to be equivalent to risk of upper gastrointestinal ulceration and bleeding. Risk of haemorrhage was ranked as the most common ADR for warfarin by patients (8.6, 3.3–9.5) and medical staff (8.8, 7.6–9.3). Conclusions Patients underrate the risk of ADRs of their medications. While there is a good level of knowledge of ADRs amongst warfarin and aspirin users, there is a clear lack of knowledge regarding the risk of upper GI bleeding in NSAID users. Increased education may reduce the incidence of ADRs but it is more likely that it will serve to meet increasing patient expectations.

The inflammatory bowel diseases require frequent hospital visits. The literature suggests that the incidence of IBD may be increasing.To investigate the pattern of admissions of patients with inflammatory bowel disease (IBD) to hospital over a five-year period (between 1996 and 2001).We obtained national data regarding admission rates for patients with IBD from the Economic and Social Research Institute (ESRI) during the years 1996 and 2001. Local data were gathered from the Hospital In-Patient Enquiry (HIPE) scheme for the same years.Over this five-year period, there has been a substantial increase in the rate of admission with IBD (58% for Crohn's disease and 25% for ulcerative colitis), in particular in the number of day-case admissions for patients with Crohn's disease (125%). There has been little change in the number of patients undergoing surgery for their disease (Crohn's disease; 24% vs 20% and Ulcerative colitis; 17% vs 16.6%) and in the length of hospital stay.Despite an increase in the rate of admission with IBD, there has been little change in the rates of surgical intervention and length of stay. The most dramatic increase was seen in the day-case admissions for patients with Crohn's disease and may reflect the use of anti-TNFalpha (infliximab) in the treatment of this disease.

Aim : In colorectal carcinomas, cyclooxygenase-2 (COX-2) is expressed predominantly by epithelial cells and is implicated in tumour progression. Tumour-associated macrophages may influence tumour growth, proliferative rate and angiogenesis and also express COX-2 when activated. Thus they may play an important stromal-epithelial role in carcinogenesis. Τhe aim of this study was to define the relationship between microvessel density (MVD), tumour COX-2 and macrophage COX-2 expression. Methods and results : Sixty-five cases of formalin-fixed paraffin-embedded colorectal cancer were included in the study. Tissues were immunostained for COX-2, CD68 (macrophage marker) and CD34 (endothelial marker to assess MVD). Thirty-six cases were grossly ulcerated cancers and 29 cases showed focal/microscopic ulceration. Macrophages were in high concentration at the base of ulcerated areas, and were also diffusely dispersed within tumoral stroma. However, the pattern of macrophage COX-2 expression revealed two populations of macrophages—those deep within the tumour (negative for COX-2) and those at the base of ulcers (positive for COX-2). In all cases, the tumour epithelial cells expressed COX-2. MVD was higher at the base of ulcers, adjacent to COX-2+ macrophages, and was lower deep within the tumour. Conclusions : In colorectal cancers, macrophages may have a dual role. Those concentrated at the base of the ulcers, where there is an associated high MVD, may induce angiogenesis, but their function may be in a healing/repair process. The lack of COX-2+ macrophages and lower MVD deep within the tumour suggests that it may be the epithelial COX-2 component that is important in tumour progression.

Hepatitis C (HCV) is a common cause of morbidity among patients who attend general practitioners (GPs) in Ireland for methadone maintenance treatment. To describe the development and content of guidelines for the management of HCV among current or former opiate users in the Eastern Regional Health Authority area attending GPs for methadone treatment. The guidelines were produced in five stages: identification of key stakeholders; development of evidence-based draft guidelines; discussion of content; determination of ‘Delphi’-facilitated consensus and review by a sample of GPs for whom the guidelines would be intended. The guidelines contain advice for GPs on all aspects of care of patients at risk of HCV, including general and preventative care, care of other bloodborne and hepatotoxic viruses, and the factors to be considered and appropriate evaluation prior to referring a patient for assessment at a hepatology unit. GPs have an important role to play in the care of patients at risk of, or Infected with, HCV.

Helicobacter pylori induces cyclooxygenase activity in the stomach, although the COX isoform and cellular source are unclear. A potential source is the vascular endothelial cell, which plays a role in regulating mucosal blood flow and inflammatory cell infiltration.We examined the effect of four strains (toxigenic and non-toxigenic) of H. pylori on COX isoform expression in vascular endothelial cells. Prostaglandin synthesis was measured by enzyme immunoassay and COX isozyme expression determined by Western blot and RT-PCR. Gene induction was examined using 5' deletion constructs of the COX-1 and COX-2 promoters coupled with luciferase.All H. pylori strains induced prostaglandin generation and expression of both COX-1 and COX-2 in HUVEC, although this was most pronounced with the highly toxigenic strain H. pylori 60190. Treatment of the cells with selective COX inhibitors demonstrated that COX-1 was predominantly responsible for the enhanced generation of prostacyclin induced by H. pylori 60190. Similar results were seen with H. pylori broth culture filtrates, suggesting that a secreted product was responsible. Induction of COX-2 reflected both enhanced gene expression and stabilization of the mRNA.H. pylori increased both COX-1 and COX-2 activity in vascular endothelial cells. This increased generation of endothelial cell prostacyclin may play a role in modulating mucosal blood flow, platelet function and inflammatory cell infiltration in response to H. pylori infection. The regulation of COX-1 at the transcriptional level by H. pylori described in this study is a novel finding and calls into question the traditional description of COX-1 as a purely constitutive, housekeeping gene.

Colorectal cancer has among the highest incidence and mortality rates in the Western world, with rates continuing to rise [1]. With five-year survival for stage I and II disease of approximately 90...

The toxic effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on the small bowel have been reported extensively. A growing number of reports of toxic effects of NSAIDs on the colon have appeared recently. The clinical presentation, endoscopic appearances and histological findings of so-called NSAID colopathy are quite varied, as illustrated by a series of four patients described in this report. Presenting symptoms and signs in this series include iron-deficiency anaemia and crampy abdominal pain, but alteration of bowel habit, weight loss, and even nausea and vomiting have also been described. One patient in this series has large-bowel diaphragms, considered by some to be pathognomonic of NSAID effects. Each of the four patients had right-sided colonic lesions only, possibly supporting a direct toxic effect of NSAIDs. Management usually involves simply stopping the offending NSAID. A review of the literature on this under-recognized entity is presented.

Proton pump inhibitors (PPIs) are used to treat upper gastrointestinal tract disorders. Their efficacy and perceived safety have led to widespread prescription. This is not without effect, in terms of adverse events and resource utilization. To prospectively assess oral PPI prescription in hospitalized patients. PPI prescription in consecutive hospitalized patients was assessed. Indication and dose were assessed by patient interview and medical record review. Comparisons with current published prescribing guidelines were made. Four hundred and forty-seven patients were included. 57.5 % were prescribed PPIs. 26.8 % prescriptions were for inappropriate or unclear indications. 68.4 % were on higher doses than guidelines recommended, of which 41.6 % could have undergone dose reduction, and 26.5 % discontinued. In a multivariate analysis, age, gender, and length of stay had no association with PPI prescription. Although aspirin use was appropriately associated with PPI prescription (RR: 1.8, 95 % CI 1.127–3.69; p

Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most widely used drugs and their widespread use is associated with increased gastro-intestinal toxic effects such as ulceration, haemorrhage, perforation and death. They result in these complications mainly by reducing cytoprotective prostaglandins (PGE2 and PGI2) in the stomach, through the inhibition of cyclo-oxygenase (COX) enzyme. The increased morbidity and mortality, in addition to enormous cost, associated with NSAID-associated side effects, necessitates a need for safer GI-friendly NSAID. Various approaches have been used to counteract NSAID associated side effects with varying degrees of success and acceptance. These include the use of alternative analgesia, anti-acid secretory agents like proton pump inhibitors, sucralfate and prostaglandin analogues. In addition, new types of NSAIDs are being developed, based on new understanding of their mechanism of action and the pathogenesis of inflammation. These include a new class of NSAIDs called "selective Cox-2 inhibitors". These agents preserve the COX-1 that is responsible for the production of cytoprotective prostaglandins in the stomach and selectively inhibit COX-2 induced at the sites of inflammation. Selective COX-2 inhibitors exert the same analgesic and anti-inflammatory effects as the existing NSAIDs but may be less toxic to the stomach. In this review the background development and well-structured clinical trials on this new generation NSAIDs are discussed.

In man, nimesulide selectively inhibits cyclooxygenase-2 (COX-2) with little effect on haemostatic function or gastric prostaglandin formation. It causes significantly less gastrointestinal injury than naproxen, but has anti-inflammatory efficacy similar to that of naproxen and other currently available non-steroidal anti-inflammatory drugs. Naproxen suppressed arachidonic-acid-mediated platelet aggregation, reduced serum thromboxane B2 levels by 98% throughout the treatment period and reduced gastric mucosal prostaglandins (PGE2 and 6-keto-PGF1alpha) production by an average of 80%. This contrasts with nimesulide: platelet aggregation was not significantly affected, thromboxane B2 levels were only 29% lower and the gastric mucosal prostaglandins were inhibited in the order of approximately 20%. During the treatment period, both nimesulide and naproxen significantly inhibited COX-2-dependent PGE2 synthesis in the whole blood; however, naproxen had a lesser effect than nimesulide.

We report a patient with clinical, biochemical and immunological indices suggestive of autoimmune hepatitis with marked transaminasaemia, raised immunoglobulins and positive anti-nuclear and anti-smooth muscle antibodies. A coagulation screen revealed a transient, markedly increased, activated, partial thromboplastin time and a normal prothrombin time, with elevated levels of anticardiolipin antibodies and the presence of lupus anticoagulant, indicating the presence of antiphospholipid antibodies. Subsequent histology confirmed moderate hepatitis with piecemeal necrosis and fibrosis. Appropriate autoimmune therapy was commenced. This presentation illustrates the rare association of anti-phospholipid antibodies with autoimmune chronic active hepatitis presenting with a temporarily abnormal coagulation screen.

Objective Key to the clinical management of colorectal cancer is identifying tools which aid in assessing patient prognosis and determining more effective and personalised treatment strategies. We evaluated whether an experimental systems biology strategy which analyses the susceptibility of cancer cells to undergo caspase activation can be exploited to predict patient responses to 5-fluorouracil-based chemotherapy and to case-specifically identify potential alternative targeted treatments to reactivate apoptosis. Design We quantified five essential apoptosis-regulating proteins (Pro-Caspases 3 and 9, APAF-1, SMAC and XIAP) in samples of Stage II (n=13) and III (n=17) tumour and normal colonic (n=8) tissue using absolute quantitative immunoblotting and employed systems simulations of apoptosis signalling to predict the susceptibility of tumour cells to execute apoptosis. Additional systems analyses assessed the efficacy of novel apoptosis-inducing therapeutics such as XIAP antagonists, proteasome inhibitors and Pro-Caspase-3-activating compounds in restoring apoptosis execution in apoptosis-incompetent tumours. Results Comparisons of caspase activity profiles demonstrated that the likelihood of colorectal tumours to undergo apoptosis decreases with advancing disease stage. Systems-level analysis correctly predicted positive or negative outcome in 85% (p=0.004) of colorectal cancer patients receiving 5-fluorouracil based chemotherapy and significantly outperformed common uni- and multi-variate statistical approaches. Modelling of individual patient responses to novel apoptosis-inducing therapeutics revealed markedly different inter-individual responses. Conclusions Our study represents the first proof-of-concept example demonstrating the significant clinical potential of systems biology-based approaches for predicting patient outcome and responsiveness to novel targeted treatment paradigms.

Spending on hospital inpatients comprises a major proportion of healthcare costs. This study assessed the impact of systematic feedback to gastroenterologists on the cost of care provided to inpatients on a gastrointestinal/hepatology (GIH) hospital service.Patients with a GIH diagnosis were randomly assigned to be cared for by one of two hospital services. Over 3 months, teams were randomized to receive feedback (GIH A) or no feedback (GIH B, control group); feedback consisted of an email sent twice weekly to all physicians on the GIH A service detailing the length of stay (LOS) and real-time cost of care accrued by each inpatient.Over 3 months, care was provided to 56 (GIH A) and 47 (GIH B) inpatients with a GIH illness. Patient complexity level was similar for both services as demonstrated by mean relative value: 1.11 (GIH A) vs. 1.27 (GIH B), p=0.2. Weighted LOS and weighted cost of care values were calculated to adjust for the respective RV of each patient. Mean weighted LOS (10.8 [GIH A] vs. 13.8 days/pt [GIH B], p=0.02) and mean weighted cost of care (9,904 [GIH A] vs. 12,654 euros/pt [GIH B], p=0.02) were significantly lower in the feedback group. Subsequent hospital readmission rates did not differ among both groups.Systematic feedback on cost of care was associated with lower healthcare costs without compromising quality. Incorporating a running total of patient costs into computer software used to order patient tests may represent one approach to controlling healthcare expenses.

Background and Aim Gastric antral vascular ectasia (GAVE) or ‘watermelon stomach’ is a rare and often misdiagnosed cause of occult upper gastrointestinal bleeding. Treatment includes conservative measures such as transfusion and endoscopic therapy. A recent report suggests that endoscopic band ligation (EBL) offers an effective alternative treatment. The aim of the present study is to demonstrate our experiences with this novel technique, and to compare argon plasma coagulation (APC) with EBL in terms of safety and efficacy. Methods A retrospective analysis of all endoscopies with a diagnosis of GAVE was carried out between 2004 and 2010. Case records were examined for information pertaining to the number of procedures carried out, mean blood transfusions, mean hemoglobin, and complications. Results A total of 23 cases of GAVE were treated. The mean age was 73.9 (55–89) years. Female to male ratio was 17:6 and mean follow up was 26 months. Eight patients were treated with EBL with a mean number of treatments of 2.5 (1–5). This resulted in a statistically significant improvement in the endoscopic appearance and a trend towards fewer transfusions. Of the eight patients treated with EBL, six (75%) patients had previously failed APC treatment despite having a mean of 4.7 sessions. Band ligation was not associated with any short- or medium-term complications. The 15 patients who had APC alone had a mean of four (1–11) treatments. Only seven (46.7%) of these patients had any endoscopic improvement with a mean of four sessions. Conclusions EBL represents a safe and effective treatment for GAVE.

Cecal intubation and polyp detection rates are objective measures of colonoscopy performance. Minimum cecal intubation rates greater than 90% have been endorsed by the American Society for Gastrointestinal Endoscopy (ASGE) and the Joint Advisory Group (JAG) UK. Performance data for medical and surgical trainee endoscopists are limited, and we used endoscopy quality parameters to compare these two groups.Retrospective review of all single-endoscopist colonoscopies done by gastroenterology and surgical trainees ("registrars," equivalent to fellows, postgraduate year 5) with more than two years' endoscopy experience, in 2006 and 2007 at a single academic medical center. Completion rates and polyp detection rates for endoscopists performing more than 50 colonoscopies during the study period were audited. Colonoscopy withdrawal time was prospectively observed in a representative subset of 140 patients.Among 3079 audited single-endoscopist colonoscopies, seven gastroenterology trainees performed 1998 procedures and six surgery trainees performed 1081. The crude completion rate was 82%, 84% for gastroenterology trainees and 78% for surgery trainees (P0.0001). Adjusted for poor bowel preparation quality and obstructing lesions, the completion rate was 89%; 93% for gastroenterology trainees, and 84% for surgical trainees (P0.0001). The polyp detection rate was 19% overall, with 21% and 14% for gastroenterology and surgical trainees, respectively (P0.0001). The adenoma detection rate in patients over 50 was 12%; gastroenterology trainees 14% and surgical trainees 9% (P = 0.0065). In the prospectively audited procedures, median withdrawal time was greater in the gastroenterology trainee group and polyp detection rates correlated closely with withdrawal time (r = 0.99).The observed disparity in endoscopic performance between surgical and gastroenterology trainees suggests the need for a combined or unitary approach to endoscopy training for specialist medical and surgical trainees.