Chasing up colorectal cancer

CRC claims more than 200,000 lives in Europe alone.

Each year, Europe’s second biggest cancer killer—colorectal cancer (CRC)—claims more than 200,000 lives in Europe alone; yet, early detection may result in a 90–95% survival rate. Implementation of CRC screening programmes across Europe is booming, but what are the nuts and bolts of a good CRC screening programme?

A press release issued by UEG in March 2014 warned that the annual incidence of CRC is predicted to have risen 12% by 2020, at which time it will potentially affect about half a million Europeans.1 CRC is currently the second and third most common cancer in European women and men, respectively, and accounts for 13% of all cancer-related deaths in Europe, resulting in one fatality every 3 minutes. Screening programmes have been implemented in several countries with a view to reducing morbidity and mortality by identifying and treating cases of early-stage CRC. It’s almost a year since a nationwide CRC screening programme was launched in Denmark, with an annual budget of approximately €50M. Starting in March 2014, all Danish citizens aged 50–74 years old are invited to participate in biannual screening.2 Those individuals who are willing to participate receive a screening kit by regular mail, and the test is free and voluntary to complete. The CRC screening programme uses a faecal occult blood (FOB) test (FOBT), and individuals with a positive FOBT are offered a colonoscopy. The Danish screening programme was implemented on the basis of a feasibility study carried out in 2005–2006, in which 2–3% of those screened tested positive for the presence of FOB; of these, 8% and 40% were found to have cancer and polyps, respectively, as demonstrated by colonoscopy.3 In the feasibility study, a chemical test with a sensitivity of only 60% was used. In the ongoing screening programme, however, the faecal immunochemical test (FIT; also known as an immunochemical FOBT) is being used, which is expected to increase sensitivity. Meanwhile, high FIT sensitivity and specificity may be difficult to achieve given the fact that not all CRCs bleed and there are causes of FOB other than cancer and polyps; hence, quite a few false-negatives and false-positives may still be expected with the FIT. Of course, there’s more to achieving a successful screening programme than safeguarding best possible intervention options and optimizing diagnostic performance parameters, such as test cut-off and predictive values. The very nature of the test itself, how the screening programme is presented to the public and overall public health awareness are all factors potentially influencing the success of a screening programme. In the case of CRC, the mere thought of having a colonoscopy may scare people off, and public health awareness may differ substantially between countries, both of which are factors that may significantly affect uptake and thereby overall success rates. Sometimes there are differences in the willingness to participate within the same country that have no obvious explanation. For example, as pointed out by Björn Rembacken in his talk on CRC screening strategies in the West, a striking difference in the uptake rate has been observed in Belgium, where the Flemish appear much more keen on participating than the Walloons.4 In the Danish feasibility study, women were more likely to participate, as were those with higher education and higher income.5 Moreover, a study carried out by The Danish Cancer Society suggests that it takes time for a population to adjust to thinking and speaking of CRC.6 In this study, the most common barriers to accepting screening invitations included:
  • Not wanting to know whether they have CRC
  • Thinking that the test is too awkward to do
  • The need for more information
  • Developing a sense of being ill merely by being offered the test
  • Feeling too old for the test to be relevant
Apart from mitigating issues that have to do with culture and tradition, by removing stigma and taboos through campaigns and the provision of information, what diagnostic tools can be developed to minimize the number of cases with a positive result for FOB but negative findings on colonoscopy? How far are we in terms of developing other non-invasive biomarkers, such as those based on microbiota signatures7 or DNA methylation, for the detection of both CRC and critical precursor lesions? To which extent may individual risk assessment replace invasive and semi-invasive diagnostic methods in terms of identifying patients with early CRC? The UEG Education Library boasts a large catalogue of presentations, abstracts and syllabi focusing on early detection of CRC as a means of improving patient survival and widening the window of therapeutic intervention. For instance, if you want to familiarise yourself with the current status of CRC screening programmes throughout Europe, simply sign in to myUEG, go the Library and search for “CRC AND screening”. I also recommend listening to the presentations included in the session on “Colorectal cancer screening: the future” from UEG Week 2014 (see Further UEG Resources below). References
  1. UEG Press Release. Europe is falling behind America in the fight against colorectal cancer due to low screening uptake. (March 2014, accessed February 2015).
  2. Danish Cancer Society. Screening for colon cancer. (2014, accessed February 2015)
  3. Research Centre for Prevention and Health—The Capital Region of Denmark. Screening for colorectal cancer in the counties of Vejle and Copenhagen—cross evaluation of pilot studies. [Article in Danish]
  4. Rembacken B. CRC screening strategies. Presentation in the East meets West: CRC Screening Strategies session at UEG Week 2013 
  5. Frederiksen BL, Jørgensen T, Brasso K, et al. Socioeconomic position and participation in colorectal cancer screening. Br J Cancer 2010; 103: 1496—1501.
  6. Meyer M. Department of Prevention and Documentation. The Danish Cancer Society. What were the barriers for participating in colorectal cancer screening? A qualitative and quantitative analysis of non-participant barriers to participating in a pilot colorectal cancer screening programme in Vejle and Copenhagen in 2005 and 2006. (April 2007) [Article in Danish].
  7. National Cancer Institute. Analyzing the gut microbiome to help detect colorectal cancer. (January 2015, accessed February 2015)
Further UEG resources “Colorectal cancer screening: The future” session at UEG Week 2014. Fight against colorectal cancer.  Colorectal cancer in Europe. Colorectal cancer incidence and mortality in Europe.  Colorectal cancer – how to spot the symptoms.

Hepatologists jump on screening bandwagon

In the UK, endoscopy is riding a wave of investment generated by population-level colorectal cancer screening. Now, it seems that hepatology is also planning to jump on the screening bandwagon.

In 2012 the US Centers for Disease Control and Prevention gave the go-ahead for population-level screening for chronic HCV infection.1 Then, in 2014, the World Health Organisation also recommended an expansion of the current screening strategy beyond those at high risk of HCV infection2. Screening for HCV infection is a sizeable undertaking as up to 150 million people worldwide are thought to have the disease. Although most are asymptomatic, all studies have found that patients infected with HCV have a reduced life expectancy. Understandably, in those countries where most HCV infections result from intravenous drug use, there is not only an increased risk of liver disease, but also an increased risk of death from alcohol, HIV infection, smoking or drug-related events such as overdose, suicide, homicide and trauma.3 In patients with iatrogenic HCV infections, an excess mortality from nonhepatic causes such as renal and heart disease and cancer has also been described.4 What do people with HCV infection usually die from? I must admit that I find it difficult to understand research papers reporting on standardised mortality rates (SMR). It seems counterintuitive that patients who have an SMR of 16.8 of dying from a liver-related cause are still far more likely to die from heart disease (SMR of 1.25).5,6 However, a slightly increased risk of dying from something that is already a frequent cause of death will obviously have a great impact on the total number of deaths. I was surprised to find that up to 85% of patients with chronic HCV infections die from nonhepatic causes.7–14 Is there anything we can do to reduce the risk of progression to liver fibrosis, cirrhosis, liver failure or hepatoma? Yes! Beneficial lifestyle interventions could include attempts to reduce intravenous drug taking, tackle alcohol dependency, help with weight reduction in the obese and treat HIV co-infection aggressively, all of which may reduce the risk of progression.15 In fact, all of the above interventions would be beneficial for patients regardless of infection status. The reason that hepatologists are so enthusiastic about screening for HCV infection is the fantastic sustained virologic response (SVR) rates achieved with the latest antiviral agents, which is now approaching 90%.16 However, it is worth pointing out that the SVR is a surrogate endpoint and sadly we don’t know if this translates into long-term clinical benefit. I find it surprising that this fundamental issue has not yet been clarified. However, I do understand that the issues surrounding antiviral therapy are complex! For example, the patients who are the most likely to achieve an SVR are those who are least likely to have risk factors for progressive disease.17–19 In other words, those who do well on treatment would probably also do well even without treatment. In addition, a proportion of patients who achieve an SVR, nevertheless develop and die from liver-related causes. In one of the largest studies with the longest follow up (8 years), patients with severe hepatic fibrosis but with an SVR, were found to have annual risk of developing hepatocellular carcinoma of 1%.20 This sounded like a good result until I realised that the background incidence of hepatocellular carcinoma in patients with HCV cirrhosis is very similar (1.4–3.3%).21 Once population-level screening for chronic HCV infection has been rolled out there will be some difficult consultations during which unsuspecting people are told that they are now patients with a chronic disease, requiring lifelong monitoring and treatment. Although the long-term clinical benefit of antiviral therapy is uncertain, I would nevertheless expect these difficult conversations to be easier if a safe and well-tolerated treatment was on offer. Sadly this is not the case. The adverse effects of interferon are well known and it is associated with a 4% increase in all-cause mortality.22 Both the guanosine analogues and the protease inhibitors may cause bone marrow suppression, skin reactions, gastrointestinal upset and insomnia in a large proportion of patients.23.24 In 2012, the US Food and Drug Administration reported that telaprevir was the most common reported cause of severe and fatal skin reactions of any drug.25 In one trial, 3% of patients randomly allocated to receive sofosbuvir experienced serious adverse events, with 1% occurring in the peginterferon plus ribavirin arm.26 In a more recent study, combination therapy with sofosbuvir plus ledipasvir was associated with a 0.5–2% rate of serious adverse events.27 As up to 85% of HCV-infected people in the population will die from nonhepatic causes, the newer antiviral therapies must be safer and better tolerated; otherwise, people will conclude that such a government screening programme turns well people into poorly patients. As an endoscopist, I find it reassuring to know that the benefit of colorectal cancer screening has been proven in several large, prospective studies. In view of the uncertainties surrounding population-level screening for HCV infection, I am not alone in wanting to see plans for large, prospective randomised controlled trials to prove it’s worthwhile.28 As a taxpayer, I would also like to be reassured that such screening would be money well spent. References
  1. Smith BD, Morgan RL, Beckett GA, et al. Recommendations for the identification of chronic hepatitis C virus infection among persons born during 1945–1965. MMWR Recomm Rep 2012; 61(RR-4): 1–32 
  2. WHO. Guidelines for the screening, care and treatment of persons with hepatitis C infection. (2014, accessed 28 January 2015)
  3. Grebely J and Dore GJ. What is killing people with hepatitis C virus infection? Semin Liver Dis 2011; 31: 331–333.
  4. Lee MH, Yang HI, Lu SN, et al. Chronic hepatitis C virus infection increases mortality from hepatic and extrahepatic diseases: a community-based long-term prospective study. J Infect Dis 2012; 206: 469–477.
  5. Amin J, Law MG, Bartlett M, et al. Causes of death after diagnosis of hepatitis B or hepatitis C infection: a large community-based linkage study. Lancet 2006; 368: 938–945.
  6. Butt AA, Xiaogiang W, Budoff M, et al. Hepatitis C virus infection and the risk of coronary disease. Clin Infect Dis 2009; 49: 225–232.
  7. Wiese M, Fischer J, Lobermann M, et al. Evaluation of liver disease progression in the German hepatitis C virus (1b)-contaminated anti-D cohort at 35 years after infection. Hepatology 2014; 59: 49–57. 
  8. Seeff LB, Hollinger FB, Alter HJ, et al. Long-term mortality and morbidity of transfusion-associated non-A, non-B, and type C hepatitis: a National Heart, Lung, and Blood Institute collaborative study. Hepatology 2001; 33: 455–463. 
  9. Vogt M, Lang T, Frosner G, et al. Prevalence and clinical outcome of hepatitis C infection in children who underwent cardiac surgery before the implementation of blood-donor screening. N Engl J Med 1999; 341: 866–870.
  10. Barrett S, Goh J, Coughlan B, et al. The natural course of hepatitis C virus infection after 22 years in a unique homogenous cohort: spontaneous viral clearance and chronic HCV infection. Gut 2001; 49: 423–430. 
  11. Casiraghi MA, De Paschale M, Romano L, et al. Long-term outcome (35 years) of hepatitis C after acquisition of infection through mini transfusions of blood given at birth. Hepatology 2004; 39: 90–96. 
  12. Seeff LB, Miller RN, Rabkin CS, et al. 45-year follow-up of hepatitis C virus infection in healthy young adults. Ann Intern Med 2000; 132: 105–111. 
  13. Locasciulli A, Testa M, Pontisso P, et al. Prevalence and natural history of hepatitis C infection in patients cured of childhood leukemia. Blood 1997; 90: 4628–4633. 
  14. Lai ME, Origa R, Danjou F, et al. Natural history of hepatitis C in thalassemia major: a long-term prospective study. Eur J Haematol 2013; 90: 501–507 
  15. Missiha SB, Ostrowski M and Heathcote EJ. Disease progression in chronic hepatitis C: modifiable and nonmodifiable factors. Gastroenterology 2008; 134: 1699–1714.
  16. Afdhal N, Reddy KR, Nelson DR, et al. Ledipasvir and sofosbuvir for previously treated HCV genotype 1 infection. N Engl J Med 2014; 370: 1483–1493.
  17. Stattermayer AF, Scherzer T, Beinhardt S, et al. Review article: genetic factors that modify the outcome of viral hepatitis. Aliment Pharmacol Ther 2014; 39: 1059–1070. 
  18. Zeuzem S, Feinman SV, Rasenack J, et al. Peginterferon alfa-2a in patients with chronic hepatitis C. N Engl J Med 2000; 343: 1666–1672. 
  19. Koretz R. Chronic hepatitis: more quotes and misquotes. In: Gitnick G (ed) Current Hepatology. Vol 15. St. Louis: Mosby-Year Book Inc., 1995, pp.49–84.
  20. Van der Meer A, Feld J, Hofer H, et al. The risk for hepatocellular carcinoma among patients with chronic HCV infection and advanced hepatic fibrosis following sustained virological response. In: 64th Annual Meeting of the American Association for the Study of Liver Diseases, Washington, DC, USA, 1 November–5 November 2013. Abstract 143. 
  21. Everson GT. Management of cirrhosis due to chronic hepatitis C. J Hepatol 2005; 42 (suppl1): S65–S74. 
  22. Di Bisceglie AM, Stoddard AM, Dienstag JL, et al. Excess mortality in patients with advanced chronic hepatitis C treated with long-term peginterferon. Hepatology 2011; 53: 1100–1108. 
  23. Brok J, Gluud LL and Gluud C. Ribavirin plus interferon versus interferon for chronic hepatitis C. Cochrane Database Syst Rev 2010; 1: CD005445. 
  24. Casey LC and Lee WM. Hepatitis C virus therapy update 2013. Curr Opin Gastroenterol 2013; 29: 243–249. 
  25. Institute for Safe Medication Practices. Perspective on drug hypersensitivity. QuarterWatch 2013 Q1, (2014, accessed 28 January 2015) 
  26. Lawitz E, Mangia A, Wyles D, et al. Sofosbuvir for previously untreated chronic hepatitis C infection. N Engl J Med 2013; 368: 1878–1887. 
  27. Kowdley KV, Gordon SC, Reddy KR, et al. Ledipasvir and sofosbuvir for 8 or 12 weeks for chronic HCV without cirrhosis. N Engl J Med 2014; 370: 1879–1888. 
  28. Koretz RL, Lin KW, Loannidis JPA, et al. Is widespread screening for hepatitis C justified? BMJ 2015; 350: g7809. 

The Intestinal Microbiome—Rosetta Stone or Tower of Babel?

One of the hot topics in modern-day research is the mapping and understanding of the human intestinal microbiome and its role in health and disease. Studies have suggested that the development of several diseases and conditions depends on how our microbiomes are influenced and shaped, but interpreting the data generated by such studies may not be that simple. Are we holding the key to understanding metabolic, immunological and pathological processes, or do the data produced so far preclude any type of generalization? Are we unraveling the code necessary to develop obesity, irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD), or are we looking at a chaos of data, different terminologies and methodologies?

UEG Week 2014 was the first UEG event that I’ve attended in person, and the meeting was so packed with interesting sessions, I felt like cloning myself and deploying my clones to follow the many parallel tracks on offer. But alas, like all my fellow attendees, I had to choose, and rarely have I felt so spoiled for choice! Luckily, accessing the UEG Education Library has allowed me to look up a lot of the material that I was unable to see in person. Of the 52 ‘microbiota’ files available from UEG Week 2014 that can be discovered in the library, 10 are video-recorded presentations. As I take a huge interest in the role of the gut microbiota in health and disease, I've been indulging in these to update myself with some of the most recent advances in the field. In one of his presentations at UEG Week 2014, Professor Antonio Gasbarrini starts out by asking several questions about the gut microbiota in relation to coeliac disease, an autoimmune enteropahty triggered by gluten proteins. Do patients with coeliac disease have a different gut microbiota to healthy people? Does the microbiota have a role in the pathogenesis of coeliac disease? Can a gluten-free diet (GFD) alter the composition of gut microbiota? He stresses that a GFD does alter the microbiota and that, in healthy individuals, just a few weeks on a GFD may in fact lead to a decrease in beneficial bacteria such as Bifidobacteria/Lactobacilli and an increase in Enterobacteriaceae, thus affecting immune-metabolic responses. Moreover, a decrease in short-chain fatty acids is seen, possibly conferring a decrease in the immunomodulatory role of the microbiota. It appears that an altered microbiota is a characteristic feature of coeliac disease, that Bifidobacteria is decreased, at least in children, along with upregulation of other bacterial species, while any causal link between microbiota composition and disease development remains to be established. At least one HLA genotype is known to select for early microbiota composition, so it is possible that this is in fact one of the mechanisms underlying the genetic component of the disease. As do so many other scientists nowadays, Professor Gasbarrini stresses that while it may be important to know the structure of the microbiome, it is probably more important to know about the function of the microbiome. He also stresses the importance of sampling by highlighting the fact that identification of microbial communities may differ in the same individual depending on whether analysis of faecal or bioptic samples (mucosal biopsies, for instance) has been performed. Regarding the function of the microbiome, there are two talks on the microbiota in the context of IBD by Professor Joël Doré, who expands on the existence of Crohn’s disease-specific signature genes that are much less abundant in Crohn’s disease patients than in healthy controls. However, single genes not being very informative, scientists of the MetaHIT Consortium recently took to ‘binning’ genes identified by metagenomic analysis of roughly 400 faecal samples into co-abundance gene groups (CAGs), enabling a comprehensive discovery of new microbial organisms, viruses and co-inherited genetic entities, and facilitating assembly of microbial genomes without the need for reference sequences.1 From these CAGs, a total of 741 metagenomic ‘units’ or ‘species’ could be derived, four of which have been identified as highly discriminatory identifiers of ulcerative colitis when compared with healthy individuals. In our lab, we have also been analysing these data, only with a view to identifying parasitic protist signatures rather than bacterial signatures in these CAGs, and we have just submitted our results for publication. Once the results are out, I’ll be back with more on this; it is safe to say already that we have found some very striking associations, with colonisation by certain parasitic protists being significantly linked to certain microbiota profiles and clinical phenotypes of study individuals. However, just like Professor Doré points out, in most cases we do not know whether such observations reflect causality or mere consequence; this is mostly due to the cross-sectional nature of such studies, but the prognostic/diagnostic value of such findings should, or course, be subject to scrutiny. Being one of the heavy mantras of recent years, Faecalibacterium prausnitzii has been shown to be a direct predictor of Crohn’s disease relapse following infliximab withdrawal. In one study, Crohn’s disease patients with F. prausnitzii levels above the median were less prone to relapse than those with F. prausnitzii levels below the median, indicating that F. prausnitzii may represent a predictive factor for relapse.2 Professor Doré highlights that this is a trend not only in Crohn’s disease but also in ulcerative colitis. In the second talk by Professor Doré, you can learn more about the anti-inflammatory properties conferred by F. prausnitzii and its potential applicability as a diagnostic/prognostic marker. Professor Doré also gave a presentation on diet as a major modulator of the gut microbiota. He included a very educational slide on the functions of the human intestinal microbiota that are essential to health and wellbeing, and a slide summarising the diseases conferred by low gut species richness/gene count, such as Crohn’s disease, ulcerative colitis, IBS, obesity, Type-1 diabetes, Type-2 diabetes, coeliac disease, allergy and autism, etc., although the situation might not be entirely clear for coeliac disease, for example, as demonstrated by the talk by Professor Gasbarrini. In this talk, you can learn more about the so-called ‘enterotypes’, and you will find a few take-home messages regarding the impact of diet on microbiota development. Four of the video-recorded presentations are from the session “The role of microbiota in non-alcoholic fatty liver disease”. If terms such as ‘microbiota’, ‘microbiome’ and ‘metagenome’, scare you off, you are offered a useful introduction from Dr Alexander Moschen. And in case these conspicuous accomplishments have slipped your attention, in this talk you are also introduced to the famous and heavily cited mouse studies by Bäckhed and colleagues3 and Turnbaugh and colleagues4 on the influence of gut microbiota on energy uptake. For me, Dr Moschen delivers one of the big take-home messages in this series of presentations, which again relates to microbiota structure and function: just because different people have different microbiota, this may not mean that these microbiota do different things. Rather, different species assemblages appear to lead to similar functional profiles (i.e. the metabolic properties of a given microbiota can be more or less identical to those metabolic properties characteristic of a microbiota of a different composition). Focusing mainly on IBS, Dr Purna Kashyap presents studies showing that the gut microbiota can influence mechanisms characteristic of IBS, including gastrointestinal motility and secretion, visceral hypersensitivity and intestinal permeability, and that the microbiota influences entero-endocrine cells, stimulates the release of neurotransmitters like GABA, and mediates activation of immune cells, all affecting CNS function. Giving a thorough account of some of his own work too, Dr Kashyap shows that the effect of the gut microbiota on intestinal motility may in part be due to the effect on the host serotonergic system and that diet-related changes in microbiota fermentation products may alter host serotonergic pathways and gastrointestinal function. Finally, I would like to recommend the presentation “Probiotics and antibiotics in IBS: Do they work?”, which was delivered by Dr Viola Andresen. Dr Andresen summarizes data from randomized controlled trials on the effect of rifaximin on non-constipated IBS patients, which includes a significant improvement of particularly (refractory) bloating, but also stool consistency and global symptoms. There may be some uncertainty as to whether the effect of rifaximin in IBS patients is due to alleviation related to unidentified small intestinal bacterial overgrowth (SIBO), and in general, the link between IBS and SIBO remains obscure, primarily due to a paucity of data. However, a study using animal experimental models that appeared in Gastroenterology almost a year ago proposed that rifaximin modulates the ileal bacterial community (leading to a relative abundance of Lactobacillus), reduces subclinical inflammation of the intestinal mucosa and improves gut barrier function to reduce visceral hypersensitivity.5 Although expensive, among its many advantages, rifaximin has few side effects, if any, and more studies on the use of this antibiotic in the management of functional bowel diseases are anticipated. The language of the intestinal microbiome is being developed. Deciphering its many signs and symbols requires patience, but hopefully, this will eventually provide us with the tools and knowledge necessary to manipulate the gut microbiota to prevent, alleviate and cure a variety of diseases and promote health. Presentations on the microbiota at UEG Week 2014 Gasbarrini A. Microbiota in coeliac disease. From New challenges in gluten sensitivity: From bench to bedside.  Dore J. Microbiota signatures in IBD. From IBD: What's new in 2014?  Dore J. Microbiota: The key player in IBD? From New insights into the pathophysiology of inflammatory bowel diseases.  Dore J. Diet: Major modulators of gut microbiota. From Diet, immunity and systemic disease.  Moschen AR. Microbiota composition in obesity and related disorders. From The role of microbiota in non-alcoholic fatty liver disease (NAFLD).  Gasbarrini A. Antibiotics, pre- and probiotics in NAFLD. From The role of microbiota in non-alcoholic fatty liver disease (NAFLD).  Tilg H. Innate immunity in NAFLD. From The role of microbiota in non-alcoholic fatty liver disease (NAFLD).  Serino M. Metabolic infection. From The role of microbiota in non-alcoholic fatty liver disease (NAFLD).  Kashyap P. Impact of gut microbiota on gut function and dysfunction. From Normal and abnormal cross-talk at the mucosal border: Relevance for GI function and dysfunction.  Andresen V. Probiotics and antibiotics in IBS: Do they work? From Altered intestinal microbiota composition in IBS: Does it affect clinical practice?  References
  1. Nielsen HB, Almeida M, Juncker AS, et al. Identification and assembly of genomes and genetic elements in complex metagenomic samples without using reference genomes. Nat Biotechnol 2014; 32: 822–828. 
  2. Rajca S, Grondin V, Louis E, et al. Alterations in the intestinal microbiome (dysbiosis) as a predictor of relapse after infliximab withdrawal in Crohn's disease. Inflamm Bowel Dis 2014; 20: 978-986. 
  3. Bäckhed F, Ding H, Wang T, et al. The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci USA 2004; 101: 15718–15723.
  4. Turnbaugh PJ, Ley RE, Mahowald MA, et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 2006; 444: 1027–1031. 
  5. Xu D, Gao J, Gillilland M 3rd, et al. Rifaximin alters intestinal bacteria and prevents stress-induced gut inflammation and visceral hyperalgesia in rats. Gastroenterology 2014; 146: 484–496. 

Postgraduate Course on the road from inflammation to cancer in the upper GI tract

During the Polish Society of Gastroenterology Congress in September 2014, EAGEN and EHMSG (formerly known as EHSG) held the joint Postgraduate Course "The road from inflammation to cancer in the upper GI tract." The aim of the course was to share knowledge and experience in this increasingly relevant field, with the participation of speakers from high-end specialty European centres, EAGEN and EHMSG. Recordings from each individual session of the course can now be found in the UEG Education library.

The Postgraduate Course was opened by Professor Jaroslaw Regula and was interactive in nature, including discussion time after the sessions and voting on questions posed by the speakers regarding the clinical cases presented.1 The relevance of inflammation leading to cancer was reinforced by Professor Peter Malfertheiner, who reported that infections leading to cancer are responsible for one out of every five cancer deaths worldwide.1 Session 1 began with an introductory lecture from Professor Tomica Milosavljević, who provided a general perspective on the inflammation and cancer axis.2 He started with the history of the field, addressing the two paradigms of the link between inflammation and cancer—chronic inflammation (extrinsic) and intratumoural inflammation (intrinsic)—as well as the molecular events and pathways regulating this axis. Professor Colm O’Morain delivered a case-based lecture, discussing therapeutic strategies to eradicate Helicobacter pylori and raising awareness of eosinophilic oesophagitis.3 Professor Lars Lundell adressed GORD, considering management and risk factors for progression, presenting and discussing two clinical cases.4 Next, Professor Heinz Hammer delivered a talk on food impaction.5 He guided the audience through the possible causes, criteria for endoscopic intervention and methods for removing impacted food. Eosinophilic oesophagitis and oesophageal eosinophilia were also discussed and an overview of treatment options provided. Dr. Jochen Weigt, presenting a case of Barrett’s esophageal cancer and dysplasia, initiated session 2.6 His presentation addressed the rationale for staging, problems with staging procedures, and treatment options, raising the discussion of the true value of chromoendoscopy (acetic acid staining) versus dedicated white-light high-definition endoscopy. Next, Professor Juan Malagelada presented two cases of dyspepsia, addressing diagnostic approaches, prevalence and also the pathophysiology of functional dyspepsia.7 He also covered the associated abdominal manifestations and putative influencing factors, as well as therapy for functional dyspepsia. Dr. Tamara Matysiak-Budnik completed session 2, by presenting three clinical cases of gastric malignancy, underscoring the relevance of early detection and the importance of multimodality treatment.8 The Healthy Stomach Initiative, which is striving to spread preventive measures for greater stomach health throughout the world, was also promoted. Session 3, the final session of the course, started with a lecture by Dr. Gunther Krejs on the topic of familial gastric cancer, providing clinical and practical advice.9 Next, Professor Malfertheiner delivered a lecture on “Helicobacter pylori and cancer: what studies are needed?”10 He indicated that we are currently still challenged by H. pylori and its consequences, highlighting the need for further studies. Professor Malfertheiner stressed that in both less developed and also in more developed regions of the world, H. pylori is the most frequent infectious agent ultimately leading to cancer, and remains as the most important risk factor for gastric cancer. The lecture also covered the general pathophysiology of gastric adenocarcinoma, atrophic gastritis and the assessment of risk of gastric cancer development, and the pathways from H. pylori infection to gastric cancer. Importantly, Professor Malfertheiner proposed several basic and clinical studies needed in this context, concluding with the message being promoted by the Healthy Stomach Initiative that what is needed is a healthy stomach that is H. pylori free. Presentations at "The road from inflammation to cancer in the upper GI tract" EAGEN and EHMSG Postgraduate Course
  1. Malfertheiner P and Regula J. Welcome. 
  2. Milosavljević T. Introductory lecture: the road from inflammation to cancer. 
  3. O’Morain C. Case based lecture: patient with heartburn: history, endoscopy, medical/interventional therapy. 
  4. Lundell L. Case based lecture: patient with severe reflux: history, diagnostic work-up, therapy. 
  5. Hammer H. Case based lecture: patient with oesophageal food impaction. 
  6. Weigt J. Case based lecture: Patient with Barrett oesophagus and cancer – history, endoscopy, medical/interventional therapy. 
  7. Malagelada J. Case based lecture: Patient with dyspeptic symptoms – how does the stomach signal discomfort and disease. History, diagnosis, endoscopy, medical/interventional therapy. 
  8. Matysiak-Budnik T. Case based lecture: Patients with gastric malignancies: history, diagnosis, endoscopy, medical/interventional therapy. 
  9. Krejs G. Case based lecture: Familial gastric cancer – clinical and practical advices. 
  10. Malfertheiner P. Helicobacter pylori and cancer: what studies are needed? 

Highlights of the ESPGHAN Pediatric Hepatology Summer School 2014

ESPGHAN aims to promote the health of children, focusing on the gastrointestinal tract, liver and nutritional status. Since its foundation in 1968, ESPGHAN has been engaging scientific exchange among trainees, young doctors and scientists involved in paediatric gastroenterology, hepatology and nutrition, by means of summer schools, research forums and workshops. The 2014 Pedriatric Hepatology Summer School, which was organized by Professor Pietro Vajro and the ESPGHAN Hepatology Committee, focused on the latest multidisciplinary approaches for the diagnosis and management of paediatric hepatobiliary disorders.

Several recordings from this year’s Pedriatric Hepatology Summer School are now available in the UEG Education library. They include state-of-the-art lectures, specifically tailored for the paediatric hepatologist, on: liver development, anatomy and biology by Professor Stefania Nori;1 liver function tests by Doctor Valerio Nobili;2 and gene therapy for inherited liver diseases by Professor Nicola Brunetti-Pierri.3 Also featured is a collection of recordings on cholestasis, introduced by Professor Thierry Lamireau.4 He explains that cholestasis is thought to affect between 1/2,500 to 1/5,000 neonates, being much more frequent in premature babies, with causes being extrahepatic, intrahepatic or even both. Intrahepatic cholestasis can be triggered by infection or by a wide range of genetic, metabolic and endocrinological factors. In his presentation, Professor Lamireau showcases step-by-step practical biological and clinical procedures for the diagnosis and treatment of each pathology.5 In turn, biliary atresia is the main pathology leading to extrahepatic cholestasis. Professor Björn Fischler illustrates disease pathogenesis and the multiple problems associated with the currently available surgical treatment for extrahepatic cholestasis, highlighting the importance of screening procedures for early diagnosis.6 So, how should cholestasis be managed? Professor Fischler addresses this issue, starting by outlining the consequences of ongoing cholestasis, namely the lack of bile acids in the gut and the retention of toxic hydrophobic bile acids in the liver, and then moving on to the specific management of cholestasis and malnutrition, as well as cholestatic pruritus.7 At the 2014 Summer School, Dr Alex Knisely hosted an interactive voting session on clinical cholestasis cases.8 He introduced the special problems in early life that may lead to cholestasis and the challenges of taking biopsy samples in young infants, before moving to the presentation and discussion of five different clinical cases based on biological and biochemical analyses, as well as liver biopsies. Dr Danièle Pariente’s presentation provides an extended and comprehensive overview of paediatric hepatology imaging modalities, namely ultrasonography, computed tomography and magnetic resonance imaging.9 She addresses each modality’s advantages and drawbacks, as well as indications and limits, in parallel with the presentation of clinical cases. Dr Pariente then goes on to define the imaging strategies in neonates and children in cases of cholestasis (with practical examples on cholelithiasis, choledochal cysts, neonatal cholestasis, biliary atresia); portal hypertension (extrahepatic portal vein obstruction, wedged cirrhosis, congenital hepatic fibrosis, obliterative portal venopathy and Budd-Chiari Syndrome); and liver tumors (hepatoblastoma; hepatic hemangioma; focal nodular hyperplasia; adenomas).   In the final presentation from this series, Professor Fischler discusses hepatitis B, highlighting the large prevalence of this disease in children, particularly in developing and more-heavily populated countries.10 He also considers the challenges of effective vaccination as a preventative measure. Four clinical cases are presented and discussed. If you’d like to discover more paediatric hepatology content from ESPGHAN, please feel free to browse the UEG Education Library, which includes presentations from the ESPGHAN 2013 Summer School and Liver Conference, as well as its 46th Annual Meeting, also held in 2013. Presentations at ESPGHAN Pediatric Hepatology Summer School 2014
  1. Nori S. The liver and the hepatobiliary tree: Development, anatomy and biology issues for the pediatric hepatologist. 
  2. Nobili V. Common LFTs in pediatric Hepatology. 
  3. Brunetti-Pierri N. Gene therapy for inherited liver diseases. 
  4. Lamireau T. Cholestasis: Generalities. 
  5. Lamireau T. Focus on INTRA-hepatic cholestasis. 
  6. Fischler B. Focus on EXTRA-hepatic cholestasis. 
  7. Fischler B. Cholestasis: Management. 
  8. Knisely A. Clinical Cases and Interactive Voting Session. 
  9. Pariente D. Interactive Overview in Pediatric Hepatology Imaging. 
  10. Fischler B. Chronic Viral Hepatitis B.

FMT: balancing scientific success with successful regulation

Eww! If the thought of gulping down helminth eggs in an effort to mitigate the symptoms of IBD, psoriasis and other autoimmune diseases wasn’t unpalatable enough, we now face the reality of having someone else’s faeces fertilizing our guts! Nevertheless, it appears that the incentive for using these types of ‘paleo’ therapeutic approaches is increasing, driven mainly by problems related to antimicrobial resistance, faltering immunological pathways and intestinal dysbiosis, all of which may be intrinsically linked. Meanwhile, authorities are struggling to develop regulations in the face of multiple trials supporting the efficacy of faecal microbiota transplantation (FMT) for the treatment of recurrent Clostridium difficile infections (CDI).

A few weeks ago, @Liz_Atchley uttered on Twitter “If I'm ever in need of a fecal transplant, just let me die”. Same week, @beardbrain went ‘"There Is No ‘Healthy’ Microbiome". So don't get that fashionable fecal transplant unless you really need it!”’ The last tweet refers to an article that appeared in the New York Times.1 What the article actually said was that it appears that there is no single healthy microbiome, that the microbiome in each individual may undergo dynamic changes, and that perfectly healthy people may differ greatly in terms of microbiota structure and diversity. In fact, each of us appears to have a unique gut microbiome that may, however, be perturbed (e.g. by antimicrobials or certain types of diets), leading to disease, possibly including metabolic syndrome. Meanwhile, there is solid scientific evidence that some patient groups, especially patients with recurrent CDI, benefit from FMT aiming to correct intestinal dysbiosis—microbiota alterations—by instilling fecal microorganisms from a healthy individual into the intestine of a patient. In the US, a total of 15%—20% of antibiotic-related cases of diarrhea and most cases of pseudomembranous colitis can be attributed to CDI, which is involved in three million cases of diarrhea and colitis per year, with many thousands succumbing to infection.2 Recurrence of CDI appears to be common, affecting around 15%—20% of cases. In their current CDI guidelines, The European Society for Clinical Microbiology and Infectious Diseases (ESCMID) recommends the use of FMT rather than vancomycin or fidaxomicin in patients who have experienced at least two CDI recurrences (i.e. three CDI episodes in a single patient).3,4 The EAGEN Gut Microbiota 2014 meeting took place in Rome in September, and some of the talks are now available in the UEG Education Library (please see below for the list of presentations). In one of the presentations, Dr Luca Pani from the Italian Medicines Agency not only ‘brutally’ explains the bread and butter of FMT and dishes out compelling facts on FMT success rates, but also expands on the vast potential applicability of FMT, which may prove valuable in preventing, mitigating, and/or treating complex disorders, such as multiple sclerosis, colorectal cancer, metabolic syndrome and disorders stemming from imbalances in the gut–brain axis.2 Moreover, Dr Pani importantly touches upon the intricate issues related to regulating FMT procedures, and asks several important questions. Should food and drug administrations control FMTs? Who are the FMT manufacturers? How about donor exclusions and testing of donor stool—which of the 40,000 species in stool should we allow to enter the recipient? Can single ‘active ingredients’ be identified or does the success of FMT rely on the combined actions/influence of diverse microbial communities? There have been discussions about whether FMTs are in fact tissue transplants or medicines, and there is also a continuum of varieties of FMT, from the infusion of donor faeces screened for pathogens prior to administration, to cocktails of enteric bacteria specifically chosen for and selectively grown on agar plates. Are we talking full-spectrum microbiota or defined microbiota ecosystems? Instead of FMT, are we moving towards ‘Next-Generation Microbiota Therapeutics’5 such as ‘RePOOPulate’, a synthetic stool produced by a ‘Robogut’6? Apparently, FMT regulations vary from being very strict, such as those developed by the US FDA, to being more or less absent in most other countries. In Austria, FMT is regarded as a therapeutic intervention that is not to be considered a pharmaceutical drug and is therefore exempt from regulation by the Austrian Medicines Act.4 As Dr Pani explains, the statistics on FMT for successfully treating C. difficile infections are clear—no need for P values anymore.2 Success stories keep coming in, which will eventually make FMT more palatable to the general public, and so it probably won’t be long before FMT will be triaged by health care professionals, medical companies, and national FDA agencies. Efforts aiming to relax regulations and ensure standardization as much as possible will be crucial in order to reduce the incidence of DIY-related mishaps and to quickly gain more insight into the therapeutic potential of FMT. Hungry for more? Then why not sit back and update yourself on FMT constituents, indications, feasibility, safety, practicality, and regulations, and—maybe first and foremost—examples of professional experience with FMT by having a look at the accepted articles section in Clinical Microbiology and Infection. I also recommend watching the talk on FMT and recurrent CDI by Lawrence Brandt given at the Gut Microbiota for Health 2nd World Summit.7
  1. Yong E. There Is No ‘Healthy’ Microbiome. The New York Times. November 1, 2014.
  2. Pani L. Microbial transplantation as a new therapy option in medicine: The views of the Italian Medicines Agency (AIFA). Opening lecture at EAGAN Gut Microbiota 2014.
  3. Debast SB, Bauer MP, Kuijper EJ, et al. European Society of Clinical Microbiology and Infectious Diseases: Update of the treatment guidance document for Clostridium difficile infection. Clin Microbiol Infect 2014; 20 (Suppl 2):1–26
  4. Kump PK, Krause R, Allerberger F, et al. Fecal microbiota transplantation—the Austrian approach. Clin Microbiol Infect Epub ahead of print 1 October 2014. DOI: 10.1111/1469-0691.12801
  5. Petrof EO and Khoruts A. From stool transplants to next-generation microbiota therapeutics. Gastroenterology 2014; 146; 1573–1582
  6. Petrof EO, Gloor GB, Vanner SJ, et al. Stool substitute transplant therapy for the eradication of Clostridium difficile infection: ‘RePOOPulating’ the gut. Microbiome 2013; 1:3
  7. Brandt L. Fecal Transplantation for the treatment of Clostridium difficile infection. Presentation at the Gut Microbiota for Health 2nd World Summit Madrid 2013.
EAGEN Gut Microbiota 2014 Presentations Pani L. Microbial transplantation as a new therapy option in medicine: the views of the Italian Medicines Agency (AIFA).  Putignani L. Gut bacteriome—Gut aerobs.  Delogu G. Gut bacteriome—Gut anaerobs.  Langella P. Gut bacteriome—Focus on Fecalibacterium prausnitziiCani P. Gut bacteriome—Focus on Akkermansia muciniphilia. Ianiro G. Gut mycome. Bruno R. Gut virome.  Gasbarrini A. The intestinal barrier in different physiological and pathological conditions.  Barbara G. Consequences of increased intestinal permeability.  Lopetuso L. Esophageal gastric barrier. Further UEG Education Resources Surawicz CM. Regulatory and safety issues. Presentation from Faecal microbial transplantation: An old therapy comes of age at UEG Week 2014 Mattila E. FMT for Clostridium difficile infection. Presentation from Faecal microbial transplantation: An old therapy comes of age at UEG Week 2014 Vermeire S. Modulation of the Intestinal Microbiota by Faecal Transplantation: What Can We Expect? Keynote Lecture at ESPGHAN Conference 2013. Further Reading Brandt LJ. American Journal of Gastroenterology Lecture: Intestinal microbiota and the role of fecal microbiota transplant (FMT) in treatment of C. difficile infection. Am J Gastroenterol 2013; 108: 177–185. DOI:10.1038/ajg.2012.450 Kapel N, Thomas M, Corcos O et al. Practical implementation of faecal transplantation. Clin Microbiol Infect Epub ahead of print 1 October 2014. DOI: 10.1111/1469-0691.12796 Kelly CR, Kunde SS and Khoruts A. Guidance on preparing an investigational new drug application for fecal microbiota transplantation studies. Clin Gastroenterol Hepatol 2014; 12: 283–288 Lagier JC. Fecal microbiota transplantation: from practices to legislation before considering industrialization. Clin Microbiol Infect Epub ahead of print 1 October 2014. DOI: 10.1111/1469-0691.12795 Singh R, Nieuwdorp M, Ten Berge IJ, et al. The potential beneficial role of faecal microbiota transplantation in diseases other than Clostridium difficile infection. Clin Microbiol Infect Epub ahead of print 7 November 2014. DOI: 10.1111/1469-0691.12799.

Medical mishaps

… mistakes also happen when providing health care.

Mistakes happen. This is the reason why my Volvo has large rubber bumpers and why pencils have rubbers. Indeed, I, amongst many others, may have been born for this very reason. It has long been recognised that mistakes also happen when providing health care. Of course, there are lots of reasons that such mistakes occur, including sleep deprivation, being rushed, having illegible hand writing, delivering complex care, language barriers and treating elderly patients who have lots of interacting comorbidities.

Estimates vary, but the now famous Harvard Study concluded that 1% of hospital admissions result in an adverse event.1 I must admit to being sceptical about this figure, which would equate to more Americans being killed in US hospitals every 6 months than died in the entire Vietnam War. By contrast, on ward rounds it is clear to me that what actually kills people is being old, frail and diseased. And herein lies the root of my scepticism. The study takes no account of the expected risk of death in the absence of a medical error. A rarely quoted study by Hayward and Hofer,2 tried to examine care more objectively. The authors derived three interesting and illuminating conclusions. First, most deaths reportedly due to medical errors occurred at the end of life or in critically ill patients in whom death was likely regardless of the care received. Indeed, two-thirds of cases reviewed in their study had a "do-not-resuscitate" order in place at the time of death. Second, the level of agreement that a death was 'preventable' was poor (kappa value 0.25). The authors concluded, "…most of the 'errors' identified represent outlier opinions in cases in which the median reviewer believed either that an error did not occur or that it had little or no effect on the outcome." They dryly commented that if there were a large enough reviewer panel, there would always be someone of the opinion that each death was preventable. Third, the probability that an error definitely had contributed to a death was considered rare. The reviewing clinicians estimated that only 0.5% (95% CI, 0.3–0.7%) of patients who died would have lived an extra 3 months if their care had been optimal. This would represent roughly 1 patient per 10,000 admissions to the seven Veterans Affairs medical centres included in the study. The above conclusions will not be surprising to doctors who look after patients. But surely we should always be alert and pounce on every medical mishap to continuously improve practices and reduce the risk of further errors? The hunt for hospital mishaps may, however, have unforeseen consequences. I am aware of three problematic issues. The first issue is that identifying particular patterns of care that result in truly preventable deaths is difficult. It's far easier to identify 'minor' problems and the 'minor' individual responsible. For this reason nursing staff are the most frequently reprimanded team members. Paradoxically, nurses are the least likely not to internalise the reprimand and forgive themselves, and are the most likely to become depressed afterwards. I have seen nurses leave our NHS after a reprimand. There is already a national shortage of nurses because young people don’t want to spend a lifetime working shifts, doing physically and emotionally draining jobs in a punitive environment that comes down hard on every mistake. Qualified nurses don't need a push through the door; they are already leaving frontline services for less demanding jobs in the private sector. Personally, I regret not going into the financial sector where, for example, bringing your bank into financial ruin or the whole world into deep recession is rewarded with a warm handshake and a fat pension. Trying to fix problems in complex settings using hindsight and anecdotes is the second issue as it may lead to processes that worsen care. British nurses now seem to spend more time completing care plans and paperwork than directly caring for patients. To reduce prescription errors, we now have a bewildering 6-page colour coded prescription chart with a myriad of tiny boxes to prescribe anything from oxygen, to compression stockings, to drugs, with ample opportunity to get confused and make a mistake. In my opinion, almost all processes that are put in place to reduce risk, result in an increase in the complexity and time it takes to achieve the task. Surely, the reverse should be the case? Never before in the history of medicine have so many patients with so much disease been given such complex care by so few nurses within such a short space of time! The third and final issue is the overestimation of life expectancy. It is often lamented that doctors overestimate the life expectancy of their patients, but sick patients and their relatives have even more unrealistic expectations—they don't expect to die at all! Paradoxically, it is the elderly who have the least to gain from receiving numerous medical interventions, are the most likely to suffer an adverse event and the least likely to survive when something goes wrong. In spite of all this, when the 'unexpected' happens, it is presumed that it must be due to an error. The creeping mistrust is fuelled by our medical obligation to disclose every medical mishap. The relatives of an octogenarian who succumbs to a hospital acquired infection after a hip replacement will have little doubt that, "The reason my grandfather died was because the nurse didn't dress his wound on time/he didn't get his tablets in the evening/the hospital gave him pneumonia." How can we continuously reduce errors, encourage more young people to become healthcare professionals and provide sufficient time to complete every task, whilst encouraging the elderly to be realistic in their expectations? Unfortunately, this is a circle that cannot easily be squared. In the future, health care will undoubtedly be provided by robots! References 
  1. Brennan TA, Leape LL, Laird NM et al. Incidence of Adverse Events and Negligence in Hospitalized Patients — Results of the Harvard Medical Practice Study I. NEJM 1991; 324: 370–376.
  2. Hayward RA and Hofer TP. Estimating hospital deaths due to medical errors: preventability is in the eye of the reviewer. JAMA 2001; 286: 415–420. 

Endoscopic happenings at UEG Week 2014

I am limbering up for a dose of endoscopy at UEG Week. The ESGE has already sent me free complimentary access to their eLearning unit "Colonoscopy – the Basics". Clearly they are trying to tell me something.

Hopefully you have now downloaded the UEG Week 2014 App, which allows you to choose between 20 different pathways. The UEG Week Vienna Pathways Tool can also be downloaded. I am particularly looking forward to the endoscopy pathway. On Saturday during the postgraduate teaching programme there will be two live endoscopy sessions in the afternoon. The live endoscopists can then relax until Tuesday morning when there will be wall-to-wall live endoscopy in Hall A. These Live sessions do not always go to plan and they are a great opportunity to see experts get into and out of difficulties. Alex Meining is in charge and has told me that he has a record 36 cases lined up. He promises "polyps, polyps, polyps (small ones, ugly ones, polyps in the ileum, polyps in the rectum, polyps in Barrett's, polyps in the stomach), several IBD patients with strictures, new endoscopes (a new gastroscope and the three-lens screening colonoscope from FUSE, Olympus brand new extra-wide-angle scope, etc.). (Only) one ESD, a POEM, pancreatic cysts (with drainage, inspection of IPMN with Spy and confocal). In addition, there are pancreatic and biliary strictures of various types, contrast-enhanced EUS and various EUS-FNAs using various needles". Sounds like the kind of real-life stuff that is always interesting to see how other approach. Don't forget UEG Week Live and UEG 24/7—streaming many sessions as they happen and then making them available later on. Note, however, that none of the live endoscopy sessions are live streamed. On Monday, I'm looking forward to the acute upper GI bleeding therapy update in Hall D. I've got high hopes for the Hemospray device, which I hope will allow me to stay in bed when injection and thermal therapy has failed. In my mind the only outstanding question is "Do we need to organise an early re-check the next morning?" My guess is yes, that white powder will not stay on forever! We have two free paper sessions on new imaging and diagnostic modalities in upper and lower GI endoscopy on Monday afternoon. Not sure why the organisers haven't put the two sessions in the same hall though? Nevertheless, it's great to see that technology arms race is still in place. Sadly, there is a clash between the upper GI update and the update on gastro and duodenal endotherapy. I have the greatest respect for duodenal endotherapy, which is Tiger country indeed. It would be great if there were something that reduces the risk of late bleeding! For a large mucosal defect I spray thrombin, but this stuff is ridiculously expensive. On Tuesday morning Lars Aabakken and I will be hosting a session dedicated to the future of colorectal cancer screening. We'll give you an update on what to do with sessile serrated lesions, and presentations on the thorny issue of how to prevent and deal with local recurrences. Hopefully we can get a consensus on how many times we should try to get rid of a local recurrence before we give up. These are just some of the endoscopic happenings at UEG Week 2014. There are lots more to choose from including updates on Barrett's, EUS, ERCP, capsule and small bowel disease. Endoscopy continues to develop in numerous simultaneous directions driven by new technologies. I think that it has overtaken radiology in complexity, variety and colour! Please give us some feedback on which endoscopy sessions you're enjoying throughout the meeting. The easiest way may be to tweet using any of the hashtags: #UEGWeek #endoscopy #UEGEducation. Alternatively, just grab me for a chat!

Moving through the oesophagus at UEG Week 2014

If this is not your first time at UEG Week, you will already know that coffee breaks and lunch are on us! Just don’t spend too much time on them, as we have an extensive programme on the oesophagus and all things related waiting for you as well!

The postgraduate teaching programme on Sunday is your entrée. It starts with novel approaches and views on dysphagia and eosinophilic oesophagitis in patients with normal endoscopy, followed by a case presentation session on new options in gastro-oesophageal reflux disease (GORD). In the afternoon, you will be served an update on the management and outcomes of upper gastrointestinal bleeding (UGIB). Starting Monday, the oesophagus offering becomes truly 'buffet style' and you may want to take a look at the UEG Week Vienna Pathways Tool to help tailor your schedule to your appetite. For instance, this might be a good opportunity to get a therapy update on acute upper GI bleeding, starting at 11:00 in Hall D. Alternatively, you may walk into Hall B for views on the optimal management of patients with belching, aerophagia, rumination and hiccups. Can't decide? Here's a tip. Look for sessions with a 'Live' symbol. These will be streaming live on the UEG website and made available after the meeting via UEG 24/7. This is also a good day for you to grab your congress lunch and join Professor Mark Fox and colleagues in a round table discussion on dysphagia, based on a case presentation. Please come early though, as seats are limited. During the afternoon, there are two free paper sessions that might interest you: "Clinical and molecular factors in oesophago-gastric cancer outcomes", starting at 14:00 in Lounge 5, and "New diagnostic modalities in upper GI endoscopy", starting at 15:45 in Hall G/H. Continuing with your oesophageal main course, Tuesday kicks off with a therapy update on GORD, the implications of molecular pathogenesis on endoscopic therapy for Barrett's oesophagus, and a session on the risk factors and management of upper GI bleeding. If you are interested in novel endoscopic interventions in the oesophagus, please be sure to attend a free paper session on this topic at 11:00 in Hall O. Right after lunch at 14:00, you might want to join the discussion on whether function tests for the upper GI tract are indeed necessary or not (Hall B) or perhaps you might rather attend a free paper session on risk stratification and ablation in Barrett's oesophagus (Hall O). Moving towards the end of the day, a symposium on evidence-based treatment of achalasia takes place. No meal is complete without dessert! On Wednesday, the oesophagus pathway wraps up, starting with fresh and innovative views on the challenges and new frontiers in GORD and Barrett's oesophagus. You are also in for an integrated pathologist's versus endoscopist's view on oesophageal squamous cell carcinoma, early Barrett's neoplasia and early gastric carcinoma in the 11:00 symposium in Hall I/K. To return home with a sweet taste in your mouth, UEG Week 2014 ends with three cherries on top of the cake: a symposium on adenocarcinomas of the oesophago-gastric junction, another on endoscopic resection of upper GI tumours, and a free paper session on eosinophilic oesophagitis and other immune-mediated upper GI diseases.      We hope you enjoy the oesophagus 'course' at this year's UEG Week and look forward to your comments and tweets! (#UEGWeek #oesophagus #UEGEducation).

Spotlight on cancer—covering all bases at UEG Week 2014

Time is ticking away to UEG Week 2014 and if fighting cancer makes you tick, you are about to enjoy a full-course week, with servings from a cutting-edge research programme on cancer screening, diagnosis and prevention, and treatment.

If you're an early bird, you might decide to start your UEG Week 2014 experience on Saturday by attending the postgraduate teaching programme, with a mid-morning session dedicated to pancreatic adenocarcinoma, which covers endoscopic ultrasound, radiology and pathology for differential diagnosis, resectability and novel systemic treatment options. Sunday is a busy day and kicks off early morning with a session on colorectal cancer (CRC), focusing on early detection and local treatment, with talks on colonoscopy and non-invasive tests in population screening, and on recognition and diagnosis of early (T1) cancer: endoscopy, histopathological diagnosis and the use of ESD or TEM. This session is followed by one on terminal GI cancer, focused on symptom management and patient care (including case presentations). If you are only arriving on Monday, no worries! You are just in time to get in gear for the opening plenary session, which includes a talk on advances in the management of CRC, and is followed later in the morning by a free paper session focusing on the clinico-pathological features of GI cancer. During the lunch break you may want to electronically browse through the posters at the E-poster exhibition, and attend the new 'Poster Champ' sessions (from Monday to Wednesday), to select and award the best posters in each category. The afternoon programme includes plenty of sessions for you to choose from, starting with a free paper session on imaging techniques in colonoscopy, followed by another on new diagnostic modalities in upper GI endoscopy. In parallel, from a cancer treatment perspective, the session on late breaking digestive oncology abstracts is very appealing, and just prior to a session on the current and future perspectives in pancreatic cancer. Tuesday begins with a session on funding available for research under the EU research framework programme (H2020), followed by a 'Posters in the Spotlight' session on "Mechanisms underlying the development of GI cancer". This format is new for UEG Week 2014, in which hot topic research E-posters are presented on stage, and an oral free paper prize will be presented to the best poster. The afternoon kicks off with a free paper session on novel mechanisms and targets in CRC, followed by two sessions focusing on endoscopic management of early colorectal neoplasia and treatment of liver metastases. Wednesday wraps up this year's exciting and vibrant UEG Week, starting with novel approaches to rectal cancer from the viewpoint of the pathologist and the endoscopist. The final afternoon starts off with a round table discussion on molecular guided therapy for GI cancer, and ends with a session on the pancreas, in which an annual review of pancreatic cancer will be presented from basic and clinic viewpoints.  To make sure you're not missing out, please do complement this brief by browsing the complete programme online or by viewing the cancer pathway, which can be accessed online or via the UEG Week App.  We'd also love to hear what cancer content you find appealing throughout the meeting. Tweet to let us know! #UEGWeek #GIcancer #UEGEducation. On a footnote, since you can't physically be in two places at once (yet!), UEG will be livestreaming many of the sessions as they happen via UEG Week Live and all recorded talks will be made available via UEG 24/7.

Hepatobiliary highlights at UEG Week 2014

There is no doubt that 2014 is witnessing a revolution in the treatment of hepatitis C. You can find out all the latest information at this year's UEG Week, starting with a dedicated session during the postgraduate teaching programme on Saturday morning (Viral hepatitis: Cure by modern regimens?). The course will further offer you the opportunity to get an update on non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease, as well as on the endoscopic management of malignant biliary obstruction challenges, and will also feature a clinical case-based session on liver function assessments.

For further insights into hepatitis C management, be sure to attend the opening plenary session on Monday morning, which includes a talk by Professor Michael Manns, followed by an overview by Professor Heiner Wedermeyer of what's new in hepatology in clinical practice in 2014. After lunch, there will be a special free paper session on the lingering clinical challenges for hepatitis C therapy, followed by an update symposium on viral hepatitis therapies. Hepatitis C may be a lead actor in this year's UEG Week liver 'play', but much more besides is being covered. For example, why not join a round table discussion on non-obstructive jaundice on Monday lunchtime (please note that numbers are limited for these sessions)? Updates on NAFLD and liver cirrhosis (in the format of a free paper session and posters in the spotlight) are also featured in the afternoon, in parallel with a session on the immunopathogenesis of pancreatitis and hepatitis, as part of UEG’s two day "Today's Science; Tomorrow's Medicine" initiative. On Tuesday morning you might find yourself undecided on which session to attend. Will it be 'Clinical management of liver cirrhosis' or 'The liver as a central regulator of inflammation'? Shortly after, there's an update on alcoholic liver disease and novel aspects of biliary tract cancer to choose between. Finally, the afternoon has new concepts in management of biliary diseases and a free paper session on biliary tract cancer occurring simultaneously. Lucky for you, UEG has your back; all recorded sessions will be made available via UEG 24/7, with many of the sessions being made available as they happen, via UEG Week Live. For the final day of the meeting, there will still be plenty to learn about cholangiocellularcarcinoma (and neuroendocrine tumours), as well as diagnosis and management of both non-cirrhotic and cirrhotic liver nodules. And you may want to return home with some new insights on biliary stenting or on the interconnecting pathways linking viral hepatitis, cytokines and liver regeneration, which you can learn all about in the last two free paper sessions of the day. And don't forget there are poster sessions running throughout the whole meeting! Last but not least, we invite to visit the online program and search for your specific topic of interest—the word 'liver’ alone returns 355 matches! Or you might want to make use of the UEG Week Vienna Pathways Tool to make sure you’re not missing out! You can also download the UEG Week App for your mobile device and have all this information and more at your fingertips. We hope you enjoy the hepatobiliary pathway and would love to hear what you find interesting at this year's meeting! Please do comment or tweet to let us know by including one or more of the following hashtags: #UEGWeek #Hepatobiliary #UEGEducation. You can also visit the UEG Education Lounge located in Hall Z and talk to us personally. Have a great meeting!

UEG Week 2014 in transit: A view from the intestine

With UEG Week 2014 just around the corner, we have forged a brief summary for your perusal that might be of interest if you're into inflammatory bowel disease (IBD), irritable bowel syndrome (IBS) or other issues related to functional and organic bowel diseases.

Unsurprisingly, IBD is one of the major topics at UEG Week 2014. If IBD is your thing, then you should kick things off with the postgraduate teaching programme on Saturday and Sunday, when you can learn more about what's important for diagnosis, the challenges of refractory IBD and also skin lesions in IBD. And do make sure you're ready for Monday because it's jam-packed! The opening plenary session includes no fewer than two talks on 'How to translate basic immunology findings into clinical reality in IBD'. You may then want to stay put in Hall A to get updates on 'What's new in 2014' and to receive highlights from Digestive Disease Week 2014. However, you might prefer to stretch your legs and explore the convention centre. Why not look up environmental factors and IBD (Hall F2), conventional therapy for IBD (Hall I/K) or the free paper session on small bowel imaging and endoscopic interventions (Lounge 6), where you can get updates on everything from the diagnostic value of faecal calprotectin to the clinical usefulness of virtual enteroscopy for Crohn’s Disease. At lunchtime there's a round table discussion on treating IBD in patients with cancer and early in the afternoon there are parallel sessions on pathophysiology and new imaging tools. After all that, move to Hall E to be updated on the new European guidelines for diagnosing IBD or to Hall L/M to find out about new therapeutics for specific targets. Tuesday and Wednesday continue in the same vein, with more than ten other IBD sessions on offer—from management of complicated Crohn's disease to the best use of biologics, new biomarkers, new drugs, epidemiology and outcomes, targeting new pathways and what's new in 2014. In order to bone up on coeliac disease and wheat allergy, you should look up the postgraduate teaching programme session in Hall E on Sunday morning. Monday sees an afternoon session on 'New Challenges in Gluten Sensitivity: From Bench to Bedside', and includes a talk on triggers and drivers of autoimmunity. Look up 'Posters in the Spotlight' on Tuesday afternoon to learn about the applicability of serological tests for the diagnosis of coeliac disease in asymptomatic children. Speaking of those who are asymptomatic—should they be put on a gluten-free diet? Find out at the round table discussion on Wednesday lunchtime! To learn more about diet, food intolerance, and nutrition you'll probably want to secure a seat in Hall G/H Wednesday from 11:00am. Diet appears to be a major modulator of gut microbiota and this is one of the topics covered in the 'Today's Science Tomorrow's Medicine' session on 'Diet, immunity and systemic disease' in Hall R late on Monday morning. Moving on to bacteria, blooming blasters of bad bugs probably don't want to miss out on the postgraduate training programme on Saturday afternoon, which covers diagnosis, management and prevention of Clostridium difficile infections. Obviously, faecal microbial transplantation is bound to attract a lot of attention—make sure you secure your seat in Hall C on Tuesday afternoon! To learn more about the gut microbiota in health and disease, the symposium on altered intestinal microbiota composition in IBS on Monday morning in Hall G/H is an absolute must. Participate in the debate on whether gut microbiota alterations in patients with IBS are a cause or a consequence. To be updated on FODMAP and gluten-free diets for IBS patients you just have to look up Hall I/K and Hall Q on Monday afternoon, and if this is not enough, a panoply of talks on restrictive diets is in store for you in Hall E just before lunch on Tuesday. Next, hurry to Hall G/H to participate in the round table discussion on how to manage the difficult IBS patient, and then, immediately after this, Hall D is certainly the place to be on Tuesday afternoon if you want to continue learning how to manage IBS patients successfully. Please, however, be aware that there is also a Translational/Basic Science pathway session on normal and abnormal cross-talk at the mucosal border and the relevance of this for GI function and dysfunction taking place on Tuesday afternoon (Hall L/M). Faecal incontinence gets attention in the postgraduate teaching programme on Sunday, while constipation takes the stage on Tuesday afternoon—these two topics are also the focus of a free paper session in Hall R on Wednesday morning. Finally, don't forget the 'Neurogastroenterology and Motility: What’s new in 2014?' symposium in Hall 2 at 11:00–12:30 on Wednesday! With so much on offer, don't forget that there are plenty of tools available to help you make the most of UEG Week 2014. Downloading the UEG Week Vienna Pathways Tool is one way of getting acquainted with the entire conference programme. Or maybe you prefer to download the UEG Week App instead? The App includes the 'Pathways' feature that enables you to identify exactly which sessions might be of particular interest for your specialty. Many of the talks will be made available as they happen via UEG Week Live, which is great if you can't make the meeting in person. All recorded sessions will also be made available via UEG 24/7—perfect if you can't decide between parallel sessions!   We'd love to hear what intestine and motility content you find interesting throughout the meeting, so please do tweet to let us know by including the hashtag #UEGEducation and one or more of the following: #Intestine #IBS #IBD #motility #microbiota #FMT (faecal microbial transplantation) #Cdiff   Happy ruminating!

How to stomach H. pylori during UEG Week 2014

UEG Week 2014 is now just a few days away, and if your research or specialty involves upper GI diseases, such as gastric ulcers or gastric cancer, you're sure to get your fill at this year’s meeting.

With more than 35 sessions of relevance to choose from, we've selected a few that you might find interesting and informative, but do consider downloading the UEG Week Vienna Pathways Tool to make sure you're not missing out! The postgraduate teaching programme on Sunday has a lot in store for you. In the morning, there is a session on advanced endoscopic techniques, including gastrointestinal imaging and submucosal endoscopy. Around noon, you'll need to choose between three practical sessions that are supported by case presentations: learn more about managing and caring for patients with terminal GI cancer, progress in dysphagia and gastroparesis or whether we've solved all the problems associated with H. pylori infection. The afternoon is completed by a session on management and outcomes of upper GI bleeding, including endoscopic management, blood transfusion, pharmacological strategies for improving outcomes in acute upper GI bleeding, and information on the impact of novel oral anticoagulants on the gastroenterologist's case load. How H. pylori alters stem cell homeostasis by direct colonization of the gastric glands is the subject of a talk by Michael Sigal in Monday morning's opening plenary session in Hall A. If you choose to stay put in Hall A, you will certainly be able to find something to your liking in the 'What's new in 2014' session. Alternatively, you may want to proceed to Hall D if you're particularly interested in issues related to acute upper GI bleeding, or to Hall B if you’re more into topics related to belching, aerophagia, hiccups, rumination or cyclic vomiting. Of course, functional dyspepsia is also on the menu. Talks on diagnostic criteria and therapeutic approaches will surely attract quite a few attendants in a symposium dedicated to new thoughts in functional dyspepsia. This symposium also includes a talk on the role of food allergy in dyspepsia, and data on the association of serum adipocytokines and gut hormone levels with gastric emptying and symptoms in patients with functional dyspepsia will be presented. Monday finishes with talks and a panel discussion on 'quality endoscopy', including upper GI diagnosis, and should give rise to some interesting discussions based on experience and data from around the world. By the way, don't forget to season your Monday with some of the 'Best of DDW' from 14.00—15.30 in Hall A. There are two free paper sessions on offer if you're up and about bright and early on Tuesday morning: one on upper GI bleeding (risk factors and management) and the other on gastric carcinogenesis (new insights into pathogenesis and management). Tuesday morning is also H. pylori galore and offers an entire symposium on H. pylori-associated gastric carcinogenesis, covering everything on how H. pylori is able to induce gastric cancer. Unsurprisingly, there will be presentations on H. pylori-induced epigenetic changes, H. pylori-mediated miRNA regulation, proteolytic activity, and how iron deficiency may be involved in H. pylori-associated carcinogenesis. Later in the day, Hall B will also host talks on function tests for the upper GI tract and this session is a must for those interested in lactose intolerance and for those who do not really know what to make of oesophageal high-resolution manometry. If you're not full by the end of Tuesday, there's still plenty on offer on the final day of the meeting. On Wednesday lunchtime there are limited spaces available at two Round Table Discussions: one on the impact of long-term PPI use and one on molecular guided therapy for GI cancer. You also have your pick of two Wednesday afternoon symposia. In case you want to update yourself on advances in obtaining a mechanistic understanding of dyspepsia, Hall B is the place to be. Here you will also get a general update on dyspepsia, including data on new drugs, psychological therapies, and diagnostic tools. If adenocarcinoma of the oesophago-gastric junction sounds more alluring, then you should proceed to Hall F1. Here, different aspects of diagnosis and treatment will be dealt with, and the session highlights the relevance of taking a multidisciplinary approach to this particular disease. Finally, don't forget to check out the poster sessions on Monday, Tuesday and Wednesday, with 'Posters in the Spotlight' available for viewing in the E-poster lounge on those days. We'd love to hear what stomach and H. pylori content you find interesting throughout the meeting, so please do tweet to let us know by including one or more of the following hashtags: #UEGWeek #Stomach #Hpylori #upperGI #UEGEducation. In case you're not attending UEG Week in person, please note that many of the talks will be made available as they happen via UEG Week Live – just follow the livestream on the UEG website ( If you can't catch every talk as it happens (in person or via the livestream), then you're in luck because all recorded sessions will be made available via UEG 24/7 ( Bon appétit!

A perfect storm

A record number of patient complaints for the 12-month.

The English Health and Social Care Information Centre recently reported a record number of patient complaints for the 12-month period from 1 April 2013—31 March 2014. The total tally was 174,872 complaints and the largest single source was complaints about inpatient care. In a country where people apologise for getting their feet stepped on, most patients do not complain about poor medical care and this figure is likely to be the tip of the iceberg.

So who is to blame for this epidemic? The West in general and the English National Health Service (NHS) in particular is seeing the beginning of a perfect storm in which several forces are converging. The first component is our increased life expectancy (lifespan), which has not been mirrored by an increase in healthy life expectancy (health span). People are now living longer in spite of accumulating health problems. Patients survive heart attacks, only to require multiple vascular interventions. Patients live with cancer longer, at huge expense, requiring close monitoring and frequent imaging. The second component of the perfect storm is patient expectation. It is paradoxical that although we now live longer than at any time before in history, we worry more about our health than ever. People are no longer content to see if that stubborn cough or sore throat will settle in a few days. After all, it may well be the beginning of something serious! Furthermore, they would rather have someone else, a 'qualified person', telling them that they have nothing to worry about. If their insomnia then turns out to be the first sign of a brain tumour, at least there is someone to sue. Many of the major IT companies are also developing smart watches with the ability to monitor health parameters and turn healthy people into nervous patients concerned about extra heart beats or poor quality of their REM sleep. In the case of the English NHS, the third component is that politicians are unwilling to pour further money into a health service that they see as inefficient. I guess that by throttling funds, they are hoping that a more efficient service will emerge. Sadly they are mistaken and instead services are increasingly managed on a shoestring. Wards are kept open with the bare minimum of nursing staff. Support services such as audiology, speech therapy, physiotherapy and occupational health are told that they have to cut expenditure by up to 20% As the above three factors are beginning to exert an irresistible force on the English health care system, managers' and politicians' eyes are increasingly turning towards the Pandora's box that is 'the marketplace'. When I first arrived in England some 30 years ago, hearing aids, dental care, retirement homes and eyesight tests were all free. However, it was soon realised that these services could be taken care of by private providers. As our creaking NHS is finding itself subjected to the unyielding effect of the above three forces, it is inevitable that this Pandora's box will be opened. Naturally, the NHS could never stop providing free emergency care for patients with serious acute disease or cancer, but this leaves plenty of scope for private providers in the marketplace. Why not ask pharmacists to see patients who develop a sore throat, wake up with a headache or simply feel tired? Pharmacists could charge patients either directly for giving them advice or indirectly by incurring a fee for the medicines that they recommend. Parents who find that their children have wonky teeth, can’t sit still in the classroom or simply don't seem to develop as well as their siblings, will in the future have to pay to have their children seen to. But why stop there? Why should the NHS provide joint replacements for free when instead it could supply patients with walking sticks? Why should the NHS provide free cataract extractions in both eyes when operating on just one eye is enough to allow people to read a book? Osteoarthritis and cataracts are neither emergency care nor cancer! Furthermore, why shouldn't patients pay for more expensive medication themselves? If patients don't like their angiotensin receptor blocker, they may opt for an angiotensin-II receptor blocker that has a different side effect profile! If patients are prepared to pay an extra €30.000 for a cytotoxic agent that gives them hope of an extra few months' survival, why stop them? The marketization of our lives is becoming omnipresent. Soon it will be possible to purchase everything. I can see three reasons why the free rein of market forces will be bad. Firstly, there will obviously be people who cannot afford care. Parents who do not have the funds or knowledge of 'the system' will not be able to obtain medication for ADHD or pay a psychologist for cognitive behavioural therapy. I predict that we will in the future see more evidence of what can go wrong when children are left unsupervised on our streets. Secondly, I would miss the fact that when I recommend a treatment to a patient, both of us know that I do not stand to gain personally from the advice. In most parts of the world, patients do not have this reassurance and may be tempted to seek an alternative and perhaps cheaper opinion. Patients seeking multiple opinions and then choosing the one that suits their own ideas best will not necessarily lead to better health outcomes. Thirdly, the 'haves' and the 'have-nots' will live completely separate lives. They will live in different parts of the city, their children will go to different schools, they will travel to work by different means and their leisure time will be spent in different places. I don’t think that this is good for society. Democracy itself will be under direct attack as those who can afford to pay for political influence and lobbyists will seek to buy the policies that favour them. Why not—it's the marketplace! In the meantime, I keep staring at those X-ray machines in the knowledge that when my own cataracts have reached maturity, and I can no longer read a book, my optician will swiftly point me in the direction of a private ophthalmologist without any involvement of the NHS. 

Cooperation and Reciprocity in Organ Transplantation

Surely one of the cornerstones of the survival of any species is how individuals participate by means of “Reciprocity” (Oxford dictionary; exchanging things or favours with others for mutual benefit) and “Cooperation” (the action or process of working together to the same end).

But what about those who try to cheat the system, deriving the benefit of others cooperating but without providing any reciprocity? I recall a study of seagulls which prune their own feathers but have to rely on other to prune their own heads. What if a pesky bird would accept others pruning its head but would rather spend his own pruning time catching more fish than pruning others in return? How does nature deal with the problem of the cheat? The observational study found that birds have a long memory and will not prune another bird if it had not returned the favour in the past.  I remembered this study when reading about the dwindling supply of organ donation. Safer cars have reduced supply and improved survival after heart attacks have increased demand for heart transplants. According to the NHS own website, between April 2011 and March 2012, 3,960 organ transplants were carried out in the UK thanks to the generosity of 2,143 donors. Unfortunately, another 7,593 people were still waiting for transplants at the end of the period. The ratio of 2.1 donors/ 3.9 organs is a little odd as in theory, one donor should provide organs for up to 6 transplantations.  There is a particular problem with tissue mismatch as Black and Asian people are three to four times more likely to develop kidney failure than the general population but are particularly unlikely to join the Organ Donor Register. This is particularly tragic as people from the same ethnic group are more likely to be a good tissue match.  To boost supply in England, a Bill has been proposed for an “opt-out transplant system” whereby everyone would automatically be included in the donor registry unless they ask to be taken off the register. Although the bill has already become law in Wales, I must admit that I am sceptical. People may still find a myriad of reasons why Nature’s law of cooperation and reciprocity does not apply to them and opt out of the donor registry. Indeed, Chile has seen an overall fall in the number of organ donors since they introduced an “active opt-out system” and evidence from other countries with an opt-out system indicates that the rise is small with only around 15 additional donors per country per year!  The Government’s proposed bill has received fierce opposition from Christian churches and from within the Muslim and Jewish communities. I would like to propose a solution which will retain people’s ability to exercise free choice, will not offend religious sensitivities and still provide a fair system, based on cooperation and reciprocity.  People will only be eligible to receive a donated organ IF they had already joined a donor registry! People would indicate which donor registry’s they would like to join and in turn be eligible to receive a transplanted kidney, liver, heart, lung, small bowel or pancreas.  It would work similarly to an insurance programme in which it would only be possible to get cover for a new disease. Without this clause, we will soon find cheats who quickly join the donor registry once they have received a diagnosis of cirrhosis. The only problem I can foresee is that of children or people with diminished capacity who are unable to choose. Perhaps in those cases, it would have to be their legal guardians who would have to make the choice on their behalf.  Wales will reassess the result of their new law in 5 years. Perhaps when they see the paltry number of extra donors, all from white middle classes rather than minorities, they will re-consider my proposal?

After the Summer School

Having returned from a hectic UEG Summer School in Prague, Bjorn has some reflections on Happiness

Professor Richard Easterlin found that more money does not make us more happy – the “Easterlin Paradox”.  This is because of “habituation” whereby the immediate thrill of buying something extravagant wears off. 

In fact, in spite of rising disposable incomes, people are less happy than they were 50 years ago.  Professor Robert Putnam blames the American unhappiness on television.  This is because the TV makes us less likely to go out and socialise and feel part of a community.  He also found, after studying some 30 000 Americans, that as communities became more diverse, people became less trusting of each other. 

Can Social Networks overcome our TV-induced isolation?  Well, Facebook may be better than TV (as a degree of communication is possible) but “competitive pressures” also increase. The “look what a fantastic life I have – effect” reduces happiness in others. 

Having spent a few fun days at the UEG Summer School in Prague, it’s clear to me that Putnam was right.  Nothing can beat meeting people face-to-face for building bridges across countries and continents.  As a total of 150 trainees and 20 specialists from 33 different countries mixed in the morning lecture theatre, afternoon workshops and over dinner an in nightclubs, a strong camaraderie developed.  

The last century has given us cars, telecommunication and globalisation.  These are firmly anchored in an economical “growth strategy” in which countries compete to continuously increase Productivity and GDP.  This is associated with depleting resources, global warming and a reduction in overall happiness.   In contrast to having more stuff, I predict that in the next 100 years, people will want and expect improved health and longevity.  In Prague I was privileged to meet some of the people who will deliver it. 

Do you have what it takes?

Every year we are hosting a one year’s Endoscopy Fellowship in Leeds. The aim is to provide one of our senior Gastroenterology Trainees with a grounding in advanced therapeutic endoscopy.

Unfortunately, it has become apparent that not every trainee is comfortable with advanced therapeutic endoscopy.  They have a problem with the unpredictability of neoplasia and therapeutics.  Sometimes the resection goes to plan but at other times there is pain, immediate bleeding, delayed bleeding or even perforations.  Unpredictability is an inherent part of endoscopic therapeutics.  In fact, it is one of the reasons that I love it.  Not two cases are the same!

However, some of our trainees find this new role deeply unsettling.  Up to this point in their careers, they have never found themselves to be the reason why their patient ends up on the ITU or admitted for live saving emergency surgery or readmitted with a haemoglobin level of 40.  

A few years ago the Christmas edition of the BMJ published a tongue-in-cheek piece of research which clearly identified the "Therapeuticians” from the “Diagnosticians” (those who dare from those who duck).  A plucky researcher hid in the car park of a large hospital and secretly timed how long it took for surgeons to park their cars compared to the medics.  There was a clear divide, whereby surgeons would park their cars 20% faster than their medical counterparts.  The reason was not that the medics were driving larger cars but because they were far more cautious.  They would pull up to a free slot but bail out because it looked a little tight, or was close to a bend or required reversing into the slot etc.  The surgeons had more confidence in their abilities and were less concerned about what could go wrong (scratched paintwork). 

I now try to dissuade the trainees from applying who are the least likely to be comfortable in a life of therapeutic endoscopy.  It is easy to identify them. They will not miss an opportunity to phone you for advice, craving reassurance that they are doing the right thing. They feel uncomfortable making decisions, particularly if it has to be based on a “best guess” rather than a treatment protocol.   Paradoxically, I regard our ability to assess large amounts of partially contradictive and confusing information and provide a sensible and educated guess, is what separates us from nurses.  This is what we are trained for! 

I do ask trainees if they think that they would be happy in a professional life of removing large and scary lesions.  Unfortunately, most trainees have little insight into their own comfort zones.   Perhaps I should change my approach and simply time how long they take to park their cars. 

Get checked out - have a full body CT?

Since my teenage years I have been afraid of radiation. Two phrases stuck in my mind: 1) “there is no safe limit for radiation exposure”, 2) “the DNA damage is cumulative and never goes away” ...

Indeed this is why I see little point in radiology for disease which can be assessed by endoscopic means.  For the same reason I am incredulous when people voluntarily expose themselves to ionising radiation as part of a health check-up.

During ERCP I diligently carried my personal radiation exposure meter for many years.  Although the device was issued for “exposure prone activities”, such as ERCP, I decided to always carry the meter with me at work.  After all, the ionising radiation is even more significant when not shielded by a lead apron. 

Last year I had an Eureka moment and also started to wear the dosimeter during flights.  In the UK the average annual background radiation dose is 2.2 millisieverts (mSv).  However, at cruising altitude (35.000 feet), the hourly radiation may be up to 50 times greater than at the surface.  In addition, those body scanners which are replacing metal detectors at airports also emit radiation.

Your precise dose depends on the number of hours spent at high altitude and the latitude of the flight.  Latitude is important as earth's magnetic field deflects charged particles. The shielding is most effective at the equator where earth's magnetic lines are parallel to earth’s surface. Conversely, the magnetic shielding disappears over the poles where the magnetic lines point perpendicular to the surface.  Not sure how do penguins manage to cope with the large amount of radiation they receive at the South Pole?  Perhaps they don't live long enough to get cancer? 

For every 200 hours in the air, you receive 1 mSv of radiation exposure (look for yourself by clicking this link).  I was therefore surprised that our radiation protection officer did not phone me after I had travelled with my radiation exposure meter for year.  It turns out that most of the radiation received in an aircraft is from neutrons which can not be detected with classical dosimeter!

Official calculations estimate that for each 1 mSv of radiation exposure (above background radiation), will give rise to another 6.3 cancers per 100.000 people/year.  It is for this reason that EU-based air crews are limited to a maximum of 100 mSv of exposure in every 5 year period.  Nevertheless, there is evidently no safe radiation limit as pilots have been found to have an increased risk of cancer. 

My Radiologist friend tried his best to reassure me and pointed out that these radiation figures must be put into context.  “For example, a trip to Mars, will give you a total of 1000 mSv  which will give you a 1:20 extra risk of dying from cancer”.   In comparison, one of our abdominal CT studies only generate some 10mSv of radiation and will not cause more than one extra cancer in 400-500 exposures…

Reassuring words indeed !

A couple of years ago, I was invited to spend a long weekend in an African city.

It was part of an initiative to teach endoscopy to the locals. Anticipating trouble, I cautiously announced to my wife that this “would provide a great opportunity to see some of the marvellous continent.” My wife agreed: “Yes this is a great opportunity, just a shame that you will NOT be going!” She continued, “it’s far too dangerous and what these poor people need is clean water and a comprehensive vaccination programme not blooming endoscopies!” As a paediatrician, my wife felt that she could speak with some authority on the needs of Africa. “And goats, lots of goats”, I retorted remembering a friend who on getting married declined wedding presents but accepted donations of goats. One of my friends thought that I gave in far too easily. “You know, if you allow your wife to cocoon you like this, with ever tighter wraps, you’ll suffocate”. I was somewhat taken aback. For me, defiance was unthinkable but this guy seemed to do as he pleased with impunity! Living with a formidable wife and three strong daughters, I had been outnumbered for more than a decade. Furthermore, I spent every working day in the company of women. Last year I concluded that the testosterone levels at home needed a boost. I bought a 50Kg male brute of a dog. At the previous owners, he used to bark gruffly at passing cars. Sadly he quickly adapted to his new surroundings and within three weeks, the dog stopped barking and became frightened of umbrellas, balloons and plastic bags. I don’t blame the poor dog, fear was inevitable. I am still OK with balloons and umbrellas but I have become afraid of my wife. After 30 years I have even come to believe that it’s the secret behind a long and successful marriage.
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