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Access over 450 recorded scientific lectures from UEG Week 2015. Free for delegates, attractive bundles for all!

Ulrike Kapp-Popov


T  +43 (0) 699 1997 16 16


E  e-learning@remove-this.ueg.eu

 

Julia Kasper


T  +43 (0) 699 1997 16 11


E  j.kasper@remove-this.medadvice.co.at

 

 

My precious!

Testing nanosilver-based preparations in preclinical conditions. What would you do next?

Preliminary findings in our laboratory indicate that preparations based on silver particles and nanolayers could be directed against inflammation in the colon.

What strategy would you recommend when testing and trying to characterize the mechanism of action of a nanosilver-based preparation in preclinical conditions?

a) An in vitro assay for antimicrobial activity of the drug (e.g. agar-cup technique)

b) An in vitro assay for antimicrobial activity of the drug (e.g. agar-cup technique), followed by an in vitro examination of its cytotoxic effect on a human cell line (e.g. CaCo-2)

c) An in vivo model of colitis, followed by flow cytometry for selected lymphocytes and basic tests for biodistribution and toxicity

d) An in vivo model of colitis, followed by examination of changes in intestinal bacteria and basic tests for biodistribution and toxicity

e) An in vivo model of colitis, followed by examination of changes in intestinal fungi and basic tests for biodistribution and toxicity

Mistakes in coeliac disease diagnosis and how to avoid them

Learn from leaders in the field!

Coeliac disease is regarded as an autoimmune disorder triggered by gluten, which activates an immune reaction against the autoantigen tissue transglutaminase (transglutaminase 2; TG2) in genetically predisposed subjects. Genetic susceptibility to coeliac disease has been proven by its close linkage with major histocompatibility complex (MHC) class II human leukocyte antigen (HLA) DQ2 and DQ8 haplotypes. The identification of biomarkers for coeliac disease (e.g. endomysial antibodies [EmA] and antibodies to TG2 [anti-TG2]) has changed the epidemiology of coeliac disease from being a rare to a frequent condition, with an expected prevalence of 1% in the worldwide population.1 Nonetheless, the majority of patients who have coeliac disease remain undiagnosed, leaving the coeliac ‘iceberg’ mostly submerged. Coeliac disease can be difficult to diagnose because symptoms vary from patient to patient. Indeed, the heterogeneity among the clinical signs and the lack of specificity of many of the presenting symptoms means that the diagnosis of coeliac disease can be a challenge even for experts.

Despite substantial differences in the mode of presentation and the availability of new diagnostic tools, small intestinal biopsy, which shows different grades of mucosal damage, remains the gold standard for coeliac disease diagnosis. A delayed diagnosis of coeliac disease in the elderly can be considered a risk factor for complications including refractory coeliac disease, ulcerative jejunoileitis, collagenous sprue, small bowel carcinoma and enteropathy-associated T-cell lymphoma (EATL). Complicated coeliac disease is not so frequent, being found only in about 1–2% of the total number of coeliac disease patients, but for those who have it the prognosis is very poor, with a low rate of survival after 5 years.2

Here we discuss the major mistakes that are made when diagnosing coeliac disease and how to avoid them. The list of mistakes and the discussion that follows is evidence based and integrated with our clinical experience of more than 30 years in this field.

Surgical hands-on training

This course enables residents & young surgeons to improve conventional and laparoscopic surgery skills.

E-learning for e-living (or “A personal perspective on kung fu”)

Education is changing...

Education is changing. It is changing because our lifestyle has changed. Information is now instantly available, wireless, mobile and, at times, even pushed as notifications or alerts to our devices and inboxes. Accessibility is the key to this change. Starting at kindergarten and first grade, teachers can use this access to enrich and diversify the students’ experience. The implications for medical education may be even more profound. 

 

Medicine is a unique type of training, made challenging by the sheer volume of knowledge required, the need to understand complex physiology and pathophysiology, literature that is constantly being updated, the need for clinical skills and reasoning, and much more. Furthermore, medical training is not just limited to students, but continues well into the professional life (e.g. specialty, subspecialty, etc.).

Medical students and interns go through an apprentice-like programme, gaining clinical experience and honing their medical reasoning based on clinical exposure. For many, good mentors at this period have a great impact on who they are today, and probably nothing will ever replace this important interaction.

However, we must also appreciate the inherent limitations of this system. Try recalling your own training. Did every lecture make sense? Could you always see the slides and hear properly? What if you wanted the last two sentences to be repeated? Could you even find a lecture on your specific topic of interest?

This is where e-learning becomes a necessary component of medical education. E-learning provides every user with a front-row seat in a class of their choice, which can be ‘attended’ in their free time, with the ability to view the learning material more than once. Such a platform can be extremely attractive to gastroenterologists and gastrointestinal researchers, and not just for viewing rare endoscopic findings and procedures.

When was the last time you (or your fellows) heard an excellent talk on the use of proton pump inhibitors (PPIs)? Understanding such a ‘bread and butter’ topic is paramount to our everyday practice, but may be considered too basic for inclusion at international meetings. This is an example of a larger potential caveat in available educational resources. Different programmes and societies may work to fill this gap, and here is one area where the UEG e-learning website comes in handy.

The UEG E-learning website now has a vast library of resources plus new e-courses; however, it also faces several challenges. The one that may prove hardest to overcome is the change in our lifestyle—the way we consume data.

In the 1999 Wachowski brothers’ blockbuster “The Matrix”, Neo is hooked up to a cable, and quickly obtains skills by means of a simple upload. This leads him to the realization “I know kung fu.” In real life this is not possible (for now!), and learning martial arts takes time, practice, dedication and more time; however, in an e-living environment, we expect everything to not just be accessible, but also high speed. This is a major challenge, as the bottom line is that this is still medicine, and topics are not always byte-size (pun intended).

The solution is flexibility, and understanding the strength of the e-learning platform, especially in gastroenterology. Indeed, the key is not to try to replace textbooks (nowadays many are also available online), but rather provide an added value, in a variety of formats. A great example of this is the upcoming “Mistakes in...” series. In this series, leading figures will cover some of the possible mistakes to avoid in their respective fields. This concise format is designed to be easy to digest, and provides distilled added value—delivering expert know-how and including insights that are not always found in textbooks.

To conclude, gastrointestinal training is a continuous process, with different requirements at various levels. UEG's e-learning platform is adaptive, designed to facilitate training and education using different formats suitable for our e-living times. While interaction with mentors is an irreplaceable experience, e-learning can undoubtedly bridge gaps and conserve local resources (as content can be adapted or translated rather than developed de novo). Looking to the future, the major milestones for e-learning in medicine will probably be inclusion as required training for fellows (in a manner that would suit local requirements), authorship recognition for academic CVs of contributors and accreditation of new non-course formats.

 

Further UEG Resources

Murray, C. UEG E-learning: The future has arrived. United European Gastroenterology Journal 2015; 3: 399.

UEG Education Website.

UEG Education Library.

UEG Education Courses.

A rapidly changing polyp

This polyp appeared radically different at the time of resection. What's your diagnosis?  

The polyp shown in figure 1 was found in the sigmoid colon of a middle-aged man who was complaining of intermittent rectal bleeding. The lesion was sampled and in view of the symptoms an endoscopic resection was organised. Six weeks later the patient attended for his polypectomy, at which time the lesion shown in figure 2 was found.

 

WHAT IS YOUR ENDOSCOPIC DIAGNOSIS?

a)     Lipoma

b)     Gastrointestinal stromal tumour (GIST)

c)     Carcinoid (neuroendocrine tumour)

d)     Leiomyoma

e)     Adenocarcinoma

Advice on Christmas Dinners...

A factual but fun article for the festive period from Mark Fox based on a Q&A session for his local newspaper

Advice on Christmas Dinners and its after effects

 “A factual but fun article for the festive period from Mark Fox based on a Q&A session for his local newspaper. Merry Christmas!”

 

 

 

 

 

Nurse endoscopists

How have nurse endoscopists benefitted endoscopy services?

I remember the incredulity on the faces on my European colleagues 20 years ago when I told them that the UK was to start training nurse endoscopists. They doubted that it was desirable (or even possible!) to train nurses. Of course, by then the American Society for Gastrointestinal Endoscopy (ASGE) had for many years endorsed flexible sigmoidoscopy by ‘nonspecialists,’1,2 but little evidence of their effectiveness had been published.3

Unsurprisingly, it was the relentlessly increasing demand for endoscopy that made the introduction of nurse endoscopists necessary in the UK.  Some 20 years ago, the demand for gastroscopy approached 10 per 1,000 population per year and the demand for colonoscopy was expected to increase from an average of 2.5 to 10 colonoscopies per 1,000 population per year.4 In addition, the implementation of the NHS National Bowel Cancer Screening programme would further inflate the demand for endoscopy.

For this reason, a British Society of Gastroenterology (BSG) Working Party5 gave the green light for nurse endoscopy, together with the United Kingdom Central Council (UKCC)6 and the General Medical Council (GMC). However, it was a cautious start because endoscopy was seen as a risky procedure that was associated with a 1:2,000 risk of death.7 The BSG, GMC and UKCC all agreed that nurse endoscopists were only to act as “technicians”. The responsibility for the patient’s management remained with “the supervising doctor” who had to be “immediately available within the hospital” (an oxymoron of course) in the event of complications or to give advice. Now we know that they were wrong and that the “interpretation of findings does not rely on the experience and training of an appropriately qualified doctor.”5 Endoscopy can be taught! Indeed, throughout the UK, nurse endoscopists now work independently, interpreting findings without the immediate supervision of a clinician.

The uptake of nurse endoscopy has been steady in the past 20 years. In Leeds we have seven nurse endoscopists who undertake about 22% of our gastroscopies, 27% of our colonoscopies and all of our flexible sigmoidoscopies. ERCP, enteroscopy, EUS and most therapeutic endoscopy procedures that pose a significant risk of complications are carried out by consultants who are increasingly dedicating their time purely to endoscopy.

Now we know more about the performance of nurse endoscopists. There is irrefutable evidence that the caecal intubation rate, adenoma detection rate, complication rate and patient satisfaction scores are comparable among nurses and doctors.8–10 In Leeds, the ‘raw’ caecal intubation rate for both our nurse endoscopists and consultants is 92% and the average polyp detection index (total number of polyps found/total number of patients) is also virtually identical (34.5 for nurses and 33.5 for consultants).

In view of the reassuring published literature that has become available over the years, I was bemused to read a recent survey from New Zealand in which only 30% of doctors welcomed the introduction of nurse endoscopists.11 A huge majority believed that doctors would always deliver a better quality of endoscopy and that overall costs would spiral out of control if nurses were to be trained in endoscopy. Of course, endoscopy is a valued source of extra income for gastroenterologists in New Zealand, which makes me wonder if this may have had an influence on the outcome of the survey.

Nevertheless, the statistics, reassuring as the may be, do not do nurse endoscopists justice. As a lead endoscopist, it is a relief to have a stable workforce that is fully committed to endoscopy. Most of my gastroenterology colleagues rush between ward rounds and outpatient clinics, phoning patients and their relatives in between. They have little time and energy to invest in endoscopy. By contrast, if an endoscopy list needs back filling, one of our nurse endoscopists will take it on. If an endoscopy audit is required, a nurse endoscopist can make the time. If there is an endoscopy-related problem, a nurse endoscopist will be willing to get involved.

The truth is that without nurse endoscopists, endoscopy services will not be able to make the quantum leap from ‘Cinderella speciality’ to a core hospital service that is on an equal footing with radiology. My advice to any anxious colleagues who worry about the emergence of the nurse endoscopist is to welcome them, because with their help we can make endoscopy bloom!

 

References 

  1. Maule WF. Screening for colorectal cancer by nurse endoscopist. NEJM 1994; 330(3):183–187. 
  2. DiSario JA and Sanowski RA. Sigmoidoscopy training for nurses and resident physicians. Gastrointest Endosc 1993; 39(1):29–32. 
  3. Committee on Training, Gross GWW, Bozymski EM, et al. Guidelines for training non-specialists in screening flexible sigmoidoscopy. Gastrointest Endosc 2000;51(6):783–785. 
  4. Barrison IG, Bramble MG, Wilkinson M, et al. Provision of endoscopy related services in district general hospitals: BSG Working Party Report 2001.
  5. British Society of Gastroenterology. Report of the British Society of Gastroenterology Working Party—The nurse endoscopist. 1994. 
  6. UKCC. The Scope Of Professional Practice. London UKCC 1992.
  7. Quine MA, Bell GD, McCloy RF, et al. Prospective audit of upper gastrointestinal endoscopy in two regions of England: safety, staffing, and sedation methods. Gut 1995; 36(3):462–467.
  8. Hui AJ, Lau JY, Lam PPY, et al. Comparison of colonoscopic performance between medical and nurse endoscopists: a non-inferiority randomised controlled study in Asia. Gut 2015; 64(7): 1058–1062. 
  9. Massl R, van Putten PG, Steyerberg EW, et al. Comparing quality, safety, and costs of colonoscopies performed by nurse vs physician trainees. Clin Gastroenterol Hepatol 2014; 12(3): 470–477. 
  10. Schoenfeld P; Lipscomb S; Crook J; et al. Accuracy of polyp detection by gastroenterologists and nurse endoscopists during flexible sigmoidoscopy: a randomized trial. Gastroenterology 1999; 117(2): 312–318. 
  11. Khan MI, Khan R and Owen W. Doctors and the nurse endoscopist issue in New Zealand. NZ Med J 2012; 125(1357): 88–97. 

Colonoscopy & Neoplasia

A new symposium in the QinE series features leaders & rising stars on pressing topics in the field.

Pretty but probably poisonous    

What is the most likely histology of the lesion?

The beautiful polyp shown in the photograph (figure 1) was found in the rectum of a middle-aged man who was on a polyp surveillance programme.

WHAT IS THE MOST LIKELY HISTOLOGY OF THE LESION?

a)    Hyperplastic polyp

b)    Tubular adenoma

c)     Tubulovillous adenoma

d)    Villous adenoma

e)    Traditional serrated adenoma

Possible pancreatitis or could it be cancer?

A retired man with an unusual cause of jaundice...

A 65-year-old man presents with obstructive jaundice. He admits to drinking up to half a bottle of wine every day. The photograph shows the findings of the abdominal CT that is organised (figure 1).  Subsequently, an endoscopic retrograde cholangiopancreatography (ERCP) is arranged to place a common bile duct (CBD) stent and obtain ampullary biopsy samples. Unfortunately the obstruction, just distal to the first part of the duodenum, prevents access to the papilla (figure 2).

 

WHAT IS THE LIKELY DIAGNOSIS?

a)     Acute pancreatitis

b)     Autoimmune pancreatitis

c)     Chronic pancreatitis

d)     Carcinoma of the head of the pancreas

e)     Duodenal adenocarcinoma

 

 

Medical writing in 4 sessions

Engage with the expert in the field, Abe Fingerhut. 4 compelling online sessions provide a formalised approach to this critical but often neglected skill.

 

 

Confusion over a rectal biopsy sample

How would you manage this nodule?    

The nodule shown in the photograph was found in the rectum of an elderly, asymptomatic patient undergoing a gastroscopy and colonoscopy because of mild iron-deficiency anaemia (figure 1). Biopsy samples were taken from the nodule and the H&E stain is shown (figure 2).

HOW WOULD YOU MANAGE THIS NODULE?

a)     Ignore the polyp

b)     Sample it again

c)     Remove it by endoscopic mucosal resection

d)     Remove it by endoscopic submucosal dissection

e)     Remove it surgically

Access Bacelona recordings

The ESDO Cancer workshop, held at UEG Week 2015, presented innovative strategies in GI cancers, with a focus on molecular pathology.
Access free of charge

Early Detection of Pancreatic Cancer—How?

What's the outlook for the development of biomarkers?

World Pancreatic Cancer Day is being held on November 13. It is estimated that 367,000 new cases of pancreatic cancer will be diagnosed worldwide in 2015 and the dismal survival rate means that only 2–10% of patients will be alive 5 years after diagnosis.

Globally, pancreatic cancer is the seventh most common cause of cancer-related death, and while death rates for many cancers are dropping, the death rate for pancreatic cancer is rising in Europe and the United States.1

The mortality of pancreatic cancer may, at least in part, be explained by the fact that early diagnosis is challenging. However, advances in the development of various biomarkers appear to hold promise for future screening of high-risk individuals, which—according to Cancer Research UK—includes patients with hereditary pancreatitis, a high incidence of pancreatic cancer in their family or a family history of at least one person with pancreatic cancer plus a linked cancer syndrome (e.g. a BRCA2 mutation).2

It has been reported that levels of serum cancer antigen 19-9 (CA19-9) are elevated in approximately 80% of patients with pancreatic cancer,3 and CA19-9 has been useful for therapeutic monitoring and early detection of recurrent disease after treatment in patients with known pancreatic cancer.4 However, CA19-9 is not a specific biomarker for pancreatic cancer. Moreover, patients who are negative for Lewis antigen a or b (approximately 10% of patients with pancreatic cancer) are unable to synthesize CA19-9. Although measurement of serum CA 19-9 levels is useful in patients with known pancreatic cancer, the use of this biomarker as a screening tool has yielded disappointing results.4

In addition to genetic alterations, dysregulation of specific epigenetic mechanisms is critical to tumour development. Comparing patients who have pancreatic cancer with healthy individuals and patients with chronic pancreatitis, Schultz et al. described differences in microRNA expression in whole blood with a view to identifying microRNA panels (classifiers) for diagnosing pancreatic cancer.3 microRNAs—non-coding 17–25-nucleotide-long RNAs that regulate gene expression—play important roles in tumour development and metastasis, and several have been described as specific to pancreatic cancer. Schultz and colleagues validated microRNA panels against CA19-9 sero-status and disease, and identified two panels for diagnosing pancreatic cancer using combinations of four and ten microRNAs in whole blood, respectively. The investigators call for further studies that could validate the use of these biomarkers as a screening tool for early-stage pancreatic cancer detection. More on the role of microRNAs in pancreatic tumour growth and progression can be found in a paper by Frampton and colleagues that was published in The Lancet in February 2015.5

Even more recently, in an article in Nature, Melo and colleagues6 suggested the use of a proteoglycan molecule (glypican-1 [GPC1]) anchored in the membrane of extracellular vesicles—exosomes—circulating in the bloodstream as a cancer biomarker. In particular, the team claimed that detection of GPC1+ exosomes in the blood could distinguish patients with early-stage and late-stage pancreatic cancer from patients with benign pancreatic disease and healthy individuals. The assay appeared more reliable than that based on CA19-9 detection. Compared with healthy donors, serum CA19-9 levels were increased in patients with cancer, but CA19-9 levels were also significantly increased in the serum of patients with benign pancreatic disease. Moreover, CA19-9 levels failed to distinguish patients with pancreatic cancer precursor lesions from healthy donors. An expanded interpretation of this important study, including a discussion of semantic issues, can be found in an accompanying News & Views article by Clotilde Théry.7

Apart from microRNAs, epigenetic features such as DNA methylation, satellite repeats and histone modifications might serve as biomarkers for early diagnosis of pancreatic cancer.8 Reviewing genes aberrantly methylated in pancreatic cancer, Henriksen and her team concluded that investigations into hypermethylated markers in cell-free DNA in plasma or serum are still limited by the availability of only a handful of small studies, which lack well-defined control groups, and that no single gene has been identified as a diagnostic marker.9

To read more about the many challenges related to identifying biomarkers for early diagnosis of pancreatic cancer, I recommend looking up a review by Jenkinson and colleagues.10 There are also a couple of interesting sessions from the recently concluded UEG Week 2015 in Barcelona that I’d like to highlight—all are available online. To learn more about ‘liquid biopsies’, including cell-free DNA, exosomes, and circulating tumour cells, you could look up the talk delivered by Aldo Scarpa, “Molecular diagnostics: From tissue biomarkers to liquid biopsies, single genes and panels”, which was part of the session “Pancreatic cancer: Where are we and what is the future?”11 There’s also an update session on therapy, including talks on chemotherapy, surgical resection, preoperative and palliative treatment, and neoadjuvant and adjuvant treatment.12 Finally, I would like to direct your attention to a talk that was given by Jean-Luc van Laethem, entitled “Pancreatic cancer in annual review”.13

Challenges aside, sensitive and specific biomarkers of early pancreatic cancer that can be obtained non-invasively appear critical to reducing the morbidity and mortality associated with pancreatic cancer. As we mark the 2015 World Pancreatic Cancer Day, we should set our hopes on it not being too long until one or more biomarkers prove valid for use in screening.

 

References

  1. http://www.worldpancreaticcancerday.org/about/
  2. http://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/pancreatic-cancer/risk-factors#heading-Eightteen
  3. Schultz NA, Dehlendorff C, Jensen BV, et al. MicroRNA biomarkers in whole blood for detection of pancreatic cancer. JAMA 2015; 311: 392–404.
  4. Hidalgo M. Pancreatic cancer. N Eng J Med 2010; 362: 1605–1617. 
  5. Frampton AE, Castellano L, Colombo T. Integrated molecular analysis to investigate the role of microRNAs in pancreatic tumour growth and progression. Lancet 2015; 385 Suppl 1: S37. 
  6. Melo SA, Luecke LB, Kahlert C, et al. Glypican-1 identifies cancer exosomes and detects early pancreatic cancer. Nature 2015; 523: 177–182. 
  7. Théry C. Cancer: Diagnosis by extracellular vesicles. Nature 2015; 523: 161–162. 
  8. Fukushige S, Horii A. Road to early detection of pancreatic cancer: Attempts to utilize epigenetic biomarkers. Cancer Lett 2014; 342: 231–237. 
  9. Henriksen SD, Madsen PH, Krarup H, et al. DNA hypermethylation as a blood-based marker for pancreatic cancer: A literature review. Pancreas 2015; 44: 1036–1045. 
  10. Jenkinson C, Earl J, Ghaneh P, et al. Biomarkers for early diagnosis of pancreatic cancer. Expert Rev Gastroenterol Hepatol 2015; 9: 309—315. 
  11. Pancreatic cancer: Where are we and what is the future? Session at UEG Week 2015. 
  12. Therapy update: Pancreatic cancer Session at UEG Week 2015.
  13. Pancreatic cancer in annual review Presentation by Jean-Luc van Laetham in the Pancreas: What’s new in 2015? Session at UEG Week 2015.

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