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Julia Kasper

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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).



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).


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

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



  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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A coeliac conundrum

What would you do next for this middle-aged woman previously diagnosed with coeliac disease?

A middle-aged woman presented with loose stool and weight loss. Initially, she refused an endoscopy and a diagnosis of coeliac disease was made on the basis of a high tissue transglutaminase (tTG) antibody titre. She was started on a gluten-free diet (GFD) but her symptoms remained despite adherence to the GFD. After several months she agreed to undergo an endoscopy. The images show the endoscopic view of the duodenal mucosa (figure 1) and the corresponding histology slide (figure 2) stained with haemotoxylin and eosin (H&E).


a)     Refer the patient for a dietary review

b)     Request a clonal analysis of the intraepithelial lymphocytes

c)     Refer for HLA DQ2/DQ8 testing

d)     Refer the patient for capsule endoscopy

e)     Add prednisolone to the dietary restrictions

An interesting ileal finding

What are the treatment options for this lesion discovered during colonoscopy?

A 50-year-old woman is undergoing a colonoscopy because of loose stool. When the tip of the endoscope enters the terminal ileum, the lesion in the photograph is found. The patient asks you if any treatment will be necessary.



a)     The lesion is likely to be a lipoma and can probably be ignored

b)     The lesion is likely to be adenomatous and should be removed by endoscopic mucosal resection (EMR)

c)     The lesion is likely to be a neuroendocrine tumour (NET) and should be removed surgically

d)     The lesion is likely to be a gastrointestinal stromal tumour (GIST), requiring annual surveillance

e)     None of the above 

Primer in Capsule Endoscopy

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Benign Focal Liver Lesions

Develop your knowledge of diagnosis and management

Small things, vast impact: gut microbiota in health & disease

All things microbiota related at UEG Week 2015!

The relevance of manipulating gut microbiota—that is using gut microbiota (e.g. faecal microbiota transplantation [FMT]), components thereof, or diet (including probiotics)—with a view to ameliorating or potentially treating diseases and syndromes is currently subject to intense scrutiny.

The number of conditions that could potentially benefit from gut microbiota manipulation is vast, ranging from autoimmune diseases, such as inflammatory bowel disease (IBD) and multiple sclerosis, to functional bowel diseases (e.g. irritable bowel syndrome [IBS]), antibiotic-induced gut dysbiosis (e.g. recurrent Clostridium difficile infection) and metabolic syndrome. Others include mental health diseases/personality disorders, including anxiety, depression, autism, and schizophrenia.

Through my own research, I have discovered that some intestinal microbes are much more common in healthy individuals than in patients with infectious diarrhoea, functional or inflammatory bowel diseases. Just to be clear, I’m not talking about Akkermansia muciniphila or Faecalibacterium prausnitzii, in fact, I’m not even talking about bacteria! I’m referring to a couple of intestinal protists (Blastocystis sp. and Dientamoeba fragilis) that once were thought by many to be gut pathogens. Well, a lot of recent data not only suggest that they are not gut pathogens, but that they also appear to be much more common than previously anticipated. At our lab, we have developed and are currently validating a gut microbiota profiling tool that enables unprecedented and exhaustive interrogation of ribosomal genes from bacteria, yeasts, moulds, and parasites (protists and helminths) in complex samples, such as stool samples. In other words, we will be able to identify all gut colonising/infecting organisms present in a stool sample to at least genus level, and very often to species level.

Given my background and interests, I was very pleased to learn that UEG Week 2015 has a specific “Gut Microbiota” pathway. I’m going to adhere to it as much as I can! Not only am I interested in being able to pin down every single organism squatting our guts, I also want to know what they do! You’ll definitely find me in Room E2 at the “From omics to better understanding of pathogenesis” session, which is being chaired by my fellow Web Editor, Rui Castro. Here, Loris Lopetuso will present and compare data on gut microbiota composition (16S NGS data) in patients with IBD, IBS, diverticular disease and healthy controls.

If you’re new to research into gut microbiota, you’d do well to attend the talk by Paul O’Toole on “Microbiota: What gastroenterologists should know.” This talk is part of the symposium “Microbiota: Evolving concepts in GI disorders” that takes place in Room F1 on Tuesday 27 October (14:00–15:30). Also in this session, you’ll be able to listen to Patricia Lepage discussing the fundamental issue of causation versus correlation in research into IBD-associated microbiota. Harry Sokol will reveal whether FMT for non-infectious GI diseases is “ready for prime time”, and Gerardo Nardone will deliver a talk with the title, “Microbiota and upper GI diseases: What is the clinical relevance?”

 “Brain–gut interactions in health and disease” is the title of a Round Table Discussion taking place in Room E4 on Tuesday 27 October (14:00–15:30). As Peter Andrey Smith says, referring to the gut-brain axis, “…the mechanisms by which gut microbes and the brain might communicate are unclear, but there are several tantalising leads for researchers to follow.” In a recent News Feature in Nature, he provides some examples as to how differences in gut microbiota may lead to differences in brain development and behaviour. Butyrate, one of the short-chain fatty acids apparently produced by gut bacteria in those of us who are not on the FODMAP diet (for more information, see my previous blog), fortifies the blood–brain barrier by tightening connections between cells, hence influencing the basic physiology of the blood–brain barrier.

I’m also really looking forward to the “Abstracts on Fire: Gut microbiota in lower GI diseases” session, which will be chaired by Antonio Gasbarrini and Herbert Tilg, and takes place at the UEG Hotspot on Wednesday 28 October (8:30–10:30). This free paper session provides us with no less than 12 talks, focusing on topics such as recurrent C. difficile infection and FMT. Among these, we will be spoiled with two talks from Gianluca Ianiro, who is going to try to convince us that surgery is no longer required in patients with C. difficile infection after FMT performed in an academic tertiary care centre.

If you’d like to come and talk to me about gut microbiota in health and disease in general, research communication, or about UEG E-learning, I’ll be at the Young GI Network “Let’s Meet” event on Sunday evening and at the UEG Booth on Monday (13:00–14:00) and Tuesday (15:30–15:45). See you there!




The hot PET

Hot spots in the descending colon. What would you do with the polyps found on subsequent colonoscopy?

A 72-year-old man previously presented with obstructive bowel symptoms. He was diagnosed with mantle cell lymphoma—a type of non-Hodgkin lymphoma—with involvement of the rectosigmoid junction and terminal ileum.

He underwent a left hemicolectomy and resection of the terminal ileum followed by chemotherapy (fludarabine, mitoxantrone, dexamethasone and rituximab). After treatment he went into prolonged remission and follow-up colonoscopies 5 years and 7 years later were both unremarkable. The findings of a gastroscopy and capsule endoscopy were also normal 7 years after treatment, at which time the patient was asymptomatic with normal blood results. His haematologist requested a surveillance FDG PET-CT scan, which demonstrated a hot spot in the descending colon (figure 1). A further colonoscopy was carried out and showed 2 polyps in the descending colon (figure 2; DC1 [15mm] and DC2 [50 mm]). The ileocolonic anastomosis and neoterminal ileum were both unremarkable.



a)     Ignore them, as they are inflammatory.

b)     Take biopsy samples only.

c)     Perform standard snare polypectomy.

d)     Organise an endoscopic mucosal resection (EMR).

e)     Organise an endoscopic submucosal dissection (ESD).

E-learning adventures at UEG Week 2015

Getting ready for a busy few days in Barcelona!

UEG Week 2015 is just around the corner and the UEG E-learning team is getting ready for a busy few days in Barcelona! As well as meeting to plan future UEG Education online courses and content, we’ll be spending time at the UEG Booth and the Young GI Lounge in Hall 8.0 during many of the session breaks on Monday, Tuesday and Wednesday. We’ll also be attending the “Young GI Network—Let’s Meet” reception on Sunday evening. If you’d like to meet the team to find out more about what we do, discuss how we can best serve you and how you might be able to get involved, then please do come and say hello!

Tomer, Rui and Bjorn will also be chairing sessions and, as one of this year’s UEG Rising Stars, Rui will be presenting his work on microRNAs in NASH in Room E1 during the first session on Wednesday morning. The team will also be attending many of the sessions to get their annual updates across the breadth of the field, and below are a few highlights that everyone is looking forward to.

Charlie’s choice: As usual there is so much excellent content that the problem will be fitting it all in. I'll certainly be attending the Rising Stars session, highlighting the best of our researchers from Europe and the USA—this is always an inspiring session. I'll also be playing close attention to the IBD free paper sessions. Like Rune, I'm looking forward to attending the microbiota-focused sessions. And for all the rest there is UEG Week Live!

Bjorn’s choice: My pick of the sessions would be “Endoscopic management of benign oesophageal strictures.” I am convinced that in treatment-resistant cases a “stricturoplasty”—whereby the stricture is cut with an endoscopic knife—can turn failure into victory. I would like to discuss this option with the presenters!

Tomer’s choice: There are many attractive learning options at the upcoming UEG Week, ranging from basic science to practical patient management. I am looking forward to “Introducing the omics: A guide for clinicians” on Monday morning, as part of the Today’s Science; Tomorrow’s Medicine lectures. This field has evolved greatly and I am looking to hear an update on the implications for clinicians.  I am also glad the Postgraduate Teaching Programme has a session dedicated to lower GI bleeding, a topic that applies to our everyday practice.

Rui’s choice: I am particularly interested in the hepatobiliary pathway, featuring different session formats on liver cirrhosis and cholestasis. And I always love the Today’s Science; Tomorrow’s Medicine sessions, showing just how much can be achieved from a well-sustained and rational basic-to-translational/clinical research plan. And speaking of research, I am also looking forward to a great panel discussion at the “How to do research?” Hotspot Symposia!

Rune’s choice: The impact of the intestinal microbiota on human health and disease is something that never ceases to fascinate me, and of course, I’ll be giving priority to the gut microbiota pathway. I’m especially looking forward to the session chaired by my colleague Mirjana Rajilic-Stojanovic and Giovanni Barbara on evolving microbiota concepts in GI disorders on Tuesday. Here, Paul O'Toole will deliver a talk with the title “Microbiota: What gastroenterologists should know.”

Natalie’s choice: I love a bit of controversy, so I’m really looking forward to visiting the UEG Week Hotspot to see some of the new session formats—Abstracts on Fire, Clinical Trials Revisited and Hotspot Symposia—in action! Coming from a basic research background, I’m also particularly interested in the sessions on the ‘omics’ and learning more about what difference they are making to practical patient care and what they might allow us to achieve in the future.

Don’t forget to look out for tweets from all of the team (@CharlieMuz, @Bjorn_Rembacken, @Eukaryotes, @RuiCastroHD, @adartom and @nataliewood06) during UEG Week (#uegweek)! Why not join the dialogue and tell us what’s got your attention? And if you like twitter debates then make sure you’re online for the #WeekChat on Sunday with Mark Hull (@mark_tbh; Diet, microbiota and colonic disease) and on Tuesday with Chris Hawkey (@chrishawkey; Updates on stem cell research in gastroenterology).

There will also be three Decide on the Spot cases published in the UEG Week News and online during UEG Week (on Saturday, Monday and Tuesday)—the answer and explanation for each case will be posted online the following day. Those of you who view the case online, sign in to myUEG and post a comment or answer in the comments section will qualify for a complimentary UEG Education Power Bank, which is perfect for charging your mobile devices on the go! To receive your UEG Education Power Bank, simply come and show us your post on the laptop at the UEG booth in Hall 8.0. Please note that comments on social media don’t count, participants are entitled to a maximum of one Power Bank and the number of Power Banks available each day is limited!

Wishing you all an enjoyable and productive time in Barcelona! 

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Quick or Quincke's thinking?

What next for a patient who's recently been feeling unwell & passing black stools?

A 40-year-old male patient went to his local A&E department with a short history of feeling unwell and passing black stools. He had a past history of chronic pancreatitis that was attributable to alcohol and a bleeding peptic ulcer some 15 years earlier. He was not taking any medication. On admission, the patient was pale with a heart rate of 75 BPM and his blood pressure was 125/80 mm Hg. The patient’s Hb level was 36 g/L, with a mean corpuscular volume of 8.93, iron 1.253 mmol/L and ferritin 0.27 pmol/L. On endoscopy, the oesophagus and stomach were unremarkable and the photographs show the appearance of the duodenal ampulla (figure 1a–c).



a)     Endoscopic retrograde cholangiopancreatography (ERCP)

b)     Percutaenous transhepatic cholangiogram

c)     Abdominal computed tomography (CT)

d)     Angiogram

e)     Abdominal ultrasound

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