Gastrointestinal pathology update report


Dr Tim Bracey 

I recently had the pleasure of attending Roger Feakins’ GI pathology update course December 10th in London. In addition to the usual suspects, Marco Novelli, Neil Shepherd, Newton Wong, and the organiser himself, we were treated to some more excellent talks from International speakers, Profs Odze and Riddell (USA and Canada) as well as Karel Geboes(Ghent Belgium). For myself, now living and working in Cornwall, even a trip to the local shops is a major undertaking, crossing the Tamar is considered risky, and the visiting the “big smoke” provokes hyperventilation and panic attacks in many! Fortunately I tied in the trip with visiting friends and getting the “Night Riviera” sleeper train which is always very relaxing; I call it time travelling!

One of the reasons I was so keen to attend this course was the venue; the stars and planets hold similar fascination to pathologists like myself as cells and molecules, and walking through the main exhibits at the Science Museum to the talks in the iMax theatre, we were treated to both.  I was also excited about finally hearing from and meeting our esteemed international speakers, and I wasn’t disappointed.  Robert Odze kicked off proceedings with an algorithmic approach to GI biopsies, the first talk about Barrett’s oesophagus. Although North American, he seemed to favour the British opinion that goblet cells shouldn’t be required for a diagnosis of Barrett’s, emphasising that biopsies without goblet cells don’t reduce risk of adenocarcinoma, but that eventually intestinal metaplasia will be revealed if sampling is extensive. 

Like Neil Shepherd he is sceptical of special stains and immuno in this setting, feeling that p53 for example is not necessary in difficult Barrett’s cases when dysplasia is queried, pointing out that even non-dysplastic Barrett’s can have aberrant expression of p53. He also however acknowledged that Barrett’s dysplasia (particularly when low grade) does not have good interobserver agreement (even among experts) and dysplasia with p53 mutations show a considerably increased risk of progression to adenocarcinoma compared with wild type cases. We are all more reliable at diagnosing high grade dysplasia and there was a discussion about how much high grade is high grade, with the answer being that limited evidence currently suggests any at all is important even within a small biopsy.  Cases of non-intestinal dysplasia of foveolar type however is even harder to identify and grade.  He also talked about sampling errors in dysplasia and highlighted that multiple biomarker testing (likely performed on scrapings rather than biopsies) might be the future.

Dr Odze next presented a pattern-based approach to inflammatory lower GI pathology. He proposed four main categories; acute, chronic, eosinophilic and paucicellular/apoptotic. This logical approach reminded me of dermatopathologists inflammatory reaction patterns, and analogous to skin it was emphasised that drug-reactions can mimic every type of inflammatory process in the GI tract, including infections and IBD. 

Dr Robert Odze showing a case of foveolar dysplasia (image property of Digestive Disease Pathology LLP) on the big iMax screen at the Science museum.

Next, Newton Wong talked about mesenchymal lesions and started by explaining that narrowing a differential based on “location, location, location” can prevent wasteful IHC, and is safer than just picking up the slide and looking at it without paying attention to the history.  Newton always manages to make complex subjects interesting and approachable and despite having heard him speak countless times I always learn something new. Although the “GIST” of his talk was familiar, with emphasis on combined morphological-molecular diagnosis, relatively new and controversial entities and important pitfalls were also discussed. Everything always comes back to morphology since examples of completely different kinds of neoplasms with different treatment and prognosis can have identical genetic driver mutations.

Morphology and clinical/endoscopic correlation was an important emphasis of Roger Feakins’ inflammatory bowel disease talk and I also learned some important pitfalls and exceptions to some of the classical teaching on idiopathic IBD as well as it’s mimics. For example only 20-30% of Crohn’s has granulomas, and even deep ulceration (less than half of the muscularis propria) can still be consistent with ulcerative colitis, and this feature doesn’t necessarily correlate with pouch surgery failure (in my experience, even classical Crohn’s disease isn’t an absolute contraindication to pouch surgery. We have patients who have done remarkably well with a pouch and known Crohn’s). New to my knowledge, Roger explained that upper GI involvement and more conspicuous granulomas is characteristic in children with Crohn’s, and that right sided colonic involvement is common in patients with UC preceding development of primary sclerosing cholangitis. Most pathologists are aware that infectious colitis can mimic IBD both clinically and histologically, but it was useful to also learn that infections can also mask typical features of CD and UC and delay their diagnosis. As we know, several infections can superimpose on IBD, most commonly CMV, but also amoebiasis and other rarer organisms in some parts of the world. 

Before lunch, Karel Geboes talked about macrophages and mast cells in the context of the normal and diseased GI tract, first continuing the theme of atypical infections and later moving on to metabolic diseases and the many clinical and histological manifestations of mast cell diseases. This was a very academically interesting talk but arguably the least relevant to the more general Histopathology audience. 

After lunch my personal favourite talk was from Prof Riddell, who despite having worked in North America since the early 1970’s (he is now at Mount Sinai, Toronto) hasn’t appeared to have picked up an accent. He covered a wide range of topics including difficult areas like hamartoma polyposis syndromes, neuroendocrine proliferations and non-intestinal dysplasias. I enjoyed his emphasis on what was clinically relevant to report and what distinctions were less important for the pathologist to recognise, and why. 

After the tea break, there were reliably excellent presentations from Profs Shepherd and Novelli covering colitis pitfalls, and BCSP polyps respectively. Both talks triggered some interesting relevant questions from the audience and I enjoyed a catch-up with both of them afterwards with an obligatory beer or two. I’m glad that Prof Shepherd seems to be gradually softening towards accepting an intramucosal stage for colorectal carcinoma, to hopefully bring diagnosis and treatment in line with all other early gastrointestinal cancers (or maybe that was the effect of the beer). 

Overall the meeting was extremely well organised, in a stimulating venue with great speakers.. I was impressed that all of the talks ran to time and the breaks were long enough to ask additional questions. If the Cheltenham racecourse meeting doesn’t continue I think this would be a more than satisfactory replacement, and even for those of us who have to travel a long way, London at the beginning or the end of the week is still convenient, especially for those with access to time travel! 

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