You can see the thin vessels crawling up the side of polyp A. This appearance is typical of a gastric NET. Polyp B has a more villous surface with a few white spots - all typical of a hyperplastic gastric polyp. Some of these may contain some malignant cells which somehow generate a hyperplastic/reactive/inflammatory reaction around themselves.  However, most hyperplastic gastric polyps are benign and arise secondary to a Helicobacter pylori gastritis. For this reason, you should always do a CLO test in these cases.  

Every few weeks, I look up the notes on Prof Pritchard's' Podcast on gastric NET's to remind myself of the workup of these cases.  As you remember, you should take samples to confirm an atrophic gastritis whenever you find a gastric NET.  In this case, the patient did NOT have an atrophic gastritis. Instead, there was a Hp associated gastritis which is the reason for the second polyp. 

We realised that what we had was a TYPE II gastric NET! Analysis confirmed that the 17mm was WHO grade II. The finding of anything else than an innocent Type I gastric NET means that further imaging was required.  A little late in the day of course but fortunately, the following imaging investigations were unremarkable: 

• CT
• 68Gallium DOTA-peptide PET/CT scan
• EUS to search for duodenal wall gastrinomas and small gastrinomas within the pancreas which CT can't see and to search for lymphadenopathy close to the NET

Anyway, below is a reminder of what to do at gastroscopy, when you have a case of gastric NET: 

• Look for atrophic gastritis 
• Consider using some pH indicator strips to measure the gastric pH (unless pt is taking PPI)
• Identify all the NETs, record their size and number and sample them for histology and grading
• Take antral and corpus biopsies and ask pathologist to do report on the presence/absence of gastric atrophy and intestinal metaplasia and also ask them to carry out immunohistochemistry stains for ‘gastrin’ in the antral biopsies and ‘chromogranin’ and ‘synaptophysin’ in the gastric body samples.
• Look into the second part of the duodenum for the small submucosal gastrinomas which occasionally are seen in MEN-I
• Consider samples for Coeliac disease if the patient has an iron deficiency anaemia

If course, this patient has 'Serrated Polyposis Syndrome'. It's important to recognise that the serrated polyp count is cumulative over multiple colonoscopies.

The recently updated 2019 WHO criteria for Serrated Polyposis Syndrome recognize two types of the syndrome: a 'proximal phenotype' with serrated polyps proximal to the rectum, all being ≥5 mm in size, with at least two being ≥10 mm in size (criterion I 2019), and a more 'distal phenotype' with more than 20 serrated polyps of any size throughout the large bowel (criterion II 2019) [Gastroenterology 2020;158:1520–23]. 

Personally, I believe that there are more than two subtypes of the Serrated Polyposis Syndrome.  There is accumulating evidence that the syndrome includes multiple conditions with variable phenotypes and with different risks of progression to CRC [Gut 2010;59:1094–1100].  This would explain the huge range of cancer risk (25%-70%) in published studies [GIE 2016;83:563–65]. 

Of course, the likely mixture of several 'syndromes', makes writing guidelines difficult. A recent consensus update by the US Multi-Society Task Force recommend offering a follow-up colonoscopy to average risk patients based on number and size of the SSL's found [GIE 2020;91:463–85].  Interestingly, the US guidelines make a distinction between 'hyperplastic polyps' and 'sessile serrated polyps' although pathologists can't reliably make that distinction.  Furthermore, the guidelines excludes patients with an increased life-time risk of cancer which of course excludes patients with Serrated Polyposis Syndrome. 

I find it all somewhat confusing!  James East's BSG guideline 2017  [ Gut 2017;0:1–16 ] recommend surveillance every other year whilst the more recent  BSG/ACPGBI guideline of 2020 [ Gut 2020;69:201– 23 ] would seem to suggest 3 yr for all 'high risk cases. But these guidelines expressively don't cover pts with hereditary cancers.   Hereditary cancers are instead covered by the BSG/ACPGBI 2019 guideline [ Gut 2019;0:1–34 ] which recommends annual surveillance until all polyps are cleared and then every 2 years. 

Finally, I admit that I also take the age of the patient into consideration as well as the presence of both serrated and adenomatous polyps. A 40 year old person is surely more likely to benefit from surveillance than a 75 year old person with multiple comorbidities?   In particular, I would worry about a young patient, perhaps 35 year old, with 1-2 large serrated polyps and perhaps only a single adenoma.  Current guidelines don't flag these individuals up but personally, I would organise another surveillance colonoscopy in a few years time.

Clearly, more research is needed to unpick the different serrated sub-pathways ! 

These polyps have a funny crypt pattern, but THERE IS A PATTERN! Accordingly, they are likely to be 'hamartomatous' (a non-sensical histological term which basically means overgrowth of normal tissue). Of course, this patient has Juvenile Polyposis syndrome. Although the polyps are 'hamartomatous', as in Peutz-Jeghers syndrome, there is a stark difference. The polyps in JP often turn dysplastic and are presumably the origin of this patients adenocarcinomas. In contrast, the polyps in PJS are extremely rarely reported to harvest dysplasia (I've never seen a dysplastic polyp in PJS). 

By the way, the WHO criteria for diagnosis of juvenile polyposis syndrome are one of either:

• More than five juvenile polyps in the colon or rectum
• Juvenile polyps find in both the upper and lower gastrointestinal tract
• Any juvenile polyps found in a person with a family history of juvenile polyposis

This is rare stuff!  I was clueless although reassured that the thing was soft and didn't feel malignant when squeezed between my fingers. 

It proved to be a (rare) 'cloacogenic polyp'!  You'd be excused if you have never heard of this (I hadn't).  Apparently these were first described as recently as 1981!  The same year that I was born ☺!  Essentially they are inflammatory polyps arising from the transitional zone of the anorectal junction.  

They can be much larger than this and even be multiple and can occur at any age. Patients are usually asymptomatic but could (naturally) present with some blood on the toilet paper (this patients complaint).  

Histology is similar to that of solitary rectal ulcers with inflammation and fibromuscular hypertrophy. For this reason it is perhaps not surprising that they are linked with constipation and straining.  Rare associations include small nearby cancers and human papillomavirus infection.

The Spigelman score is a little peculiar in that patients with scores of 0 to 3 have a very low risk of developing cancer. However, when patients accumulate a score of 4, surgery should be considered as there is a high risk of cancer.  

Of course, many patients with FAP have desmoids which precludes surgery. In those cases I consider intervening endoscopically if: 1) the patient is fit enough to survive emergency surgery to sort out a perforation or cope with a 4+ unit blood loss AND/OR  2) there is a higher than average risk of cancer, for example in a patient with extensive HGD or confirmed IMca. Of course, the lesion also has to be 'resectable' within your level of expertise. Personally, I find lesions situated at 12 O'clock the most challenging to remove.  Furthermore, a general anaesthetic is probably a prerequisite for resections taking longer than 20 min or so (which they always seem to do). 

Thus, I consider the "correct" answer to be 'Abort'!  I decided that the lesion was likely to be too large for me to resect.  Fortunately, the patient was a good surgical candidate.  A 'pancreas sparing duodenectomy' was carried out and a TVA with mainly LGD but also areas with HGD was completely removed. Postoperatively the patient developed pancreatitis and was discharged 4 months later...  Clearly this is 'Tiger Country' for surgeons as well !  

​The nail dystrophy is not due fungal infection (onychogryphosis).  In fact, this patient has Cronkhite-Canada syndrome.   This enigmatic acquired syndrome is characterised by malabsorption, gastrointestinal polyposis, nail dystrophy, alopecia, cutaneous pigmentation, diarrhoea and weight loss.  The nail dystrophy and skin pigmentation is clearly seen in the photograph.  Other common symptoms include abdominal discomfort and a protein loosing enteropathy.  The underlying cause is unknown.  The cutaneous manifestations are probably all secondary to severe malnutrition due to diffuse small bowel mucosal involvement.  

Histologically the mucosa is oedematous with dilated glands and an inflammatory cell infiltrate of the lamina propria.  Gastrointestinal polyps are hamartomatous but may contain foci of adenomatous epithelium.  The histopathologists will struggle in interpreting the biopsy findings and will mention things like 'marked foveolar hyperplasia',  'cystically dilated irregular glands', 'oedematous stroma' and 'scattered mixed inflammatory cells'. The differential diagnosis of such hamartomatous findings includes juvenile polyposis syndrome, Cronkhite-Canada syndrome, hyperplastic polyposis and Menetrier's disease.  Of course, it will help them to know about the nails and hairloss etc!!! 

Malignant transformation has been reported and may not be as rare as initially thought .  The prognosis is said to be poor but I'm not sure that this is still the case with 'modern management'.   Interestingly, in this case a suspicious nodule was found (image below).  It was removed endoscopically and found to be an early gastric cancer!  

There lots of "cystic fundic polyps" and there is also at least one duodenal adenoma. Such findings in a 55-year-old man is suggestive of the "attenuated" form of familial adenomatous polyposis (FAP).  In the absence of a family history, presumably this is a new mutation. Of course this means that the most likely reason for the iron deficiency anaemia is a colorectal cancer. This patient needs an urgent colonoscopy! 

To remind you, the APC gene is located on the long arm of chromosome 5 and encodes a tumour suppressor protein. APC is a huge protein that no doubt acts in many different ways to help control cell division and cell attachment and preserve the chromosome number through cell division. Normally, APC mops up intracellular ß-catenin. The newly formed “APC– ß-catenin complex” is quickly destroyed. The removal of intracellular ß-catenin is a good thing!  Because when a mutated APC gene is less capable of mopping up intracellular ß-catenin, cell-to-cell adhesion is reduced and cells are allowed to stay non-differentiated and immature.  That's not good! 

Of course there is a second possibility.  This could also be a new MYH gene mutation. Briefly, the MUTYH gene encodes 'MUTYH glycosylase', which is a DNA repair enzyme. Similarly to attenuated FAP, patients with MUTYH gene mutations develop multiple colonic polyps in adulthood. However, in contrast to attenuated FAP, patients with MUTYH gene mutations have both an markedly increased risk of both colonic and gastric cancer. 

Characteristics of 'attenuated FAP' compared with 'classic FAP' are:

• Fewer colonic polyps (the average is 30)
• Polyps and cancers are more frequent on the right side of colon
• Patients are older at presentation (average age ~44 years)
• The risk of cancer is lower (70% at the age of 80 years)
• Cancer develops at a later age (average age 56 years)
• Mutations towards the 5´ end of the APC gene

This proved to be a difficult question and only 15% of our facebook group got the correct answer of:  Serrated Polyposis Syndrome !!! 

The odd thing about this polyp is that it appears to be a tubular adenoma (slit-like crypts) arising from a broad somewhat odd looking fold.  The 'fold' is actually a larger hyperplastic polyp.  Of course large hyperplastic polyps are now referred to as 'sessile serrated lesions' (SSL's). You are looking at an SSL, sprouting a TA !?   A 'purist' histopathologist may refer to this entity as a 'mixed serrated, adenomatous polyp'.  

Do you know of a polyp syndrome where patients have a mixture of SSL's and adenomatous polyps? Of course, the  serrated polyposis syndrome 'SPS' (previously called the sessile serrated polyposis syndrome).   It's now realised that many patients with serrated polyposis syndrome actually have a mixture of serrated and adenomatous polyps. It's possible that these patients have a greater risk of developing cancer.    The correct answer is therefore 'A' ! 

The BSG has published a 'position statement' on the topic of SSL's which is well worth reading.  The BSG sensibly recommend annual surveillance until all serrated polyps above 5mm have been cleared, following which the surveillance interval may be reduced. This is because patients with SPS do not seem to have a higher risk of developing cancer than patients with Lynch syndrome.