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<2cm visible lesion without deep invasion: Offer EMR first and then ablation for Barretts eradication if lesion has been cured

Low grade dysplasia is a difficult diagnosis and should be always  confirmed by at second endoscopy and ideally by two pathologist (sometime LGD is actually downgraded to non displasia , or sometimes when reviewed can be upgraded to HGD)

HGD, on the contrary, does not necessarily need repeating endoscopy but always needs to be confirmed by a expert GI pathologist.  If any doubt, it is always reasonable to repeat endoscopy.

Patients with early-stage esophageal adenocarcinoma need treatment depending on many factors ( EMR, ESD, surgery or Radio-chemotherapy , discuss in the MDT)

If Check the guidelines

Check the guidelines

In general, EMR recurrence  (presence of residual polypoid tissue at the level of the scar in control colonoscopy) is described as high as 20-30%.    Currently it is recommended to treat the margins of the scar immediately after polyp resection to reduce this rate.  Treating with APC or soft snare coagulation (this latter is preferred in the ESGE guidelines) help significantly reduce the recurrence

See Bourkes group RCT

See metanalisis

We need to differenciate between non dysplastic (the majority of Barrett's do not have any dysplasia, just metaplasia) versus dysplastic changes (proliferative changes that is characterized by a loss in the uniformity of individual cells in a tissue and loss in the architectural orientation )

The overall yearly incidence of  eosphageal adenocarcinoma in non dysplasitc  is 0.3% (. This is approximate and based on a metanalysis, although we know that factors such a age, smoking or obesity increase the overall risk of adenocarcinoma in Barrett's patients, and equally, the risk lowers when short segment (<3cm) - down to 0.19 % per year)

9.1% is the overall incidence of progression (to either HGD or adenoca) in those who already present low grade dysplasia, up to   9.1% per patient/year  with pooled annual incidence of adenocarcinoma of 0.54% per year

ALD is the most common diagnose on referral for liver transplant in men but the second for women after MASLD.  MASLD is the most rapidly increasing indication for liver transplant worldwide.

It is not 2 times higher, it is actually > 10 times higher!!

This is the reason ADR is probably  the most important surrogate marker of a good  quality colonoscopy, (others are bowel preparation, caecal intubation and withdrawal time) and we need to maintain ADR  at least >20%

According to the  2020 BSG  post-polypectomy surveillance guidelines   we recommend no surveillance if life expectancy is less than 10 y or patient older than 75 yo.  However this can be flexible depending on the patient situation. For example, if histology show incomplete resection margins or colonoscopy was suboptimally prepared then it could be reasonable to repeat the test in 1 year.

If this same case was in a fit and younger patient (e.g  65 yo patient ) then given that we removed 5  adenomas (premalignant) - this would be the cutoff to have another colonoscopy in 3 years

In fact, the majority of the guidelines suggest 3 year follow up if 5 or more small(<10mm)  adenomas are removed.  2020 AGA recommend 3 years followup if 5-10 adenomas, 5 years if 3-4 adenomas and up to 7-10 years if only 1-2 adenomas (or SSL).

For example, if a 65 yo patient had only 4 small adenomas with en bloc resection and good bowel cleaning,  no further surveillance and return to bowel screening according to the British guidelines but would need 5 year colonoscopy according to the AGA guidelines. 

The majority of pancreatic cancers are due to spontaneous mutations in a complex combination of usually several mutations ((KRAS) mutations are common in 90% of pancreatic cancers, but in combination with different other mutations, DNA damage and usually other risk factors.

There is however a very important percentage (5%-10%) of new PC which associate familial pancreatic cancer (Defined by two first-degree-relatives with pancreatic cancer), There are indeed genes involved such as BRCA2 gene  mutations  ( 3.5-fold increased risk of pancreatic cancer ).  Other inherited mutations in the STK11 gene cause the Peutz-Jeghers syndrome, and individuals with Peutz-Jeghers have a 130-fold increased risk of pancreatic cancer

To put in context,

One degree relative with PC  makes relative having an 80% increased risk of developing pancreatic adenocarcinoma (this is RR: 1.8)

individuals with 2 degree relatives with PC have a nine fold risk , and this rises to thirty-two times greater risk if three or more first degree relatives have been previously diagnosed

Smoking and obesity are probably the most important modifiable risk factors for panc cancer (Smoking 74% higher risk, whereas every 5 points of increased BMI  increases risk in 10% )

Diabetes is an independent factor associated with higer risk of pancreatic cancer.

Alcohol is known to increase the risk although there is different evidence in regards of the association (It is known to be dose dependant, plus also alcohol can increase the risk of adquired chronic pancreatitis, which in itself increases the overal risk of cancer in about 4%)

The evidence of Hpylori is controversia, it was described in this review however further evidence fails to suppor this. It is thought to be  through secondary mucosal inflammation and immune evasion rather than Hpylori per se.

However it is known that there is an association with ABO blood groups in several large epidemiological studies. Non 0 blood types have a higher risk of developing pancreatic cancer compared to A/B/AB

In this article they summarised the current evidence.