Final Precancerous Lesions of the Digestive Tract

7/30/2019 Final Precancerous Lesions of the Digestive Tract

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PRECANCEROUS LESIONS OF

THE DIGESTIVE TRACT

An Evidence-Based Review

Zvi Bernstein M.D. LISSOD, Ukraine - Israel

30.07.2012 LISSOD Endoscopists Conference 1


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Grading recommendations


Guyatt G , Gutterman D , Baumann MH et al. Grading strength of recommendations and quality of evidence in

clinical guidelines: report from an American College of Chest Physicians Task Force. Chest 2006 ; 129 : 174 81.


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Fecal Occult Blood Testing



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BARRETTS ESOPHAGUS



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Incidence of Esophageal Adenocarcinoma

& Other Malignancies 1975-2001


Pohl H & Welch G. JNCI 2005;97:142-6

Esophageal AdenoCa

Melanoma

Prostate

BreastLung

Colorectal


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Key questions Do current medical and surgical GERD treatments prevent

esophageal adenocarcinomas?

Are current screening and surveillance recommendationsevidence-based?

Have current screening and surveillance practices made apositive difference in preventing cancers and saving lives?

Are current screening and surveillance practices justifiedbased on the evidence?



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Estimated prevalence of Barretts esophagus

6-12% of patients who undergo EGD for GERD.

Short-segment BE: 6-12% Long-segment BE: 1-5%

1-2% of unselected patients who undergo EGD

Most cases go undetected in the general population

[Autopsy data]. Perhaps 5% of patients with BE arecurrently being diagnosed.



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Is Helicobacter pylori infection a risk

factor of Barretts esophagus?

No.

Individuals with H. pylori infection/gastritistend to have less problems with GERD.

Thus, H. pylori infection may even have aprotective effect against GERD and BE.



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Potential ways of reducing the cancer risk

associated with Barretts esophagus

Aggressive anti-reflux medical therapy or

surgical fundoplication.

Screen individuals with chronic GERD for BE.

In patients known to have BE, performsurveillance to take biopsies to look for

dysplasia.



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Does aggressive medical therapy for GERD

reduce the cancer risk in patients with BE?

Proton pump inhibitors are the cornerstone ofmedical therapy for BE. They consistently result insymptomatic GERD relief and heal esophagitis.

PPI therapy rarely results in significant regression ofBE.

While it makes theoretical sense that PPIs might

reduce cancer risk in BE, there is little proof to date.



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Does anti-reflux surgery reduce

cancer risk in patients with BE?

Anti-reflux surgery effectively alleviates GERDsymptoms in BE patients. Effectivenessdepends on the skill of the particular surgeon.

Incomplete regression of BE is occasionallyseen after surgery, but complete regression israre.

No credible evidence to date that anti-refluxsurgery decreases cancer risk.



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Chemoprevention in BE?

Chemoprevention strategies in BE are just

starting to be examined (e.g. COX-2inhibitors).

However, there is no current proof thatchemopreventive agents effectively reduce

cancer risk.



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Rationale for surveillance (EGD with Bx)

Endoscopic surveillance can detect dysplasia in BE,

which is a further marker of cancer risk:

No dysplasia-- cancer risk 2%Low-grade dysplasia-- cancer risk 7%

High-grade dysplasia-- cancer risk 22%

Asymptomatic cancers detected during surveillance

are less advanced than those which present withsymptoms. [If wait for symptoms, 5-year survival

only 14%.]



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ACG Practice Guideline:

Surveillance in Barretts esophagus



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Critical issues relating to screening and

surveillance in Barretts esophagus

No data proving effectiveness of current strategies.

Currently


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So, where do we stand as regards our Key

Questions?

Do current medical and surgical GERD treatments preventesophageal adenocarcinomas? Sounds appealing, but no

data to show that they do.

Are current screening and surveillance recommendationsevidence-based? No.

Have current screening and surveillance practices made apositive difference in preventing cancers and saving lives?Their overall impact has been quite small.

Are current screening and surveillance practices justifiedbased on the evidence? Modification of current practiceguidelines is needed.



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GASTRIC LESIONS



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Endoscopy. 2012 Jan;44(1):74-94.


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The basic principle


From: Potet F, Barge J. Ann Pathol. 1991. Review [Dysplasia in the digestive tract].


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Gastric carcinogenesis

Gastric cancer is believed to arise via a multistage

process that includes chronic gastritis, gastricatrophy, usually with intestinal metaplasia, and

finally dysplasia.


Correa P. Human gastric carcinogenesis: a multistep and multifactorial processfirst

American Cancer Society award lecture on cancer epidemiology and prevention.

Cancer Res 1992;52:673540.

Sobala GM, OConnor HJ, Dewar EP, et al. Bile reflux and intestinal metaplasia ingastric mucosa.J Clin Pathol1993; 46:23540.

Correa P, Duque E, Duque E, et al. Gastric cancer in Colombia. III. Natural history of

precursor lesions.J Natl Cancer Inst1976; 57:102735.


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Intestinal metaplasia Morson & Belcher 1952

Intestinal metaplasia (IM) and gastric dysplasia are

the main precancerous lesions of the stomach andusually found in patients infected with H. pylori.

Helicobacter pylori(H. pylori) eradication isrecommended as it is able to reduce gastric cancer

incidence up to 35%Parsonnet J, Friedman GD, et al. Helicobacter pylori infection and the risk of gastric carcinoma. NEngl J Med1991;325:112731.

Fuccio L, Eusebi LH, et al. Gastric cancer, Helicobacter pylori infection and other risk factors.World J Gastrointest Oncol2010; 2: 342-347

de Vries AC, Kuipers EJ. Epidemiology of premalignant gastric lesions: implications for thedevelopment of screening and surveillance strategies. Helicobacter2007; 12 Suppl 2: 22-31



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Reports on the effect of H. pylori

eradication on intestinal metaplasia



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Summary of results

Consistent reports of either stable disease or

disease-progression in H. pylori-positive controls

No disease progression after H. pylorieradication



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Endoscopic surveillance of gastric premalignant

lesions improves cancer survival


Whiting et al. Gut 2002; 50: 278-81


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A pragmatic endoscopic surveillance for

IM patients


Angelo Zullo, Cesare Hassan, et al. Follow-up of intestinal metaplasia in the stomach: When,

how and why. World J Gastrointest Oncol2012 March 15; 4(3): 30-36


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Types of gastric polyps


Fundic gland polyps

Hyperplastic Adenomatous

Hamartomatous polyps (Juvenile polyp, Peutz-

Jeghers syndrome and Cowdens syndrome) Polyposis syndromes (non Hamartomatous

polyps as in Juvenile polyposis, Familial

adenomatous polyposis) Subepithelial masses presenting as polyp


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Fundic gland polyps (FGP)

Located in the body and fundus

Uncertain cause. FGP may regress or evendisappear in time

Unlikely to be related to PPI use (howeverconflicting reports)

Dysplasia occur in < 1% of sporadic FGPs



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Management of FGP

Polypectomy is not required for sporadic FGPs.

Biopsy is recommended to exclude dysplasiaor adenocarcinoma (and possible FAP)

In patients with numerous FGP who are under40 years of age, or with dysplasia, colonicinvestigation should be performed to exclude

FAP



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Hyperplastic polyps

Majority of gastric polyps are hyperplastic in

nature (30-93%) Multiple hyperplastic polyps occur in

Menetriers disease

Up to 80% of hyperplastic polyps regree aftereradication of H pylori before endoscopic

removal



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Management of hyperplastic polyps

Hyperplastic polyps should be biopsied

The risk of adenocarcinoma in the surroundingmucosa is probably higher than in the polyp

itself.

Test for H Pylori and eradicate when present

Symptomatic polyp or polyp with dysplastic

foci should be removed



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Adenomatous polyps

These are true neoplasms and are precursors

of gastric cancer Frequently arise on a background of atrophic

gastritis and intestinal metaplasia, but there is

no proven association with H. Pylori infection.



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Management of adenomatous polyps

Complete removal of the adenoma should be

performed when safe to do so. Endoscopic follow-up is required

Endoscopy should be repeated at 6 monthsfor incompletely resected polyps or those withhigh grade dysplasia and after 1 year for all

other polyps



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Gastric polyps associated with polyposis syndromes


BSG recommendations: A. Goddard, R.Badreldin et al. The management of gastric polyps.Guidelines. Gut 2010;59:1270 - 1276.

Endoscopy 2012 Jan;44(1):74 94 Epub 2011 Dec 23


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Endoscopy. 2012 Jan;44(1):74-94. Epub 2011 Dec 23.


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BSG algorithm for the management of gastric polyps



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COLON POLYPS



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EVIDENCE THAT COLONOSCOPIC


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EVIDENCE THAT COLONOSCOPIC

POLYPECTOMY PREVENTS CANCER


The USA National Polyp Studyobserved a 70%90% lower than

expected incidence of CRC in

patients undergoing colonoscopic

surveillance compared with threereference populations.

Non-neoplastic polyps


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Non-neoplastic polyps

90% of all epithelial polyps in large intestineare found in more than 50% of all people

over 60 years of age

Hyperplastic (metaplastic) polyps

Hamartomatous polyps

-Juvenilie polyps

-Peutz-Jeghers polyps

Reactive polyps-Inflammatory polyps

-Lymphoid polyps30.07.2012 LISSOD Endoscopists Conference 44


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Neoplastic polyps

Adenomas:

Tubular

Villous

Tubulovillous

Serrated

Dysplasia (intraepithelial neoplasia) is necessary todiagnose adenomas

Adenomas are precusor lesions for adenocarcinomas20-30% before the age of 40, 40-50% after the age of 60



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Adenomas/carcinomas

The malignant risk is depended on: polyp size,histologic type and severity of epithelilal

dysplasia

Cancer is rare in tubular adenoma 4cm

Severe dysplasia is connected with high risk

of malignant transformation and often isfound in villous adenomas



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ACG Screening Recommendations


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ACG Postpolipectomy recommendations


S ill id li i k


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UK Surveillance guidelines risk groups

Low riskPatients with only 12, small (1 cm

High riskIf either of the following are detected at any single

examination (at baseline or follow up): >5 adenomas or

>3 adenomas at least one of which is >1cm.


W S Atkin, B P Saunders. Surveillance guidelines after removal of colorectal

adenomatous polyps. Gut 2002;51(Suppl V):v6v9

(Recommendation Grade B)


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Final Precancerous Lesions of the Digestive Tract