Prevention and Diagnosis of Oesophageal and Pancreatic Cancer

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Prevention and Diagnosis of Oesophageal and Pancreatic Cancer

Dr Sameer Zar MBBS, FRCP, PhD

Consultant Gastroenterologist

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Case Studies

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Case 1

– 61 year old male presents with loss of appetite,

abdominal discomfort and back pain, weight loss

two stones over previous 3 months and progressive

jaundice for 2 weeks

– On enquiry, he has dark urine, pale stools and

complains of generalized pruritis

– US Scan abdomen shows intrahepatic biliary

dilatation. Stones in gall bladder, no stones in bile

duct but lower end of bile duct and pancreas not

adequately visualized due to bowel gas

2

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Case 1

What is the best next investigation to confirm diagnosis?

1 MRCP

2 CT Scan

3 ERCP

4 Ca 19-9

5 Endoscopic ultrasound

6 None of the above

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Case 2

– 50 year old male presents with 1 months history of

dysphagia to solids

– He has restricted his diet to liquids and soft mashed

solids and has lost one stone in weight.

– He has a long standing history of heartburn and

takes regular omeprazole 20mg once a day

– A previous endoscopy showed Barrett’s oesophagus

10 years ago and he is on surveillance every 2 years

but failed to attend his last appointment for

surveillance endoscopy 2 years ago

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Case 2

What is the best next best step?

1 Increase Omeprazole to 20mg bid x 2 weeks

2 Review history of drug compliance and give dietary

advice

3 CT Scan

4 Upper GI endoscopy

5 Refer for anti-reflux surgery

6 None of the above

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Prevention and diagnosis of early pancreatic cancer

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Operability and Survival in Pancreatic Cancer

- Best outcome in pancreatic cancer is from curative

surgical resection

- 45% of patients have metastases at diagnosis

- 40% of patients do not have distant metastases but

have locally advanced inoperable disease

- Only 15% have localised, non-metastatic potentially

resectable disease

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Operability and Survival in Pancreatic Cancer

- Survival at 5 years is only 4-5%

- 5 year survival after surgery

- 25% for node negative patients

- 10% for node positive patients

It means that even in operable cases, majority die of

the disease and this has not improved greatly over

the decades

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4

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Pancreatic cancer:Stage at the time of diagnosis

Localised% o

f to

tal

cases

Baxter et al, SEER database

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Size of pancreatic tumor at diagnosis over past few decades

First Author Year of

Publication

Patient

accrual

Institution Mean

tumour size at diagnosis

Yeo 1995 1970-1994 JHMI 3.0 cm

Nitecki 1995 1981-1991 Mayo 3.1 cm

Fortner 1996 1979-1991 MSKCC 3.9 cm

Sohn 2001 1984-1999 JHMI 3.2 cm

Schmidt 2004 1980-2002 IUPUI 3.2 cm

Agarwal 2004 2000-2002 MDACC 3.0 cm

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Usual Progression of Pancreatic Cancer

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Goal of Screening/Surveillance is to intervene at a curative stage


We need alternative strategies to diagnose Early Pancreatic Cancers!

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Issues in Screening for Pancreatic Cancer

– Late presentation:

– Symptoms = Advanced disease

– Will require screening asymptomatic individuals

– Uncommon disease:

– Age >50 yr: Incidence 38/100,000

– Is it cost effective to screen general population

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Screening for PC in the general population -Specificity determines screening 10,000 people

Specificity True Positive False Positive

100% 1 0

99% 1 99

95% 1 499

90% 1 999

80% 1 1999

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Using enriched cohorts: When incidence is 1 in 1000 Specificity range of Screening Test can expand

Specificity True Positive False Positive

100% 1 0

99% 1 9

95% 1 49

90% 1 99

80% 1 199

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Pancreatic cancer screening test: What to do?

Two possible solutions:

– The test should be of high sensitivity and

specificity (99%)

– The target population screened should have a

high incidence

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Potential Screening Tools:

- Tumour markers: Ca 19-9

- CT scan

- Endoscopic Ultrasound

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Sensitivity and Specificity of Tumour Markers

Diagnostic test Sensitivity Specificity

Ca 19-9 60-70% 70-85%

CEA 30-60% 80-90%

Ca 125 30-60% 80-90%

Proteomics 71% 91%

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Journal of Surgical Oncology 2013;107

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CT scan: Sensitivity for detection of pancreatic cancer

Year of

Publication

Number of

subjects

Sensitivity (%)

Muller et al 1993 49 69

Ichikawa et al 1997 21 76

Palazzo L et al 1993 64 66

Sheridan et al 1999 33 93.5

Amin et al 2006 276 68

Ahn et al 2009 20 75

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Endoscopic Ultrasound and FNA biopsy

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EUS and FNA of Pancreatic Adenocarcinoma

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Sensitivity of EUS for detecting pancreatic cancer

First

Author

Year Tumour size Number of

patients (n)

Sensitivity for tumour

detection (%)

Palazzo 1993 < 25 mm 7 100

Nakaizumi 1995<20mm

20-30 mm

>30 mm

88

12

88100

100

Legmann 1998<15 mm

15-35 mm

>35 mm

614

7

100100

100

Krishna 2012

<15 mm

16-20 mm21-25 mm

29

3644

100

100100

9

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Sensitivity of Pancreatic protocol CT and EUS for detecting Pancreatic Cancer

PPCT EUS

≤ 20 mm 40% 100%

21-30 mm 84% 100%

Agarwal et al 2004, AJG

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Lessons learned from Familial Pancreatic Cancer surveillance

– CA19-9 and CT scan not able to detect early

mass lesions

– EUS is effective in detecting early lesions

– Cost-effectiveness is excellent as long as the

lifetime risk of PC is >16%

– Surveillance of the general population would

not be cost effective by EUS

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Solutions in Future:

– New biomarkers

– Gene testing

– Molecular CT/PET

– Molecular Endoscopic Ultrasound

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Approach to Detect Early Pancreatic Cancer

At present, detection of ‘early pancreatic

cancer’ will require:

– screening/surveillance of asymptomatic

subjects

– in a ‘high-risk population’

– with EUS

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Pancreatic Cancer: Environmental Risk Factors

Which of the following is not associated with

increased risk of pancreatic cancer

1 Obesity

2 Physical inactivity

3 Alcohol and coffee

4 Western diet (high in fat and processed meat)

5 History of partial gastrectomy & cholecystectomy

6 Smoking

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Screening vs Surveillance

– Screening: Asymptomatic persons with no known precancerous pancreatic disease

– Surveillance: Persons with known

precancerous pancreatic disease

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Surveillance of Pre-cancerous lesionsof the Pancreas

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Pancreatic Cancer: Surveillance

Persons with known precancerous condition:

– Cystic lesions

– IPMN (Intraductal Papillary Mucinous Tumour)

– MCN (Mucinous Cystic Neoplasm)

– Pancreatic Intraepithelial Neoplasia (PanIn)

– Family history + abnormal pancreas


Mucinous Cystic Neoplasm of Pancreas

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Mucinous Cystic Neoplasm (MCN)

– >95% female

– mean age at diagnosis is 45 (range 16-82) years

– >95% in body/tail of pancreas; single lesions

– >50% asymptomatic or minimal (?unrelated)

symptoms;

– When symptomatic: pain, weight loss

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Mucinous Cystic Neoplasm (MCN)

– Histology at resection:

– 18% carcinoma

– 10% borderline

– 72% adenoma

– Practically all malignant MCN are > 4 cm or

have nodules

– Slow progression from adenoma to invasive carcinoma (~11 years).


Intra-ductal MucinousPapillary Neoplasm of Pancreas

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Intraductal Papillary Mucinous Neoplasms

Branch-duct IPMNs Main-duct IPMNs


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Main-duct Branch-duct

– Rate of malignancy 70%

– Rate of invasive cancer

40%

– Mostly

intestinal/pb/oncoytic

phenotype (70%)

– Likely tumor progression

from adenoma to

carcinoma

– Always surgery !!!

– Rate of malignancy 25%

– Rate of invasive cancer

12%

– Mostly gastric phenotype

(71%)

– Tumor progression from

adenoma to cancer

uncertain

– Observation vs surgery

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Main Duct IPMN

– Uncommon disease

– Sometimes incidentally discovered (~ 25%),

but not infrequently patients have had

symptoms for years

– When malignant, often is colloid carcinoma,

which is very indolent.

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Branch Duct IPMNs

– In absence of “worrisome features” (i.e.

nodules, thickened wall, dilated pancreatic

duct, size > 3 cm) likelihood of invasive

cancer was zero in >700 pts, although HGD

was present in 7%.

– In patients who require resection during

follow up, risk of invasive cancer was 10%,

and the majority of lesions were stage I

Sahora et al, Ann Surg 2013, in press


Pancreatic Intra-epithelial Neoplasia (PanIN)

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Pancreatic Intraepithelial Neoplasia(PanIN) vs. IPMN

Hruban RH, et al. Am J Surg Pathol 2004

PanIN Branch duct

< 0.5 cm in greatest ductal diameter > 1.0 cm in greatest ductal diameter

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Link between PanIN and Pancreatic Cancer

– Prevalence of PanIn increases with age

(present in >50% of 80 year olds)

– 3x more common in pts with pancreatic

cancer.

– More common in pts with family history of

pancreatic cancer

– Stepwise increase in mutations parallels

progression of PanIn and those same

mutations present in pancreatic cancer Poruk et al, Ann Surg 2013; 257:17-26

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PanIN (Pancreatic Intra-epithelial Neoplasia)

– PanIn is a microscopic lesion without

radiological or endoscopic correlate

– Identification of PanIn 3 (i.e. in-situ cancer)

is not possible with currently available tests

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Familial Pancreatic Cancer

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Pancreatic Cancer: Hereditary Risk Factors

Which of the following is associated with

increased risk of pancreatic cancer

1 Lynch Syndrome and FAP

2 Peutz-Jaegher’s syndrome

3 Hereditary Ovarian Cancer

4 Familial pancreatic cancer

5 Ataxia Telangiectasia

6 Hereditary Breast Cancer

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Familial Pancreatic Cancer: Screening

– Strength of Family History:

– ≥3 affected, 2 or more 1o relative

– ≥2 affected, one 1o relative

– 2 affected relatives with 1o relative

– Mutation Carriers

– Patients with Peutz–Jeghers syndrome

– BRCA2 mutation carriers with one or more

affected FDR with PC

– p16 mutation carriers with one or more

affected FDR with PC

– Lynch syndrome and one affected FDR with PC

Gut doi:10. 1136/gutjnl-2012-303108

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Familial Pancreatic Cancer: Screening Modality

– MRI

– Multiple cystic lesions

– Ductal stricture

– Solid mass

– EUS

– Chronic pancreatitis-like changes

– Cystic lesions

– Indeterminate solid lesion (<10 mm)

– Solid lesion (>10 mm)

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Familial Pancreatic Cancer

– Who should have resection?

– There is little consensus about which lesions

detected by screening require surgery

– Solid lesions >1 cm: Yes

– All the rest: no consensus

Gut doi:10.1136/gutjnl-2012-303108

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Familial Pancreatic Cancer: F/U Surveillance

– Non-suspicious cyst

– EUS/MRI after 6–12 months

– Newly detected indeterminate solid lesion

– F/U imaging at 3 months

– Indeterminate main pancreatic duct

stricture:

– Repeat imaging within 3 months

Gut doi:10.1136/gutjnl-2012-303108

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Screening for Familial Pancreatic Cancer

– Abnormal on EUS and MRCP or ERCP reflect

present of underlying pre-neoplastic lesions

(PanINs)

– Such changes are very common in FPC

kindreds

– Prevalence of such changes far exceeds life

time risk of Pancreatic Cancer

– Changes may occur many decades before

development of cancer


Screening for Familial Pancreatic Cancer

– Currently no way to distinguish low-grade

from high-grade PanINs

– Total pancreatectomy required to eliminate

risk

– Choice between uncertain risk of Pancreatic

Cancer and brittle DM

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Screening/Surveillance in Familial Pancreatic Cancer

Family Hx of PaCOr Mutation carrier

Family Hx of PaCOr Mutation carrier

Endoscopic US/MRIEndoscopic US/MRI

CP-like changesSmall and large cysts (IPMN)Indeterminate/Solid lesions

CP-like changesSmall and large cysts (IPMN)Indeterminate/Solid lesions

Watchful Waiting vs SurgeryWatchful Waiting vs Surgery

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Approach to Detecting Resectable Sporadic Pancreatic Cancer

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Pancreatic Cancer: Screening

Screening can be potentially considered in:

– Asymptomatic adults with

– New-onset DM >age 50 years

– Chronic pancreatitis

– ?1st attack of AP >age 50 years

– Subjects with family history of pancreatic cancer


Pancreatic Cancer and Diabetes: What’s the Connection?

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Diabetes in Pancreatic Cancer

– 85% have hyperglycemia

– 50% have diabetes

– 75% is new-onset

– Median interval between onset of DM and diagnosis

of cancer is 13 months (0-36 months)

– New-onset diabetes resolves with cancer resection

Pannala et al Gastroenterology 2008;134:981-7Chari et al Gastroenterology 2008;134:95-101


Probability of Pancreatic Cancer in New-onset DM

– In Rochester population

– 18/2,122 (0.85%) with new-onset DM > 50 yrs

of age developed Pancreatic cancer within 3

years of first meeting criteria for diabetes

– Overall risk ~8 times compared to age

matched general population

– 1 in 125 subjects with new DM had

Pancreatic cancer

Chari et al Gastroenterology 2005;129:504-11


Weight Change and New-Onset DM

– 65% of subjects new-onset DM associated

with PC lose weight prior to DM onset

– 65% of type 2 DM gain weight at onset of DM.

– Weight loss in PC-DM precedes cancer-

specific symptoms

– Weight loss continues till cancer diagnosis

despite worsening DM

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Pancreatic cancer diagnosis following a new diagnosis of chronic pancreatitis


Risk of pancreatic cancer after new diagnosis of chronic pancreatitis

– 462 patients with new diagnosis of CP

– Pancreatic cancer diagnosed in 27 (5.8%)

within 2 years

– 4546 patients with new diagnosis of CP

– Pancreatic cancer diagnosed in

– 110 (2.42%) in <1 year

– 46 (1.01%) in 1-4 years

– 24 (0.52%) in 4-24 years

Lowenfels et al. New England Journal of Medicine 1993

Britt Marie Karlson et al. Gastroenterology 1997


Incidence of PaCa following a new diagnosis of chronic pancreatitis

Agarwal et al, APA 2012

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Summary

– More early stage tumors can potentially be

diagnosed by

– Being more accepting of false positive diagnoses

in order not to miss opportunity for timely

treatment of early pancreatic cancers

– Using the right imaging test to diagnose early

stage pancreatic cancer

– Identifying clinical presentations associated

with early stage tumors


Diagnosis and Prevention of Oesopahgeal Cancer

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Differences in Oesophageal SCC and Adenocarcinoma

SCC Adenocarcinoma

Proportion of total 40% 60%

Male:Female 3:1 7:1

Black:White ratio 6:1 1:4

Location Mid oesophagus Lower oesophagus

Major risk factors Smoking, alcohol GORD, Barrett’s

108

23


0

0.5

1

1.5

2

2.5

3

3.5

4

4.5

1974 1978 1982 1986 1990 1994 1998

Ra

te p

er 1

00

,000

Incidence of Oesophageal Adenocarcinoma is on the rise in White Men


Oesophageal Cancer is a Lethal

Disease

Shaheen NJ et al. Am J Gastroenterol 2006; 101: 2128-38


Treatment Outcome in Oesophageal Cancer

60% of patients have metastatic or locally advanced

disease at presentation

Outcome strongly correlates to stage of disease

Only 15% of patients with localised disease can

achieve long term cure with multi-modality

approach due to presence of early lymph node

metastases

Best outcome is for patients with early mucosal disease

who are usually asymptomatic at presentation

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Treatment Outcome in Oesophageal Cancer

Patients who present with dysphagia usually have

advanced disease

Best outcome is for patients with early mucosal disease

who are usually asymptomatic at presentation

Barrett’s metaplasia is the only precursor lesion which

can be identified endoscopically

It provides an opportunity to screen for dysplasia and

early cancer

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Barrett’s Oesophagus

Barrett's oesophagus is a condition in which

stratified squamous epithelium in the distal

oesophagus is replaced by metaplastic

columnar epithelium to a varying extent

The condition develops as a consequence of

chronic gastroesophageal reflux disease

(GORD)


Diagnosis of Barrett’s Oesophagus

Diagnosis of Barrett’s oesophagus is based on two criteria

– Endoscopic examination

Location of squamocolumnar junction in relationship

to the gastroesophageal junction

– Histological confirmation

Replacement of stratified squamous epithelium with

intestinal metaplasia (columnar lined epithelium)


Barrett’s Oesophagus - Diagnosis

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Risk factors for Barrett’s Oesophagus


Risk Factors Associated with Oesophageal Adenocarcinoma in Barrett’s Oesophagus

Which of the following is not a risk factor for Barrett’s

Oesophagus:

1. Age 50 years or older

2. Male sex

3. White race

4. Chronic GORD (>10yrs)

5. Hiatus hernia

6. H pylori infection

Screening for Barrett’s should be considered in patients with

multiple risk factors

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Barrett’s Oesophagus

– Caucasian male disease

– 40–100 x increased risk of oesophageal cancer

– Annual progression rate 0.5%/year

(Shaheen, Am J Gastro 2000)

– Average age at diagnosis=55

(Spechler, NEJM 1986)

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Cancer Risk in Barrett’s Oesophagus – Case for Screening and Surveillance


Cancer Risk in Barrett’s Oesophagus

– Observational studies show that endoscopic

surveillance can detect curable dysplasia in Barrett's

– Asymptomatic cancers discovered during

surveillance are less advanced than those found in

patients who present with cancer symptoms


Surveillance Detects Cancer at Early Stage

BarrettBarrett’’s Surveillance associated with better cancer stage and s Surveillance associated with better cancer stage and

survival (Corley, Gastro 2002)survival (Corley, Gastro 2002)

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Risk Factors Associated with Oesophageal Adenocarcinoma in Barrett’s Oesophagus

Which of the following is not a risk factor for

adenocarcinoma in Barrett’s Oesophagus:

1. Length of Barrett’s segment (>8cm)

2. Severity of reflux symptoms

3. Frequency of reflux symptoms (>3 times/week)

4. Ulceration or stricture in Barrett’s segment

5. NSAIDs, Aspirin and COX -2 inhibitors

6. Duodeno-gastro-oesophageal (Biliary) reflux


Strategies to Manage Cancer Risk in Barrett’s Oesophagus

Screening

– General population

– GORD patients

Surveillance

– Barrett’s oesophagus

– Barrett’s oesophagus with risk factors


Screening For Barrett’s Oesophagus

General population

– 1.6% of general population has Barrett’sRonkainen J, Gastroenterology 2005; 129:1825.

GORD patient

– In patients with GORD symptoms, long-segment

Barrett's oesophagus is found in 3 - 5 % and short-

segment Barrett's in 10 - 15 %Winters C Jr,. Gastroenterology 1987; 92:118.

Spechler SJ. N Engl J Med 2002; 346:836.

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Screening and Surveillance for OesophagealAdenocarcinoma

How many patients with early oesophageal

adenocarcinoma can be potentially indentified

through screening and surveillance?

1 90-100%

2 75%

3 50%

4 20-25%

5 10%

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Screening for Barrett’s Oesophagus

>40% of patients diagnosed with oesophageal adeno-

carcinoma have no history of heartburn

Chak, Cancer 2006

Majority (>90%) Barrett’s pts will NOT develop

adenocarcinoma

Barrett’s diagnosis negatively impacts Quality of Life

Gerson, GI Endo 2007; Hur, Health Rel QoL 2007

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Screening and Surveillance for OesophagealAdenocarcinoma

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How to Improve Screening for Barrett’s Oesophagus– Review guidelines for

screening

– Identify risk factors for Barrett’s

– Heartburn / 4 weeks / most of the

time – triggers endoscopy

– Improve screening methods

– Videocapsule

– Cytosponge

– Prescribing practices

– Repeat prescriptions for PPI

– Educating public, pharmacists

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Management of Barrett’s Oesophagus


The current screening & surveillance

practice for Oesophageal Adenocarcinoma?

31


Managing Cancer Risk in Barrett’s Oesophagus

The management of patients with Barrett's oesophagus involves following components:

– Treatment of the associated GORD

– Endoscopic surveillance to detect dysplasia

– Treatment of dysplasia

– Chemoprevention


How to Screen for Dysplasia in Barrett’s Oesophagus

Endoscopic evaluation using white light endoscopy

– Four-quadrant biopsy specimens be taken every 2

cm

– Specific biopsy specimens of any mucosal

irregularities


Management of Barrett’s Oesophagus

Management of patients with Barrett’s can be divided in three categories

– Barrett’s oesophagus without dysplasia

– Barrett’s oesophagus with Low Grade Dysplasia

– Barrett’s with High Grade Dysplasia

32



Barrett’s oesophagus

– Risk of cancer 0.3 - 0.5% per yearShaheen. Gastroenterology 2000:119:333

Barrett’s oesophagus with Low Grade Dysplasia

– Probably 0.6 - 5%

Barrett’s with High Grade Dysplasia

– Risk of cancer 5-8% per yearSpechler: Am J Gastroenterol 2005;100:927

– 12% harbour invasive carcinoma at diagnosis

– Lymph node metastases is <1% in intramucosal

cancer



Endoscopic surveillance is suggested for patients with

Barrett's oesophagus using the following surveillance

intervals:

– No dysplasia: 3 to 5 years

– Low-grade dysplasia: 6 to 12 months

– High-grade dysplasia - eradication therapy or 3

months


Management options in Barrett’s with High Grade Dysplasia

Surgery

Increased frequency of surveillance

Endotherapy

– Endoscopic Ablation (RFA, PDT, APC,

Cryotherapy)

– Endoscopic Mucosal Resection (EMR)

– Endoscopic Submucosal Dissection (ESD)

33


Radiofrequency Ablation


Radiofrequency Ablation

– A bipolar device containing 60 separate 250-µm

electrodes circumferentially oriented on the outer

surface of a balloon for circumferential ablation in

the esophagus

– It delivers heat to the mucosa at a controlled depth

(down to muscularis mucosae, with no involvement

of the submucosa).

– A related device (HALO90; Barrx) is designed for

focal ablation.


Radiofrequency AblationBarrx Halo

34


Endoscopic Mucosal Resection



Endoscopic Mucosal Resection (EMR)

– EMR is an endoscopic alternative to surgical

resection of mucosal and submucosal neoplastic

lesions

– EMR involves snare resection of the dysplastic lesion

– Two methods: Cap suction and Band ligation

followed by snare resection

– Lesion is excised rather than ablated – allows

histological diagnosis and staging

35


Endoscopic SubmucosalDissection


Endoscopic Submucosal Dissection (ESD)

– Large oesophageal lesions are removed en bloc by

dissecting through the submucosal plane

– Specially designed needle-knives

– Facilitated by submucosal injection of viscous

substances such as hyaluronidate, which provide

prolonged submucosal lifting

– High level of endoscopic expertise required


ESD for Barrett’s and High Grade Dysplasia

36


ESD for Barrett’s and High Grade Dysplasia

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Primary Prevention

- Surveillance Dietary factors (not proven):

- Ample fruit and vegetables

- Effect of dietary supplements not clear

- Weight Gain and Obesity

Documents

Prevention and Diagnosis of Oesophageal and Pancreatic Cancer