ATILLA ERTAN, MD, FACP, AGAF, MACG - PowerPoint PPT Presentation

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ATILLA ERTAN, MD, FACP, AGAF, MACG. F.G.# 02020323-8. A 87 y/o male with a h/o mild fluctuating HTN & over 50 yrs GERD who was diagnosed as having S.S. Barrett’s esophagus with intramucosal ca & multifocal HGD on 07/22/03. MED: Aciphex, Lisinopril & ASA.

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F.G.# 02020323-8

A 87 y/o male with a h/o mild fluctuating HTN & over 50 yrs GERD who was diagnosed as having S.S. Barrett’s esophagus with intramucosal ca & multifocal HGD on 07/22/03.

MED: Aciphex, Lisinopril & ASA.

PMH, PSH, SH, FH, ROS & PE: Essentially unremarkable.

Chest/abd./pelvic CT scan & esophageal EUS findings were c/w intramucosal Barrett’s cancer.

He was referred for PDT & performed on 08/23/03.

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F G # 02020323-8

Barrett’s Ca, T1N0MX, 8/23/2003

PDT, 8/23/2003

Post-PDT F/U EGD, 3/01/2004

Post-PDT F/U EGD, 2/03/2005

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F. G. # 02020323-8

S.S. Barrett’s with recurrent HGD


S/P HALO-360 ablation


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F. G. # 02020323-8S/P HALO-90 ablation, 12/04/2007

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A.P.# 01911497-4

A 47 y/o male with a more than 9 yrs h/o GERD & intermittent dysphagia who has had 6-7 episodes of food impaction within last 2 years. He has been diagnosed as having L.S. Barrett’s with HGD/LGD & eosinophilic esophagitis.

MED: Zegerid 40 mg BID

PMH/PSH & FH: Unremarkable.

SH: Married, IT technician, no tobacco, ETOH or IVDA.

ROS: Gained 40 lbs within last 10 yrs.

PE: Essentially unremarkable except moderate obesity.

LAB: Unremarkable CBC-diff, SMA-6 & other blood tests. Chest/abd CT scan


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Case AP

Previous history of food impactions:

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A.P. #01911497-4L.S. Barrett’s esophagus & E.E. with transient circular rings

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Case AP

  • Pathology

Basal zone hyperplasia, increased eosinophilsLuminal accumulation

of eosinophils

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What would you do next?

  • Stage:

  • T3N0M0 Esophageal Cancer

  • GEJxn Type II Tumor

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A.P. # 019114974 L.S. Barrett’s with HGD & E.E. , S/P HALO-360

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  • “Barrett’s esophagus or esophageal adenocarcinoma has not been reported in patients with EE” (1,2).

  • “EE is not a disease characterized by mucosal ulceration or destruction. Therefore, it seems likely that the pathologic process of EE is different from that of GERD and that adenocarcinoma or squamous cancer of the esophagus are

    not the spectrum of EE, other than perhaps as coincidental occurences” (2).

    Natural history & long-term follow-up studies are needed to provide more information in this relation.

    1. Am J Gastroenterol, 101: 1900, 2006.

    2. Gastroenterology, 133: 1342, 2007.

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D.W.S.# 1740111-8

A 37 y/o male with a 5 yrs h/o intermittent solid food dysphagia, food impaction episodes who had many related ER visits. He has had minimal GERD complaints between

these episodes. During one of these episodes, he came to TMH ER.

MED: None

ALL: Penn, shellfish

PMH/PSH: Unremarkable

SH: Married, lawyer, denied T, ETOH & IVDA

FH: Noncontributory

ROS/PE: Unremarkable

Emergent EGD & biopsy findings

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D.W.S. # 1740111-8

Post food impaction 3-20-2003

Food impaction 3-20-2003

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D.W.S. # 1740111-8Linear furrowing, vertical lines & white specks

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D.W.S. # 1740111-8Duodenal adenoma Duodenal ulcer

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___________________________________________________During the last decade, we saw a rapid increase of patients with esophageal intraepithelial eosinophilia who were thought to be GERD but who did not respond to GERD management. Subsequent studies showed that these patients had a “new “ disease termed EE which is a disease characterized by:

Symptoms including but not restricted to food impaction & dysphagia in adults , and feeding intolerance & GERD symptoms in children.

≥15 intraepithelial eosinophilis/HPF

Exclusion of other disorders associated with similar clinical, histological, or endoscopic features, especially GERD.


FIGERS; Gastroenterol 133:1342-63, 2007.

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  • Unremarkable endoscopic mucosa & lumen.

  • Circular rings, transient or fixed, “feline esophagus”

  • Linear furrowing, vertical lines of the mucosa

  • Linear shearing/crepe paper mucosa with passage of endoscope or dilator

  • White exudates, white specks, nodules or granularity

  • Stricture/rings: proximal, middle, or distal.


    FIGERS: Gastroenterol, 133: 1342, 2007 (modified).

    * None of the features are pathogonomic of EE.

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J.M.H. # 2096026-6Linear shearing

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A.E. # 2096036-5Circular rings, “feline esophagus”

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I.E. # 3659813-1Barrett’s islands & E.E. with transient circular rings

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Differential Diagnosis of Eosinophilic Esophagitis


Crohn’s disease*

Connective tissue disorders*

Hypereosinophilia syndrome

Infections [herpes & candida]*

Drug sensitivity response

Eosinophilic gastroenteritis


*These diseases may have intraepithelial eosinophilia but less than

15/HPF in one or more biopsy specimens.

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  • The majority of patients with EE is atopic based on the coexistence of atophic dermatitis, allergic rhinitis, and/or bronchial asthma & the presence of allergic antigen skin sensitization or measurement of plasma antigen-specific IgE.

  • 10%-50% of adults had peripheral eosinophilia.

  • Most patients improve on allergen-free diets.

  • Allergist consultation may be recommended.

    ClinGastroenterol Hepatol 3:1198-206, 2005.

    J Pediatr Gastroenterol Nutr 42:22-6, 2006.

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  • Removal of allergenic foods [diary, eggs, wheat, soy, peanuts, fish/shellfish], without unpredictive allergy testing, demonstrated significant efficacy (1). The elemental diet was very effective in severe cases with EE (1).

  • Only 16% of patients with EE showed symptomatic improvement with PPI treatment (2).

  • Systemic and topical corticosteroids resolve acute symptoms of EE. Fluticasone propionate 440 mcg BID for 6-8 weeks may be effective for induction therapy (3).

  • Endoscopic dilatation is useful in patients with fixed strictures/rings causing food impaction. However, the risk of mucosal tearing and perforation are relatively higher (4,5).

    1. Clin Gastroenterol Hepatol 4: 1097-102, 2006.

    2. Am J Gastroenterol 101: 1666-70, 2006.

    3. Gastrointest Endosc 63:3-12, 2006.

    4 & 5. Gastroenterology 127: 364-5, 2004; 133:1342, 2007.

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