plicated the postoperative period leading to death on the 12th postoperativeday.Summary: This 37 year–old man presented with massive upper GI bleed-ing thought to be caused by changes in the proximal jejunum due tosarcoidosis. Although bleeding appeared to resolve spontaneously, multipletransfusions and underlying changes in the lung contributed to his demise.

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EOSINOPHILIC ESOPHAGITISNader Dababneh, M.D. and Joseph DePasquale, M.D.*. Division ofGastroenterology, Seton Hall University School of Graduate MedicalEducation, South Orange,NJ; St.Michael’s Medical Center, Newark, NJ.

Introduction: Eosinophils are often found in the esophagus associatedwith gastro–esophageal reflux disease (GERD). Eosinophilic esophagitis(EE) is characterized by a diffuse eosinophilic infiltrative process. It can bean unrecognized cause of dysphagia or heartburn that is unresponsive toantireflux measures. The majority of affected adults have been men be-tween the ages of 20 and 30. A history of allergies with peripheraleosinophilia is common. Endoscopic findings have included multiple whit-ish papules representing eosinophilic abscesses.Case Report: A 42 year–old male presented with ten–day history ofdysphagia to solids. He denied weight loss, nausea or vomiting. His pastmedical history was significant for weight loss at age 12. An extensivegastrointestinal work–up was done at that time following which he wasdiagnosed with celiac disease and placed on a gluten–free diet for one anda half years ; his symptoms resolved completely. There was no history ofasthma, hay fever or other allergies. Physical exam was negative. Labora-tory studies were normal; in particular, there was no eosinophilia. Upperendoscopy was performed which showed whitish papules without sur-rounding erythema. Biopsies and brushing were obtained. No hyphae orevidence of candida was found. Sheets of eosinophils were noted, consis-tent with EE.Discussion: The pathogenesis of EE is unknown. One hypothesis postu-lates that antigens may exert their effect systemically. The recruitment ofthe local esophageal immune system occurs as a byproduct. However, theinconsistent response to measures aimed at limiting antigen exposuresuggests that other mechanisms may be involved. Alternatively, the re-cruitment of esophageal eosinophils may represent the footprint of an acuteinfectious process. The eosinophils may cause local inflammation by re-lease of eosinophil major basic protein, a cytotoxic cationic protein. Theongoing inflammatory response is responsible for the development ofdysphagia. EE should be considered in patients with dysphagia withoutobjective evidence of GERD and in those with a history of allergies andperipheral eosinophilia. The diagnosis can be confirmed histologically; thedegree of eosinophilic infiltration is significantly greater in EE than inreflux esophagitis. Thus, the presence of excessive numbers of eosinophil-s,notably in the proximal esophagus, distinguishes EE from GERD. Opti-mal medical treatment has not been well defined . EE remains an under–recognized disease.

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AN IDIOPATHIC OROPHARYNGEAL AND ESOPHAGEALINFLAMMATORY MUCOSAL DISORDER: DISTALESOPHAGEAL SPARING IN ULCERATIVE ESOPHAGITISMAY INDICATE AN AUTOIMMUNE DISORDERMichael S. Shapiro, M.D.*, Catherine E. Harmon, M.D., Mark V. Dahl,M.D., Cuong C. Nguyen, M.D., Nizar N. Ramzan, M.D., Ray F. Keate,M.D. and Kevin W. Olden, M.D. Gastroenterology and Hepatology,Mayo Clinic Scottsdale, Scottsdale, AZ; Rheumatology, Mayo ClinicScottsdale, Scottsdale, AZ; Thoracic Surgery, Mayo Clinic Scottsdale,Scottsdale, AZ and Dermatology, Mayo Clinic Scottsdale, Scottsdale,AZ.

Purpose: A 70 year old man with progressive solid and liquid dysphagia,pyrosis, regurgitation and weight loss over 10 years. Was referred to a

tertiary medical center because of a mid to distal esophageal stricture,suspected Barrett’s esophagus and ulcerative esophagitis refractory tomedical management. Prior failed therapy included aggressive PPI Rx,prokinetic Rx, discontinuation of all potential ulcerogenic medication andnumerous dilations. Physical exam was otherwise unremarkable. EGDrevealed a 4 cm ulcerated stricture in mid to distal esophagus with 2 cmdistal sparing and no intestinal metaplasia. Esophageal manometry showednon–specific esophageal dysmotility. After multiple additional failed at-tempts at medical Rx, Collis–Nissen gastroplasty was performed. However,the esophageal ulceration and stricture remained refractory to this inter-vention.

Physical exam 1 year later revealed:a) new erosions in the throat and palateb) normal: gastrin, ESR, SB x–ray, HIV, SPEP, Cac) marked increase: ENA,ANA, Anti Ds DNAd) colonoscopy: diverticulosise) labial punch Bx: negative immunofluorescent markers for SLE, vas-

culitis, lichen planus, pemphigoid or immunobullous disease.Empiric steroid therapy using prednisone 40 mg per day resulted in rapid

improvement in symptoms and esophageal inflammation.Conclusions: This case represents an idiopathic oropharyngeal and esoph-ageal inflammatory disorder responsive to steroid therapy of possibleautoimmune nature. Distal esophageal sparing in the setting of ulcerativeesophagitis may indicate presence of an autoimmune disorder.

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METASTATIC BREAST CANCER PRESENTING AS A GIBLEED IN A MANBryan Contreras, M.D. and Mazen Jamal, M.D.*. Department ofGastroenterology, Veterans Affairs Medical Center, Long Beach, CA.

Purpose: Mr. QT is an 81 y/o man who presented to the VA MedicalCenter with 3–4 days of black and maroon colored stools. Mr. QT has ahistory of PUD, CHF and MVR. The patient had an upper and lowerendoscopy 4 yrs prior after his mitral valve replacement when he had somemelena while in the ICU. He was diagnosed with a small gastric ulcer andhis colonoscopy was normal. Upon this admission, the patient was noted tobe anemic and iron deficient, with a Hbg of 7 and ferritin of 20. The patientwas also complaining of some mild SOB and left chest pain upon thisadmission. Mr. QT was admitted to the ICU and stablilized and prepped foran EGD and colonoscopy in the AM. He was also ruled out for an MI overthe evening. The next morning he underwent both an EGD and colonos-copy to find his source of bleeding. The EGD showed a 2–3 cm red, raisedlesion along the angularis. There was no active bleeding and this lesion wasbiopsied. This was then followed by a colonoscopy which showed twodiscrete lesions in his ascending colon. Both lesions measured about 2–3cm in size and appeared endoscopically like the gastric lesion. Theselesions were also biopsied. Mr. QT was then dischared 1 day later and hadfollow–up in the GI clinic to discuss his biopsy results. The pathologyresults from both the stomach and colon showed undifferentiated anaplasticmalignant cells consistent with a metastatic cancer. Upon further discussionwith the patient in the clinic, he still complained of left chest pain. He statedthat he had this pain for about 4 months and it appeared to be getting worse.His chest was then examined showing a hard palpable mass in his leftbreast. A mammogram was done which showed a 6x4 cm. mass consistentwith a breast/chest wall malignancy. Fine needle aspiration of the breastmass was then done which showed cells consistent with the colon andstomach lesions, undifferentiated anaplastic malignant cells.

Futher work–up, including chest CT, confirmed that this was a breastmalignancy as the primary with metastasis to both the stomach and colon.Although, Mr. QT had several more episodes of bleeding, he refusedsurgery and chemoradiation and died 9 months after his diagnosis.

It has been well described that breast cancer can have metastasis to theGI tract in women. This is a rare and interesting case of a breast malignancypresenting as a GI bleed in a man.

S216 Abstracts AJG – Vol. 97, No. 9, Suppl., 2002