DIAGNOSIS AND TREATMENT OF POST PRANDIAL NAUSEA, ALLERGY AND EOSINOPHILIA. D. Coleman 1 , J.S. Scolapio 1 , J.R. Cangemi 1 , J.C. Guarderas 1 ; 1 Mayo Clinic Jacksonville, Jacksonville, FL (Tracking ID #76262) LEARNING OBJECTIVES: Eosinophilic gastroenteritis, is a disorder characterized by infiltration of eosinophils into the mucosa of the gastrointestinal tract. As a clinical entity with recognizable symptoms it is a rare disorder. Here we discuss the extensive treatment course of a refractory case of eosinophilic gastroenteritis. CASE INFORMATION: A 16-year-old male patient who presented with post-prandial fullness and nausea. He had a history of seasonal allergies, asthma, and peripheral eosinophilia. Endoscopy of the stomach with mucosal biopsies revealed predominate eosinophils. A diagnosis of eosinophilic gastroenteritis was made. He was treated with a proton pump inhibitor (Prilosec) an oral cromolyn (for gastrointestinal symptoms), initially. After no response, he began on high dose prednisone with a gradual taper, with clinical response, to every other day prednisone indefinitely. Several years later, he again experienced symptoms of dysphagia, early satiety, nausea and occasional vomiting. He had been compliant with his medications. The oral steroids (20 mg every other day) had not been tapered because of recurrent symptoms upon dose reduction. As a result of his prolonged predisone use, bone mineral analysis was performed and showed signs of early osteoporosis. He was treated with Fosamax 5 mg a day, vitmain D 50,000 IU twice a week, and Calcium 1000 mg a day. A trial of an elemental nutrition formula was attempted in hopes of reducing his gastrointestinal eosinophilia. Although his peripheral eosinophil count significantly decreased on this elemental diet (Vivonex) he was unable to continue with it because of its poor taste. Given his refractory symptoms and continued risk of complications from chronic steroid use he was treated with Interferon Alpha, starting at a low dose and gradually increased to a dose of 1 million units per day. His peripheral blood eosinophils initially dropped from 5410 to 1020 but then slowly began to increase. In early 2002 his gastrointestinal symptoms recurred and his peripheral blood eosinophils began to rise. He had been compliant with medications. Because the majority of his symptoms were gastroesophageal, we elected to try oral flonase. Since this newest therapy was begun, he has experienced a marked drop in peripheral blood eosinophils (the lowest to date) and his gastrointestinal symptoms have markedly improved. IMPLICATIONS/DISCUSSION: This case is unique because it illustrates an unusual approach to a refractory case of eosinophilic gastroenteritis. Most known and reported therapies had failed in our patient with the exception of high dose steroids and, more recently, oral Flonase. Unfortunately his dependence upon corticosteroids resulted in the serious sequelae of osteoporosis. Although a systemic illness with marked peripheral eosinophils, the symptomatology of this patient was predominantly gastrointestinal. RAPIDLY PROGRESSIVE HEPATOSPLENOMEGALY. K. Cooke 1 , S. Rusch 1 ; 1 University of Illinois, Peoria, IL (Tracking ID #76040) LEARNING OBJECTIVES: Discuss the differential diagnosis of rapidly progressive hepatosplenomegaly while highlighting a typical presentation of an uncommon lymphoma. CASE INFORMATION: A previously healthy 32-year-old woman initially presented to her primary care physician with pleuritic left shoulder pain and a normal physical exam. Laboratory results then included platelets of 104,000/L; alkaline phosphatase of 125 U/L; alanine aminotransferase of 58 U/L; and aspartate aminotransferase of 65 U/L. Two weeks later, the patient returned with acute onset of fevers, fatigue and nausea. Physical examination was benign except for marked hepatosplenomegaly. The liver was palpable 11cm below the right costal margin and the spleen 5cm below the left costal margin. Laboratory results included platelets of 42,000/L; alkaline phosphatase of 1,045 U/L; alanine aminotransferase of 285 U/L; and aspartate aminotransferase of 610 U/L. Admission computed tomography showed diffuse homogenous enlargement of the liver, spleen and kidney with a few mildly enlarged retroperitoneal lymph nodes. Serologic evaluation was negative for hepatitis A, B and C viruses, cytomegalovirus, Epstein Barr virus, herpes simplex virus, toxoplasmosis and human immunodeficiency virus. Bone marrow biopsy on day two of admission was negative for malignancy, infection and amyloid. Screening for antinuclear antibody and extractable nuclear antigen antibodies was negative. The patient's history did not reveal risk factors for unusual infections or toxins. Noninvasive doppler ultrasound was not consistent with Budd Chiari. Blood cultures were negative and alpha-fetoprotein level was within normal limits. During the ensuing four days, the patient rapidly deteriorated with additional liver enlargement of 4cm, falling platelet count and metabolic acidosis. On day five of admission, a transjugular liver biopsy demonstrated alphabeta-hepatosplenic T-cell lymphoma. IMPLICATIONS/DISCUSSION: Rapidly progressive hepatosplenomegaly is not widely discussed in the literature. However, reviewing MEDLINE and EMBASE databases, one can conclude that it is most common in hematologic malignancies and infection. The above typical presentation of an uncommon peripheral T-cell lymphoma illustrates that lymphoma can present without lymphadenopathy or bone marrow involvement. Hepatosplenic T-cell lymphoma is an aggressive cancer with a poor prognosis. Despite aggressive treatment, our patient died on the 28th hospital day.