patient reported extensive travel through parts of Ohio when he worked asa salesman. He denied travel to the south and southwest. Fungal cultureswere sent for aspergillus, blastomyces, coccidoides and histoplasma. Aserum cryptococcal antigen was also checked. All these tests were negative.A CT scan of the chest was done which showed multiple, diffuse 1–2 mmnodules present in both lungs. The patient was placed in isolation forsuspected tuberculosis. Blood, urine and stool cultures were negative foracid fast bacilli. A fiberoptic bronchoscopy was performed for broncho-alveolar lavage, brushings and transbronchial lung biopsy. The transbron-chial biopsies showed multiple small pulmonary interstitial caseating gran-ulomas. Acid fast bacteria were seen with ziehl-neelsen stain. The patientwas started on a four drug tuberculosis regimen. The skin biopsy culturesgrew mycobacterium tuberculosis from both sites.Discussion: Tuberculosis reactivation associated with infliximab treatmenthas been well reported recently. To date, there are no reports of cutaneoustuberculosis associated with infliximab treatment reported in the Englishliterature. We report a case of cutaneous and miliary tuberculosis associatedwith infliximab treatment.

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ERITROPOIETIC PROTOPORPHYRIA: FAVORABLEEVOLUTION WITH UDCA?Jose Alexandre Sarmento, M.D.*, Manuel Correia, M.D.,Teresa Baudrier, M.D., Alberto Mota, M.D., Fatima Carneiro, Ph.D.,Tavarela Veloso, Ph.D. Hospital S. Joao, Porto, Portugal andUniversidade do Porto, Porto, Portugal.

Background: Eritropoietic Protoporphyria is a rare disease resulting frominherited ferrochelatase deficiency that can present liver involvement, withdeposition of protoporphyrin in the liver. Patients with severe acute oradvanced liver disease may need liver transplantation. There is little ex-perience of treatment modalities.Clinical Case: DB, a 27 years old male caucasian, had eritropoieticprotoporphyria diagnosed in late childhood, because of cutaneous com-plains (burning sensation when exposed to sunlight). In 1995 he presentedfor the first time high vales of AST, ALT and gama-GT, especially duringsummer time. A complete diagnostic work-up was done, with negativity ofviral and autoimmune markers, as well as normal iron and ferritin, ceru-loplasmin and alfa 1 antitrypsin; a liver biopsy was performed, withelectron microscopy (with no signs of deposition of porfirins). As liverenzymes were high for almost three years we decide to introduce UDCA(URSOFALK) 750mg/day in 2.1998, with observation of progressive nor-malisation of ALT, yet with peaks in July of 1998 and 1999. Since then, wenoted a complete normalisation of liver enzymes levels, without seasonalpeak; in October 1999 UDCA dose was raised to 1gr /day, and a liverbiopsy was repeated in 2002.

UDCA seams to be a very good alternative to maintain patients with EPwith normal liver enzymes levels, wish presumably should slow down theprogression to severe liver lesions, eventually interfering with deposition ofprotoporphyrin.

558

PEGYLATED INTERFERON ALFA-2B AND RIBAVIRIN FORACUTE HEPATITIS CSandeep Mukherjee, M.D.* University of Nebraska Medical Center,Omaha, NE.

A 27 year-old lady developed elevated liver tests after a suicidal attemptwith acetaminophen and alcohol. Transaminases were elevated (ALT 455U/L, AST 500 U/L) but she was negative for hepatitis A, B and C. Livertests normalized with N-acetylcysteine therapy .She was discharged onanti-depressants and participated in weekly counselling sessions and alco-hol abstinence. She developed flu-like symptoms three months later.Transaminases were elevated again (ALT 129 U/L, AST 64 U/L) but shewas now hepatitis C (HCV)antibody positive. Other causes of abnormalliver tests were unremarkable and she was diagnosed with acute hepatitisC. HCVRNA viral load was 515,000 iu/ml and genotype was 1a. Her riskfactor was exposure to a significant other with hepatitis C six weeks priorto her presentation. The patient was eager to initiate treatment for acuteHCV despite being informed of the relative contraindications of treatment,namely her history of significant depression and past alcohol use. Afterpsychiatry consultation, she was started on pegylated interferon alfa-2b(Schering-Plough, Kenilworth, New Jersey) at a dose of 1.0 microgramsper kilogram. Ribavirin (Schering-Plough, Kenilworth, New Jersey) wasnot prescribed due to the lack of data on combination therapy for acutehepatitis C and its known teratogenic effects in women of reproductive age.One month later she developed neutropenia (absolute neutrophil count400/mm

3and pharygitis. Pegylated-interferon was discontinued and she

was prescribed levoquin 400mg per day for one week. White cell countnormalized but liver tests deteriorated.The patient was still eager to trytreatment with lower dose of pegylated interferon (50mcg per week) butthree months later her transaminases were still elevated and HCVRNA hadincreased to 2,500,000 iu/ml. Pegylated interferon alpha 2b was increasedto 64mcg per week and ribavirin 800mg per day. She was treated for sixmonths. One month later, transaminases normalized and three months latershe was HCVRNA negative. At end of treatment transaminases werenormal and HCVRNA undetectable.Six months later, transaminases re-mained normal with undetectable HCVRNA satisfying criteria for sus-tained HCV eradication. The optimum duration of treatment for acutehepatitis C is unknown. However, pegylated-interferon alfa-2b and riba-virin succesfully eradicated acute hepatitis C in a young patient withrelative contra-indications to treatment, highlighting the importance of amulti-disciplinary team.

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ENTEROSCOPY AS A DIAGNOSTIC MODALITY IN THEDIAGNOSIS OF CHYLOUS ASCITES!Gonzalo Pandolfi, M.D., Sanjay Nayyar, M.D., Franjo Vladic, M.D.,Gijo Vettiankal, M.D., Melchor Demetria, M.D.,Bashar M. Attar, M.D., FACG* John H. Stroger Hospital of CookCounty, Rush Medical College, Chicago, IL.

Chylous ascites is an uncommon cause of ascites and its etiology could bea diagnostic challenge. We present one such case of chylous ascites thatwas diagnosed in a 44 year-old African-American woman who presentedwith new onset of ascites and abdominal pain. Physical examination wasremarkable for generalized lymphadenopathy and a 8 cm periumblical masslesion. There was no hepatosplenomegaly. Laboratory data was significantfor a normocytic anemia (Hb�8.5) and leucocytosis with a left shift andthrombocytosis. . Abnormalities on liver function test were a total protein4.1, albumin 1.9, cholesterol 128, Alk Phos 371 and GGT 185. Ascitic fluidanalysis showed a low SAAG ascites (0.9), TG 341 with WBC count of 610(L: 73%, N: 5%). Cytology of the fluid was non conclusive. CT abdomenshowed large ascites and bulky retroperitoneal lymphadenopathy. With aclinical suspicion of malignancy/lymphoma, an axillary lymph node biopsywas planned for tissue diagnosis, which was inconclusive even after flowcytometry. Hence an open laparotomy was performed. It showed a large 8

S186 Abstracts AJG – Vol. 98, No. 9, Suppl., 2003