Results: Since 1982, 70 patients at the Mayo Clinic were diagnosed withIPMT (mean age of 66.3 years) typically presenting with abdominal painmimicking chronic pancreatitis or cancer. We identified 5 patients (3women, 2 men) under the age of 50 (range 36–46, mean 41.6 years) withhistologically proven IPMT. Three patients presented with recurrent acutepancreatitis; two patients presented with chronic pancreatitis. Typical eti-ologies of pancreatitis were excluded in all patients. The length of timebetween presentation and diagnosis ranged between 8 weeks and 10 years,with a median of 1 year. The diagnosis was suspected in all patients basedon localized (4) or diffuse (1) ductal dilation seen by CT or ERCP. Initialsurgical management consisted of localized resection in 4 of 5 patients. Todate, 1 patient with benign IPMT has had a localized benign recurrencerequiring completion pancreatectomy 36 months after initial surgery. Onepatient of five (20%) had invasive carcinoma at diagnosis (requiring totalpancreatectomy) compared to 29 out of 70 (45%) with invasive cancer atdiagnosis in the total cohort. One year later this patient developed perito-neal carcinomatosis. The remaining 3 patients have been symptom free.Conclusion: IPMT occurs in young patients and is often confused withother pancreatic disorders, delaying the diagnosis. IPMT must be consid-ered in the differential diagnosis of idiopathic pancreatitis. If discoveredearly, surgical management offers freedom from relapsing pancreatitis andthe later development of invasive carcinoma.

503

Indolent Wegener’s granulomatosis with intestinal involvementAgrawal MD Sanjay, Kelfer MD Michael, Levey MD* John M.University of Massachusetts Medical School, Worcester Medical Center,The Fallon Clinic, Worcester, MA.

Purpose: Wegener’s Granulomatosis (WG) is a systemic vasculitis ofunknown etiology characterized by involvement of the upper airways, lungand kidneys, although any organ may be affected. There are several casereports of intestinal involvement in aggressive WG. We report a case ofWG with colonic involvement in a patient with indolent disease, sparing thekidneys and lungs.Methods: Thirty months prior to admission this 31-year white female hadpresented with chronic sinusitis, epistaxis, polyarthralgia and a non-healingright thigh ulcer. Ulcer biopsies revealed giant cells and leukoclasticvasculitis with granulomas. Cytoplasmic antineutrophilic cytoplasmic an-tibody was positive in titers of 1:64. A urinalysis, and CT scans of thesinuses and chest were normal. She was treated for WG with prednisoneand methotrexate, with good results. At the time of this admission shepresented with subacute onset of localized right lower quadrant pain andconstipation for three days. She denied nausea, vomiting, abdominal dis-tention, GI bleeding, recent antibiotics, fever, chills, arthralgia, and car-diopulmonary or genitourinary complaints. Past medical history was sig-nificant for WG, seizures with normal MRI and EEG, anxiety, depression,and congenital absence of uterine appendages with normal chromosomalstudies. Current medications included methotrexate 15 mg/week and pred-nisone 15 mg/d. On physical examination she was in moderate distress,afebrile, with oral ulcerations, a healing right thigh ulcer with granulationtissue, decreased bowel sounds, right lower quadrant tenderness withguarding, and guaiac negative stools. Laboratory investigations revealednormal CBC, chem 7, liver enzymes, urinalysis, abdominal and chest Xray.Stool culture, stool leukocytes, Clostridium difficile toxin, ova and para-sites were negative. Contrast enhanced abdominal CT showed a thickenedcecum and ascending colon. The rest of the colon, terminal ileum andappendix were normal. Colonoscopic findings demonstrated congestededematous mucosa with superficial ulcerations and exudate in the cecumand ascending colon. The terminal ileum was not visualized. Biopsies fromthe right colon were notable for extensive acute ischemic changes. Novasculitis or granulomas were identified on biopsy.Results:A diagnosis of WG with right colonic involvement was made. Shereceived antibiotics for a week and the dose of prednisone was increased to60 mg/day. Methotrexate was continued. She gradually recovered to herbaseline status in a month.

Conclusions:Intestinal involvement in WG is rare. This diagnosis shouldbe considered in any patient with indolent WG presenting with abdominalpain, change in bowel habits or perforation.

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Human Immunodeficiency Virus (HIV) protease inhibitor-inducedacute pancreatitis secondary to hypertriglyceridemia—A case reportAhmad MD Jawad, Martin MD John. University of Pittsburgh MedicalCenter, Pittsburgh, PA.

HIV protease inhibitor therapy is associated with hyperlipidemia and alsoidiosyncratic acute pancreatitis. We present an unusual case of predictablehypertriglyceridemia secondary to protease inhibitor therapy that led to asevere episode of acute pancreatitis, and the patient continues to developasymptomatic hypertriglyceridemia whenever challenged with these drugs.Case Report:A 32 year old homosexual male with AIDS was admittedwith acute pancreatitis in September 1998 which resolved after 2 weekswith conservative therapy. Four months prior to admission his anti-HIVmedications were changed from indinavir (I), lamivudine (L), and stavu-dine (St) to ritonavir (R), saquinavir (Sa), lamivudine, stavudine, andnevirapine (N) following a rising HIV viral load. The table below shows hisresponse to HIV therapy and effect on his lipids.Other meds.-Amprenavir(Am), efavirenz (E), adefovir (Ad).

Date MedicationsViral load(copies/ml)

Trig.(mg/dl)

Chol.(mg/dl)

5/98 I, L, St 105062 488 1296/98 R, Sa, L, St, N ,400 2930 4538/98 R, Sa, L, St, N ,400 3970 12110/98 Off HIV meds. 35250 141 9612/98 R, Sa, L, St, N 1424 610 2291/99 R, Sa, L, St, N — 2982 4842/99 Off HIV meds. 41038 180 1035/99 Am, St, L, E, Ad 1921 332 12911/99 R added ,50 681 —1/00 Am, St, L, E, Ad, R ,50 865 1692/00 Am, St, L, E, Ad, R — 3520 4053/00 Off HIV meds. — 286 2094/00 Am, St, L, E, Ad, R ,50 1090 286

Discussion:The pattern of medication use would suggest that ritonavir wasresponsible. Despite the very high TG levels, the patient has not hadanother episode of pancreatitis. Monitoring of lipids is essential for patientson protease inhibitor therapy.

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Ecstasy induced severe acute hepatitis among young adultsJamil Akhras, MD, Joseph L Kinzie, MD, FACG*. Wayne StateUniversity, Detroit, MI.

Purpose and Case:A 21 year old Caucasian female was referred to for 4weeks history of progressive jaundice associated with lethargy, anorexia,pruritus, nausea, dark urine and clay-colored stool, other symptoms arenegative. She was taking no medication. Patient drank alcohol socially,admitted the use of oral ecstasy (MDMA) 4–5 times over the past 10 weeksprior to her illness, at interval of 2 weeks apart. Before a trip to India 10months prior to her presentation, she had been vaccinated against typhoid,meningitis, hepatitis B, and received hepatitis A immune globulin. Herheight was 5 feet 6 inches, weight was 121 pounds, and other vitals werestable. She was deeply jaundiced with icteric sclera, no evidence of hep-atosplenomegaly, shifting dullness, or flapping tremor. Sensorium wasclear.Results: Albumin 4.2 (g/dl), Alkaline Phosphatase 232 (U/L) Total Bili-rubin 5.9 peaked to 31 (mg/dl), Direct Bilirubin 3.6 (mg/dl), AST 1745(U/L), ALT 2250 (U/L), PT 14.6 (Sec), HbsAg, HbcAb, HAAB (IgM),HCV Ab, HEV Ab (IgM), HCV PCR/RNA, ANA, AMA, and ASMA arenegative, but total HAAB, and HbsAb are positive. Ceruloplasmin level

2558 Abstracts AJG – Vol. 95, No. 9, 2000