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Hepatic infarction in pregnancy associated with the antiphospholipid syndrome
AJG – September, Suppl., 2003
Introduction: Burkitt’s lymphoma is a highly aggressive non-Hodgkin’s lymphoma. It is most commonly seen in its endemic form as a childhood disease in Africa, presenting as a facial bone tumor with spread to extranodal sites. It also has a sporadic presentation involving predominantly the gastrointestinal tract, primarily the stomach, cecum and distal ileum. Additionally, it may manifest itself as part of an immunodeficiency syndrome. Burkitt’s lymphoma of the colon is an extremely rare disease in the Western world. Case Report: A 45 year-old white male with a two year history of ulcerative colitis presented with bloody diarrhea, crampy abdominal pain and a 15lb weight loss. Medications included mesalamine and antidepressants. Physical examination was remarkable for left lower quadrant tenderness. Laboratory findings were significant for iron deficiency anemia. A colonoscopy showed evidence of marked colitis with large nodular exophytic lesions extending from the rectum to the splenic flexure. Rectal biopsies revealed a diffuse infiltration of lymphoid cells with a starry sky pattern and extensive necrosis consistent with a malignant B cell lymphoma. Flow cytometry confirmed absolute lymphocytosis with a pattern usually seen in certain viral infections including Epstein Barr virus. CT scan of the abdomen demonstrated extensive diffuse wall thickening throughout the left colon with slight infiltration of the pericolonic fat consistent with our clinical and immunohistochemical diagnosis of Burkitt’s lymphoma. The patient tested negative for human immunodeficiency virus. Conclusion: Burkitt’s lymphoma is an extremely rare yet potentially curable disease mandating an accurate diagnosis. It may present primarily in the gastrointestinal tract mimicking other conditions such as inflammatory bowel disease. This case represents a unique and atypical presentation of an uncommon disease.
604 REVERSAL OF ADVANCE LIVER FIBROSIS WITH PHLEBOTOMY IN A PATIENT WITH PORPHYRIA CUTANEA TARDA AND HEPATITIS C Muhammad K. Hasan, M.D., Ali A. Siddiqui, M.D., Sikander Mesiya, M.D.*, Javid Fazili, M.D., Jan Pitha, M.D., Michael Talbert, M.D. University of Oklahoma, Oklahoma City, OK. Introduction: Porphyria cutanea tarda (PCT) is characterized by skin rash, iron overload and chronic hepatitis. Cirrhosis is a known complication of chronic liver disease. Once established, cirrhosis has generally been considered irreversible. We here describe a case of PCT with hepatic iron overload that had a reversal of advance hepatic fibrosis and resolution of cutaneous lesions with iron reduction therapy. Case: A 47 year-old Caucasian man with five-month history of recurring, fragile vesicles and bullae over the dorsal aspect of both forearms and hands. Patient denied history of jaundice, hepatitis or family history of chronic liver disease. Physical examination revealed several tense bullae overlying normal appearing skin on the dorsal aspect of the patient’s forearms, hands and fingers. There was no clinical evidence of hepatomegaly and ascites. Laboratory findings were noted for elevated serum transaminases ALT and AST 218 IU/L and 203 IU/L, respectively. Serum ferritin was 320 ng/ml, albumin 4.1 gm/dl, platelet 270,000, prothrombin time 10.3 seconds. Patient had a positive hepatitis C antibody with viral RNA of 515,540 copies/ml. Hemochromatosis gene test was negative for both C282Y and H63D mutations. The 24-hour urine noted to have abnormally high uroporphyrin at 874 nmol/24 h. Patient underwent a percutaneous liver biopsy that showed moderate piecemeal necrosis, portal inflammation and bridging fibrosis, hepatic activity index (HAI) score of 12. Moderate degree of hemosiderosis and steatosis were present. The patient underwent biweekly phlebotomy for 8 months that resulted in decreased skin fragility with moderate improvement in serum transaminases. Four years later patient was referred for treatment of hepatitis C. A repeat liver biopsy showed marked improvement of hepatic inflammation, fibrosis and resolution of hemosiderosis with HAI score of 6.
Abstracts
S201
Discussion: There is growing evidence that clinically silent cirrhosis can be reversed with appropriate treatment of the underlying cause of the cirrhosis. Patients with PCT with hepatitis C usually undergo iron reduction therapy followed by definitive antiviral therapy for hepatitis C. Iron reduction therapy improves skin lesions, transaminases and the response to interferon in patient with hepatitis C and PCT. This case is unique as it demonstrates the importance of iron reduction therapy in achieving improvement of liver histology.
605 ISOLATED ESOPHAGEAL PEMPHIGUS VULGARIS Ziad Salem, M.D., Anthony Strippoli, M.D., Joseph R. DePasquale, M.D., FACG*. Seton Hall University School of Graduate Medical Education, South Orange, NJ and St. Michael’s Medical Center, Newark, NJ. Introduction: Pemphigus vulgaris is a rare autoimmune blistering disease of the skin and mucous membranes. Studies have indicated that most patients with the cutaneous form of the disease will have an oropharyngeal component. When the esophagus is involved, erosions secondary to mucosal sloughing may mask the blistering nature of the disease. Isolated esophageal disease is rarely seen. Case Report: A 55 year-old white female with a past medical history significant for asthma presented with evaluation of unremitting dysphagia to solids and liquids without heartburn. Physical examination and laboratory studies were unremarkable; there was no evidence of oral or cutaneous lesions. Previous endoscopy had revealed esophagitis with a distal esophageal stricture. Subsequently, she underwent balloon dilatation with a trial of high dose proton inhibitors with minimal symptom relief. Repeat endoscopy showed persistent esophagitis with recurrent stricture formation requiring repeat dilatation . On follow-up visit, the patient reported worsening of her symptoms; re-endoscopy revealed sloughing of the esophageal mucosa suggestive of a bullous disease. Esophageal biopsies showed subepidermal blistering confirming our clinical impression of pemphigus vulgaris. Steroid therapy was initiated with a dramatic response. Conclusion: Isolated esophageal pemphigus vulgaris without concomitant oral or skin involvement is seldom reported and ultimately presents a clinical challenge to the most experienced endoscopist. This case represents an extremely rare presentation of a rare disease.
606 HEPATIC INFARCTION IN PREGNANCY ASSOCIATED WITH THE ANTIPHOSPHOLIPID SYNDROME Kiran Jagarlamudi, M.D., Bakul Patel, M.D., Walid Baddoura, M.D.*. Seton Hall University School of Graduate Medical Education, South Orange, NJ and St. Joseph’s Regional Medical Center, Paterson, NJ. Introduction: Antiphospholipid syndrome is associated with vascular thrombosis, recurrent pregnancy loss and thrombocytopenia. Patients have an increased risk of thromboembolic phenomena in venous and arterial systems. We describe a 16 year-old pregnant female who developed hepatic infarction in the setting of antiphospholipid syndrome. Case Report: A 16 year-old female in her second trimester of pregnancy was admitted with a three-week history of epigastric pain, nausea and vomiting. She had a previous history of spontaneous abortion at six weeks of gestation.Her physical examination was remarkable for epigastric and right upper quadrant tenderness. Significant laboratory findings at the time of admission included: platelet count 125,000, LDH 1742, AST 111, ALT 63, and PTT 73.4. Abdominal ultrasound revealed no evidence of cholelithiasis or hepatic lesion. On the next day, leukocytosis was noted with a further increase in the LDH, AST and ALT; VDRL was reactive. Post delivery, the abdominal pain decreased; due to elevation of liver enzymes, a CT scan of the abdomen was done which showed a 7 cm well-circumscribed irregularly shaped focus of low attenuation occupying the right lobe
S202
Abstracts
AJG – Vol. 98, No. 9, Suppl., 2003
of the liver with smaller satellite areas of low attenuation scattered throughout the more anterior aspect of the right lobe highly suggestive of hepatic infarction. Steroids and heparin were started. Additional labs included a positive lupus anticoagulant and an elevated anticardiolipin IgM antibody. She was discharged home on warfarin after attaining therapeutic INR levels. Follow-up CT scan done a month later showed resolution of the infarction. Discussion: The liver is a very vascular organ, with a dual blood supply from both hepatic and portal circulation. As such, hepatic infarction is rare. Patients diagnosed with the antiphospholipid syndrome are at increased risk for thromboembolic phenomena, both in the venous and arterial systems thus requiring long term anticoagulation. Antiphospholipid syndrome is a rare cause of hepatic infarction. As illustrated in this case, this syndrome should be entertained in the differential diagnosis of hepatic infarction.
607 RECURRENT PORTOSYSTEMIC ENCEPHALOPATHY DESPITE MEDICAL THERAPY Christian M. Mendez, M.D.*, Luis S. Marsano, M.D., Craig J. McClain, M.D., Aronson Brian, M.D. University of Louisville School of Medicine, Louisville, KY. A 60 year-old white male presents with a 2 month history of recurrent episodes of innapropiate behavior and disorientation. Past medical history included ulcerative colitis in remission and abnormal liver tests. An ERCP and percutaneous liver biopsy were performed as part of the work up for abnormal liver tests. ERCP showed sclerosis of the secondary and tertiary biliary ducts and no strictures. The liver biopsy showed mild portal fibrosis and positive PAS staining consistent with alpha 1 antitrypsin deficiency. Phenotype PiMZ. Physical exam revealed an obese male with asterixis and no stigmata of chronic liver disease. Work-up performed showed mild anemia, normal platelet count, ALT 156, AST 116, total bilirrubin 2.3, albumin 4.1, PT 11, INR 1.0. Ammonia level was elevated in 95. HCV and HBV serologies were negative. CSF exam and CT and MRI of the head were normal. Patient had received treatment for hepatic encephalopathy with metronidazol/lactulose with recurrence of symptoms. Further work-up included a hepatic doppler ultrasound that was normal and an arteriovenous phase CT of the abdomen that showed an intrahepatic arteriovenous shunt located in the right hepatic lobe. A mesenteric angiography did confirm the diagnosis and allowed the successful embolization and closure of the shunt using steel coils. Resolution of the symptoms was noted and there were no more episodes of confusion during follow-up. Learning points: recurrent episodes of encephalopathy despite medical therapy and no precipitating factors may be secondary to portosystemic shunts; and vascular complications of liver biopsy are rare events and are amenable to angiographic therapy.
608 MASSIVE GASTRIC BLEEDING AS INITIAL PRESENTATION OF PANCREATIC CANCER Ziad Salem, M.D., Walid Baddoura, M.D., Michael Martino, M.D., Ralph Demaio, M.D.*. Seton Hall University School of Medical Education, South Orange, NJ and Saint Joseph’s Regional Medical Center, Paterson, NJ. Introduction: Neoplasm as a cause of massive upper gastrointestinal bleeding is uncommon. It is mostly caused by gastric cancer; it is also well established that pancreatic cancer can directly invade the duodenum and present as bleeding. Case Report: A 79 year-old man with history of coronary artery bypass, congestive heart failure, hypertriglyceridemia, cardiovascular accident and prostate cancer was hospitalized with peri-umbilical pain, lightheadedness and two episodes of melena. He denied back pain or weight loss. His medications included metoprolol, furosemide and gemfibrozil. His physical examination was only remarkable for mid-abdominal tenderness. Nasogastric tube revealed a coffee-ground return. Laboratory findings on admission were significant for Hgb 9.1 with an MCV of 96. Upper endoscopy showed a large amount of coffee-ground material and pre-pyloric erosions with no demonstrable active bleeding site; the proximal duodenum was clear. The patient was treated with a proton pump inhibitor for presumptive ulcer disease. Due to a two-gram drop in Hgb, a repeat endoscopic examination was performed; frank bleeding was noted in the fundic area which could not be controlled. This prompted an emergency laparotomy which showed a pancreatic mass invading the proximal stomach wall; bleeding vessels were ligated as the tumor was found to be unresectable. Pathological analysis revealed a well differentiated mucin-producing pancreatic adenocarcinoma with metastasis to the small bowel mesentery. The post operative course was complicated by a transient coagulopathy and a change in mental status. Palliative therapy was subsequently initiated. Conclusion: Although pancreatic cancer is known to impinge on adjacent structures such as the duodenum and the stomach, it seldom presents with active upper gastrointestinal bleeding; massive gastric bleeding is exceedingly rare. Our case illustrates such a rare presentation of locally invasive pancreatic cancer.
609 DOUBLE DUCT SIGN DUE TO PANCREATIC LYMPHOMA IN AIDS Joanne M. Silvia, Graham Gardner, M.D., Samir A. Shah, M.D., FACG, Edward R. Feller, M.D., FACG*. Brown Medical School, Providence, RI and Beth Israel Deaconess Medical Center, Boston, MA. Pancreatic lymphoma is a rare cause of biliary obstruction. We report a case of obstructive jaundice due to large-cell, non-Hodgkin’s lymphoma to alert
Introduction: Burkitt’s lymphoma is a highly aggressive non-Hodgkin’s lymphoma. It is most commonly seen in its endemic form as a childhood disease in Africa, presenting as a facial bone tumor with spread to extranodal sites. It also has a sporadic presentation involving predominantly the gastrointestinal tract, primarily the stomach, cecum and distal ileum. Additionally, it may manifest itself as part of an immunodeficiency syndrome. Burkitt’s lymphoma of the colon is an extremely rare disease in the Western world. Case Report: A 45 year-old white male with a two year history of ulcerative colitis presented with bloody diarrhea, crampy abdominal pain and a 15lb weight loss. Medications included mesalamine and antidepressants. Physical examination was remarkable for left lower quadrant tenderness. Laboratory findings were significant for iron deficiency anemia. A colonoscopy showed evidence of marked colitis with large nodular exophytic lesions extending from the rectum to the splenic flexure. Rectal biopsies revealed a diffuse infiltration of lymphoid cells with a starry sky pattern and extensive necrosis consistent with a malignant B cell lymphoma. Flow cytometry confirmed absolute lymphocytosis with a pattern usually seen in certain viral infections including Epstein Barr virus. CT scan of the abdomen demonstrated extensive diffuse wall thickening throughout the left colon with slight infiltration of the pericolonic fat consistent with our clinical and immunohistochemical diagnosis of Burkitt’s lymphoma. The patient tested negative for human immunodeficiency virus. Conclusion: Burkitt’s lymphoma is an extremely rare yet potentially curable disease mandating an accurate diagnosis. It may present primarily in the gastrointestinal tract mimicking other conditions such as inflammatory bowel disease. This case represents a unique and atypical presentation of an uncommon disease.
604 REVERSAL OF ADVANCE LIVER FIBROSIS WITH PHLEBOTOMY IN A PATIENT WITH PORPHYRIA CUTANEA TARDA AND HEPATITIS C Muhammad K. Hasan, M.D., Ali A. Siddiqui, M.D., Sikander Mesiya, M.D.*, Javid Fazili, M.D., Jan Pitha, M.D., Michael Talbert, M.D. University of Oklahoma, Oklahoma City, OK. Introduction: Porphyria cutanea tarda (PCT) is characterized by skin rash, iron overload and chronic hepatitis. Cirrhosis is a known complication of chronic liver disease. Once established, cirrhosis has generally been considered irreversible. We here describe a case of PCT with hepatic iron overload that had a reversal of advance hepatic fibrosis and resolution of cutaneous lesions with iron reduction therapy. Case: A 47 year-old Caucasian man with five-month history of recurring, fragile vesicles and bullae over the dorsal aspect of both forearms and hands. Patient denied history of jaundice, hepatitis or family history of chronic liver disease. Physical examination revealed several tense bullae overlying normal appearing skin on the dorsal aspect of the patient’s forearms, hands and fingers. There was no clinical evidence of hepatomegaly and ascites. Laboratory findings were noted for elevated serum transaminases ALT and AST 218 IU/L and 203 IU/L, respectively. Serum ferritin was 320 ng/ml, albumin 4.1 gm/dl, platelet 270,000, prothrombin time 10.3 seconds. Patient had a positive hepatitis C antibody with viral RNA of 515,540 copies/ml. Hemochromatosis gene test was negative for both C282Y and H63D mutations. The 24-hour urine noted to have abnormally high uroporphyrin at 874 nmol/24 h. Patient underwent a percutaneous liver biopsy that showed moderate piecemeal necrosis, portal inflammation and bridging fibrosis, hepatic activity index (HAI) score of 12. Moderate degree of hemosiderosis and steatosis were present. The patient underwent biweekly phlebotomy for 8 months that resulted in decreased skin fragility with moderate improvement in serum transaminases. Four years later patient was referred for treatment of hepatitis C. A repeat liver biopsy showed marked improvement of hepatic inflammation, fibrosis and resolution of hemosiderosis with HAI score of 6.
Abstracts
S201
Discussion: There is growing evidence that clinically silent cirrhosis can be reversed with appropriate treatment of the underlying cause of the cirrhosis. Patients with PCT with hepatitis C usually undergo iron reduction therapy followed by definitive antiviral therapy for hepatitis C. Iron reduction therapy improves skin lesions, transaminases and the response to interferon in patient with hepatitis C and PCT. This case is unique as it demonstrates the importance of iron reduction therapy in achieving improvement of liver histology.
605 ISOLATED ESOPHAGEAL PEMPHIGUS VULGARIS Ziad Salem, M.D., Anthony Strippoli, M.D., Joseph R. DePasquale, M.D., FACG*. Seton Hall University School of Graduate Medical Education, South Orange, NJ and St. Michael’s Medical Center, Newark, NJ. Introduction: Pemphigus vulgaris is a rare autoimmune blistering disease of the skin and mucous membranes. Studies have indicated that most patients with the cutaneous form of the disease will have an oropharyngeal component. When the esophagus is involved, erosions secondary to mucosal sloughing may mask the blistering nature of the disease. Isolated esophageal disease is rarely seen. Case Report: A 55 year-old white female with a past medical history significant for asthma presented with evaluation of unremitting dysphagia to solids and liquids without heartburn. Physical examination and laboratory studies were unremarkable; there was no evidence of oral or cutaneous lesions. Previous endoscopy had revealed esophagitis with a distal esophageal stricture. Subsequently, she underwent balloon dilatation with a trial of high dose proton inhibitors with minimal symptom relief. Repeat endoscopy showed persistent esophagitis with recurrent stricture formation requiring repeat dilatation . On follow-up visit, the patient reported worsening of her symptoms; re-endoscopy revealed sloughing of the esophageal mucosa suggestive of a bullous disease. Esophageal biopsies showed subepidermal blistering confirming our clinical impression of pemphigus vulgaris. Steroid therapy was initiated with a dramatic response. Conclusion: Isolated esophageal pemphigus vulgaris without concomitant oral or skin involvement is seldom reported and ultimately presents a clinical challenge to the most experienced endoscopist. This case represents an extremely rare presentation of a rare disease.
606 HEPATIC INFARCTION IN PREGNANCY ASSOCIATED WITH THE ANTIPHOSPHOLIPID SYNDROME Kiran Jagarlamudi, M.D., Bakul Patel, M.D., Walid Baddoura, M.D.*. Seton Hall University School of Graduate Medical Education, South Orange, NJ and St. Joseph’s Regional Medical Center, Paterson, NJ. Introduction: Antiphospholipid syndrome is associated with vascular thrombosis, recurrent pregnancy loss and thrombocytopenia. Patients have an increased risk of thromboembolic phenomena in venous and arterial systems. We describe a 16 year-old pregnant female who developed hepatic infarction in the setting of antiphospholipid syndrome. Case Report: A 16 year-old female in her second trimester of pregnancy was admitted with a three-week history of epigastric pain, nausea and vomiting. She had a previous history of spontaneous abortion at six weeks of gestation.Her physical examination was remarkable for epigastric and right upper quadrant tenderness. Significant laboratory findings at the time of admission included: platelet count 125,000, LDH 1742, AST 111, ALT 63, and PTT 73.4. Abdominal ultrasound revealed no evidence of cholelithiasis or hepatic lesion. On the next day, leukocytosis was noted with a further increase in the LDH, AST and ALT; VDRL was reactive. Post delivery, the abdominal pain decreased; due to elevation of liver enzymes, a CT scan of the abdomen was done which showed a 7 cm well-circumscribed irregularly shaped focus of low attenuation occupying the right lobe
S202
Abstracts
AJG – Vol. 98, No. 9, Suppl., 2003
of the liver with smaller satellite areas of low attenuation scattered throughout the more anterior aspect of the right lobe highly suggestive of hepatic infarction. Steroids and heparin were started. Additional labs included a positive lupus anticoagulant and an elevated anticardiolipin IgM antibody. She was discharged home on warfarin after attaining therapeutic INR levels. Follow-up CT scan done a month later showed resolution of the infarction. Discussion: The liver is a very vascular organ, with a dual blood supply from both hepatic and portal circulation. As such, hepatic infarction is rare. Patients diagnosed with the antiphospholipid syndrome are at increased risk for thromboembolic phenomena, both in the venous and arterial systems thus requiring long term anticoagulation. Antiphospholipid syndrome is a rare cause of hepatic infarction. As illustrated in this case, this syndrome should be entertained in the differential diagnosis of hepatic infarction.
607 RECURRENT PORTOSYSTEMIC ENCEPHALOPATHY DESPITE MEDICAL THERAPY Christian M. Mendez, M.D.*, Luis S. Marsano, M.D., Craig J. McClain, M.D., Aronson Brian, M.D. University of Louisville School of Medicine, Louisville, KY. A 60 year-old white male presents with a 2 month history of recurrent episodes of innapropiate behavior and disorientation. Past medical history included ulcerative colitis in remission and abnormal liver tests. An ERCP and percutaneous liver biopsy were performed as part of the work up for abnormal liver tests. ERCP showed sclerosis of the secondary and tertiary biliary ducts and no strictures. The liver biopsy showed mild portal fibrosis and positive PAS staining consistent with alpha 1 antitrypsin deficiency. Phenotype PiMZ. Physical exam revealed an obese male with asterixis and no stigmata of chronic liver disease. Work-up performed showed mild anemia, normal platelet count, ALT 156, AST 116, total bilirrubin 2.3, albumin 4.1, PT 11, INR 1.0. Ammonia level was elevated in 95. HCV and HBV serologies were negative. CSF exam and CT and MRI of the head were normal. Patient had received treatment for hepatic encephalopathy with metronidazol/lactulose with recurrence of symptoms. Further work-up included a hepatic doppler ultrasound that was normal and an arteriovenous phase CT of the abdomen that showed an intrahepatic arteriovenous shunt located in the right hepatic lobe. A mesenteric angiography did confirm the diagnosis and allowed the successful embolization and closure of the shunt using steel coils. Resolution of the symptoms was noted and there were no more episodes of confusion during follow-up. Learning points: recurrent episodes of encephalopathy despite medical therapy and no precipitating factors may be secondary to portosystemic shunts; and vascular complications of liver biopsy are rare events and are amenable to angiographic therapy.
608 MASSIVE GASTRIC BLEEDING AS INITIAL PRESENTATION OF PANCREATIC CANCER Ziad Salem, M.D., Walid Baddoura, M.D., Michael Martino, M.D., Ralph Demaio, M.D.*. Seton Hall University School of Medical Education, South Orange, NJ and Saint Joseph’s Regional Medical Center, Paterson, NJ. Introduction: Neoplasm as a cause of massive upper gastrointestinal bleeding is uncommon. It is mostly caused by gastric cancer; it is also well established that pancreatic cancer can directly invade the duodenum and present as bleeding. Case Report: A 79 year-old man with history of coronary artery bypass, congestive heart failure, hypertriglyceridemia, cardiovascular accident and prostate cancer was hospitalized with peri-umbilical pain, lightheadedness and two episodes of melena. He denied back pain or weight loss. His medications included metoprolol, furosemide and gemfibrozil. His physical examination was only remarkable for mid-abdominal tenderness. Nasogastric tube revealed a coffee-ground return. Laboratory findings on admission were significant for Hgb 9.1 with an MCV of 96. Upper endoscopy showed a large amount of coffee-ground material and pre-pyloric erosions with no demonstrable active bleeding site; the proximal duodenum was clear. The patient was treated with a proton pump inhibitor for presumptive ulcer disease. Due to a two-gram drop in Hgb, a repeat endoscopic examination was performed; frank bleeding was noted in the fundic area which could not be controlled. This prompted an emergency laparotomy which showed a pancreatic mass invading the proximal stomach wall; bleeding vessels were ligated as the tumor was found to be unresectable. Pathological analysis revealed a well differentiated mucin-producing pancreatic adenocarcinoma with metastasis to the small bowel mesentery. The post operative course was complicated by a transient coagulopathy and a change in mental status. Palliative therapy was subsequently initiated. Conclusion: Although pancreatic cancer is known to impinge on adjacent structures such as the duodenum and the stomach, it seldom presents with active upper gastrointestinal bleeding; massive gastric bleeding is exceedingly rare. Our case illustrates such a rare presentation of locally invasive pancreatic cancer.
609 DOUBLE DUCT SIGN DUE TO PANCREATIC LYMPHOMA IN AIDS Joanne M. Silvia, Graham Gardner, M.D., Samir A. Shah, M.D., FACG, Edward R. Feller, M.D., FACG*. Brown Medical School, Providence, RI and Beth Israel Deaconess Medical Center, Boston, MA. Pancreatic lymphoma is a rare cause of biliary obstruction. We report a case of obstructive jaundice due to large-cell, non-Hodgkin’s lymphoma to alert