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Colitis induced by glutaraldehyde
AJG – September, Suppl., 2001
bination of gastrostomy feedings and parenteral nutrition appear to be the most effective strategy available to ameliorate the patient’s symptoms. 729 Santorinicele with recurrent acute pancreatitis—an argument for observation Pamela Ojha, MD1, Michele D Bishop, MD2 and Stephen M Lange, MD2*. 1Medicine, Mayo Clinic, Jacksonville, FL, United States; and 2 Gastroenterology, Mayo Clinic, Jacksonville, FL, United States. Purpose: A pancreatic dorsal duct cyst, Santorinicele, has been reported as an unusual cause of recurrent pancreatitis. All ten previously published cases were discovered after recurrent attacks of pancreatitis, and all were treated endoscopically. We report a case of Santorinicele diagnosed after the first episode of acute pancreatitis, not treated, and six-year follow up. This emphasizes the individuality required for endoscopic treatment decisions. Methods: Our patient, a 67 year old Caucasian man, was initially referred to Mayo Clinic one month after his first episode of idiopathic acute pancreatitis (lipase 23,793 with peripancreatic inflammation on CT scan, normal LFTs). His gallbladder had been removed 20 years earlier. Other medical history included coronary artery disease. There was no family history of pancreatitis or cancer. ERCP was performed finding a small ventral pancreatic duct suggesting pancreas divisum. After IV secretin was used, the minor papilla was identified and cannulated, and a bulbous dilatation was seen distally, consistent with Santorinicele. No endoscopic treatment was elected. Results: Five years later, he experienced his second attack of acute pancreatitis. His symptoms were mild, lipase 428, abdominal ultrasound was normal, and no pancreatic inflammation was seen on CT scan. He was again referred to our clinic 2 months later for follow up. Endoscopic ultrasound of the pancreas was performed, with no evidence of tumor or chronic pancreatitis. Ductal measurements were 1.6 mm in the body and tail, 3.3 mm in the head. After consideration, the patient declined endoscopic treatment. Conclusions: The term, Santorinicele, was first used in 1994 by Eisen and colleagues (Gastrointest Endosc 1994; 40:73–76). Occuring with a prominent dorsal anatomy of the ductal system in pancreas divisum, Santoriniceles are thought to result from a congenital or acquired variation from normal anatomy. As an acquired variation, it may be related to stenosis of the minor papilla and increased dorsal duct pressure, combined with a weakened distal duct wall. A cyst then forms, similar to a choledochocele. No data has been published on the prevalence of Santoriniceles in the general population. Of the ten published case reports (9 adults median age 69 years and one pediatric case, a 7 year-old boy), all cases were found after multiple attacks of pancreatitis and all were treated at the time of diagnosis with papillotomy or balloon dilation. All reportedly had resolution of symptoms, but follow up was less than one year in six pts, and two to three years in four pts. 730 Visceral varicella-zoster after bone marrow transplant: an obscure cause of severe abdominal pain Colm J O’Loughlin, Umaprasanna S Karnam and Jamie S Barkin MACG*. 1Division of Gastroenterology, Mount Sinai Medical Center/ University of Miami, Miami, FL; 2Division of Gastroenterology, Mount Sinai Medical Center/University of Miami, Miami, FL; and 3Division of Gastroenterology, Mount Sinai Medical Center/University of Miami, Miami, FL. Purpose: Visceral varicella-zoster virus (VZV) infection has been reported in approximately 1% of Bone Marrow Transplant recipients. Although relatively uncommon, Visceral VZV infection is most likely underdiagnosed and is frequently lethal-with a 50% mortality from ARDS, MOF, fulminant hepatic failure and severe pancreatitis. Described below is a case of visceral VZV infection ocurring post autologous BMT.
Abstracts
S229
Case Report: A 58-year-old white male diagnosed with IgA Myeloma was treated with Tandem Autologous Bone Marrow Transplants 10 and 4 months prior to presentation. Chemotherapy (Vincristine, Adriamycin and Dexamethasone) preceded the first BMT. He presented with 8 hours of acute generalized abdominal pain associated with nausea, vomiting and diarrhea. He had undergone a sigmoid resection and colostomy (with subsequent closure) for perforated diverticulitis 14 months prior. Abdominal examination revealed a non-distended mildly tender abdomen without guarding or rebound, with midline and left lower quadrant surgical scars. The severity of the patient’s pain was incongruous to the findings on physical examination. Flat and upright abdominal radiographs revealed no dilated bowel loops with gas and stool in a non-dilated colon. Twelve hours later he developed a vesicular erythematous rash on the anterior chest, abdomen, groin and back. Serum AST, ALT, ALP, Total Bilirubin and Lipase levels, which were within normal limits on presentation, were elevated to 704u/l, 965u/l, 230u/l, 2.1mg/dl and 605u/l respectively. The possibility of visceral VZV infection post BMT was raised and empiric therapy with intravenous Acyclovir(15mg/kg/day) was instituted. Clinical symptoms improved and serum transaminases, total bilirubin and lipase levels trended downward within 48 hours. The diagnosis of visceral VZV was confirmed by positive VZV direct flourescence assay (DEA) from skin vesicular fluid. Discussion: Visceral involvement with VZV infection after bone marrow transplant is a common cause of morbidity and mortality. Presenting symptoms include abdominal pain, fever, nausea, vomiting, pneumonitis, rash and diarrhea. Abominal pain is most likely due to stretching of Glisson’s capsule secondary to hepatitis, VZV-induced pancreatitis, or VZV gastritis. Central to the management of visceral VZV is the early recognition and prompt therapy of this infection, as often the abdominal pain precedes the characteristic rash. Conclusion: As this case exemplifies, visceral VZV infection should be considered in immunocompromised patients having abdominal pain with elevated aminotransferases and biochemical evidence of pancreatitis.
731 Colitis induced by glutaraldehyde Fredrick Oni, M.D., Vlado Simko, M.D. VA NY Harbor Health Care System and SUNY Health Science Center at Brooklyn, NY. Potential life threatening complications during endoscopic procedures are well documented. Less known are cases of chemical colitis resulting from disinfecting agents. We report here a case of colitis induced by glutaraldehyde: A non-alcoholic 45 y old man regularly taking fluoxetine but no tobacco or illicit drugs and no recent antibiotics had an uneventful screening colonoscopy because of family history of colon cancer. Twelve hours later he presented to the emergency room with abdominal cramps, bloody diarrhea and diffuse abdominal tenderness. Bright red blood on rectal examination was noted, WBC was 19,000/cu mm with a left shift, CT scan of the abdomen revealed left colonic wall thickening. Flexible sigmoidoscopy two days after colonoscopy revealed an edematous mucosa with exudates and ulcerations suggestive of ischemic colitis. The biopsy documented necrosis and well formed exudates of neutrophils and fibrin. A special stain was negative for gonococcus. Mesalamine and ciprofloxacin were commenced. MRA of the abdomen was normal. Blood cultures and stool for Clostridium dificile were negative. Repeated flexible sigmoidoscopy nine days after colonoscopy was normal. This rapid recovery makes ischemic colitis unlikely and it favors chemical colitis. The instruments in our institution which annually performs over 900 lower GI endoscopies are first manually cleansed with Endozyme (Ruhoff, Long Island, NY) then automatically processed in a Medivator using six cycles which include glutaraldehyde (Cidex plus, Johnson and Johnson, Irvine, CA), Endozyme, ethanol and a flush with air. This is the first time we observed a case of chemical colitis. There have been several reports in the literature of colitis induced by various disinfecting agents, with different mechanisms inducing colitis.
S230
Abstracts
Conclusion: Glutaraldehyde causes direct injury to the crypt epithelium with histopathologic findings that cannot be differentiated from ischemic or pseudomembraneous colitis. An acute onset after a lower GI endoscopy and rapid resolution documented by follow-up procedures confirms this unusual type of colitis which has a more favorable prognosis. 732 AIDS cholangiopathy: ultrasound, ERCP and CT findings in HIV cholangitis David J. Ott, M.D., F.A.C.G.*, Michael Y. Chen, M.D. Department of Radiology, Wake Forest University School Medicine, Winston-Salem, NC 27157. HIV cholangiopathy is one of many multi-system disorders that occurs in patients with AIDS. We present a 28 year-old female with HIV cholangitis, likely related to cryptosporidium infection, who had multiple imaging examinations which showed a variety of abnormalities that may be seen in this disorder. In this exhibit, the clinical history, laboratory results, and imaging findings in this patient are presented more thoroughly and illustrated. The etiology, pathology, and clinical features of AIDS cholangiopathy are discussed and differential considerations, such as sclerosing cholangitis, are outlined. The imaging findings in these biliary tract disorders are compared and the efficacy and role of these modalities in evaluating patients with AIDS and biliary tract signs and symptoms are reviewed and updated. 733 Islet cell tumor: ERCP and CT correlation in patient with hypoglycemia David J. Ott, M.D., F.A.C.G.*, Michael Y. Chen, M.D. Department of Radiology, Wake Forest University School Medicine, Winston-Salem, NC 27157. Islet cell tumors of the pancreas are rare; insulinoma is the most common but is often small (⬍2 cm) and may be difficult to identify preoperatively. We present a 64 year-old man with hypoglycemic episodes who had an insulinoma in the head of the pancreas. Biochemical evidence of the tumor was present, and multiple imaging examinations were performed, including an ERCP which showed a ‘mass’ effect; pancreatic ductal stenting was performed before surgical removal of the mass to help prevent ductal injury. In this exhibit, the clinical history and operative procedure are discussed more thoroughly and imaging findings are illustrated. The classification, pathology and clinical features of islet cell tumors are discussed in general with an emphasis on insulinomas. The imaging modalities used to identify these neoplasms are compared and more recent imaging techniques updated.
AJG – Vol. 96, No. 9, Suppl., 2001
temperature of 101.3F, hepatomegaly and jaundice. Otherwise the patient had stable vital signs, no lymphadenopathy or asterixis, and normal mental status. Laboratory data showed: WBC 16.9 th/cmm, Hgb 7.3 g/dl, Plt 213 th/cmm, T Bili 15.6 mg/dl, D Bili 12.8 mg/dl, ALT 511 u/l, AST 587 u/l, Alk Phos 845 u/l, PT 20.9 sec. Ultrasound of the liver showed multiple “bull’s-eye” lesions, and CT showed diffuse hypodense hepatic lesions. A CT-guided biopsy of the liver was significant for Non-Hodgkin’s lymphoma (NHL), diffuse large B-cell type. Soon after admission, the patient developed worsening coagulopathy and severe encephalopathy progressing to the point of death within a week of hospitalization. A bone marrow evaluation was not done. However, the normal WBC and platelet counts, and lack of intraabdominal or peripheral lymphadenopathy are consistent with primary hepatic lymphoma. While the association of NHL and HIV is well established, hepatic involvement is often associated with systemic disease. Primary hepatic lymphoma is uncommon. Our case reports a rare presentation of primary hepatic lymphoma with FHF. 735 Celiac disease (CD) presenting as chronic unexplained elevation of liver enzymes Nuri Ozden1, John K DiBaise1* and Frederick F Paustian1. 1Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska, United States. Purpose: The wide spectrum of clinical presentations associated with CD oftentimes makes for a challenging diagnosis. Methods: We report an unusual presentation of CD in a 40 year-old Caucasian woman with SLE who we were asked to see for evaluation of chronically elevated liver enzymes (AST 225, ALT 157, AP 736) and a gradually declining albumin (2.5 g/dl). Results: Previous workup was as follows: Hepatitis A, B, C serologies, antismooth muscle, anti-LKM, ANA, anti-dsDNA, and AMA were negative; abdominal CTscan revealed splenic atrophy and multiple 1-cm size mesenteric lymph nodes; and, percutaneous liver biopsy identified nonspecific portal lymphocytic infiltration. Upon further evaluation, we identified history of intermittent diarrhea and mild iron deficiency anemia (Hgb 10.6 g/dl, MCV 73). Peripheral blood smear revealed anisocytosis, Heinz bodies and poikilocytosis. Anti-gliadin, anti-reticulin and anti-endomysial antibody titers were subsequently obtained and were positive. Upper endoscopy with small bowel biopsy confirmed the diagnosis of CD. After a year on a gluten free diet, her clinical condition had improved considerably; liver enzymes and hemoglobin had returned to normal after 3 months. Conclusions: This case highlights the importance of including celiac disease as a potential cause of chronically elevated liver enzymes of unknown etiology. Elevated liver tests, most commonly seen in CD cases of long duration, usually normalize within 6 months of initiating a gluten free diet. Interestingly, CD patients with liver test abnormalities seem to have a higher incidence of lymphoma and small intestinal adenocarcinoma.
734 Fulminant hepatic failure in a patient with primary hepatic lymphoma and HIV Oubre, B., MD, Sood, G., MD, Donelson, S., MD. University of Mississippi/VA Medical Center, Jackson, MS. Hepatic involvement in HIV disease is common. Viral pathogens (Hepatitis A, B, C, CMV, Herpes virus) are the most common cause of HIV associated hepatobiliary disease, followed by opportunistic pathogens (Cryptosporidium, Candida, MAC), neoplasms (Kaposi’s Sarcoma, NonHodgkin’s Lymphoma), and hepatotoxic drugs. Abnormal liver chemistries are seen in two-thirds of HIV patients, jaundice in five to ten percent, and fulminant hepatic failure (FHF) rarely. We present a case of FHF caused by primary hepatic lymphoma in an HIV positive patient. A 39 y/o white man with HIV, a CD4 count of 400, and a viral load of 3,501 copies, on antiretroviral therapy (lamivudine, zidovudine, and nelfinavir) presented with 10 lb. weight loss over 4 weeks, abdominal distention, early satiety, fever, chills, and jaundice. Physical examination was remarkable for a
736 Ecstasy induced fulminant liver failure— half is enough Nuri Ozden, M.D.1, Jesus Carale, M.D.1, Sandeep Mukherjee, M.D.1 and Rowen Zetterman, M.D. FACG, FACP1*. 1Medicine/Hepatology, University of Nebraska Medical Center, Omaha, NE, United States. Purpose: 3,4-Methylenedioxymethamphetamine (MDMA or Ecstasy) is a synthetic amphetamine widely used as weekend recreational drug during RAVE parties. Toxicity ranges from hepatitis like presentation (mimicking viral hepatitis) to fulminant hepatitis with hepatic necrosis and multisystem failure. Methods: A 24 yr old Caucasian female was transferred to our hepatology unit with 48 hour duration of progressive jaundice and Grade II hepatic encephalopathy. She admitted taking half tablet of ecstasy 24 hour prior to initial presentation to an outside facility. She denied using any street drugs or alcohol prior to this incident. Her labs during hospitalization at our facility were AST 2100 ALT 4069, PT/INR ⬎ 10, Cr 4.5 mg/dl. Her
bination of gastrostomy feedings and parenteral nutrition appear to be the most effective strategy available to ameliorate the patient’s symptoms. 729 Santorinicele with recurrent acute pancreatitis—an argument for observation Pamela Ojha, MD1, Michele D Bishop, MD2 and Stephen M Lange, MD2*. 1Medicine, Mayo Clinic, Jacksonville, FL, United States; and 2 Gastroenterology, Mayo Clinic, Jacksonville, FL, United States. Purpose: A pancreatic dorsal duct cyst, Santorinicele, has been reported as an unusual cause of recurrent pancreatitis. All ten previously published cases were discovered after recurrent attacks of pancreatitis, and all were treated endoscopically. We report a case of Santorinicele diagnosed after the first episode of acute pancreatitis, not treated, and six-year follow up. This emphasizes the individuality required for endoscopic treatment decisions. Methods: Our patient, a 67 year old Caucasian man, was initially referred to Mayo Clinic one month after his first episode of idiopathic acute pancreatitis (lipase 23,793 with peripancreatic inflammation on CT scan, normal LFTs). His gallbladder had been removed 20 years earlier. Other medical history included coronary artery disease. There was no family history of pancreatitis or cancer. ERCP was performed finding a small ventral pancreatic duct suggesting pancreas divisum. After IV secretin was used, the minor papilla was identified and cannulated, and a bulbous dilatation was seen distally, consistent with Santorinicele. No endoscopic treatment was elected. Results: Five years later, he experienced his second attack of acute pancreatitis. His symptoms were mild, lipase 428, abdominal ultrasound was normal, and no pancreatic inflammation was seen on CT scan. He was again referred to our clinic 2 months later for follow up. Endoscopic ultrasound of the pancreas was performed, with no evidence of tumor or chronic pancreatitis. Ductal measurements were 1.6 mm in the body and tail, 3.3 mm in the head. After consideration, the patient declined endoscopic treatment. Conclusions: The term, Santorinicele, was first used in 1994 by Eisen and colleagues (Gastrointest Endosc 1994; 40:73–76). Occuring with a prominent dorsal anatomy of the ductal system in pancreas divisum, Santoriniceles are thought to result from a congenital or acquired variation from normal anatomy. As an acquired variation, it may be related to stenosis of the minor papilla and increased dorsal duct pressure, combined with a weakened distal duct wall. A cyst then forms, similar to a choledochocele. No data has been published on the prevalence of Santoriniceles in the general population. Of the ten published case reports (9 adults median age 69 years and one pediatric case, a 7 year-old boy), all cases were found after multiple attacks of pancreatitis and all were treated at the time of diagnosis with papillotomy or balloon dilation. All reportedly had resolution of symptoms, but follow up was less than one year in six pts, and two to three years in four pts. 730 Visceral varicella-zoster after bone marrow transplant: an obscure cause of severe abdominal pain Colm J O’Loughlin, Umaprasanna S Karnam and Jamie S Barkin MACG*. 1Division of Gastroenterology, Mount Sinai Medical Center/ University of Miami, Miami, FL; 2Division of Gastroenterology, Mount Sinai Medical Center/University of Miami, Miami, FL; and 3Division of Gastroenterology, Mount Sinai Medical Center/University of Miami, Miami, FL. Purpose: Visceral varicella-zoster virus (VZV) infection has been reported in approximately 1% of Bone Marrow Transplant recipients. Although relatively uncommon, Visceral VZV infection is most likely underdiagnosed and is frequently lethal-with a 50% mortality from ARDS, MOF, fulminant hepatic failure and severe pancreatitis. Described below is a case of visceral VZV infection ocurring post autologous BMT.
Abstracts
S229
Case Report: A 58-year-old white male diagnosed with IgA Myeloma was treated with Tandem Autologous Bone Marrow Transplants 10 and 4 months prior to presentation. Chemotherapy (Vincristine, Adriamycin and Dexamethasone) preceded the first BMT. He presented with 8 hours of acute generalized abdominal pain associated with nausea, vomiting and diarrhea. He had undergone a sigmoid resection and colostomy (with subsequent closure) for perforated diverticulitis 14 months prior. Abdominal examination revealed a non-distended mildly tender abdomen without guarding or rebound, with midline and left lower quadrant surgical scars. The severity of the patient’s pain was incongruous to the findings on physical examination. Flat and upright abdominal radiographs revealed no dilated bowel loops with gas and stool in a non-dilated colon. Twelve hours later he developed a vesicular erythematous rash on the anterior chest, abdomen, groin and back. Serum AST, ALT, ALP, Total Bilirubin and Lipase levels, which were within normal limits on presentation, were elevated to 704u/l, 965u/l, 230u/l, 2.1mg/dl and 605u/l respectively. The possibility of visceral VZV infection post BMT was raised and empiric therapy with intravenous Acyclovir(15mg/kg/day) was instituted. Clinical symptoms improved and serum transaminases, total bilirubin and lipase levels trended downward within 48 hours. The diagnosis of visceral VZV was confirmed by positive VZV direct flourescence assay (DEA) from skin vesicular fluid. Discussion: Visceral involvement with VZV infection after bone marrow transplant is a common cause of morbidity and mortality. Presenting symptoms include abdominal pain, fever, nausea, vomiting, pneumonitis, rash and diarrhea. Abominal pain is most likely due to stretching of Glisson’s capsule secondary to hepatitis, VZV-induced pancreatitis, or VZV gastritis. Central to the management of visceral VZV is the early recognition and prompt therapy of this infection, as often the abdominal pain precedes the characteristic rash. Conclusion: As this case exemplifies, visceral VZV infection should be considered in immunocompromised patients having abdominal pain with elevated aminotransferases and biochemical evidence of pancreatitis.
731 Colitis induced by glutaraldehyde Fredrick Oni, M.D., Vlado Simko, M.D. VA NY Harbor Health Care System and SUNY Health Science Center at Brooklyn, NY. Potential life threatening complications during endoscopic procedures are well documented. Less known are cases of chemical colitis resulting from disinfecting agents. We report here a case of colitis induced by glutaraldehyde: A non-alcoholic 45 y old man regularly taking fluoxetine but no tobacco or illicit drugs and no recent antibiotics had an uneventful screening colonoscopy because of family history of colon cancer. Twelve hours later he presented to the emergency room with abdominal cramps, bloody diarrhea and diffuse abdominal tenderness. Bright red blood on rectal examination was noted, WBC was 19,000/cu mm with a left shift, CT scan of the abdomen revealed left colonic wall thickening. Flexible sigmoidoscopy two days after colonoscopy revealed an edematous mucosa with exudates and ulcerations suggestive of ischemic colitis. The biopsy documented necrosis and well formed exudates of neutrophils and fibrin. A special stain was negative for gonococcus. Mesalamine and ciprofloxacin were commenced. MRA of the abdomen was normal. Blood cultures and stool for Clostridium dificile were negative. Repeated flexible sigmoidoscopy nine days after colonoscopy was normal. This rapid recovery makes ischemic colitis unlikely and it favors chemical colitis. The instruments in our institution which annually performs over 900 lower GI endoscopies are first manually cleansed with Endozyme (Ruhoff, Long Island, NY) then automatically processed in a Medivator using six cycles which include glutaraldehyde (Cidex plus, Johnson and Johnson, Irvine, CA), Endozyme, ethanol and a flush with air. This is the first time we observed a case of chemical colitis. There have been several reports in the literature of colitis induced by various disinfecting agents, with different mechanisms inducing colitis.
S230
Abstracts
Conclusion: Glutaraldehyde causes direct injury to the crypt epithelium with histopathologic findings that cannot be differentiated from ischemic or pseudomembraneous colitis. An acute onset after a lower GI endoscopy and rapid resolution documented by follow-up procedures confirms this unusual type of colitis which has a more favorable prognosis. 732 AIDS cholangiopathy: ultrasound, ERCP and CT findings in HIV cholangitis David J. Ott, M.D., F.A.C.G.*, Michael Y. Chen, M.D. Department of Radiology, Wake Forest University School Medicine, Winston-Salem, NC 27157. HIV cholangiopathy is one of many multi-system disorders that occurs in patients with AIDS. We present a 28 year-old female with HIV cholangitis, likely related to cryptosporidium infection, who had multiple imaging examinations which showed a variety of abnormalities that may be seen in this disorder. In this exhibit, the clinical history, laboratory results, and imaging findings in this patient are presented more thoroughly and illustrated. The etiology, pathology, and clinical features of AIDS cholangiopathy are discussed and differential considerations, such as sclerosing cholangitis, are outlined. The imaging findings in these biliary tract disorders are compared and the efficacy and role of these modalities in evaluating patients with AIDS and biliary tract signs and symptoms are reviewed and updated. 733 Islet cell tumor: ERCP and CT correlation in patient with hypoglycemia David J. Ott, M.D., F.A.C.G.*, Michael Y. Chen, M.D. Department of Radiology, Wake Forest University School Medicine, Winston-Salem, NC 27157. Islet cell tumors of the pancreas are rare; insulinoma is the most common but is often small (⬍2 cm) and may be difficult to identify preoperatively. We present a 64 year-old man with hypoglycemic episodes who had an insulinoma in the head of the pancreas. Biochemical evidence of the tumor was present, and multiple imaging examinations were performed, including an ERCP which showed a ‘mass’ effect; pancreatic ductal stenting was performed before surgical removal of the mass to help prevent ductal injury. In this exhibit, the clinical history and operative procedure are discussed more thoroughly and imaging findings are illustrated. The classification, pathology and clinical features of islet cell tumors are discussed in general with an emphasis on insulinomas. The imaging modalities used to identify these neoplasms are compared and more recent imaging techniques updated.
AJG – Vol. 96, No. 9, Suppl., 2001
temperature of 101.3F, hepatomegaly and jaundice. Otherwise the patient had stable vital signs, no lymphadenopathy or asterixis, and normal mental status. Laboratory data showed: WBC 16.9 th/cmm, Hgb 7.3 g/dl, Plt 213 th/cmm, T Bili 15.6 mg/dl, D Bili 12.8 mg/dl, ALT 511 u/l, AST 587 u/l, Alk Phos 845 u/l, PT 20.9 sec. Ultrasound of the liver showed multiple “bull’s-eye” lesions, and CT showed diffuse hypodense hepatic lesions. A CT-guided biopsy of the liver was significant for Non-Hodgkin’s lymphoma (NHL), diffuse large B-cell type. Soon after admission, the patient developed worsening coagulopathy and severe encephalopathy progressing to the point of death within a week of hospitalization. A bone marrow evaluation was not done. However, the normal WBC and platelet counts, and lack of intraabdominal or peripheral lymphadenopathy are consistent with primary hepatic lymphoma. While the association of NHL and HIV is well established, hepatic involvement is often associated with systemic disease. Primary hepatic lymphoma is uncommon. Our case reports a rare presentation of primary hepatic lymphoma with FHF. 735 Celiac disease (CD) presenting as chronic unexplained elevation of liver enzymes Nuri Ozden1, John K DiBaise1* and Frederick F Paustian1. 1Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska, United States. Purpose: The wide spectrum of clinical presentations associated with CD oftentimes makes for a challenging diagnosis. Methods: We report an unusual presentation of CD in a 40 year-old Caucasian woman with SLE who we were asked to see for evaluation of chronically elevated liver enzymes (AST 225, ALT 157, AP 736) and a gradually declining albumin (2.5 g/dl). Results: Previous workup was as follows: Hepatitis A, B, C serologies, antismooth muscle, anti-LKM, ANA, anti-dsDNA, and AMA were negative; abdominal CTscan revealed splenic atrophy and multiple 1-cm size mesenteric lymph nodes; and, percutaneous liver biopsy identified nonspecific portal lymphocytic infiltration. Upon further evaluation, we identified history of intermittent diarrhea and mild iron deficiency anemia (Hgb 10.6 g/dl, MCV 73). Peripheral blood smear revealed anisocytosis, Heinz bodies and poikilocytosis. Anti-gliadin, anti-reticulin and anti-endomysial antibody titers were subsequently obtained and were positive. Upper endoscopy with small bowel biopsy confirmed the diagnosis of CD. After a year on a gluten free diet, her clinical condition had improved considerably; liver enzymes and hemoglobin had returned to normal after 3 months. Conclusions: This case highlights the importance of including celiac disease as a potential cause of chronically elevated liver enzymes of unknown etiology. Elevated liver tests, most commonly seen in CD cases of long duration, usually normalize within 6 months of initiating a gluten free diet. Interestingly, CD patients with liver test abnormalities seem to have a higher incidence of lymphoma and small intestinal adenocarcinoma.
734 Fulminant hepatic failure in a patient with primary hepatic lymphoma and HIV Oubre, B., MD, Sood, G., MD, Donelson, S., MD. University of Mississippi/VA Medical Center, Jackson, MS. Hepatic involvement in HIV disease is common. Viral pathogens (Hepatitis A, B, C, CMV, Herpes virus) are the most common cause of HIV associated hepatobiliary disease, followed by opportunistic pathogens (Cryptosporidium, Candida, MAC), neoplasms (Kaposi’s Sarcoma, NonHodgkin’s Lymphoma), and hepatotoxic drugs. Abnormal liver chemistries are seen in two-thirds of HIV patients, jaundice in five to ten percent, and fulminant hepatic failure (FHF) rarely. We present a case of FHF caused by primary hepatic lymphoma in an HIV positive patient. A 39 y/o white man with HIV, a CD4 count of 400, and a viral load of 3,501 copies, on antiretroviral therapy (lamivudine, zidovudine, and nelfinavir) presented with 10 lb. weight loss over 4 weeks, abdominal distention, early satiety, fever, chills, and jaundice. Physical examination was remarkable for a
736 Ecstasy induced fulminant liver failure— half is enough Nuri Ozden, M.D.1, Jesus Carale, M.D.1, Sandeep Mukherjee, M.D.1 and Rowen Zetterman, M.D. FACG, FACP1*. 1Medicine/Hepatology, University of Nebraska Medical Center, Omaha, NE, United States. Purpose: 3,4-Methylenedioxymethamphetamine (MDMA or Ecstasy) is a synthetic amphetamine widely used as weekend recreational drug during RAVE parties. Toxicity ranges from hepatitis like presentation (mimicking viral hepatitis) to fulminant hepatitis with hepatic necrosis and multisystem failure. Methods: A 24 yr old Caucasian female was transferred to our hepatology unit with 48 hour duration of progressive jaundice and Grade II hepatic encephalopathy. She admitted taking half tablet of ecstasy 24 hour prior to initial presentation to an outside facility. She denied using any street drugs or alcohol prior to this incident. Her labs during hospitalization at our facility were AST 2100 ALT 4069, PT/INR ⬎ 10, Cr 4.5 mg/dl. Her