Antral mass due to cytomegalovirus infection requiring gastrectomy in a liver transplant recipient.

The incidence of cytomegalovirus (CMV) infection after liver transplantation (LT) has decreased in recent years. Advances in immunosuppression and CMV prophylaxis have improved the management of CMV disease. Organ involvement is infrequent and gastrointestinal CMV disease is quite rare. Few cases of an antral mass due to CMV infection have been described; those reported to date have mostly been in patients with acquired immunodeficiency syndrome. We describe a case of a CMV-seronegative liver transplant patient who received a seropositive liver graft. Owing to gastrointestinal complaints, CMV prophylaxis was stopped one month after LT. The patient developed an antral mass due to CMV infection and an anastomotic biliary stricture. Antigenemia became negative with ganciclovir, but this treatment did not eliminate the mass. Ganciclovir resistance was ruled out as well as other causes of antral mass, especially malignancy. The patient finally required gastrectomy and hepaticojejunostomy. We conclude that CMV disease is less common today but should be included in the diagnosis of gastrointestinal mass after transplantation.

Cytomegalovirus infection and development of biliary complications after liver transplantation.

BACKGROUND: Cytomegalovirus (CMV) infection is known to cause ulceration and mucosal hemorrhage in the gastrointestinal tract. Gastroduodenal and biliary complications were prospectively evaluated in 100 consecutive liver transplant patients in whom CMV was monitored during the first posttransplant year. METHOD: Gastroduodenal biopsy specimens were taken from 36 patients by endoscopies and in 28 patients by endoscopic retrograde cholangiopancreatography, and bile duct specimens were taken from three patients who underwent surgical reconstruction because of biliary complication. CMV was demonstrated from blood by the pp65 antigenemia test and from frozen sections of tissue specimens by immunohistochemistry and in situ hybridization. RESULTS: Symptomatic CMV infection, treated with ganciclovir, developed in 49 recipients: 13 (100%) of CMV seropositive donor (D+) seronegative recipient (R-) cases, 29 (45%) D+/R+ cases, and 7 (32%) D-/R+ cases. Duodenal ulcer developed in three and hemorrhagic gastritis in three recipients. CMV antigens were found from the gastroduodenal mucosa in 37 (69%) of the 54 studied recipients. The biliary complication rate was 24%. Preceding or concomitant CMV antigenemia was demonstrated in 75% of patients with a biliary complication (68% in CMV D+/R+ or D-/R+ and 100% in D+/R- recipients). The biliary complication rate was higher among recipients with CMV antigenemia, compared with recipients without (P<0.05). CMV antigenemia, CMV infection, or both in the duodenal mucosa was found in 96% of patients with a biliary complication. In two patients who underwent surgical reconstruction, CMV antigens and DNA were demonstrated in the bile ducts. CONCLUSIONS: Liver transplant patients are at risk of developing biliary complications after CMV infection, especially those with primary CMV infection.

[Orthotopic liver transplantation for end-stage liver diseases in 71 cases].

OBJECTIVE: To assess the role of orthotopic liver transplantation (OLT) in the treatment of end-stage liver diseases and to discuss the experience of the operation. METHODS: Retrospective analysis of clinical data of 71 cases of liver transplantation was performed in our hospital from April 1993 to August 2001. RESULTS: One year survival rate of recipients with benign hepatic disease was over 75%. The survival time and life quality of malignant recipients were also improved. Lamivudine monotherapy during the operation period could reduce HBV reinfection rate. The practice of OLT without veno-venous bypass (VVB) was associated with a shorter operating time, less hemorrhape, and thus less blood transfusion during the operation compared with standard technique of OLT with routine use of VVB. The occurrence rate of biliary complications was 5.98% and vascular complication 8.96%. CONCLUSIONS: OLT should become a routine therapeutic choice for end-stage liver diseases. Lamivudine is helpful to reduce HBV reinfection after OLT in HBV-related liver diseases. OLT without VVB is safe and can be performed in the majority of adult patients. The early diagnosis and timely application of interventional radiological technique are important for the treatment of biliary and vascular complications.

Cytomegalovirus infection and proinflammatory cytokine activation modulate the surface immune determinant expression and immunogenicity of cultured murine extrahepatic bile duct epithelial cells.

Murine extrahepatic bile duct epithelial cells (MEBEC) were isolated from extrahepatic bile ducts of BALB/c mice and established in primary culture. The epithelial origin was confirmed by positive cytokeratin 19 staining for these cells and the presence of microvilli and tight junctions under electron microscopy. By immunofluorescent staining with monoclonal antibodies and flow-cytometric analysis, MEBEC in culture constitutively express low levels of intercellular adhesion molecule (ICAM)-1, class I and class II major histocompatibility (MHC) antigens. The expression of ICAM-1 was significantly increased by interferon gamma (INF-gamma) or tumour necrosis factor alpha (TNF-alpha) stimulation. Class I and class II antigen expression were significantly enhanced by INF-gamma and in vitro murine cytomegalovirus (MCMV) infection. MEBEC infected with MCMV revealed a progressive cytopathic effect. MEBEC activated by INF-gamma or infected by MCMV induced a low but significant proliferation of allogeneic T cells and displayed a significant decrease in the absorbance at O.D. 550 nm in a microtitre tetrazolium assay after these treated cells were co-cultured with allogeneic T cells. These results suggest that following the up-regulation of surface MHC antigen and adhesion molecule expression with cytokines or MCMV, the MEBEC can function as antigen-presenting cells and initiate T-cell proliferation, which in turn trigger the recognition of MEBEC by effector T-cell-mediated cytotoxic responses. These findings may be implicated in the pathogenesis of virally induced, immune-mediated extrahepatic bile duct damage disorders.

Gastrointestinal manifestations of HIV infection.

Since the beginning of the AIDS pandemic, gastrointestinal (GI) problems have been among the most common features of the disease. Despite the introduction of highly active antiretroviral therapy (HAART) in 1995 and 1996, most HIV-infected patients continue to have GI complications. The clinician must be able to diagnose and treat the opportunistic gastrointestinal infections and neoplasms that occur in the advanced AIDS patient, as well as the treatment-induced symptoms and non-HIV-related GI disorders that predominate in early HIV disease. This review addresses the GI manifestations of HIV, with particular emphasis on new developments in the era of highly effective therapy.

Biliary complications in pediatric living related liver transplantation.

BACKGROUND: The goal of this study was to evaluate cause and outcome of biliary complications occurring after pediatric living related liver transplantation (LRLT). METHODS: A database of 205 pediatric patients (71 male and 134 female) undergoing 208 LRLT from June 1990 to April 1996 was reviewed. RESULTS: The overall incidence of bile duct complications was 13.9% (29 patients). There were 19 bile leaks, 7 anastomotic strictures, 8 intrahepatic biliary complications, and the bile duct was ligated inadvertently in 2 cases. Logistic regression analysis revealed hepatic artery thrombosis, ABO incompatible transplantation, intrapulmonary shunting in recipients, mode of artery reconstruction, and cytomegalovirus infection were all significant risk factors for biliary complications. CONCLUSIONS: Avoidance of ABO incompatible transplantation where possible, routine use of microvascular techniques for hepatic artery reconstruction to minimize the risk of artery thrombosis, earlier transplantation for patients with intrapulmonary shunt, and prophylaxis against cytomegalovirus infection should all reduce the rate of biliary complications after LRLT in pediatric recipients.

Identification of an Enterocytozoon bieneusi-like microsporidian parasite in simian-immunodeficiency-virus-inoculated macaques with hepatobiliary disease.

Enterocytozoon bieneusi is a common opportunistic pathogen of human patients with acquired immune deficiency syndrome (AIDS) causing significant morbidity and mortality. In a retrospective analysis utilizing conventional histochemical techniques, in situ hybridization, polymerase chain reaction, and ultrastructural examination, we identified 18 simian-immunodeficiency-virus-infected macaques (16 Macaca mulatta, 1 M. nemestrina, and 1 M. cyclopis) with Enterocytozoon infection of the hepatobiliary system and small intestine. The organisms were readily identified in the bile ducts and gall bladder by special stains and by in situ hybridization using a probe directed against the small subunit ribosomal RNA of human origin E. bieneusi. Infection of the biliary system was associated with a nonsuppurative and proliferative cholecystitis and choledochitis. Hepatic involvement was characterized by bridging portal fibrosis and nodular hepatocellular regeneration accompanied by marked bile ductular and septal duct hyperplasia. Ultrastructurally, all developmental stages of the organism were found in direct contact with the host cell cytoplasm; spores and sporoblasts contained a double layer of polar tubes. Sequencing of a 607-bp segment of the small subunit ribosomal RNA revealed 97 and 100% identity to two clones of small subunit ribosomal RNA derived from E. bieneusi of human origin. Extensive morphological and genetic similarities between the simian and human enterocytozoons suggest that experimentally infected macaques may serve as a useful model of microsporidial infection in AIDS.

Neonatal hepatobiliary disorders.

Neonatal hepatobiliary disorders are now better understood due primarily to new discoveries in molecular genetics, virology, and immunology. Because they are almost always pathologic and require early intervention, the neonatologist must recognize infants with these hepatocellular and ductal cholestatic problems occurring in the first few weeks of life. This article focuses mainly on new developments regarding neonatal metabolic disorders and their potential for gene therapy; perinatal infections, especially those caused by hepatitis B virus, hepatitis C virus, and human immunodeficiency virus; and recent concepts of neonatal hepatitis and biliary atresia, including a review of predictors that influence outcome for infants undergoing Kasai portoenterostomy and liver transplantation.