1/9. Cholestatic jaundice caused by sequential carbimazole and propylthiouracil treatment for thyrotoxicosis.A 36-year-old Chinese man presented to the Queen Mary Hospital in August 1999 with a 2-week history of jaundice due to propylthiouracil treatment for thyrotoxicosis. He had previously received carbimazole but had developed an urticarial skin rash after 2 weeks of treatment. The patient developed liver failure and fulminant pneumonitis shortly after hospital admission. Despite receiving treatment with broad-spectrum antibiotics and intravenous immunoglobulin, he died 11 days after the onset of the respiratory symptoms. Postmortem examination using electron microscopy showed typical glycogen bodies within the cytoplasm of the hepatocytes, which corresponded to eosinophilic cytoplasmic inclusion bodies visible under light microscopy. Immunohistochemical studies of the inclusion bodies were positive for carcinoembryonic antigen and albumin, and negative for fibrinogen, complement protein C3, immunoglobulins G, M, and A, alpha-fetoprotein, and alpha-1-antitrypsin. This is the first report of a patient who received two sequential antithyroid drugs and developed predominate cholestasis with unique histological features. Extreme caution should be taken when a patient develops allergy to one type of antithyroid drug, because cross-reactivity may develop to the other type.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/9. Fulminant hepatitis B associated with a specific insertion in the basal core promoter region of hepatitis b virus dna after immunosuppressive treatment.We report a case of hepatitis b virus reactivation that occurred after immunosuppressive treatment in a hepatitis B surface antigen-negative patient with detectable antibodies to hepatitis B core antigen and hepatitis B surface antigen. sequence analysis revealed an 11-bp insertion in the core promoter region of hepatitis virus dna, creating a novel hepatocyte nuclear factor-1 binding site. This led to enhanced viral replication and fulminant hepatitis.- - - - - - - - - - ranking = 3keywords = antigen (Clic here for more details about this article) |
3/9. Fatal fulminant hepatitis B after withdrawal of prophylactic lamivudine in hematopoietic stem cell transplantation patients.hepatitis b virus (HBV) reactivation can give rise to acute hepatitis and even fatal fulminant hepatitis in patients receiving immunosuppressive or cytostatic treatment. Recently, the prophylactic use of lamivudine for HBV reactivation in HBV surface antigen-positive chronic-disease patients undergoing hematopoietic stem cell transplantation (HSCT) has been reported. However, the appropriate duration for this prophylactic therapy is unclear. Here, we report 2 cases of fatal fulminant hepatitis B reactivation in HSCT patients after lamivudine withdrawal. One patient with non-Hodgkin's lymphoma completed 6 courses of CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine [Oncovin], and prednisone) and autologous peripheral blood SCT (PBSCT). lamivudine was discontinued 3 months after transplantation. The second patient had acute myeloid leukemia. He received induction chemotherapy and postremission allogeneic PBSCT as late intensified consolidation therapy. lamivudine treatment was discontinued 10 months after transplantation. In both patients, HBV reactivation 2 to 3 months following lamivudine cessation led to fatal fulminant hepatitis. We suggest that the duration of prophylactic use of lamivudine in chronic HBV carriers receiving HSCT be prolonged until the patient's immune system has been reconstituted.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
4/9. Langerhans' cell histiocytosis after living donor liver transplantation: report of a case.We report a case of Langerhans' cell histiocytosis (LCH) occurring after a living donor liver transplantation (LDLT) for fulminant hepatitis. A 9-month-old girl underwent an LDLT for fulminant hepatitis of an unknown cause. The histology of the native liver did not show any findings of LCH. On postoperative day 42, her Epstein-Barr virus (EBV)-dna and cytomegalovirus antigenemia were both found to be positive. As a result, she was treated with antiviral agents and a reduction of the immunosuppression dosage. On postoperative day 98, acute rejection occurred, and she was treated with FK506, methylprednisolone, and finally, anti-CD3 murine monoclonal antibody was added. Subsequently, the EBV was re-activated. Thereafter, skin eruptions, swelling of the systemic lymph nodes, and pancytopenia appeared on postoperative day 127. LCH was diagnosed based on the typical histological findings as LCH, CD1a, and S-100-positive cells in her skin and a lymph nodes biopsy. She was treated by chemotherapy. The symptoms disappeared a few weeks after the start of the chemotherapy, and a clinical remission of LCH was obtained. We could not detect any evidence of EBV infection in the tumor cells. In spite of the fact that her LCH lesions thereafter remained in remission, she died of hepatic failure at 22 months after undergoing the liver transplantation. In conclusion, we discuss the factors influencing the occurrence of LCH in our patient after LDLT, while also evaluating the relationship between LCH and the immunosuppressive therapy administered to this patient.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
5/9. Acute fulminant hepatitis B in a patient with diabetic nephropathy treated successfully with concomitant lamivudine and molecular adsorbents recirculating system.A 36-year-old man with type 2 diabetes and diabetic nephropathy treated with hemodialysis developed hepatitis b virus (HBV)-induced acute fulminant hepatic failure (FHF). Despite supportive treatment, the condition rapidly progressed as manifested by severe jaundice, coagulopathy and hepatic coma. He was placed on the waiting list for liver transplantation and was treated with lamivudine and extracoporeal liver support with the molecular adsorbent recirculating system (mars). After three 8-h sessions of mars treatment in 1 week, he had remarkable improvement in clinical symptoms and serum biochemistry. On the 14th hospital day, surface antigen seroconversion was noted with undetectable hepatitis b virus surface antigen (HBs Ag) and low titre of anti-HBs antibody, indicating a complete recovery from acute fulminant hepatitis B. mars treatment has been reported to benefit patients with liver failure from different causes including acute exacerbation of chronic hepatitis B, poisoning, post transplantation and Wilson's disease. The present case suggests its potential benefit when combined with lamivudine in treating uremic patients with acute fulminant hepatitis B.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
6/9. ABO-incompatible deceased donor liver transplantation with the use of antigen-specific immunoadsorption and anti-CD20 monoclonal antibody.In patients with fulminant liver failure requiring emergency liver transplantation, the only donor organ that becomes available may be ABO incompatible. The risk of graft failure because of antibody-mediated acute rejection is high, but can be reduced by various means. We reported a deceased donor ABO-incompatible liver allograft recipient who was treated with antigen-specific immunoadsorption in combination with anti-CD20 monoclonal antibody and conventional plasmapheresis and immunosuppression. The patient was a 33-yr-old male with blood group A who presented with subacute liver failure of unknown aetiology and received a blood group AB liver graft. Pretransplant he underwent plasmapheresis and received one dose of rituximab. The immunosuppressive regimen consisted of methylprednisolone, tacrolimus and mycophenolate mofetil. Despite regular post-operative plasmapheresis sessions, anti-B antibody titres increased. Antigen-specific immunoadsorption with depletion of anti-B antibodies was performed from day nine to day 17. Thereafter, anti-B IgM and IgG antibody titres remained low. After one month the patient was reoperated with hepaticojejunostomy because of bile duct necrosis and with reconstruction of a stenotic hepatic artery. A mild rejection was successfully treated with methylprednisolone four months post-transplant. At six months post-transplant there was a stricture of the biliary-enteric anastomosis, but the graft was well functioning. We conclude that antigen-specific immunoadsorption can be an important adjuvant therapy to control recipient anti-A/B antibody levels and prevent acute rejection in ABO-incompatible deceased donor liver transplantation.- - - - - - - - - - ranking = 6keywords = antigen (Clic here for more details about this article) |
7/9. Possible association of vigorous hepatitis b virus replication with the development of fulminant hepatitis.A 49 year-old man was referred to our hospital for fear of developing fulminant hepatic failure. There had been an outbreak of fulminant hepatitis B in a dialysis clinic in the western part of Honshu, japan, that resulted in four deaths among six patients. After the sixth patient contracted severe hepatitis, all patients in the unit were screened biweekly for hepatitis B surface antigen (HBsAg) to detect newly infected patients as soon as possible. Our patient was the seventh victim, and on the day he gave a positive result for HBsAg, his hepatitis b virus (HBV) dna level had reached 1.1 x 10(11) copies/ml as assessed by real time polymerase chain reaction. sequence analysis of the causal HBV revealed the presence of a mutation in the precore region (nt 1896), two mutations in the core promoter (nt 1762 and nt 1764), and some minor mutations in the P gene that were restricted to the upstream region. These mutations are indicative of a virus with a high replicative rate that cannot secrete HBeAg. Taken together, these findings indicate that it is very likely that the replicative ability of the causal virus was as vigorous as that of HBV in hepatitis B e antigen-positive asymptomatic carriers with markedly high viral titers. The present case report provides clinical evidence of a possible association between the rapid spread of highly replicative HBV before host immunological recognition and the development of fulminant hepatitis.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
8/9. Breakthrough of hepatitis b virus escape mutants after vaccination and virus reactivation.Escape mutants of hepatitis b virus (HBV) carry mutations in the major antigenic region of the hepatitis B surface antigen (HBsAg). They are able to grow in the presence of antibodies against HBsAg (anti-HBs) and may escape detection by immuno assays for HBsAg. antibodies against HBV core antigen (anti-HBc) are considered to be a universal marker for active or resolved HBV infections but they may appear very late. Highly sensitive detection of HBV dna is the most universal reliable marker of infectivity, but in the blood donation setting even the most sensitive assay for HBV dna may not detect all infectious donations. This brief report describes three cases of HBV infections caused by HBV escape mutants. The implications of the findings for the prevention of HBV transmission through donor blood are discussed.- - - - - - - - - - ranking = 3keywords = antigen (Clic here for more details about this article) |
9/9. Severe hepatitis E infection during pregnancy.In areas with endemic hepatitis e virus (HEV), acute liver failure secondary to hepatitis E infection is common in pregnancy and associated with a mortality rate of up to 20%. However, there is little information on the clinical course of severe hepatitis E infection during pregnancy in non-endemic areas such as the UK. Here we describe two cases of severe hepatitis E in pregnancy in patients returning from the Indian subcontinent. These cases were diagnosed by the detection of IgM anti-HEV antibody using an enzyme immunoassay with recombinant hepatitis E viral antigens. The first case describes acute hepatic failure, with coagulopathy and encephalopathy, warranting intensive therapy and elective ventilation. In the other case, the patient had severe hepatitis with coagulopathy. Both cases spontaneously resolved with no foetal loss. These cases highlight the need for suspicion of HEV infection in patients returning from endemic areas and presenting with acute non-A non-B hepatitis, especially when pregnant. Furthermore, the intensive treatment of acute liver failure caused by HEV may reduce the high mortality reported in asia.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |