1/76. Falsely low calcium measurements after high volume plasma exchange in a patient with liver failure.A 63-year-old male with lactic acidosis secondary to fialuridine-induced liver failure underwent seven plasma exchanges while awaiting orthotopic liver transplantation. Following plasma exchange, total serum calcium concentrations measured by conventional clinical chemistry methods were significantly lower than the elemental calciums determined by atomic absorption spectroscopy (P = 0.004). The difference in calcium measured by atomic absorption and by conventional methods correlated with serum citrate concentration (R = 0.77) Following the first exchange, the serum lactic acid concentration decreased from 10.2 to 4.4 mmol/L. These results suggest that plasma exchange may aid in the removal of metabolic products such as lactic acid in patients with liver failure. However, the accumulation of unmetabolized citrate may also result in falsely low total calcium measurements in some patients who undergo plasma exchange.- - - - - - - - - - ranking = 1keywords = acid (Clic here for more details about this article) |
2/76. Selection of hepatitis B surface "escape" mutants during passive immune prophylaxis following liver transplantation: potential impact of genetic changes on polymerase protein function.CASE REPORT: A patient is described who developed hepatitis b virus (HBV) reinfection five months following liver transplantation. Failure of hepatitis B immunoglobulin prophylaxis was associated with the emergence of mutations. HBV gene sequencing identified nucleotide substitutions associated with amino acid changes, one within the major hydrophilic region (MHR) of the HBV surface antigen at amino acid position 144 and one outside the MHR. Because of the overlapping reading frames of surface and polymerase genes, the latter surface antigen change was associated with an amino acid change in the polymerase protein. The patient developed significant allograft hepatitis and was treated with lamivudine (3TC) 100 mg daily. Rapid decline of serum HBV dna was observed with loss of HBV e antigen and HBV surface antigen from serum. There was normalisation of liver biochemistry, and liver immunohistochemistry showed a reduction in HBV core and disappearance of HBs antigen staining. CONCLUSION: Surface antigen encoding gene mutations associated with HBIg escape may be associated with alteration of the polymerase protein. The polymerase changes may affect sensitivity to antiviral treatment. Selection pressure on one HBV reading frame (for example, HBIg pressure on HBsAg, or nucleoside analogue pressure on polymerase protein) may alter the gene product of the overlapping frame. Such interactions are relevant to strategies employing passive immune prophylaxis and antiviral treatment.- - - - - - - - - - ranking = 1keywords = acid (Clic here for more details about this article) |
3/76. Clearance of HCV rna in a chronic hepatitis c virus-infected patient during acute hepatitis b virus superinfection.The routes of hepatitis b virus and hepatitis c virus transmission are quite similar and coexistence of both viruses in one patient is not a rare phenomenon. Until now, the natural course of liver diseases induced by coinfections has not been well documented and the mechanisms of interaction between the two viruses and the human host have not been fully clarified. We report the case of a patient suffering from chronic hepatitis due to hepatitis c virus who developed an acute hepatitis b virus superinfection. serum hepatitis c virus ribonucleic acid became undetectable by reverse transcriptase/polymerase chain reaction at diagnosis of acute hepatitis b virus infection. At the same time, there was a striking increase in the serum concentrations of the antibodies against C22 and C33c hepatitis c virus antigens. Four months after clinical resolution of the acute hepatitis, hepatitis B surface antigen was undetectable in serum and three months later antibodies against hepatitis B surface antigen appeared. Two years after acute hepatitis b virus infection, the patient has had no relapse of markers for viral replication of hepatitis b virus. transaminases are within the reference range and hepatitis c virus ribonucleic acid is undetectable in both serum and liver tissue. We hypothesize that acute hepatitis b virus infection stimulated a specific humoral response against hepatitis c virus as well as triggering non-specific defense mechanisms which finally eliminated both viruses.- - - - - - - - - - ranking = 28157.999957762keywords = nucleic acid, acid (Clic here for more details about this article) |
4/76. Nosocomial transmission of hepatitis b virus infection through multiple-dose vials.The source of acute hepatitis b virus (HBV) infection in two women (55 and 72 years old) was investigated. They displayed no risk factors for acquiring HBV infection, other than treatment with local anaesthetic injections some months previously. The HBV strains were sequenced and showed distinct homology to strains seen in Swedish intravenous drug users (IVDU). Prior to these patients' acute infection, an outbreak of HBV had occurred among IVDU in the same county. Analysis of the HBV strains from six of these IVDUs showed their core promoter, precore and pre-S sequences (679 nucleotides) to be identical to those from the two patients. Cross-contamination between samples was excluded and the most likely source of infection was thought to be multiple-dose vials of local anaesthetic that had been contaminated with the HBV strain circulating among the IVDU population in the community. We believe that multiple-dose vials have no place in modern healthcare and recommend sequence homology analysis as an alternative or additional way to trace a source of HBV infection.- - - - - - - - - - ranking = 3.7901745908168keywords = rna (Clic here for more details about this article) |
5/76. Multi-system cytomegalovirus fetopathy by recurrent infection in a pregnant woman with hepatitis B.A pregnant woman with acute hepatitis b virus (HBV) infection had her second pregnancy terminated at 25 weeks' gestation because of fetal ascites and ventriculitis. meconium peritonitis was also found at autopsy. No HBV dna but cytomegalovirus (CMV) dna was detected in the fetal liver and ascitic fluid. Recurrent maternal CMV infection was demonstrated by pre-existing CMV IgG antibodies, high IgG avidity and low IgM levels. After abortion, the patient developed chronic active hepatitis. Nevertheless, having become pregnant again with a new partner, she had an uneventful third pregnancy and gave birth to a healthy boy.- - - - - - - - - - ranking = 3.7901745908168keywords = rna (Clic here for more details about this article) |
6/76. Outcome of lamivudine resistant hepatitis b virus infection in the liver transplant recipient.BACKGROUND: In many transplant centres lamivudine is an important component of prophylaxis against, and treatment of, hepatitis b virus (HBV) graft infection. Drug resistant HBV species with specific polymerase mutations may emerge during lamivudine treatment. AIMS: To examine the clinical consequences of graft infection by lamivudine resistant virus. methods: The clinical course of four liver transplant patients who developed graft infection with lamivudine resistant virus was reviewed. The response of HBV infection to reduction of immunosuppression and to manipulation of antiviral therapy was assessed. For each patient, serum viral titre was measured and the viral polymerase gene was sequenced at multiple time points. RESULTS: High serum titres were observed following emergence of the lamivudine resistant species. Wild type HBV re-emerged as the dominant serum species after lamivudine withdrawal. All patients developed liver failure, and onset of liver dysfunction was observed when resistant virus was the dominant serum species. In three patients, liver recovery was observed when immunosuppression was stopped and when alternative antivirals were given. Wild type virus appeared to respond to ganciclovir, and to reintroduction of lamivudine. For one patient, introduction of famciclovir was associated with clinical, virological, and histological response. CONCLUSIONS: Failure of lamivudine prophylaxis may identify patients at special risk for the development of severe graft infection. Treatment of graft reinfection should include reduction of immunosuppression, and systematic exposure to alternative antivirals. Viral quantitation and genetic sequencing are essential components of therapeutic monitoring.- - - - - - - - - - ranking = 7.5803491816335keywords = rna (Clic here for more details about this article) |
7/76. Failed adoptive immunity transfer: reactivation or reinfection?A 26-year-old female bone marrow transplant (BMT) recipient was hepatitis B surface antigen (HBsAg) and hepatitis B e antibody (HBeAb) positive. The donor, her human leucocyte antigen (HLA)-compatible sister, was HBsAg negative but hepatitis B surface antibody (HBsAb) and hepatitis B core antibody (HBcAb) positive. Twelve weeks post-BMT the patient became HBsAg negative, as determined using a monoclonal antibody-based assay. At 16 weeks post-BMT, HBsAg became undetectable by monoclonal and polyclonal immunoassay with seroconversion to HBsAb; however, at 24 weeks post-BMT the patient again became HBsAg positive. Both the recipient and the donor were retrospectively tested by hepatitis b virus (HBV) polymerase chain reaction (PCR) and found to be positive. The recipient displayed variants at amino acids 4 and 47 of the surface (S) gene prior to BMT. These mutations were not detected 32 weeks post-BMT when the S gene sequence was identical to that of an adr prototype. The donor was found to have four unique amino acid substitutions at positions 30, 98, 101 and 210 of the S gene. However, in vitro-expressed HBsAg from the donor was detected by commercial kits and an immunofluorescence assay, indicating that antigenic alteration did not explain HBsAg negativity. This donor highlights the value of PCR as the gold standard test for current HBV infection. It also demonstrates that discordance between two commercial HBsAg assays may not always be caused by antigenic variants. The second episode of hepatitis may theoretically have been caused by reactivation, selection of an escape mutant by HBsAb, reinfection or recombination. We suggest it was reactivation because none of the donor variants was seen in the recipient post-BMT.- - - - - - - - - - ranking = 0.66666666666667keywords = acid (Clic here for more details about this article) |
8/76. Emergency adult to adult living donor liver transplantation for fulminant hepatic failure.BACKGROUND: The high mortality rate associated with fulminant hepatic failure combined with the limited availability of cadaveric organs requires consideration of alternatives to conventional cadaveric transplantation. Use of the donor right lobe in adult-to-adult living donor transplantation holds promise in a variety of circumstances, including high-acuity situations. methods: A 28-year-old male with fulminant hepatic failure secondary to hepatitis B was referred to our institution. He rapidly progressed to grade IV encephalopathy, and laboratory values were indicative of a poor prognosis without transplantation. He was listed for transplantation as UNOS status I. Three siblings were simultaneously evaluated for living liver donation. Following established protocols, we completed donor evaluation in less than 24 hr, and donor right lobectomy and living donor transplantation were performed within 36 hr of the recipient's admission to our center. RESULTS: The donor surgery was uncomplicated, and the patient was discharged on postoperative day 4. The recipient experienced full recovery and was discharged home on postoperative day 14. Of note, the first offer for a cadaveric liver came more than 60 hr after living donor transplantation. CONCLUSIONS: Thorough donor workup can be completed in less than 24 hr without inappropriate abbreviation of the evaluation. Simultaneous workup of willing individuals prevents unnecessary delay. Living donor transplantation should be considered for patients with fulminant hepatic failure who are appropriate transplant candidates.- - - - - - - - - - ranking = 3.7901745908168keywords = rna (Clic here for more details about this article) |
9/76. tacrolimus (FK 506) induced thrombotic thrombocytopenic purpura after ABO mismatched second liver transplantation: salvage with plasmapheresis and prostacyclin.We report the course of thrombotic thrombocytopenic purpura (TTP) in a patient receiving tacrolimus (FK506) immunosuppression for an ABO mismatched second liver graft. A Chinese woman with fulminant hepatitis-B reactivation failed a living-related orthotopic liver transplantation (OLT) due to portal vein thrombosis. An ABO mismatched cadaveric OLT (group A to O) was performed, with peri-operative plasmapheresis to reduce anti-A hemagglutinin titers. On day 30, she developed fever, hemolysis, thrombocytopenia and neurologic dulling. Prominent microangiopathic features in peripheral blood film, and characteristic brain lesions on magnetic resonance imaging confirmed TTP. She responded initially to intensive plasmapheresis with cryosupernatant replacement, and withdrawal of FK506. An attempted reintroduction of FK506 for threatened rejection led to TTP exacerbation. This was controlled with prolonged plasmapheresis and a ten-day infusion of prostacyclin. immunosuppression was changed to mycophenolate mofetil. By day 53, the peripheral film and lactate dehydrogenase level had returned to baseline and plasmapheresis was stopped.- - - - - - - - - - ranking = 3.7901745908168keywords = rna (Clic here for more details about this article) |
10/76. life-threatening haemorrhage from a sternal metastatic hepatocellular carcinoma.rupture of the tumour is a catastrophic complication of hepatocellular carcinoma. The prognosis in patients with a ruptured hepatocellular carcinoma is usually unfavourable. We describe a 46-year-old man who suffered from visible massive tumour haemorrhage due to a hepatitis B-related hepatocellular carcinoma that metastasized to the sternal bone. The prominent tumour mass was bulging over the anterior chest wall on the sternum of the patient, and bled spontaneously. This episode of life-threatening haemorrhage was stopped by surgical ligation of the bleeding site. Palliative radiotherapy shrank the tumour mass size and prevented further possible bleeding. This is likely to be the first reported case with a visible spontaneous tumour bleeding from a sternal metastatic hepatocellular carcinoma.- - - - - - - - - - ranking = 22.741047544901keywords = rna (Clic here for more details about this article) |
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