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Biomedical subjects

R Tur-Kaspa

Publications and source records attributed to R Tur-Kaspa.

At least 91 records · Page 5Linked to original sources
PubMed1995

Acquired hepatocerebral degeneration in a liver transplant recipient.

A 47-year-old-man lapsed into coma 12 h after liver transplantation, and remained comatose until death 38 days later. Prior to transplantation he had repeated episodes of hepatic encephalopathy, but no fixed neurological signs. Autopsy revealed typical features of acquired hepatocerebral degeneration with diffuse but patchy pseudolaminar cortical necrosis, variable amount of neuronal loss in the cerebral cortex, basal ganglia and other areas, and proliferation of Alzheimer type II glia. In addition, there was central pontine and extensive extrapontine myelinolysis involving the lateral and medical geniculate bodies, the thalamus, internal capsule, fornix, mamillothalamic tract, white matter bundles in the caudate and pallidum, the oculomotor nuclei and the foliar white matter of the cerebellum. The distinction between myelinolytic lesions and lesions due to hepatocerebral degeneration was not always clear. Although neurological complications and brain lesions are rather common after liver transplantation, there have been no reports of acquired hepatocerebral degeneration in liver transplant recipients. Our data lend support to the idea that a single prolonged comatose episode, due to hepatic dysfunction, may induce permanent parenchymal brain damage.

Autopsy↗
PubMed1995

Disseminated Nocardia transvalensis infection resembling pulmonary infarction in a liver transplant recipient.

Infections due to Nocardia transvalensis are extremely rare: only four disseminated infections with this pathogen have been reported, three of which ended fatally. This is the first report of a liver transplant recipient with Nocardia transvalensis infection. The patient had disseminated infection with pulmonary involvement, which presented as pulmonary infarction. Despite a ten-day delay in the administration of correct therapy, he responded rapidly to trimethoprim-sulfamethoxazole. The pitfalls of differentiating nocardial infection from pulmonary thromboembolism in solid organ transplant recipients and the diagnostic considerations unique to liver transplant recipients are discussed.

Bacteremia↗
PubMed1995

Long-term prevention of recurrent hepatitis B virus after liver transplantation.

Hepatitis B virus (HBV) reinfection is a major threat to HBV-infected patients undergoing orthotopic liver transplantation. Eleven HBsAg-positive patients with end-stage liver disease underwent liver transplantation. All were treated with high doses of anti-HBs antibodies, initiated first during the anhepatic stage of the operation and continued every 2-8 weeks thereafter according to anti-HBs levels in the serum. Attempts were made to keep anti-HBs levels above 400 IU/ml. Patients were followed for 8-42 months and only one of them had any evidence for recurrence of HBV infection 40 months post-transplantation. We conclude that continuous administration of anti-HBs and maintenance of high levels of anti-HBs in the serum prevent recurrence of HBV infection.

Adolescent↗
PubMed1995

A study of Israeli blood donors, asymptomatic carriers of hepatitis C virus, in relation to liver disease, cryoglobulinemia and transmission.

In order to study the asymptomatic hepatitis C virus (HCV)-positive blood donors in Israel we analyzed their sera for HCV-RNA using the polymerase chain reaction technique. We found that 0.44% of blood donors were anti-HCV positive. Of those who had repeatedly positive anti-HCV, 82% had evidence of HCV-RNA. One-third of them had elevated liver enzymes, but no detectable cryoglobulins were found in their sera. Although HCV-RNA was detected in the majority of the patients, we were unable to demonstrate vertical or horizontal transmission among the family members of our carrier population.

Adult↗
PubMed1994

Systemic chimerism in sex-mismatched liver transplant recipients detected by fluorescence in situ hybridization.

Fluorescent in situ hybridization (FISH) is a reliable, rapid, sensitive, and quantitative method for detection of residual host cells following sex-mismatched bone marrow transplantation. Recently, donor-derived long-term multilineage hematopoiesis was detected in a sex-mismatched liver transplant recipient. We therefore assessed chimeric status in 12 patients (F 9, M3), mean age 42.5 years (range 16-57), for a median period of 18 months (range 7-32) following sex-mismatched liver transplantation. Peripheral blood hematolymphoid cells were hybridized with Y- or X-chromosome fluorescently labeled specific probes, and the donor-typed hematopoietic cells were enumerated. In two F recipients 4-5% male hematolymphoid cells were detected in the peripheral blood at 15 and 22 months after sex-mismatched liver transplantation, respectively. These two patients with systemic chimerism suffered from primary biliary cirrhosis and fulminant Wilson's disease before transplantation. One of them had evidence of graft rejection only once during the posttransplant course and the other had no episode of graft rejection. Two other female patients who were found to have approximately 2% male hematolymphoid cells, which is considered to be in the false-positive range, also had no signs of graft rejection during the posttransplant follow-up period. Among the remaining eight patients, in whom systemic chimerism was undetectable, there was at least one episode of acute cellular rejection during the posttransplant period. In summary, the FISH technique enables us to detect systemic chimerism following sex-mismatched liver allografts. Inasmuch as balanced systemic chimerism after organ transplantation is of major importance for self tolerance, our findings may enable us to treat patients after liver transplantation without the need for immunosuppression.

Adult↗
PubMed1994

Chronic hepatitis C virus infection with exposure to hepatitis B virus.

The prevalence of hepatitis C virus (HCV) infection in patients with chronic liver disease (CLD) in Israel has not yet been reported. A retrospective analysis was performed on the first 92 consecutive patients referred to our Liver Unit with serologically confirmed antibodies to hepatitis C virus (anti-HCV) who had evidence for chronic hepatitis, cirrhosis, and hepatocellular carcinoma. We compared 31 patients who were anti-HCV positive with 61 patients who had evidence for both previous or present infection with hepatitis B virus (HBV) as well as HCV. Dual infection was significantly more prevalent in Jewish patients of non-Ashkenazi origin, who were also characterized by higher rates of portal hypertension manifested by ascites, bleeding esophageal varices as well as hepatic encephalopathy and spontaneous bacterial peritonitis. We conclude that dual infection of HBV and HCV was found in 66% of patients with anti-HCV positive liver disease in Jerusalem, and that these patients develop more serious complications than CLD patients with anti-HCV alone.

Adolescent↗
PubMed1994

Clinical, serological and molecular characteristics of 471 hepatitis B virus carriers.

A total of 471 Israel Defense Forces (IDF) blood donors identified as hepatitis B virus (HBV) carriers were examined a few months after blood donation. When compared to the general population of IDF blood donors the HBV carriers were older, belonged to certain ethnic groups and were predominantly males. Physical examination revealed minimal findings: 1 (0.3%) had splenomegaly and 5 (1.6%) had hepatomegaly. Fifty-two individuals (11.1%) had elevated liver enzymes. E antigen was present in 3.2% of HBV carriers, 94% had anti-e antibodies and 1.9% had anti-delta antibodies. Of 258 carriers tested for HBV DNA, 29 (11.2%) were positive. Abnormal liver enzymes were significantly associated with the presence of e antigen as well as with the presence of HBV DNA.

Adult↗
PubMed1993

Ablation of persistent hepatitis B by bone marrow transplantation from a hepatitis B-immune donor.

Chronic hepatitis B virus (HBV) infection is still a major cause of liver disease for which no definite therapy is available. We describe here a hepatitis B surface antigen (HBsAg) carrier patient with active viral replication (HBV DNA positive) who was treated for leukemia by bone marrow transplantation (BMT) from an HBV immune donor. Following BMT from the antibody to hepatitis B core antigen (anti-HBc) positive/anti-HBs positive bone marrow donor, immune reconstitution of the recipient's bone marrow resulted in clearance of the circulating HBsAg, as well as HBV DNA. The patient acquired immunity against HBV, which lasted for more than 8 months posttransplantation. Therefore, this report provides evidence that adoptive transfer of specific immunity against HBV through allogeneic BMT may lead to clearance of persistent HBV infection. Furthermore, the data support the hypothesis that the HBsAg carrier state is most probably the result of an inefficient immune response against HBV, implying that clearance of HBV may be facilitated by adoptive cellular immunotherapy.

Bone Marrow Transplantation↗
PubMed1993

Idiopathic unconjugated hyperbilirubinemia (Gilbert's syndrome) and concurrent psychotropic drug administration.

Gilbert's Syndrome is a benign familial condition in which unconjugated hyperbilirubinemia occurs in the absence of structural liver disease or hemolysis. Phenothiazines and tricyclic medications are often withheld in patients with preexisting liver disease. The authors present four patients with Gilbert's Syndrome and concurrent psychiatric illness. Administration of phenothiazine antipsychotics or tricyclic antidepressants proved beneficial and produced no adverse effects on hepatic function. The authors discuss clinical aspects of Gilbert's Syndrome in psychiatric patients and conclude that phenothiazine antipsychotic medication should not necessarily be withheld from these patients.

Adult↗
PubMed1992

Estrogen suppresses hepatitis B virus expression in male athymic mice transplanted with HBV transfected Hep G-2 cells.

Hormones are known to regulate both viral and cellular genes. It has been shown previously that estrogen has an effect on liver gene transcription and mRNA stability. Sex hormones might have a role in the chronic persistence of hepatitis B virus (HBV) infection. In fact, there is a male preponderance in the incidence of chronic HBV infection, and HBsAg expression was reported to be much higher in male transgenic mice than in the females. We investigated the effect of estrogen on HBV gene expression and regulation in athymic mice bearing 2.2.15 cells, a human hepatoblastoma cell line derived from Hep G-2 transfected with HBV sequences. Both male and female mice were treated with estradiol after tumors could be observed. Episomal DNA was extracted from the tumors and hybridized with 32P-labelled HBV DNA. Southern blot and slot blot analyses demonstrated that male mice had higher expression of HBV DNA. Estrogen treatment suppressed HBV DNA expression in males, but had only a minor effect on females. HBeAg production in male mice was also inhibited by estrogen treatment. HBV RNA extracted from 2.2.15 cells showed 2-3-fold reduction following beta-estradiol treatment. Moreover, inhibition of HBV transcription by estrogen was demonstrated by an RNA pulse-labelling experiment. These data indicate that estrogen inhibits HBV expression in the in vivo model presented in this study. These results might contribute to a better understanding of the effect of sex hormones on the pathogenesis of HBV-induced liver disease.

Animals↗
PubMed1992

Hepatitis B virus precore mutants are identical in carriers from various ethnic origins and are associated with a range of liver disease severity.

Hepatitis B virus carriers in Israel are mostly HBeAg negative, of whom 5% to 10% have circulating hepatitis B virus. Recently, a hepatitis B virus variant with a stop codon in the precore region was identified, and it was suggested that specific mutations are associated with fulminant or severe chronic active hepatitis. We have analyzed serum samples from HBeAg-positive and HBeAg-negative patients by polymerase chain reaction, using primers spanning the precore/core region. Nucleotide sequence analysis (by direct sequencing) from amplified hepatitis B virus DNA demonstrated that viral genomes from all HBeAg-negative patients contain G to A mutation (nucleotide 1896), leading to the formation of a stop codon. An additional G to A mutation was identified three nucleotides downstream (nucleotide 1899). These patients are of various ethnic origins, with no unique clinical characteristics and with normal liver histology, chronic hepatitis or cirrhosis. No mutation at the precore/core region was observed in the HBeAg-positive patients. In conclusion, the precore mutations identified in hepatitis B virus carriers in Israel are identical regardless of the carrier's ethnic origin and are associated with mild-to-severe liver disease.

Adult↗
PubMed1992

Resistance of hepatitis delta virus replication to interferon-alpha treatment in transfected human cells.

Interferon-alpha (IFN-alpha) is known to inhibit both DNA and RNA viruses, including hepatitis B virus (HBV). In humans the antiviral effect, if any, of IFN-alpha on hepatitis delta virus (HDV) is complicated by the fact that HDV is spread only to patients already infected with HBV. An in vitro model system was used to assay for an antiviral effect of IFN-alpha on HDV genome replication. Hep G2 cells were transfected with a plasmid containing a trimer of HDV and treated with IFN (20 or 100 units/mL) starting 1-7 days after transfection. RNA extracted from treated and nontreated cells was assayed by both slot blot and Northern analyses. The IFN-alpha treatment as expected increased the 2'-5' oligo A synthetase RNA activity, but it did not affect HDV genome replication. Thus, in the absence of HBV, it appears that HDV is resistant to IFN-alpha.

2',5'-Oligoadenylate Synthetase↗
PubMed1992

Relapsing hepatitis A. Review of 14 cases and literature survey.

We have reviewed our experience with 14 cases of relapsing hepatitis A (RH-A), as well as 68 cases reported in the literature. Relapse occurs in 3 to 20% of patients with acute hepatitis A, and rarely takes the form of a polyphasic disease (multiple relapses). After a stage of typical hepatitis A, remission phase ensues, with partial or complete resolution of clinical and biochemical manifestations. Relapse usually occurs after a short period (usually less than 3 weeks). Relapse is usually clinically milder than the first phase, with variable liver function abnormalities and a tendency toward more marked cholestatic features. Not uncommonly, immune manifestations occur during this phase, including purpura, nephritis, and arthralgia, with common laboratory findings of rheumatoid factor as well as false-positive reaction to HCV-EIA tests. The clinical course in relapsing hepatitis A is almost always benign, and uneventful recovery is the rule with few exceptions. Steroid treatment, first reported in the present series, resulted in marked clinical improvement. Preliminary results suggest that R-HA is associated with a continuing viremia as well as shedding of virus in stools during the relapse phase. The pathogenesis of R-HA probably involves an interaction between persistent viral infection and immune mechanisms responding to the continuing antigenic stimulation.

Adult↗
PubMed1992

[Kaposi's sarcoma following liver transplantation].

A 54-year-old man developed Kaposi's sarcoma 2 months following orthotopic liver transplantation for hepatitis B-associated liver cirrhosis. At that time he was on combined immunosuppressive therapy (azathioprine, prednisone and cyclosporine A). The disease is very prevalent among immunosuppressed patients following renal transplantation, but is considered to be relatively rare following liver transplantation. The patient ran a relatively benign course without organ involvement and with only the skin disease. This is the first case of Kaposi's sarcoma following liver transplantation reported in Israel.

Humans↗