摘要:

AbstractA previously healthy but obese 26‐yr‐old woman was diagnosed as having hepatic dysfunction 17 days after the third of three consecutive exposures to isoflurane anesthesia for paranasal sinus surgery. Serum laboratory findings included elevated aminotransferases and bilirubin. Radiographical evaluations showed no evidence of extrahepatic disease. Serological studies were negative for acute viral infections, and serum copper was normal. The patient's condition deteriorated over the ensuing 17 days, with hyperreflexia, hypoglycemia and a rapid fall in serum aminotransferases with a concomitant rise in bilirubin level and prothrombin time despite maximal medical support. The liver volume as shown by computed tomography fell from 1,290 cm3to 680 cm3over 6 days. The patient underwent successful orthotopic liver transplantation 25 days after onset of symptoms. Histopathological examination of the resected liver showed submassive and massive necrosis, with a few foci of microvesicular steatosis and ultrastructural evidence of mitochondrial abnormalities. Although we found insufficient evidence to prove that this case was caused by isoflurane anesthesia, the clinical course and histopathological findings are similar to those in hepatic injury caused by halothane anesthesia. Therefore we report this as a possible case of fulminant hepatic failure resulting from isoflurane anesthesia. (HEPATOLOGY1991;13:1017–

ISSN:0270-9139    

DOI:10.1002/hep.1840130602

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractWe investigated the effects of interferon therapy on hepatocyte human leukocyte antigen class I and class II antigen expression and intrahepatic lymphocyte subsets in patients with chronic viral hepatitis B (n = 11) and C (n = 10). Interferon‐α was administered intramuscularly in doses ranging from 3 to 18 million international units daily for 4 wk. Liver biopsy specimens were obtained just before and immediately after treatment, and the specimens were stained by the indirect immunoperoxidase method for evaluation of human leukocyte antigen expression and lymphocyte subsets. Before therapy, no significant difference was noted between hepatitis B and C in human leukocyte antigen class I antigen expression on hepatocytes or in the lymphocyte subsets in the intralobular and portal areas. After interferon‐α treatment, hepatocyte expression of human leukocyte antigen class I antigens and serum β2‐microglobulin levels were virtually unchanged in chronic viral hepatitis C patients, but both were increased in chronic viral hepatitis B patients. Human leukocyte antigen class II antigens were not expressed during treatment. The mean number of intralobular CD3+ and CD8+ cells and the mean serum ALT level decreased significantly in chronic viral hepatitis C patients (p<0.05) but not in chronic viral hepatitis B patients. The mean number of intralobular CD4+ cells was unaffected by interferon therapy in both groups. In all 21 patients, the changes in CD8+ cell numbers paralleled the changes in serum ALT levels. Our findings suggest that T‐cell cytotoxicity may play an important role in hepatocyte damage in both chronic viral hepatitis C and chronic viral hepatitis B and that the response to interferon‐α differs in these two types of hepatitis. (HEPATOLOGY1991;

ISSN:0270-9139    

DOI:10.1002/hep.1840130603

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractIn this study we have examined the localization of interferon‐α in liver tissue from acute and chronic hepatitis B virus carriers to establish whether the defect in interferon‐α production reported in chronic hepatitis B virus infection is at a pretranscriptional or posttranscriptional level usingin situhybridization and immunohistochemical techniques. Interferon‐α messenger RNA transcripts and the immunoreactive protein were abundant in liver tissue and in particular in hepatocytes from patients with acute hepatitis B virus infection who ubsequently recovered. In contrast interferon‐α polypeptide was present in a significantly lower number of sinusoidal cells, mononuclear cells and hepatocytes in chronic hepatitis B virus carriers. Although a high proportion of patients with chronic hepatitis B virus infection had cells that expressed interferon‐α messenger RNA transcripts, the number of such cells was significantly less than in acute hepatitis B virus infection, indicating that the defect in the hepatic interferon‐α synthesis is at the level of gene activation. Furthermore, using double immunohistochemical staining, the number of hepatocytes containing HBcAg correlated inversely with the proportion of neighboring sinusoidal cells expressing interferon‐α These data support previous observations that interferon‐α production is reduced in chronic hepatitis B virus infection and are consistent with the view that this cytokine is important in the clearance of the virus. (HEPAT

ISSN:0270-9139    

DOI:10.1002/hep.1840130604

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractThirty‐six children with chronic hepatitis B were entered into a randomized controlled trial of recombinant human interferon‐α All patients had hepatitis B virus DNA and increased levels of aminotransferases in serum for at least 1 yr. Twelve children received 10 MU of interferon‐α 2b/m2body surface area three times a week (group I); 12 children received 5 MU/m2under the same conditions (group II); and 12 children served as controls (group III). During 6 mo of therapy, 12 of 24 (50%) treated patients (7 from group I, 58%, and 5 from group II, 42%) and 2 of 12 (17%) controls lost hepatitis B virus DNA from serum and subsequently remained negative. Comparison of the rate of response in group I vs. controls showed a statistically significant difference (p<0.05). Eleven of 12 (92%) treated patients who cleared hepatitis B virus DNA from serum lost HBeAg, seroconverted to anti‐HBe and had improvement in liver histological findings with loss of hepatitis B virus DNA from liver. In 10, serum ALT levels became normal. Interferon‐α was well tolerated and all children finished therapy. These findings indicate that a 6‐mo course of interferon‐α is effective in inducing a serological, biochemical and histological remission of disease in approximately 50% of children with chronic hepatitis B. (HEPATOLOGY1

ISSN:0270-9139    

DOI:10.1002/hep.1840130605

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractHepatitis C virus RNA as detected by reverse transcription and nested polymerase chain reaction was monitored in 16 patients with chronic hepatitis C treated with interferon. Hepatitis C virus RNA became undetectable after 4 to 8 wk of interferon administration in 13 of the 16 patients. During 6 mo of follow‐up, 5 of the 13 patients who became negative for hepatitis C virus RNA after interferon administration remained negative, and all five continued to have normal ALT levels. Repeat liver biopsy in these five patients revealed histological improvement. Antibody to hepatitis C virus, which was initially positive in all treated patients, fell to undetectable levels in three of the five patients. In contrast, aminotransferase levels rose again in all eight patients who had become hepatitis C virus RNA negative but had again exhibited hepatitis C virus RNA after completion of therapy. In 16 untreated patients, hepatitis C virus RNA remained detectable. These results indicate that detection of hepatitis C virus RNA may be useful as a marker of viral replication in chronic hepatitis C; they also suggest that interferon should again be administered to patients who become hepatitis C virus RNA negative on treatment but again exhibit this marker of viral replication when treatment is stopped. (HEPATOLOGY1991;13:1040–10

ISSN:0270-9139    

DOI:10.1002/hep.1840130606

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractWe studied 67 HBsAg‐negative Israeli patients (36 negative for all HBV serological markers as group 1 and 31 positive for antibodies to HBs and HBc as group 2) with chronic liver disease and cirrhosis of unknown origin using a rapid, sensitive and specific assay for the detection of low levels of hepatitis B virus in serum. This technique uses a high‐affinity monoclonal antibody to HBs against an a domain epitope of HBsAg to capture the virion, followed by hepatitis B virus DNA amplification with the polymerase chain reaction. In addition, 55 subjects without liver disease served as controls: Group 3 (n = 32) was negative for all hepatitis B virus markers; group 4 (n = 23) was positive for antibodies to HBs and HBc. We found 11 individuals in group 1 (31%) and 10 in group 2 (29%) harboring low levels of hepatitis B virus DNA in serum. In contrast, no one in group 3 or group 4 was positive by this technique (p<0.0001). Using polymerase chain reaction primers spanning other regions of the hepatitis B virus genome and a method of restriction‐fragment analysis of polymerase chain reaction–amplified sequences, we detected significant DNA sequence heterogeneity, suggesting infection with distinct hepatitis B virus strains. DNA extracted from paraffin‐embedded liver biopsy specimens of 42 patients from groups 1 and 2 was shown to contain hepatitis B virus DNA by polymerase chain reaction in 11 of 12 patients with circulating virion DNA. More important, 18 additional patients whose sera were negative by HBs‐antibody capture/polymerase chain reaction amplification had hepatitis B virus DNA sequences in their livers. Hepatitis C virus antibodies were found in 71% of group 1, in 65% of group 2, in 3% of group 3 and in 4% of group 4 (p30%). We conclude that infection with hepatitis B virus undetectable by conventional assays and with hepatitis C virus may represent important unrecognized causes of idiopathic chronic liver disease in Israel, accounting for the possible origin in more than 90% of patients. (HEPATOLOGY1991;13

ISSN:0270-9139    

DOI:10.1002/hep.1840130607

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractTo determine whether long‐term therapy with recombinant interferon‐α can improve the course of chronic delta hepatitis, 61 Italian patients with this disease were randomly assigned to receive either interferon‐α‐2b three times a week (5 MU/m2for 4 mo and then 3 MU/m2for another 8 mo) or no treatment. At the end of the 12‐mo study, all patients were followed‐up for 12 additional months. Normalization or decrease of more than 50% from baseline of serum ALT levels occurred in 42% of treated patients the fourth month of therapy, 26% the twelfth month and 3% the twenty‐fourth month vs. 7%, 7% and 0%, respectively, in the control group. However, relapses occurred in 7 of 8 (87.5%) responders 1 to 10 mo (mean = 3.5 mo) after cessation of therapy.Liver biopsies were carried out at baseline and during the twelfth month of treatment. Histological improvement, mostly caused by decrease of portal inflammation, was observed in 57% of treated and 36% of untreated patients. Measures of antiviral activity (serum hepatitis delta virus RNA and intrahepatic hepatitis delta antigen) showed similar levels in treated and control patients. In treated patients the percentage of patients who were negative for HDV RNA never exceeded that of baseline.Although interferon‐α in the dosage given in this study had no antiviral effect on patients with chronic hepatitis D, it reduced hepatic inflammation as measured by ALT levels. Whether a longer duration or reinstitution of interferon‐α therapy would achieve longterm control of ALT levels and prevent chronic liver damage is not known. (HEPATOL

ISSN:0270-9139    

DOI:10.1002/hep.1840130608

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractWe have separated circulating HBeAg into small and large molecular forms by agarose gel electrophoresis and analyzed the relationship between the two forms and other clinical features of chronic hepatitis B, especially in regard to liver cell damage. The large HBeAg accounted for 7.3% ± 3.4% of serum HBeAg in 9 subjects with normal liver histological findings or nonspecific reactive hepatitis, 38.0% ± 27.8% in 32 patients with chronic persistent hepatitis and 65.6% ± 23.3% in 21 patients with chronic active hepatitis (p<0.01). A positive correlation was seen between the height of aminotransferase elevations and the percentage of large HBeAg. Three patients who progressed from histologically normal liver or nonspecific reactive hepatitis to chronic active hepatitis had dramatic increases in the percentage of large HBeAg. The finding that the presence of large HBeAg in serum correlated with the severity of hepatitis suggests that HBeAg may play an important role in determining the degree of liver injury in chronic hepatitis B. (HEPATOLOGY1991;13:1057–1

ISSN:0270-9139    

DOI:10.1002/hep.1840130609

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractBetween 1986 and 1989, orthotopic liver transplantations were performed in our unit for 17 patients with incurable alveolar echinococcosis. Ten patients had hilar involvement (group I), and seven patients had posterior localization (five of them had chronic Budd‐Chiari syndrome) (group II). The delay between diagnosis and the orthotopic liver transplantation was more than 48 mo in group Ia (six patients), less than 24 mo in group Ib (four patients) and less than 48 mo in group II. Previous operations were more common in group Ia than in group Ib and II. Five patients have died–four in group I and one in group II. The actuarial survival rate at 15 mo was 75%. Early reoperations were frequent (69%), mainly caused by rebleeding. Bacterial and fungal infections occurred only in group Ia (four cases) and group II (three cases). In eight patients (palliative group), residual foci of infected nonhepatic tissue occurred after surgery. The titer of specific antibodies decreased during the first 3 mo in all the patients but one. In patients with radical liver transplantation, the complete disappearance of specific antibodies occurred within 2 yr in four cases. In the remaining five patients, specific antibodies remained detectable, but no evidence of recurrence has been obtained up to now. In the palliative group, a peak of specific IgM occurred at 3 mo; an increase of specific IgG was observed later. The growth of residual parasitic foci was relatively slow, and all these patients remained asymptomatic with a mean follow‐up of 19 mo. We conclude that orthotopic liver transplantation is feasible in incurable alveolar echinococcosis and could be proposed without delay to patients with parasitic Budd‐Chiari syndrome or complicated secondary biliary cirrhosis. In the other cases, the best time to perform an orthotopic liver transplantation is more difficult to determine. Nevertheless, in the perspective of an orthotopic liver transplantation, the management of these patients has to change, and repetitive laparotomies for palliative surgical procedures have to be replaced by interventional radiology. (HEPATOLOGY1991;13:106

ISSN:0270-9139    

DOI:10.1002/hep.1840130610

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractTo clarify the pathogenetic role of acetaldehyde in the development of alcoholic liver disease, genotyping of aldehyde dehydrogenase‐2 genes was performed and the clinical features of the alcoholic liver disease patients with different genotypes were compared. Genotyping of aldehyde dehydrogenase‐2 was performed in 47 patients with alcoholic liver disease using the polymerase chain reaction and slot‐blot hybridization. Of the 47 patients with alcoholic liver disease, 40 were homozygous for the normal aldehyde dehydrogenase‐2 gene and the remaining seven cases were heterozygous for the normal and mutant aldehyde dehydrogenase‐2 genes. No homozygote was found for the mutant aldehyde dehydrogenase‐2 genes. Daily alcohol intake was less than 100 gm in all heterozygotes without relation to the type of alcoholic liver disease. On the other hand, all but four patients homozygotic for the normal aldehyde dehydrogenase‐2 gene drank more than 100 gm alcohol/day. The mean daily alcohol intake in the heterozygotes was significantly lower than that in the normal homozygotes. The incidence of alcoholic fibrosis tended to be lower in the heterozygotes than in the normal homozygotes (14.2% vs. 52.5%). On the other hand, the incidence of alcoholic hepatitis and/or cirrhosis tended to be higher in the heterozygotes than in the normal homozygotes. These results indicate that alcoholic liver disease develops even with moderate amounts of alcohol intake in heterozygotes of the aldehyde dehydrogenase‐2 genes, in which acetaldehyde metabolism in the liver is impaired and liver damage in the heterozygotes is more severe than that in the normal homozygotes, suggesting that habitual drinkers who are heterozygotes of the aldehyde dehydrogenase‐2 genes may be at high risk for alcoholic liver disease. (HEPATOLOGY1

ISSN:0270-9139    

DOI:10.1002/hep.1840130611

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY