摘要:

AbstractSerum human hepatocyte growth factor levels were measured using a newly developed enzyme‐linked immunosorbent assay kit in patients with liver diseases. Serum human hepatocyte growth factor levels were increased in correlation with derangements of prothrombin time, total bilirubin and other parameters reflecting hepatocellular dysfunction in 112 patients with chronic liver disease. The levels were positively correlated with serum AST and ALT levels in 59 of these patients whose prothrombin times were within the normal range. Abnormally increased serum human hepatocyte growth factor levels were found in 100% of the determinations in 16 patients with fulminant hepatic failure and in 80% of the determinations in 16 patients with chronic hepatic failure. The levels greater than 1 ng/ml, however, were found in 94% of determinations in the former group, but only in 16% of the determinations in the latter group. This difference was seen irrespective of prothrombin time or hepatic coma grades. In patients with fulminant hepatic failure serum human hepatocyte growth factor levels were increased immediately after plasma exchange using heparin as the anticoagulant in 71% of the determinations. This increase disappeared 12 hr after discontinuation of plasma exchange. In 17 of 39 patients with chronic renal failure who had no liver disease, serum human hepatocyte growth factor levels were abnormally increased before hemodialysis using heparin, and the levels were elevated immediately after hemodialysis in all the patients. The increase of serum human hepatocyte growth factor levels in hepatic failure may be the result of hepatocellular dysfunction and necrosis. Renal failure and extracorporeal circulation may also increase serum human hepatocyte growth factor levels. The determination of the levels may be useful to differentiate fulminant and chronic types of hepatic failure. (HEPATOLOGY1992;15: 1

ISSN:0270-9139    

DOI:10.1002/hep.1840150102

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY

摘要:

AbstractHepatocyte growth factor/hepatopoietin A is a complete mitogen for parenchymal liver cells, and its expression is increased as an early response to acute liver injury. To identify the liver cell population responsible for hepatocyte growth factor gene expression, we investigated tissue sections and isolated and purified cell fractions from normal rat liver byin situand Northern blot hybridization. Hepatocyte growth factor transcripts were present in sinusoidal liver cells, which were preferentially located in the periportal parenchyma. Northern hybridization analysis of RNA isolated from purified liver cell fractions demonstrated that HGF messenger RNA is present only in fat‐storing cells. No specific hepatocyte growth factor gene expression was detected in parenchymal cells, endothelial cells and Kupffer cells. Myofibroblast‐like transition of fat‐storing cells, which is linked to fibrogenesis in chronic liver disease, results in the loss of hepatocyte growth factor expression. Hepatocyte growth factor gene expression in the normal liver, a new function of fat‐storing cells, suggests that this growth factor may play a role in the physiological balance between cell death and replacement in the liver and that hepatocyte growth factor may also act in a paracrine manner. Furthermore, loss of hepatocyte growth factor expression in myofibroblast‐like cells derived from fat‐storing cells may be responsible for reduced parenchymal cell regeneration in chronic liver disease. (HEPATOLOGY19

ISSN:0270-9139    

DOI:10.1002/hep.1840150103

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY

摘要:

AbstractThe aim of this work was to evaluate the effect of intrasplenic hepatocellular transplantation on hepatic encephalopathy in an experimental model of chronic liver failure induced by end‐to‐side portacaval shunt in the rat. Inbred male Wistar Furth rats were divided into three groups: rats subjected to portacaval shunt (n = 10), rats subjected to portacaval shunt and intrasplenic hepatocellular transplantation of 107hepatocytes isolated from livers of syngeneic rats (n = 10) and sham‐operated rats (n = 10). Behavior tests were performed in a blind fashion at 3 wk, at 2 mo and at 3 mo after surgery. Spontaneous activity and nose‐poke exploration by individual rats were studied in automated open field boxes equipped with infrared cells. Each cell beam interruption was automatically recorded on a microcomputer and transformed into a score index (counts/hour). Plasma levels of amino acids, ammonia and total biliary acids were measured. Portacaval shunt rats showed reduced spontaneous activity and nose‐poke exploration scores. Intrasplenic hepatocellular transplantation significantly increased spontaneous activity after 2 mo and improved nose‐poke exploration after 3 wk. At 3 mo, spontaneous activity and nose‐poke exploration in portacaval shunt/intrasplenic hepatocellular transplantation rats were not significantly different from those of sham rats. Increases in plasma ammonia levels after portacaval shunt were not corrected. Amino acid imbalance and bile acid concentration in plasma were partially corrected by intrasplenic hepatocellular transplantation. These data show that intrasplenic hepatocellular transplantation can correct the neurological symptoms of hepatic encephalopathy in an experimental model of chronic liver failure and suggest that intrasplenic hepatocellular transplantation might be of therapeutic interest in chronic liver failure. (HERATOLOGY1

ISSN:0270-9139    

DOI:10.1002/hep.1840150104

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY

摘要:

AbstractSera from 483 patients at high (group 1, n = 313) and lower (group 2, n = 170) risk for exposure to hepatitis C were tested for antibodies to hepatitis C using first‐generation (c100‐3) and second‐generation enzyme‐linked immunosorbent assays and four‐antigen recombinant immunoblot assay. The second‐generation enzyme‐linked immunosorbent assay and nitrocellulose‐based immunoblot assay differ from c100‐3‐based systems in the addition of expression products from the NS3/NS4 (c33c, c200) and putative nucleocapsid (c22‐3) region of the hepatitis C genome. In group 1, the sensitivity of detection of hepatitis C antibodies was 45%, 55% and 46% by the first‐ and second‐generation enzyme‐linked immunosorbent assays and recombinant immunoblot assay, respectively. In group 2, antibodies were detected by each test system in 26%, 32% and 7% of patients, respectively. Most sera (99%) reactive with the first‐generation enzyme‐linked immunosorbent assay were reactive with the second‐generation enzyme‐linked immunosorbent assay (in group 1, 89% of these specimens demonstrated reactivity to at least one antigen with the immunoblot assay, compared with only 31% in group 2). An additional 12% (group 1) and 6% (group 2) of specimens demonstrated reactivity with the second‐generation enzyme‐linked immunosorbent assay only (of these, 75% [group 1] and 9% [group 2]demonstrated reactivity to at least one antigen with the immunoblot assay). Ninety‐eight percent of specimens not reactive with both enzyme‐linked immunosorbent assay test systems were also nonreactive by recombinant immunoblot assay. Antibodies to c22‐3 and c33c were more frequently detected in chronic hepatitis C virus infection and appeared earlier in acute hepatitis C virus infection, compared with 5‐1‐1 and c100‐3. These results indicate that the addition of structural and nonstructural hepatitis C virus antigens in the second‐generation enzyme‐linked immunosorbent assay improves the sensitivity of detecti

ISSN:0270-9139    

DOI:10.1002/hep.1840150105

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY

摘要:

AbstractSerial sera were collected prospectively during the clinical course of 13 HBsAg carriers with chronic liver disease and analyzed for ALT levels, pre‐S1and pre‐S2antigens and corresponding antibodies and other serological hepatitis B virus markers. In five patients, anti—pre‐S1and anti—pre‐S2antibodies became detectable in multiple serum samples, whereas in eight patients anti—pre‐S was never detected or only appeared transiently during the follow‐up. The first pattern was associated with normalization of ALT levels and undetectable pre‐S antigens and viral DNA by the polymerase chain reaction assay at final follow‐up. HBsAg clearance occurred in two of the five patients. The second pattern was one of persistence of HBsAg and pre‐S antigens, associated with the presence of serum HBV DNA detectable by spot hybridization or polymerase chain reaction regardless of clinical outcome. These findings demonstrate the occurrence of anti—pre‐S antibodies in chronic hepatitis B virus—induced liver disease and associate anti—pre‐S appearance with the clearance of hepatitis B virus from

ISSN:0270-9139    

DOI:10.1002/hep.1840150106

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY

摘要:

AbstractThe objective was to determine the proportion of patients with chronic hepatitis B in whom hepatitis B virus DNA is demonstrated by polymerase chain reaction after HBeAg to anti‐HBe or HBsAg to anti‐HBs spontaneous or therapeutically induced seroconversion.Polymerase chain reaction was performed on serum 6 and 12 mo after HBeAg to anti‐HBe seroconversion in 12 patients and 2, 6 and 12 mo after HBsAg to anti‐HBs seroconversion in 13 patients. Polymerase chain reaction was performed on liver tissue after HBeAg to anti‐HBe seroconversion in five patients and after HBsAg to anti‐HBs seroconversion in one patient.Serum HBV DNA was demonstrated by polymerase chain reaction in 83% of patients 6 or 12 mo after HBeAg to anti‐HBe seroconversion and in 58%, 31% and 15% of patients at 2, 6 and 12 mo, respectively, after HEsAg to anti‐HBs seroconversion. Liver HBV DNA was demonstrated by polymerase chain reaction in all patients tested.Our results show that (a) a reduced level of hepatitis B virus replication persists in most of the patients after HBeAg to anti‐HBe seroconversion and might be predictive of reactivation, and (b) in contrast, hepatitis B virus replication progressively disappears in most of the patients after HBsAg to anti‐HBs seroconversion. (HEPAT

ISSN:0270-9139    

DOI:10.1002/hep.1840150107

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY

摘要:

AbstractWe tested serial serum samples for hepatitis C virus RNA from patients undergoing treatment for chronic hepatitis C with interferon‐α using an assay that combined reverse transcription and polymerase chain reaction. The subjects studied were 20 patients with chronic hepatitis who had serum antibody to hepatitis C virus (anti‐C100–3). Before therapy, hepatitis C virus RNA was detected in 18 (90%) and 20 (100%) patients using primer sets derived from the NS3 region or the 5′‐noncoding region of hepatitis C virus, respectively. Hepatitis C virus RNA became undetectable in all patients whose ALT level fell into the normal range during therapy. However, hepatitis C virus RNA reappeared in all patients whose ALT levels rose again after therapy, usually before the relapse. In patients whose ALT levels did not become normal, hepatitis C virus RNA did not disappear during therapy. Thus therapy with interferon‐α appears to be beneficial in chronic hepatitis C because of its suppressive effects on hepatitis C virus replication. Detection of hepatitis C virus RNA in serum is useful for evaluating the antiviral effect of interferon (HEPATOLOGY1

ISSN:0270-9139    

DOI:10.1002/hep.1840150108

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY

摘要:

AbstractChronic hepatitis frequently occurs after liver transplantation. The role of hepatitis C virus infection in patients after liver transplantation is unknown, although antibodies to HCV are detected in some of these cases. The use of polymerase chain reaction techniques for the detection of hepatitis C virus RNA should improve sensitivity and specificity, particularly in these immunosuppressed patients. Our goal was to further clarify the role of hepatitis C virus infection in chronic hepatitis occurring after liver transplantation. Patients with chronic hepatitis of uncertain origin after transplantation were identified. Serum samples taken at the time of the most recent liver biopsy that showed chronic hepatitis were tested for anti‐hepatitis C virus using enzyme‐linked immunoassay and supplemented by recombinant immunoblot assay (recombinant immunoblot assay I and recombinant immunoblot assay II). The samples were also tested for the presence of hepatitis C virus RNA using polymerase chain reaction. Of the 25 patients with chronic hepatitis, 15 (60%) had hepatitis C virus RNA present. Only seven (47%) of these 15 patients had anti‐hepatitis C virus detected. Hepatitis C virus is a major cause of chronic hepatitis occurring after liver transplantation. The magnitude of hepatitis C virus infection will be underestimated if only currently available assays for anti‐hepatitis C virus are used. (HEPATOLOGY1992; 15

ISSN:0270-9139    

DOI:10.1002/hep.1840150109

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY

摘要:

AbstractUltrastructural identification of light microscopic giant mitochondria was performed on the same specimens for light and electron microscopic observations. The liver tissue specimens were fixed in OsO4, embedded in epoxy resin, cut 4 μm thick and stained with polychrome. At the beginning of the study a light microscopic observation was made, and a microphotograph was taken. The identification of light microscopic giant mitochondria by conventional microscopy was identified by the occupation rate in liver cells, the negative findings of stainability and the morphological consistency (round, cigar‐shaped and granular). The specimens were subsequently embedded again in epoxy resin and cut into ultrathin sections of 400 Å. A transillumination electron microscope was used for the observation, and ultrastructural images of light microscopic giant mitochondria revealed that they were crystalloid bodies with a crystalline latticelike structure. The occupation rates within liver cells and the morphological shapes of the crystalloid bodies corresponded with those of light microscopic giant mitochondria. The light microscopic giant mitochondria obviously had different features from those of electron microscopic giant mitochondria and Mallory bodies (Yokoo's type II), although Mallory bodies showed the same staining properties as light microscopic giant mitochondria. (HEPATOLOGY1992; 15:46

ISSN:0270-9139    

DOI:10.1002/hep.1840150110

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY

摘要:

AbstractWe studied the size of the liver graft and the host liver in six consecutive patients undergoing auxiliary heterotopic liver transplantation for chronic endstage liver disease. In all cases, a liver reduced in size by left lateral hepatectomy was inserted. The sizes of the graft and host liver were estimated by planimetry of two‐dimensional di‐isopropyl iminodiacetic acid scintigrams taken 3, 7, 21, 90 and 180 days after surgery.Graft size increased from a mean of 12.2 cm2(95% confidence interval = 10.2 to 14.1) on day 3 to a maximum of 14.8 cm2(95% confidence interval = 13.4 to 16.1) on day 21 and remained stable thereafter; in contrast, the host liver decreased in size from 9.6 cm2(95% confidence interval = 6.8 to 12.3) on day 3 to 3.9 cm2(95% confidence interval = 3.0 to 4.8) at mo 6.We conclude that in patients with chronic liver failure, an auxiliary allograft reduced in size and placed adjacent to the host liver shows regenerative growth within 3 wk, whereas the host liver atrophies in 3 to 6 mo. (HEPATOLOGY1992;15:54

ISSN:0270-9139    

DOI:10.1002/hep.1840150111

出版商:W.B. Saunders    

年代:1992

数据来源: WILEY