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PubMedDate not supplied

Pseudolesion in segment IV of the liver on MRI: prevalence and morphology in 250 cirrhotic livers compared with 250 normal livers.

PURPOSE: The goal of our study was to assess the prevalence of pseudolesion in segment IV of the liver on MRI in patients with and without liver cirrhosis. METHOD: Patients were divided into three groups: 10 patients with angiographically confirmed aberrant gastric venous drainage and liver cirrhosis (Group 1), 250 consecutively selected patients with liver cirrhosis (Group 2), and 250 with normal liver (Group 3). The signal intensity of pseudolesion in segment IV on T1- and T2-weighted MRI in the 510 patients was analyzed. RESULTS: In Group 1, five pseudolesions were visible and hyperintense on T1-weighted images. On T2-weighted images, four were visible and hypointense. In Group 2, 11 were seen (4.4%). All were hyperintense on T1-weighted images. Five were hypointense on T2-weighted images. In Group 3, one pseudolesion was seen (0.4%). CONCLUSION: The prevalence of pseudolesion in segment IV on MRI is higher in liver cirrhosis than in normal liver. The lesion is hyperintense on T1-weighted images when visible.

Adult↗
PubMed1984

Estrogen biosynthesis in human liver--a comparison of aromatase activity for C-19 steroids in fetal liver, adult liver and hepatoma tissues of human subjects.

After incubation of various tritiated C-19 steroids (androstenedione, testosterone, dehydroepiandrosterone, dehydroepiandrosterone sulfate) with human fetal liver, adult liver and hepatoma tissue homogenates, estrone, estradiol and estriol were analysed after a series of purification steps involving column chromatography, thin layer chromatography and co-crystallization. The findings indicated that the human fetal liver extensively aromatized various C-19 steroids to estrogens, whereas human adult liver and hepatoma tissues exhibited little or no aromatase activities. The formation of estradiol from androstenedione in human fetal liver indicated the presence of 17 beta-hydroxysteroid dehydrogenase in this tissue. It was therefore concluded that although the liver participated in the aromatization process during the fetal stage, extensive aromatization did not take place in the adult liver.

Aged↗
PubMed2003

Orthotopic liver transplantation for acute liver failure resulting from "acute fatty liver of pregnancy".

Steatosis of the liver, demonstrating itself as the acute liver failure during the third trimester of pregnancy (Acute Fatty Liver of Pregnancy--AFLP) is a rarely observed liver pathology. Herewith we describe the case of a 19-years old pregnant patient with this rare disease. The authors present the clinical course, dynamics, diagnostics, and outcome of treatment in this unique case. In this patient the ultimate treatment chosen was the liver transplantation. The opinions, concerning liver transplantation in AFLP (expressed in the world literature) are somewhat controversial. This paper presents the first case of AFLP treatment with orthotopic liver transplantation (OLTx) in Poland.

Acute Disease↗
PubMed1991

Detection of human hepatitis anti-liver kidney microsomes (LKM2) autoantibodies on rat liver sections is predominantly due to reactivity with rat liver P-450 IIC11.

Anti-liver kidney microsomes (anti-LKM2) autoantibodies, appearing in patients treated with tienilic acid and suffering from hepatitis, react with proteins in rat liver sections. The nature of the rat proteins responsible for this recognition and detection of anti-LKM2 has been investigated. Immunoblot testing of the anti-LKM2 with liver microsomes from diversely treated rats and with purified rat liver cytochromes P450 (IA1, IA2, IIB1, IIB2, IIC6, IIC11 and IVA1) showed that these antibodies cross-reacted with cytochrome P450IIC11 and also with phenobarbital-induced cytochromes P450IIB1 and IIB2. Moreover, metabolic activation of tienilic acid and of a tienilic acid isomer by untreated rat liver microsomes was partially inhibited by anti-LKM2. On the other hand, monospecific polyclonal anti-rat P450IIC11 antibodies cross-reacted with human microsomal cytochromes P450 and recognized the same cytochromes P450 as anti-LKM2. This antibody also gave an immunofluorescence pattern on rat and mouse liver and kidney sections very similar to anti-LKM2. The data presented here show that anti-LKM2 recognize epitopes shared by rat P450 IIC11, and a human P450 of the family IIC. All the results indicate rat P450 IIC11, the major isoenzyme present in normal adult male rat liver, as the main antigen recognized by human anti-LKM2 autoantibodies; this is the basis of the immunofluorescence test for detection of these antibodies.

Animals↗
PubMed1988

The role of liver biopsy in evaluating acute allograft dysfunction following liver transplantation: a clinical histologic correlation of 34 liver transplants.

One hundred six liver biopsy specimens from 34 orthotopic liver transplant (OLT) patients were examined and the histologic findings correlated with the clinical course of the patients to determine if specific morphologic patterns were associated with specific causes of acute allograft dysfunction. The principle causes of allograft injury in these patients appeared to be acute rejection and ischemic injury, with rarer cases of viral infection and biliary obstruction. Graft rejection causing transient liver dysfunction was associated with a mixed inflammatory infiltrate in the portal tracts and involving the interlobular bile ducts. Rejection resulting in severe, persistent dysfunction was associated with destruction and loss of the interlobular bile ducts or portal inflammation, followed by acute centrilobular hepatocyte necrosis. Ischemic liver injury was characterized by hepatocyte ballooning and/or hepatocyte necrosis. Ischemic injury causing transient graft dysfunction demonstrated focal, limited areas of hepatocyte necrosis or transient centrilobular hepatocyte ballooning. Severe ischemic injury resulting in persistent dysfunction caused diffuse hepatocyte necrosis or centrilobular ballooning followed by centrilobular hepatocyte loss and severe cholestasis with evidence of bile duct epithelial injury. The histologic patterns observed were not pathognomonic; radiologic studies, bile cultures, and other laboratory tests were necessary to rule out biliary or vascular obstruction and bacterial cholangitis. However, liver biopsies, especially serial biopsies, were helpful in suggesting the probable cause of liver dysfunction and in predicting subsequent allograft recovery or failure.

Adolescent↗
PubMed1999

[Solitary liver cysts and polycystic liver disease: aspects of surgical management of congenital cystic liver disease].

Congenital cystic liver disease represents a rare entity and only in 5%-20% the cysts cause symptoms or complications that demand therapy. In the past decades several therapeutic approaches have been developed with variable long-term outcome. We report herein our results and the postoperative outcome of 26 patients treated from 1987 to 1998 in our department because of symptomatic or complicated congenital cystic liver disease. In cases of symptom-producing solitary liver cysts our therapy of choice was laparoscopic fenestration. In cases of adult polycystic liver disease we mostly performed partial hepatic resection and fenestration. Both therapeutic approaches have proven a favorable long-term outcome. However, some types of adult polycystic liver disease possess a high risk of reappearance. Preoperative pathomorphological assessment of polycystic liver disease should be performed to choose the operative procedure in relation to the expected recurrence rate. Because of the progresses made in dialysis therapy and transplantation surgery in patients with adult polycystic kidney disease, an increase of patients with symptomatic polycystic liver disease has to be expected in the near future.

Adult↗
PubMed2000

Primary liver resection and salvage transplantation or primary liver transplantation in patients with single, small hepatocellular carcinoma and preserved liver function: an outcome-oriented decision analysis.

Two treatments are accepted for patients with solitary hepatocellular carcinoma </=5 cm in size and with preserved hepatic function: (1) liver resection, which can be performed without delay but has a high recurrence rate, and (2) liver transplantation, which has a better long-term survival, but is not easily available because grafts are scarce. A third possibility is to offer liver resection first and liver transplantation for tumor recurrence or deteriorating liver function ("salvage" transplantation). We investigated the implications of such a strategy with a Markov-based decision analytic model. In a scenario assuming intermediate values for 4 main variables (12-month waiting list; tumor progression outside transplantation criteria: 4% per month; recurrence after resection: 20% per year; recurrences eligible for transplantation: 60%), the life expectancy was 8.8 years for primary transplantation versus 7.8 years for primary resection and salvage transplantation, with a calculated use of grafts at 5 years of 52% for primary transplantation versus 23% for salvage transplantation. This study estimates of the survival and graft-saving of a strategy of primary resection and salvage transplantation according to variables that are to some extent predictable. This strategy may be a rational way to cope with lengthening waiting lists, especially for patients with tumors close to the limit for transplantation criteria, if the results of liver resection are good, if patients with the lowest risks of recurrence can be selected, and if a strict follow-up can detect recurrences when the patients are still transplantable.

Carcinoma, Hepatocellular↗
PubMed1982

Radioimmunoassay of serum glycocholic acid, standard laboratory tests of liver function and liver biopsy findings: comparative study of children with liver disease.

Serum glycocholic acid (SGC) was measured by radioimmunoassay in 277 samples from 122 children with hepatobiliary disorders and from 23 healthy age-matched controls. In patients with hepatobiliary disease the SGC was more frequently abnormal (83%) than values for serum albumin (7%), prothrombin time (17%), bilirubin (22%), alkaline phosphatase (45%), aspartate transaminase (57%) and gammaglutamyl transpeptidase (63%). The cumulative frequency of abnormality of these six tests was equal to that of SGC alone. Serum glycocholic acid concentrations were raised in 13 patients in whom all other tests of liver function were normal. Two of these had clinical and histological evidence of liver disease, while four had biopsy-proven hepatic fibrosis or cirrhosis, and two of three with chronic active hepatitis in remission subsequently relapsed. Four patients have as yet, no other clinical or biochemical evidence of continuing liver disease. Serum glycocholic acid was normal in seven children with abnormal aspartate transaminase or gammaglutamyl transpeptidase in whom there is strong suspicion of significant hepatic disease. A wide range of values of SGC was found with marked overlap between the values found in the different disease entities studied. The SGC value was related to the serum concentration of aspartate transaminase and gammaglutamyl transpeptidase but not to other tests of liver function. Serum glycocholic acid concentration was considered in relation to the severity of histological abnormality in 25 percutaneous liver biopsies. The extent of the rise in SGC was related to the presence or degree of histological severity of oedema in the portal tracts, disruption of the limiting plate, parenchymal fibrosis and hepatocellular necrosis but not to other histological features. The very high incidence of abnormal SGC values found in this study does suggest that in an ordinary inpatient and outpatient service SGC determination is a practical and sensitive indicator of the presence of significant liver disease but for its comprehensive identification aspartate transaminase and gammaglutamyl transpeptidase must also be determined.

Adolescent↗
PubMed1980

Cell-mediated immunity to liver antigen in toxic liver injury. II. Role in pathogenesis of liver damage.

The possible pathogenetic role of lymphocytes sensitized to liver antigens was investigated in CBA mice in which sublethal hepatic necrosis had been induced by carbon tetrachloride (CCl4). Sensitized lymphocytes from CCl4-treated mice were administered to syngeneic recipients. The recipients developed sensitivity to liver antigens but showed no evidence of liver damage. The cell mediating the immune response both in the donor and the recipient was a T cell. This was demonstrated further by studies involving mice rendered T cell deficient. These mice did not develop sensitized lymphocytes when they were treated with CCl4 but the extent of liver damage was similar in both T cell-depleted and intact animals. These findings suggest that T cell sensitization to liver antigens occurs as a result of toxic liver damage and does not play a role in the pathogenesis of the hepatic necrosis.

Animals↗
PubMed1994

Decreased prostacyclin production by liver non-parenchymal cells precedes liver injury in experimental alcoholic liver disease.

We used the intragastric feeding rat model for alcoholic liver disease to investigate the relationship between prostacyclin and liver injury. Rats were fed the following diets for periods ranging from 1 to 8 weeks: corn oil plus ethanol (CO+E), corn oil plus dextrose (CO+D), saturated fat plus ethanol (SF+E) and saturated fat plus dextrose (SF+D). Prostacyclin production (assessed by 6-ketoprostaglandin F1 alpha) by liver non-parenchymal cells decreased steadily over the 8 week period in animals fed CO+E (liver injury present) whereas in animals fed SF+E (no liver injury) there was no change in prostacyclin production. Plasma levels of 6-ketoprostaglandin F1 alpha were also significantly lower in the CO+E group compared to the other groups studied. We propose that decreased prostacyclin production by liver non-parenchymal cells may contribute to the hepatotoxic effect of ethanol.

6-Ketoprostaglandin F1 alpha↗
PubMed2005

Phosphorus-31 MR spectroscopy in pediatric liver transplant recipients: a noninvasive assessment of graft status with correlation with liver function tests and liver biopsy.

OBJECTIVE: Noninvasive in vivo hepatic phosphorus-31 MR spectroscopy has recently been shown to provide information about hepatic functional status. We sought to show the correlation of phosphorus-31 MR spectroscopy with blood biochemistry and liver biopsy results in pediatric patients after liver transplantation. MATERIALS AND METHODS: Eleven pediatric transplant recipients (eight with good graft function, two with chronic hepatitis, and one with acute rejection) and four healthy control subjects were studied with in vivo 31P MR spectroscopy. Ratios of phosphomonoesters (PME) to total phosphorus (TP), phosphodiester (PDE) to TP, nucleotide triphosphates (NTP), inorganic phosphate (Pi), and intracellular acid-base status (pH) were measured. Liver function test (n = 11) and biopsy (n = 3) results were obtained for correlation with spectroscopic findings. RESULTS: The eight patients with good graft function displayed spectral profiles similar to those of the healthy subjects, and no significant difference in the metabolic ratios of these patients compared with the control subjects was detected. Three patients with abnormal liver function and biopsy-proven hepatic complications showed elevated PME/TP ratios when compared with those of both the control subjects and the group with good graft function. CONCLUSION: Phosphorus-31 MR spectroscopy is a feasible technique for the noninvasive assessment of host-related complications in pediatric patients after liver transplantation. Our preliminary data suggest that the technique may be integrated with MRI for the investigation of impaired liver function in transplant recipients when neither a biliary complication nor a vascular complication is identified.

Adolescent↗
PubMed1983

Liver cell membrane antibody detected by protein A and isolated rabbit liver plasma membrane in sera of patients with chronic liver diseases.

Using the plasma membrane fraction isolated from rabbit liver (RLPM), we detected non-species specific IgG antibody against liver cell surface membrane in the sera from the patients with chronic liver diseases. The sea were treated with dithiothreitol and iodoacetamide, and absorbed with sufficient amount of actin isolated from rabbit striated muscles. The antibody was detected by incubation of RLPM with the treated and absorbed sera and subsequent determination of IgG bound to RLPM by 125I-staphylococcal protein A. It was found mainly in the patients with autoimmune hepatitis (12 of 28) and liver cirrhosis (eight of 24). It occurred more frequently in HBsAg negative liver cirrhosis than in HBsAg positive forms (six of 13 vs two of 11). The frequency of the antibody was low in chronic hepatitis except autoimmune hepatitis, and primary biliary cirrhosis. Thus the antibody against RLPM was an immunological marker of autoimmune hepatitis and HBsAg negative liver cirrhosis. The occurrence did not correlate with those of anti-smooth muscle antibody, anti-nuclear antibody and anti-mitochondrial antibody. In two cases of autoimmune hepatitis, the antibody against RLPM decreased with clinical improvement induced by corticosteroids.

Adrenal Cortex Hormones↗
PubMed1981

Role of the liver in the degradation of very low density lipoproteins: a study of lipolysis by heparin releasable liver lipase and uptake during isolated rat liver perfusion.

The role of the liver and of a heparin-releasable liver lipase in the metabolism of very low density lipoprotein (VLDL) was investigated in vitro and during recycling rat liver perfusion. Rat plasma VLDL and nascent hepatic VLDL were labelled biosynthetically in their lipid moieties. Incubation in vitro of VLDL with the lipase caused hydrolysis of VLDL-triglycerides (greater than 80%) and VLDL-phosphatidylcholine (greater than 30%). Nascent VLDL was a better substrate for the enzyme. The hydrolytic activities were inhibited by 70--90% when rat plasma (10--30 vol%) was added to the incubation mixture. VLDL-triglycerides and cholesterol esters were taken up by the liver during 180 min recycling perfusion. The rate of disappearance of nascent VLDL was faster than that of plasma VLDL (half-life times of 56.2 +/- 13.9 and 125.0 +/- 24.8 min respectively). Injection of heparin into the perfusion medium caused accelerated uptake of the hydrolysed VLDL-triglyceride by the liver. Addition of plasma (d greater than 1.006 g/ml) to the perfusion at a concentration of 10 vol% delayed the rate of disappearance of VLDL from the perfusate by about 50--75%. These studies have established the capacity of the hepatic lipase to hydrolyse VLDL-lipids and the ability of the liver to degrade nascent and plasma VLDL particles. These two activities, however, are depressed by plasma and therefore previous studies of VLDL metabolism may have to be re-examined when based on incubations or perfusions in the absence of plasma.

Animals↗
PubMed2004

Improved characterization of liver lesions with liver-phase uptake of liver-specific microbubbles: prospective multicenter study.

PURPOSE: To evaluate in a prospective multicenter study whether conventional ultrasonographic (US) characterization of liver lesions can be improved by imaging during the liver-specific phase of SH U 508A uptake in the microbubble-specific agent detection imaging mode. MATERIALS AND METHODS: One hundred forty-two patients with liver lesions underwent conventional gray-scale and color Doppler US and SH U 508A-enhanced US. Two radiologists blindly read digital cine clips and assigned scores for confidence in diagnosis of benignancy or malignancy, diagnosis of specific lesion types, and relative difference in SH U 508A uptake between the lesion and the liver parenchyma (ie, subjective conspicuity score [SCS]). Comparisons were made to see whether the addition of agent detection imaging led to improved diagnostic performance. RESULTS: Receiver operating characteristic analysis revealed improved discrimination of benign and malignant lesions for readers 1 (P =.049) and 2 (P <.001). The number of patients with a correct diagnosis of benignancy or malignancy assigned by readers 1 and 2, respectively, improved from 114 and 113 to 125 and 128 with agent detection imaging (reader 1: P =.027; reader 2: P =.008; McNemar test). Specific diagnoses were made more accurately with agent detection imaging: At McNemar testing, the number of correct lesion type determinations increased from 83 to 92 (P =.022) for reader 1 and from 85 to 99 (P <.001) for reader 2. Both readers assigned high scores for differences in SH U 508A uptake between the liver parenchyma and the lesion for metastases and cholangiocarcinomas and low scores for uptake differences in most of the benign lesions. Hepatocellular carcinomas (HCCs), hemangiomas, and adenomas had more variable uptake differences. Fourteen of 22 hemangiomas were assigned an SCS of less than 50%, and 22 (reader 1) and 15 (reader 2) of 31 HCCs were assigned an SCS of greater than 50%. CONCLUSION: With use of SH U 508A-enhanced agent detection imaging, liver lesion characterization and diagnostic performance are significantly improved.

Adult↗
PubMed1995

New techniques for liver transplantation: reduced-size, split-liver, living-related and auxiliary liver transplantation.

Mortality among patients on a waiting list for orthotopic liver transplantation continues to be 10-15%; this is of particular concern in the pediatric population and may become more problematic in adult patients as longer waiting lists for cadaveric transplantation accrue. The longer cold ischemia times afforded by use of University of Wisconsin (UW) solution and improved hepatic surgery techniques have allowed the development of reduced-size liver transplantation (RSLT), split-liver transplantation (SLT), and living-related liver transplantation (LRLT). These new surgical techniques have been predominantly employed in children, up to 40% of whom may be candidates for one of these modified procedures. With the exception of SLT, these approaches have been associated with comparable rates of biliary tract and vascular complications, rejection episodes and graft and patient survival when compared to whole organ transplantation. Right hepatic lobe graft recipients have approximately 15% decreased graft survival rates, limiting the acceptance of SLT as a standard approach to decrease waiting list times. Application of LRLT to the adult population, where 5-10% of recipients are potential candidates, is expected to increase. Over 100 LRLTs have been performed worldwide and while recipient survival with LRLT is excellent, concerns about donor morbidity and mortality, psychosocial factors and reimbursement issues remain obstacles. Living-unrelated liver transplantation and auxiliary orthotopic partial liver transplantation are developing approaches to be considered only in highly selected cases.

Humans↗
PubMed1981

Integration of hepatitis B virus DNA into the genome of liver cells in chronic liver disease and hepatocellular carcinoma. Studies in percutaneous liver biopsies and post-mortem tissue specimens.

We used recombinant-DNA technology and gel electrophoresis to find hepatitis B virus DNA (HBV-DNA) in liver and tumor tissue from patients with hepatocellular carcinoma and chronic liver disease, and to study the integration of HBV-DNA into the genome of these tissues' cells. In 12 patients with hepatocellular carcinoma who had hepatitis B surface antigen (HBsAg) in their serum, integrated HBV-DNA was identified in the tumors; it was also found in tumors from three of eight patients who were seronegative for HBsAg but positive for antibody to HBsAg. In some cases, integrated HBV-DNA was also present in nontumorous liver tissue that had the same hybridization pattern or one different from that of the tumor. In five carriers of HBsAg who had evidence of the carrier state and chronic liver disease for less than two years, HBV-DNA was present but not integrated in liver tissue. In the two patients who had carried HBsAg for more than eight years, HBV-DNA was integrated into the host genome. These data suggest that integration of HBV-DNA into hepatocytes occurs during the course of persistent HBV infection and precedes development of gross neoplasm.

Biopsy↗