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PubMed1999

Transverse hepatectomy for symptomatic polycystic liver disease.

Polycystic liver disease can result in massive enlargement of the liver with resultant debilitating symptoms of abdominal pain, chronic fatigue, and severely compromised functional status. Fenestration of hepatic cysts has been advocated as a treatment for polycystic disease. However, in patients with predominant small cyst replacement, fenestration alone often results in limited hepatic volume reduction without improvement in patient functional status. Liver transplantation has also been previously advocated for polycystic liver disease with predominant small cyst replacement, but, with the severe shortage of donor organs, alternative treatment should be considered. In this report we present a case of massive enlargement of the liver with severe clinical debilitation due to polycystic liver disease. Transverse hepatectomy provided a safe and effective alternative to fenestration or liver transplantation.

Cysts↗
PubMed2002

Living related liver transplantation for polycystic liver disease.

Polycystic liver disease (PCLD) is a rare inherited disorder, often associated with polycystic disease of the kidney. Although liver failure is unusual, some patients suffer from hepatic enlargement associated with severe complications such as abdominal distention, cachexia and dyspnea. Until recently, many surgical attempts had been made to reduce hepatic size, however, results have been unsatisfactory [3, 9, 10]. Today, liver transplantation is recommended as a therapeutic option, and excellent outcome has been demonstrated [1, 2, 4, 5, 6, 8, 11]. In this paper, we present the first case study of total hepatectomy and partial liver transplantation for PCLD, from a living, related donor. The patient is a 38-year-old man with PCLD who underwent living related liver transplantation (LRLT). He is alive and well 21 months after the operation, with complete resolution of the symptoms. He has returned to his previous job, with a marked improvement in his quality of life. Our experience demonstrates that LRLT can be an option for treatment of PCLD.

Adult↗
PubMed1985

Abnormal phenylalanine hydroxylation and tyrosine oxidation in a patient with acute fulminant liver disease with correction by liver transplantation.

Phenylalanine hydroxylation, tyrosine oxidation, and plasma appearance of phenylalanine and tyrosine were evaluated in a 49-yr-old woman with fulminant non-A, non-B hepatitis and encephalopathy using a continuous intravenous infusion of L-[ring-D5]phenylalanine and L-[U-14C]tyrosine. Despite marked elevations in plasma phenylalanine and tyrosine appearance and normal apparent albumin synthetic rates, phenylalanine clearance and hydroxylation to tyrosine were only 12% and 60%, respectively, of values observed in individuals with normal liver function. Three days after orthotopic liver transplantation, plasma phenylalanine and tyrosine appearances were not markedly changed. Phenylalanine clearance and conversion to tyrosine, however, were restored to normal. In addition, tyrosine oxidation and apparent albumin synthesis were increased. This case report represents the first in vivo demonstration of a selective diminution of enzyme function in an individual with fulminant liver disease. Liver replacement restored aromatic amino acid degradative capacity and increased albumin synthesis.

Female↗
PubMed1999

Immunohistochemical study on phenotypical changes of hepatocytes in liver disease with reference to extracellular matrix composition.

AIMS/BACKGROUND: Extracellular matrix (ECM) may affect the function and phenotype of hepatocytes. Phenotypic changes of hepatocytes in diseased liver were investigated with reference to ECM composition. METHODS: Immunohistochemistry was performed on biopsied liver samples from chronic viral hepatitis (CVH), primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) and normal patients, using monoclonal antibodies for laminin, type IV collagen, cytokeratin 19 (CK19) and epithelial glycoprotein (EGP), a protein homologous to nidogen. RESULTS: In normal controls, both EGP and CK 19 were expressed exclusively on biliary epithelia. Laminin and type IV collagen were expressed around portal bile ducts and blood vessels. Although type IV collagen was expressed in Disse's space, laminin was scarcely expressed. In all pathological livers, both EGP and CK 19 were expressed in proliferated bile ductules. In CVH with piecemeal necrosis, EGP was expressed on periportal hepatocytes, while CK19 expression was limited to a few hepatocytes. Laminin was expressed in Disse's space of periportal sinusoids, where EGP was expressed on hepatocytes. EGP expression on hepatocytes and laminin deposition in Disse's space were rare in PBC and PSC liver. CONCLUSION: These results suggest that hepatocytes transform into a phenotype similar to biliary epithelia and, laminin deposition in Disse's space (capillarization of sinusoids) may play a role in this phenotypic change.

Cholangitis, Sclerosing↗
PubMed1987

Correlations of sound speed with tissue constituents in normal and diffuse liver disease.

The speed of sound in normal and diffusely-diseased liver specimens was measured. There were four experimental groups, consisting of normal (n = 21), fatty (n = 7), fibrotic (n = 7) and mixed fatty and fibrotic (n = 9). These classifications were based on histological grading. We found that the results corroborate and extend most of the results of Bamber and coworkers. Specifically, no significant correlation was found between speed of sound and fibrosis score; a moderate correlation was found between speed of sound and tissue water content; and a relatively good correlation (r = -0.670, p less than 0.1%) was found between the speed of sound and the histological fat score, which increased to r = -0.819 (p less than 0.1%) when a correction for variations in water content was used.

Fatty Liver↗
PubMedDate not supplied

The occurrence and properties of a serum hepatic antigen in various liver diseases.

A liver antigen, LA-1, was detected by immunoelectrophoresis in the sera of 79 percent of patients with viral hepatitis A, 77 percent of patients with viral hepatitis B, and 62 percent of patients with alcoholic hepatitis. The occurrence of LA-1 was lower in liver cirrhosis (28 percent) and primary extra-hepatic disorders (18 percent) and absent in the sera of healthy subjects. Liver antigen, LA-1, is detectable in human kidney, lung, spleen, heart and skeletal muscle, and rhesus monkey liver; however, it is not found in the livers from dog, rat, cat, or pig. This antigen is characterized as a protein with beta-globulin electrophoretic mobility and a molecular weight in the range 67,000 to 80,000, which distinguishes it from liver ferritin and previously defined bile antigens and liver-specific antigens detected in sera from patients with liver diseases. The presence of LA-1 in serum appears to denote non-specific liver injury.

Animals↗
PubMed1996

Carnitine metabolism in chronic liver disease.

The liver is a central organ for carnitine metabolism and for the distribution of carnitine to the body. It is therefore not surprising that carnitine metabolism is impaired in patients and experimental animals with certain types of chronic liver disease. In this review, the changes in carnitine metabolism associated with chronic liver disease and the role of carnitine as a therapeutic agent in some of these conditions are discussed.

Animals↗
PubMed1986

Phospholipid transmethylation and choline phosphotransferase in microsomal fraction of human diseased liver.

The activities of three enzymes catalyzing the production or degradation of phosphatidylcholine, a major structural phospholipid of cell membranes, were assessed in hepatocyte membrane microsomal preparation from patients with various types of liver disease. Choline phosphotransferase activity of preparation from patients with chronic aggressive, chronic active, chronic persistent, alcoholic hepatitis and cirrhosis accompanied by marked necrosis and relatively slight fibrosis was markedly decreased, compared with normal liver; the activity from patients with fatty liver and chronic inactive hepatitis was slightly decreased. Specimens from patients with acute transient hepatitis were not significantly different from normal. Methyltransferase and phospholipase A2 activities tended to parallel that of choline phosphotransferase, although the degree of changes was generally less marked. Our studies indicate that enzyme activities that are critical for hepatic cell membrane integrity and activity are attenuated in liver specimens from patients with disease in which there is marked hepatic cell necrosis.

Adult↗
PubMed1999

Therapeutic liver repopulation for the treatment of metabolic liver diseases.

Orthotopic liver transplantation is the treatment of choice for many inherited and acquired liver diseases. Unfortunately, the supply of donor organs is limiting and therefore many patients cannot benefit from this therapy. In contrast, hepatocyte suspensions can be isolated from a single donor liver can be transplanted into several hosts, and this procedure may help overcome the shortage in donor livers. In classic hepatocyte transplantation, however, only 1% of the liver mass or less can be replaced by donor cells. Recently though, we have used a mouse model of hereditary tyrosinemia to show that > 90% of host hepatocytes can be replaced by a small number of transplanted donor cells in a process we term "therapeutic liver repopulation". This phenomenon is analogous to repopulation of the hematopoietic system after bone marrow transplantation. Liver repopulation occurs when transplanted cells have a growth advantage in the setting of damage to recipient liver cells. Here we will review the current knowledge of this process and discuss the hopeful implications for treatment of liver diseases.

Animals↗
PubMed1999

Pharmacokinetics of opioids in liver disease.

The liver is the major site of biotransformation for most opioids. Thus, the disposition of these drugs may be affected in patients with liver insufficiency. The major metabolic pathway for most opioids is oxidation. The exceptions are morphine and buprenorphine, which primarily undergo glucuronidation, and remifentanil, which is cleared by ester hydrolysis. Oxidation of opioids is reduced in patients with hepatic cirrhosis, resulting in decreased drug clearance [for pethidine (meperidine), dextropropoxyphene, pentazocine, tramadol and alfentanil] and/or increased oral bioavailability caused by a reduced first-pass metabolism (for pethidine, dextropropoxyphene, pentazocine and dihydrocodeine). Although glucuronidation is thought to be less affected in liver cirrhosis, and clearance of morphine was found to be decreased and oral bioavailability increased. The consequence of reduced drug metabolism is the risk of accumulation in the body, especially with repeated administration. Lower doses or longer administration intervals should be used to remedy this risk. Special risks are known for pethidine, with the potential for the accumulation of norpethidine, a metabolite that can cause seizures, and for dextropropoxyphene, for which several cases of hepatotoxicity have been reported. On the other hand, the analgesic activity of codeine and tilidine depends on transformation into the active metabolites, morphine and nortilidine, respectively. If metabolism is decreased in patients with chronic liver disease, the analgesic action of these drugs may be compromised. Finally, the disposition of a few opioids, such as fentanyl, sufentanil and remifentanil, appears to be unaffected in liver disease.

Administration, Oral↗
PubMed2002

Animal models of autoimmune liver disease.

Autoimmune liver diseases in humans are characterized by chronic active hepatitis with serum autoantibodies, hypergammaglobulinemia and liver pathology showing necroinflammatory disease and fibrosis. There are an increasing number of autoantigens believed to be associated with various autoimmune liver diseases. This review will briefly outline human autoimmune hepatitis and the immunology of the liver. Various murine models of liver inflammation will be discussed, including transgenic and non-transgenic models, with emphasis on how these models aid in our knowledge of the mechanisms of disease development and chronicity. There are limitations with all of the models, including a preponderance of T-cell-focused responses. Murine models do not easily develop fibrosis, a hallmark of autoimmune hepatitis in humans. Different experimental models may not reach the same conclusions with differences between immune responses. However, this multiplicity of responses does not necessarily imply that these models are inappropriate for the study of liver immunology and autoimmune liver diseases, as different autoantigens may induce different liver responses. Knowledge of how the liver differs from other immune organs is essential to further our understanding of liver-specific autoimmunity. The plethora of antigens implicated in autoimmune hepatitis in humans predicts that multiple mechanisms may play a role in precipitating disease in the susceptible individual.

Animals↗
PubMed2002

Coagulation disorders in liver disease.

The liver plays a central role in the clotting process, and acute and chronic liver diseases are invariably associated with coagulation disorders due to multiple causes: decreased synthesis of clotting and inhibitor factors, decreased clearance of activated factors, quantitative and qualitative platelet defects, hyperfibrinolysis, and accelerated intravascular coagulation. The bleeding tendency accounts for increased risk of morbidity and mortality in patients with liver disease undergoing diagnostic or therapeutic invasive procedures. Peculiar coagulation disorders are prevalent in patients with acute fatty liver of pregnancy or undergoing liver transplantation. Emerging evidence shows that sepsis further impairs hemostasis in patients with liver cirrhosis bleeding from esophageal varices. Thrombotic events, even if rare in cirrhotic patients, occur mainly in the portal and mesenteric veins. The therapeutic approach to coagulative disorders is also discussed.

Bacterial Infections↗
PubMed1978

Hepatic cholesterol ester hydrolase in human liver disease.

Human liver contains an acid cholesterol ester hydrolase (CEH) of presumed lysosomal origin, but its significance is unknown. We developed a modified CEH radioassay suitable for needle biopsy specimens and measured hepatic activity of this enzyme in 69 patients undergoing percutaneous liver biopsy. Histologically normal livers hydrolyzed 5.80 +/- 0.78 SEM mumoles of cholesterol ester per hr per g of liver protein (n, 10). Values were similar in alcoholic liver disease (n, 17), obstructive jaundice (n, 9), and miscellaneous hepatic disorders (n, 21). In contrast, mean hepatic CEH activity was more than 3-fold elevated in 12 patients with acute hepatitis, 21.05 +/- 2.45 SEM mumoles per hr per g of protein (P less than 0.01). In 2 patients studied serially, CEH returned to normal as hepatitis resolved. CEH activity in all patients paralleled SGOT levels (r, 0.84; P less than 0.01). There was no correlation with serum levels of free or esterified cholesterol nor with serum activity of lecithin-cholesterol acyltransferase, the enzyme responsible for cholesterol esterification in plasma. These studies confirm the presence of CEH activity in human liver and show markedly increased activity in acute hepatitis. The pathogenesis and clinical significance of altered hepatic CEH activity in liver disease require further study.

Acute Disease↗
PubMed1998

Growth, insulin-like growth factor I (IGF-I), and IGF-binding proteins 1 and 3 in children with severe liver disease before and after liver transplantation: a longitudinal and cross-sectional study.

We aimed to study the growth and growth factors of children with liver disease before and after liver transplantation (LT). Three observation intervals: 1) before LT (preLT), 2) after LT on daily prednisone treatment (dP), and 3) on alternate day prednisone (adP). A longitudinal study (LS) involved 17 infants (9 male) aged 0.73-2.38 y at LT; mean (+/- SD) height (Ht) SD score (SDS) at LT was -2.02 (+/- 1.25). In a cross-sectional study, there were 123 children (73 male) aged 0.16-14.88 y (mean 3.72 y). IGF-I and IGF binding proteins (BP) 1 and 3 were measured at the same intervals. The results were, for LS, preLT height velocity (HV) SDS (X +/- SD -0.8+/-1.4) lower (p < 0.01) than adP-HV SDS (3.1+/-1.8) but not different from dP-HV SDS (-1.0+/-1.9). For the cross-sectional study, dP-Ht SDS (X+/-SD -1.94+/-1.31) lower (p < 0.001) than preLT-Ht SDS (-1.03+/-1.06) and adP-Ht SDS (-0.98+/-1.20). Parental target SDS was not different from adP-Ht SDS. (Similar observations were made in the LS.) The dP- sitting height (SH) and subischial leg length (SLL) SDS were significantly lower than both preLT- and adP-SH SDS and SLL SDS (p = 0.02 and 0.002, respectively). There was a significant improvement of head circumference SDS and arm circumference SDS from preLT to adP. The dP and adP IGF-I and IGF-BP3 levels were greater than preLT levels (p < 0.001); no differences were found between preLT, dP, and adP IGF-BP1 levels. We conclude that growth in children with liver disease does not improve after LT on dP, but catch-up growth is shown on adP, appearing to depend mainly on the clinical course and corticosteroid regimen. IGF-I and IGF-BP3 increment on dP (and sustained on adP) is possibly due to liver regeneration, in contrast with inhibition of body growth on dP, possibly due to central and peripheral effects of corticosteroid.

Adolescent↗
PubMed1979

The mechanism of release of hepatic enzymes in various liver diseases. II. Altered activity ratios of GOT to GPT in serum and liver of patients with liver diseases.

The activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT) and glutamate dehydrogenase (GLD) were determined in liver biopsy specimens and sera of patients with various liver diseases. Mitochondrial and cytosol isozymes of GOT were also separated for their assay. The activity ratio of GOT/GPT in serum was found to reflect the ratio in liver cytosol. The increased ratio in advanced or severe liver diseases, such as liver cirrhosis, was due to the greater decrease in liver cytosol GPT activity, this being pronounced in primary hepatoma. The activity of GLD decreased similarly but less markedly. The relatively greater decrease in GPT compared with GOT in advanced liver diseases was not mainly due to leakage of the enzyme from the liver, but to a specific mechanism associated with hepatic injury or its progression. Other pathological conditions of the liver such as those in obstructive jaundice and alcoholic liver injury also appeared to result in reduced liver GPT activity, which was reflected in the serum as an increased GOT/GPT ratio.

Alanine Transaminase↗
PubMed1995

Bone disease in cholestatic liver disease.

Osteopenia in the form of osteoporosis is a common clinical problem associated with chronic cholestatic liver disease, and clinical morbidity from atraumatic fractures is increasing as more patients with PBC and PSC undergo successful liver transplantation. In the absence of symptomatic fractures, the clinical diagnosis may not be evident and must be sought by specific means to assess bone mineral density. The clinical problem has now been defined, but much remains unknown, from etiologic mechanisms to effective therapies. At present, it seems reasonable to provide aggressive supportive therapy in an attempt to maximize skeletal well-being until more effective therapies for osteopenia become available.

Bone Diseases↗
PubMed2005

Screening for hepatitis A and B antibodies in patients with chronic liver disease.

Chronic liver disease (CLD) is highly prevalent, and hepatitis C is one of the leading causes. Acute hepatitis A or B in patients with chronic hepatitis C can lead to more severe hepatic injury and a higher fatality rate than in patients without hepatitis C. Thus, the Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control and Prevention and the World Health Organization recommend that persons with CLD be vaccinated against hepatitis A virus (HAV), and the ACIP and the National Institutes of Health recommend vaccination against both HAV and hepatitis B virus (HBV) in patients with chronic hepatitis C. Because coinfection with HAV or HBV in patients with chronic hepatitis C or CLD is common, antibody screening prior to hepatitis A or B vaccination can identify patients who are already immune to these viruses and thus do not need to be vaccinated. Selective hepatitis A vaccination (i.e., vaccination of patients who test negative for either HAV antibody immunoglobulin G or total antibodies to HAV) is most cost-effective in areas where the local prevalence of hepatitis A is higher than the national prevalence and in populations with higher background rates of HAV exposure compared with the general population, such as older adults, foreign-born patients, African Americans, and persons with CLD or hepatitis C. Although not usually recommended for healthy adults or those with compensated CLD because of virtually 100% postvaccination seroconversion, serologic testing after hepatitis A vaccination is recommended in patients with decompensated or advanced end-stage liver disease because of the much lower seroconversion rates in these patients. Selective vaccination against HBV in patients with CLD or hepatitis C is also recommended. Testing for hepatitis B surface antigen (HBsAg) and antibodies to HBsAg (anti-HBs) is considered the most efficient and reasonably cost-effective method to screen for hepatitis B serologic markers because HBsAg identifies individuals with both acute and chronic HBV infection, and anti-HBs identify those who are immune secondary to vaccination or past infection. Testing for antibodies to hepatitis B core antigen is needed to further distinguish between immunity due to vaccination and immunity due to past infection, but it is not recommended as the only screening test for HBV immunity. Postvaccination testing for hepatitis B seroconversion is recommended in all patients with CLD, especially in those with more advanced disease, because the rate of seroconversion is generally lower than in healthy adults. If patients with CLD are not adequately protected after a standard course of hepatitis B vaccination, a repeat course of vaccination using the standard schedule or an accelerated schedule (days 0, 7, and 21) should be considered.

Chronic Disease↗