[Proceedings: Radioisotope diagnosis of liver, gallbladder and pancreatic diseases--liver diseases and folic acid metabolism].
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Animals↗
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[Extrahepatic manifestations of chronic liver diseases].
Chronic liver diseases are commonly associated with extrahepatic disease manifestations. Liver cirrhosis, the end stage of chronic liver diseases of different etiologies, can result in severe neurological, renal and pulmonary complications. Hepatic encephalopathy plays an important socio-economic role, since it affects daily functioning and fitness to drive. During the clinical course of chronic viral hepatitis, many patients develop extrahepatic disease manifestations, which lead to significant morbidity and mortality. In particular, mixed cryoglobulinemia, membranoproliferative glomerulonephritis and polyarteriitis nodosa are strongly associated with chronic viral hepatitis. Most extrahepatic manifestations are due to immunological and lymphoproliferative pathomechanisms. Knowledge of extrahepatic disease manifestations is important for adequate medical care and risk assessment of patients with chronic liver diseases by insurance companies.
Chronic Disease↗
Hyperasialoglycoproteinemia in patients with chronic liver diseases and/or liver cell carcinoma. Asialoglycoprotein receptor in cirrhosis and liver cell carcinoma.
The pathogenesis of hyperasialoglycoproteinemia in cirrhosis and liver cell carcinoma was investigated by measuring the amount of asialoglycoprotein receptor in hepatic tissues from 30 patients with either cirrhosis or a malignancy. The asialoglycoprotein receptor activity in the cirrhotic liver was 770 +/- 423 U/g liver, i.e., 28% of the control value (2770 +/- 731 U/g liver). Receptor activity was negligible in tissues from patients with either liver cell carcinoma or metastatic tumor. The receptor levels in noncirrhotic and cirrhotic tissues in close proximity to liver cell carcinoma were 2281 +/- 659 and 1134 +/- 473 U/g liver, respectively. There was a close correlation between serum asialoglycoprotein levels and the size of the tumor mass in patients with liver cell carcinoma. Our results suggest that decreases in the asialoglycoprotein receptor levels may lead to an accumulation of serum asialoglycoproteins in patients with cirrhosis or liver cell carcinoma, or both.
Asialoglycoprotein Receptor↗
Neonatal lupus liver disease.
Neonatal lupus erythematosus (NLE) is an autoimmune disease characterized by complete congenital heart block and/or transient skin lesions of subacute cutaneous lupus erythematosus. We report that in approximately 10% of cases of NLE with heart block or skin disease, liver disease also occurs (4 of 35 cases in our series). Cholestasis was the major feature in our cases. Although the cholestasis may be severe, the disease process appears to be transient and surviving babies have been healthy on follow-up. In one liver examined for antibody deposition, IgG antibody deposits, presumably of maternal origin, were present. Three maternal sera were examined for autoantibodies, including liver-specific autoantibodies. No liver-specific autoantibodies were found. Rather, the maternal autoantibodies too were the ubiquitous Ro/SSA-associated autoantigens. The autoantibodies bound the 60 kDa SSA/Ro ribonuclear protein (three of three sera), the 52 kDa SSA/Ro protein (two of three sera) and the SSB/La ribonuclear protein (two of three sera).
Antibodies, Antinuclear↗
Surgery in the patient with liver disease.
This article deals with the effects of anesthesia and surgery on the healthy and diseased liver and the preoperative assessment of patients with liver disease. Emphasis is placed on estimating surgical risk. Guidelines for optimal preoperative preparation are discussed.
Humans↗
Treatment of osteoporosis in patients with chronic liver disease and in liver transplant recipients.
The pathogenesis of osteoporosis in chronic liver disease and post-liver transplantation is complex and heterogeneous. The development of hepatic osteodystrophy may be related to both increased bone resorption and decreased bone formation. Available medical treatments can be broadly classified into antiresorptive and bone-stimulating agents. Most published studies on the treatment of osteoporosis in patients with liver disease have used the commonly prescribed antiosteoporosis drugs approved for postmenopausal osteoporosis. These studies have included a small number of subjects and used bone mineral density (BMD) changes rather than fracture occurrence as an endpoint because of the short follow-up. Although the increases in BMD are promising, no intervention is proven to have antifracture efficacy in hepatic osteodystrophy. The natural history of bone disease following liver transplantation has not been fully investigated, although studies suggest that bone mineral loss is transient and generally reverses within a year following transplantation. The approach to treatment in liver transplant recipients should be targeted at preventing the early bone loss without interfering with the later recovery. Based on the available data, no single available agent can be considered as first-line therapy. In our opinion, the best treatment approach involves the elucidation of modifiable risk factors and the selection of agents targeted at the underlying derangements.
Journal Article↗
High-resolution light microscopy. Its use in the study of liver diseases.
Tissue processing methods using methacrylate and epoxy resins, which were developed for transmission electron microscopy, allow histopathologic study of specimens by light microscopy with a degree of resolution unavailable with wax methods. We have routinely used epoxy resins in the study of specimens of diseased liver; this is, to our knowledge, the first reported study of such a procedure. Use of epoxy resins allows optimal tissue preservation and maximum use of the resolving power of the light microscope, and the use of polychromatic stains obviates the need for routine use of special stains. We believe that reexamination of specimens of diseased liver using high-resolution light microscopy will provide additional morphologic information for a better understanding of the pathology of liver and more accurate morphologic diagnosis.
Histological Techniques↗
Lymphocyte subpopulations at the site of "piecemeal" necrosis in end stage chronic liver diseases and rejecting liver allografts in cyclosporine-treated patients.
Mononuclear cells in the areas of "piecemeal" necrosis in hepatic tissues from patients with different liver diseases were subtyped using monoclonal antibodies and the avidin-biotin-peroxidase complex method. T lymphocytes were the predominant infiltrating cell type in this lesion (greater than 75% of mononuclear cells) regardless of the etiology of the liver disease. M1-positive cells represented about 20% of the infiltrate. B cells were absent and rare Leu-7-positive cells (killer, natural killer) showed random tissue distribution in both the periportal areas and the parenchyma. In contrast, the T8+ (suppressor-cytotoxic) lymphocytes accumulated selectively in the areas of piecemeal necrosis, where the tissue T4/T8 ratios were consistently less than 1. T8+ lymphocytes were also more numerous than T4+ cells around the hepatitis B surface antigen-positive hepatocytes in piecemeal necrotic areas of livers from patients with hepatitis B surface antigen-positive chronic active hepatitis. In liver tissues of patients with primary biliary cirrhosis, alcoholic cirrhosis, chronic active hepatitis, and rejecting liver allografts, selective accumulations of T8+ lymphocytes at the sites of hepatocyte necrosis were a characteristic and uniform finding. This subpopulation of lymphocytes may be an important part of the immunologically mediated destruction of hepatocytes that occurs in chronic active liver diseases and is characterized by piecemeal necrosis.
Adolescent↗
[The therapy of chronic liver diseases. The therapy of chronic liver diseases and acute threatening states of liver insufficiency].
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Hepatic Insufficiency↗
Phenotypic and functional characteristics of lymphocytes isolated from liver biopsy specimens from patients with active liver disease.
Liver-derived lymphocytes were isolated from 73 liver biopsy specimens obtained from patients with chronic active liver disease and from six samples of normal liver. Mean absolute numbers (+/- S.E.M) of liver-derived lymphocytes recovered from needle biopsy specimens by mild enzymatic digestion of the liver tissue varied from 0.7 +/- 0.3 x 10(3)/mm3 in allografts being rejected to 8.9 +/- 0.9 X 10(3)/mm3 in chronic non-A, non-B hepatitis. By two-color flow cytometry, T lymphocytes (CD3+) were the major liver-derived lymphocyte population in all biopsy specimens. The mean CD4/CD8 ratio (0.6 +/- 0.2) was similar for liver-derived lymphocytes obtained from samples of normal or diseased liver. However, activated (human leukocyte antigen DR+) T cells were significantly (p less than 0.05) increased in liver-derived lymphocytes obtained from liver disease specimens than they were in samples from normal livers. Natural killer cells were less numerous than T cells in specimens obtained from diseased livers, with the mean natural killer/T cell ratio ranging from a low of 0.1 in allograft rejection to a high of 0.8 +/- 0.3 in primary sclerosing cholangitis. Liver-derived lymphocytes isolated from diseased liver contained significantly fewer (p less than 0.05) CD3-CD56+ or CD56+CD16-natural killer cells than did those obtained from normal liver samples. Natural killer activity was consistently detectable in liver-derived lymphocytes obtained from specimens of normal or diseased livers. Moreover, natural killer activity in the liver did not differ significantly from that in either normal or patient peripheral blood.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Experimental and clinical studies on enzymes of mitochondria in various liver diseases; with special reference to alcoholic liver disease (author's transl)].
Mitochondrial enzymes in rat livers or intestines were investigated in experimental models with ethanol- or other hepatotoxic agent-induced liver injuries and extrahepatic cholestasis. In clinical experiment, activities of mitochondrial GOT (mGOT) and ornithine carbasmyl transferase (OCT) were examined in alcoholisms and patients with other various liver diseases. Results obtained are as follows; 1) The activities of OCT and mGOT were increased particularly at onset of acute hepatitis, in chronic active hepatitis and intrahepatic cholestasis, showing that mitochondria were injured strikingly in these diseases. The activities in alcoholics were not so great, however mGOT/total-GOT ratio was increased in level than in other diseases. 2) Changes in mitochondrial enzymes of rat liver treated with ethanol were too varied to catch the actual tendency in this pathologic state. 3) Administration of galactosamine, carbon tetrachloride, or alpha-naphthyl isothiocyanate (ANIT) caused a significant fall in activities of succinate cytochrome C reductase and OCT, along with increase in serum activity of OCT, indicating severe mitochondrial injury with these drugs. Extrahepatic cholestasis following bile duct ligation showed the same changes of mitochondrial enzymes in liver tissue and serum. 4) These data indicate that observation of activities of serum OCT, mGOT, along with mGOT/total-GOT ratio are useful for estimation of mitochondrial damage in extra- and intra-hepatic cholestasis, and acute or chronic active hepatitis. The changes in alcoholic fatty liver was not so subtle as compared with other liver diseases. 5) It is surmized that smooth endoplasmic reticulum was increased in content and pentose phosphate shunt was inhibited by chronic ethanol treatment, estimating from increased activities of NADH-ferricyanide reductase and gamma-glutamyl transpeptidase, and decreased activity of glucose-6-phosphate dehydrogenase. 6) The changes in hepatic enzymes with ethanol treatment were paralleled with those of intestinal ones, indicating that metabolic changes in intestine contribute someway in the formation of alcoholic fatty liver. 7) Chronic ethanol treatment induced lowered active transport in intestinal mucosa, which indicates inhibition in absorption of various nutrients by ethanol.
1-Naphthylisothiocyanate↗
Expression patterns and action analysis of genes associated with drug-induced liver diseases during rat liver regeneration.
AIM: To study the action of the genes associated with drug-induced liver diseases at the gene transcriptional level during liver regeneration (LR) in rats. METHODS: The genes associated with drug-induced liver diseases were obtained by collecting the data from databases and literature, and the gene expression changes in the regenerating liver were checked by the Rat Genome 230 2.0 array. RESULTS: The initial and total expression numbers of genes occurring in phases of 0.5-4 h after partial hepatectomy (PH), 4-6 h after PH (G0/G1 transition), 6-66 h after PH (cell proliferation), 66-168 h after PH (cell differentiation and structure-function reconstruction) were 21, 3, 9, 2 and 21, 9, 19, 18, respectively. It is illustrated that the associated genes were mainly triggered at the initial stage of LR and worked at different phases. According to their expression similarity, these genes were classified into 5 types: only up-regulated (12 genes), predominantly up-regulated (4 genes), only down-regulated (11 genes), predominantly down-regulated (3 genes), and approximately up-/down-regulated (2 genes). The total times of their up- and down-expression were 130 and 79, respectively, demonstrating that expression of most of the genes was increased during LR, while a few decreased. The cell physiological and biochemical activities during LR were staggered according to the time relevance and were diverse and complicated in gene expression patterns. CONCLUSION: Drug metabolic capacity in regenerating liver was enhanced. Thirty-two genes play important roles during liver regeneration in rats.
Animals↗
Serum type III procollagen peptide, type IV collagen 7S domain, central triple-helix of type IV collagen and tissue inhibitor of metalloproteinases in patients with chronic viral liver disease: relationship to liver histology.
To assess the clinical value of serum biochemical markers, the aminoterminal peptide of type III procollagen, type IV collagen 7S domain, the central triple-helix of type IV collagen and tissue inhibitor of metalloproteinases, as a marker of hepatic fibrosis, we measured these four serum markers in 132 patients with chronic viral liver disease and compared these serum markers with liver histological findings. Serum levels of these markers increased closely with the progress of liver disease, and the abnormal percentages of type III procollagen peptide, type IV collagen 7S domain, central triple-helix of type IV collagen and tissue inhibitor of metalloproteinases in patients with cirrhosis were 97%, 95%, 83% and 48%, respectively. These four serum markers strongly correlated with the histological degree of periportal with or without bridging hepatocellular necrosis and of liver fibrosis and correlated weakly with the degree of intralobular degeneration and focal necrosis and the degree of portal inflammation. The correlation coefficients of serum type IV collagen 7S domain with periportal with or without bridging hepatocellular necrosis and with liver fibrosis were the highest among these four serum markers, suggesting that serum type IV collagen 7S domain is the most valuable diagnostic marker to assess the degree of liver fibrosis in chronic viral liver disease. When we assessed the ability of each serum marker to detect cirrhosis with a receiver operating curve, the best test was type IV collagen 7S domain, and the second best was type III procollagen peptide.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Lifestyle guidance for patients with chronic liver diseases; information provision via educational classes on liver diseases.
Patients with chronic liver disease need information on the disease to keep their good quality of life. Educational class on liver disease is one of solutions for that. We have started the class in 1992, and continued to run it once per month. Exchange of information among patients at group work is also helpful to relief their anxiety related to their disease. Many hospitals are now preparing to establish such classes in Japan. In this article, we present tips on providing information to patients with chronic liver diseases and advice on class management.
Journal Article↗
Expression and distribution of a human colon-carcinoma-associated antigen in normal and diseased liver tissue.
Expression and distribution of 17-1A, a human colon-carcinoma-associated antigen as defined by a monoclonal antibody (17-1A mAb), were evaluated in liver tissues from normal subjects and patients with inflammatory and noninflammatory liver diseases. The antigen recognized by 17-1A mAb is a 41-kD protein that does not belong to the proteins of the cytoskeleton. Using a streptavidin-biotin-peroxidase method on frozen sections of liver tissue, it was located in the cytoplasm of bile duct epithelial cells in normal livers, whereas the hepatocytes were completely unreactive. When diseased liver tissue was examined, a strong 17-1A Ag expression was demonstrable in the epithelium of typical and atypical bile ductules in portal areas. In addition, periportal or periseptal hepatocytes revealed variable staining for 17-1A Ag directly related to acute and chronic inflammatory changes. 17-1A Ag expression in hepatocytes reached the highest frequency in acute hepatitis (5/5) and chronic active hepatitis (17/19). These results indicate that periportal hepatocytes are capable of acquiring antigen expression common to bile ductular cells in inflammatory liver diseases, further supporting the view that these ductules represent transformed hepatocytes. Furthermore, two distinct pictures were found in primary liver malignancies. Neoplastic bile duct epithelium did not maintain 17-1A Ag expression in cholangiocarcinoma, whereas neoplastic liver cells acquired cytoplasmic 17-1A Ag expression in clustered areas in hepatocellular carcinoma and the intensity of staining and antigen distribution were inversely related to the grade of tumor differentiation.
Antigens, Neoplasm↗
Ultrasound in the detection of chronic liver disease (the "bright liver").
The association of high amplitude echoes returned from the liver and advanced cirrhosis is well recognized. We have become increasingly aware of a bright liver echo pattern in relatively mild cases of cirrhosis and in other chronic liver diseases. The pattern is very characteristic but non-specific in pathological terms. We have undertaken a small pilot study based on the observation of this characteristic ultrasound appearance to assess its clinical significance. Recognition of this pattern has always corresponded with liver disease of one of five types: cirrhosis, fatty infiltration, portal tract fibrosis, severe hepatitis or longstanding congestive cardiac failure. Although the use of ultrasound appears to be sensitive in the detection of generalized liver disease, it is relatively non-specific.
Chronic Disease↗
[Polycystic liver disease without autosomal dominant polycystic kidney disease].
Polycystic liver disease is characterized by the presence of multiple bile duct-derived epithelial cysts scattered in the liver parenchyma. The natural history and clinical manifestations of polycystic liver disease are based on the disease as it manifests in patients with autosomal dominant polycystic kidney disease (ADPKD). The occurrence of polycystic liver disease independently from polycystic kidney disease has been known for a long time. More recently, a gene for autosomal dominant polycystic liver disease has been identified on chromosome 19p 13.2-13.1. Isolated polycystic liver disease is underdiagnosed and genetically distinct from polycystic liver disease associated with ADPKD but with similar pathogenesis and clinical manifestations. We report here two men with polycystic liver disease no associated with ADPKD. Ultrasound and computed tomography imaging were effective in documenting the underlying lesions non-invasively.
Adult↗
The hands in alcoholic liver disease.
Chronic liver disease is frequently associated with a hyperdynamic circulation, with warm hands and capillary pulsations. In our experience, however, a significant number of patients with alcoholic liver disease complain of cold hands. In this study, we have investigated the presence of the subjective feeling of hand temperature in 114 patients with alcoholic liver disease compared with 96 healthy controls, and studied possible correlations of this subjective feeling with the severity of liver disease. Significantly more patients with alcoholic liver disease complained of cold hands than did normals, and these differences were more prominent in the male group. The awareness of cold hands appears to be commoner in an intermediate group of patients, between those with noncirrhotic liver disease without varices and those with cirrhosis with varices. A similar pattern of awareness of hand temperature was found when patients were staged according to the severity of their liver disease. We conclude that a staging can be made; at an early stage of liver disease, patients tend to have warm hands, subsequently develop cold hands, and at a later stage, their hands become warm again.
Adult↗