Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protein FV, a human sialoprotein recently described in the stools of patients suffering from liver diseases, binds the variable domain of the heavy chains of immunoglobulins. We show here that preincubation of this protein with monoclonal human IgG1 and IgM activates the complement cascade by forming non-immune complexes, as evidenced by haemolysis inhibition of antibody-coated sheep erythrocytes. As negative controls, no inhibition was observed after incubation either with immunoglobulins or with protein FV alone, and with the protein FV-depleted medium. Activation was due to the binding of immunoglobulins with protein FV, as shown by inhibition of protein FV-induced agglutination of the sensitized erythrocytes in the absence of complement. Activation of the classical pathway was demonstrated both by using a human IgG4 or F(ab')2 fragments unable to activate C1q, and by Western blot analysis of the cleavage of C4 in human serum. These results confirm that protein FV-binding mimics antigen-antibody reactions, and suggest its involvement in hepatitis-associated vasculitis and in local lesions of some inflammatory gut diseases.
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PMID:Activation of the classical pathway of complement by non-immune complexes of immunoglobulins with human protein FV (FV fragment-binding protein). 809 Nov 37

Met-enkephalin is known to circulate in human and animal plasma in low levels. However, the source(s) of plasma met-enkephalin have not been completely elucidated. It has been proposed that the adrenal gland, sympathetic nerves, pancreas and the gut might be implicated. Recently, markedly elevated levels of met-enkephalin have been documented in the presence of liver disease. To investigate potential sources of met-enkephalin in liver disease, rats with acute cholestatic hepatitis 24 h after gavage with alpha naphthylisothiocyanate (ANIT) 100 mg/kg were studied. Plasma met-enkephalin levels were determined by radioimmunoassay in plasma samples from normal, adrenalectomized, or chemically sympathectomized animals. In control rats, ANIT treatment resulted in a striking 8.7-fold increase in systemic venous met-enkephalin levels (inferior vena cava) (P < or = 0.0005) and a significant increase in peptidase-derived met-enkephalin levels (determined after trypsin/carboxypeptidase B digestion of plasma samples) (P < or = 0.05). ANIT-treatment also resulted in a 5.6-fold increase in portal vein met-enkephalin levels (P < or = 0.005). Portal vein met-enkephalin levels were only 1.2-fold higher than IVC levels in ANIT-treated rats (P < or = 0.05). Plasma activities of the two main enkephalin degrading enzymes, aminopeptidase and enkephalinase, were similar in control and ANIT-treated rats. Chemical sympathectomy, prior to ANIT treatment, decreased the elevation in inferior vena caval met-enkephalin levels by 35% (P < or = 0.005). Adrenalectomy did not alter ANIT-induced increases in circulating met-enkephalin levels (pNS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetic nerves, but not the adrenal gland, contribute to elevated plasma levels of met-enkephalin in rats with acute cholestatic hepatitis. 821 May 12

In acute liver failure following hepatitis, toxic insults, or after major liver surgery, there is an increased bacterial translocation from the gut. This may explain some of the infectious complications seen in these conditions. To elucidate mechanisms and find possible preventive measures, we investigated the effect of rectal administration of arginine and probiotic bacteria (Lactobacillus spp.) on bacterial translocation and the extent of liver failure. Sprague-Dawley rats were used and five different Lactobacillus strains (Lb. reuteri R2LC, Lb. rhamnosus DSM 6594 (= strain 271), Lb. plantarum DSM 9843 (= strain 299v), Lb. fermentum 8704:3 (= strain 245), and Lb. reuteri (= strain 108) were administered rectally once daily for 8 days with and without 2% arginine. Acute liver injury (ALI) was induced on the eighth day by intraperitoneal injection of D-galactosamine (1.1 g/kg body weight), and samples were collected after 24 and 48 hours. Bacterial translocation was evaluated by bacterial culture from portal and arterial blood, mesenteric lymph nodes, and liver tissue. Liver enzymes and bilirubin were evaluated in the serum. The bacterial load in the cecum and colon was determined and the liver histopathological changes were studied. There was no mortality at any time. The liver enzymes and bilirubin decreased in some of the groups supplemented with lactobacilli with and without arginine compared with the ALI control group. The incidence of bacterial translocation and the number of the translocated bacteria decreased significantly in some of the supplemented groups. Lb. plantarum + arginine administration significantly reduced the level of the released liver enzymes, hepatocellular necrosis and inflammatory cell infiltration, bacterial translocation, and the number of Enterobacteriaceae in the cecum and colon. Rectal administration of different Lactobacillus strains with and without arginine in an ALI model significantly modulates the extent of the liver failure and reduces bacterial translocation. Lb. plantarum DSM 9843 (= strain 299v) with or without arginine seemed superior to the other Lactobacillus strains. The beneficial effect of arginine administration alone indicates a possible role of nitric oxide and polyamines in this process, and the lactobacilli may execute their action via the same mechanisms or via bacterial antagonism and/or enhancement of systemic and intestinal mucosal immunity.
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PMID:Effect of Lactobacillus supplementation with and without arginine on liver damage and bacterial translocation in an acute liver injury model in the rat. 904 12

Extraintestinal manifestations and metabolic complications are very frequent in patients with idiopathic inflammations of the gut and are encountered in at least 35% of these patients. In Crohn's disease extraintestinal manifestations are more frequent than in ulcerative colitis, in particular when the large bowel is affected. Metabolic complications are the result of inflammatory changes of the small intestine or develop as a result of the reduced reabsorption surface of the gut. As to the relationship to the activity of the idiopathic inflammation of the gut, extraintestinal manifestations can be differentiated into those which depend on the activity of the basic disease and those which lack this dependence. From the aspect of a long-term prognosis extraintestinal manifestation independent on the activity of the inflammation of the gut are much more serious, because as a rule they have a long-term and usually progressive trend. The most serious extraintestinal complication is primary sclerotizing cholangitis which in the majority of patients leads to destruction of the biliary pathways and the development of biliary cirrhosis. Depending on the predominantly affected site of the biliary system, primary sclerotizing cholangitis is divided into three types. It is encountered much more frequently in ulcerative colitis than in Crohn's disease. Treatment of primary sclerotizing cholangitis is not very effective. At present it appears that the only drug with an effect on the course of the disease is long-term administration of urodesoxycholic acid. For patients with manifestations of hepatic insufficiency the only solution is transplantation of the liver. In all patients where the diagnosis of primary sclerotizing cholangitis was established, at the same time the possibility of inclusion in a transplantation programme should be considered. The relationship between sclerotizing cholangitis and pericholangitis has not been resolved conclusively. At present the majority of authors is inclined to believe that pericholangitis is part of changes associated with sclerotizing cholangitis. Other hepatobiliary complications of idiopathic inflammations of the gut such as cholelithiasis and parenchymatous liver damage, steatosis of the liver and chronic autoimmune hepatitis are not such a serious problem as sclerotizing cholangitis.
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PMID:[Hepatobiliary complications of idiopathic intestinal inflammations]. 922 Nov 79

The largest lymphoid organ in the body is the gut and the gut-associated lymphoid tissue. The mucosal immune system faces many challenges in protecting the body from microbial invasion. Its chief function is to maintain a diverse population of mature lymphocytes capable of responding to foreign antigens. This task is accomplished with a variety of unique features that distinguish the mucosal from the systemic immune system. In addition, the mucosal immune system plays a role in inflammatory bowel disease, Whipple disease, autoimmune gastritis, Helicobacter pylori infection, immunoproliferative small intestinal disease, hepatitis A, B, C, D, E, F, and G, autoimmune hepatitis, primary biliary cirrhosis, progressive sclerosing cholangitis, and vanishing bile duct syndrome.
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PMID:Immunopathogenesis of gastrointestinal and hepatobiliary diseases. 939 57

This case demonstrates that excluded gut may be a reservoir for bacterial translocation and recurrent sepsis. Translocation may contribute to cholestatic hepatitis, and restoration of bowel continuity is fundamental to reversing these pathologic changes. It also emphasizes that parenteral nutrition even when used as interim supportive treatment is not without serious hazard.
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PMID:Potential hazards of excluded bowel and use of parenteral nutrition: a case report. 959 13

It is well known that females show a greater susceptibility to alcohol-induced liver injury than males. Additionally, females who consume alcohol regularly and have been obese for 10 years or more are at greater risk for both hepatitis and cirrhosis. Female rats on an enteral alcohol protocol exhibit injury more quickly than males, with widespread fatty changes over a larger portion of the liver lobule. Levels of plasma endotoxin, intercellular adhesion molecule-1, free radical adducts, infiltrating neutrophils, and nuclear factor-kappaB are increased about twofold more in livers from female than male rats after enteral alcohol treatment. Estrogen treatment in vivo increases the sensitivity of Kupffer cells to endotoxin. Evidence has been presented that Kupffer cells are pivotal in the development of alcohol-induced liver injury. Destruction of Kupffer cells with gadolinium chloride (GdCl3) or reduction of bacterial endotoxin by sterilization of the gut with antibiotics blocks early inflammation due to alcohol. Similar results have been obtained with anti-tumor necrosis factor-alpha antibody. These findings led to the hypothesis that alcohol-induced liver injury involves increases in circulating endotoxin, leading to activation of Kupffer cells, which causes a hypoxia-reoxygenation injury. This idea has been tested using pimonidazole, a nitroimidazole marker, to quantitate hypoxia in downstream pericentral regions of the liver lobule. After chronic enteral alcohol, pimonidazole binding increases twofold. Enteral alcohol also increases free radicals detected with electron spin resonance. Importantly, hepatic hypoxia and radical production detected in bile are decreased by destruction of Kupffer cells with GdCl3. These data are consistent with the hypothesis that Kupffer cells participate in important gender differences in liver injury caused by alcohol.
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PMID:II. Alcoholic liver injury involves activation of Kupffer cells by endotoxin. 975 87

Reactive biliary hepatitis is a defined morphological entity, which is a result of chronic diseases of the gall bladder, biliary ducts or pancreas. The aim of the present study was to describe the morphology of reactive biliary hepatitis and its significance for progression of liver fibrosis, and in particular Ito cell (fat storing cell) transformation and occurrence of collagen type III and IV in the liver. Liver tissue from 19 patients with reactive biliary hepatitis was investigated light microscopically and immunohistochemically. Histologically, the liver showed features of mild to severe portal and lobular inflammation. The number of Ito cells increased periportally and pericentrally. Deposition of collagen type III and IV was increased in portal tracts, septa and perisinusoidal spaces, mainly in periportal zones of the lobules. Ultrastructurally, collagen type III immunoreactive fibrillar networks were found to be increased in the space of Disse around transitional cells. Collagen type IV immunoreactive deposits were detected around newly proliferating bile ducts in portal stroma and in the space of Disse. Ito cells were mainly transformed into transitional and myofibroblast-like cells. We discuss here the role of Ito cells and certain cytokines in the process of fibrosis of the liver in the course of reactive biliary hepatitis. It is proposed that bile acid retention in bile ducts during non-specific reactive inflammation or a gut endotoxin may cause transformation of Ito cells and increased collagen type III and IV in this type of hepatitis.
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PMID:Immunohistochemical detection of collagen type III and IV in relation with transformation of Ito cells in liver sinusoids of patients with reactive biliary hepatitis. 1033 64

Biliary glycoproteins are members of the carcinoembryonic antigen (CEA) family and behave as cell adhesion molecules. The mouse genome contains two very similar Bgp genes, Bgp1 and Bgp2, whereas the human and rat genomes contain only one BGP gene. A Bgp2 isoform was previously identified as an alternative receptor for the mouse coronavirus mouse hepatitis virus. This isoform consists of two extracellular immunoglobulin domains, a transmembrane domain and a cytoplasmic tail of five amino acids. In this report, we have examined whether the Bgp2 gene can express other isoforms in different mouse tissues. We found only one other isoform, which has a long cytoplasmic tail of 73 amino acids. The long cytodomain of the Bgp2 protein is highly similar to that of the Bgp1/4L isoform. The Bgp2 protein is expressed in low amounts in kidney and in a rectal carcinoma cell line. Antibodies specific to Bgp2 detected a 42-kDa protein, which is expressed at the cell surface of these samples. Bgp2 was found by immunocytochemistry in smooth muscle layers of the kidney, the uterus, in gut mononuclear cells and in the crypt epithelia of intestinal tissues. Transfection studies showed that, in contrast with Bgp1, the Bgp2 glycoprotein was not directly involved in intercellular adhesion. However, this protein is found in the proliferative compartment of the intestinal crypts and in cells involved in immune recognition. This suggests that the Bgp2 protein represents a distinctive member of the CEA family; its unusual expression patterns in mouse tissues and the unique functions it may be fulfilling may provide novel clues about the multiple functions mediated by a common BGP protein in humans and rats.
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PMID:Comparison of expression patterns and cell adhesion properties of the mouse biliary glycoproteins Bbgp1 and Bbgp2. 1049 Nov 1

High-resolution real-time ultrasonography (US) serves as an important tool for differentiation of obstructive and nonobstructive causes of jaundice in infants and children, independent of liver function. Unconjugated hyperbilirubinemia occurs in approximately 60% of normal term infants and in 80% of preterm infants. Persistence of neonatal jaundice beyond 2 weeks of age demands US evaluation to differentiate between the three most common causes: hepatitis, biliary atresia, and choledochal cyst. In all three conditions, the hepatic echotexture is diffusely coarse and hyperechoic, but this appearance may be seen in a variety of hepatic inflammatory, obstructive, and metabolic processes. Thus, hepatic scintigraphy and at times percutaneous liver biopsy are necessary to narrow the differential diagnosis and to identify patients who require more invasive techniques (eg, intraoperative cholangiography). US is useful for demonstrating inspissated bile and biliary duct stones. In infants, stones are usually secondary to obstructive congenital anomalies of the biliary tract, total parenteral nutrition, furosemide treatment, phototherapy, dehydration, infection, hemolytic anemia, and short-gut syndrome, whereas in older children, stones are usually associated with sickle cell disease, bowel resection, hemolytic anemia, and choledochal cyst. Jaundice in infants and children may also be due to cirrhosis, benign strictures, and neoplastic processes.
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PMID:US approach to jaundice in infants and children. 1068 80


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