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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interpretation of the morphological features of alcoholic hepatitis is discussed in terms of a comparison with the results of an ultrastructural and histoenzymological study of the liver biopsies of nine patients. In these patients liver biopsies were performed in the initial stage of the illness and fifteen days after five were re-biopsied, when the clinical and biological signs were improved. The correlations between morphological and biological data were good, especially for the levels of serological and histoenzymological alkaline phosphatase and gamma-glutamyltranspeptidase evaluations. However, when histological appearances had returned to normal, after two weeks of abstinence from alcohol several histological and ultrastructural features of the initial hepatitis persisted. The presence of evolving cirrhosis was a contributing factor to the severity of the changes seen. Morphologically, apart from the changes due to chronic alcoholic intoxication (steatosis, mitochondrial alteration), the hepatitic lesions comprise Mallory's bodies, cytoplasmic oedema and mitochondrial swelling. Cholestasis was invariably present. Histo-enzymologically there was a reduction in ATPase activity suggesting a metabolic failure in the energy producing pathways. In addition, in the periphery of lobules an active cirrhotic process was present, with tubular de-differentiation of hepatocytes and an increase in gamma-glutamyltranspeptidase on the cytoplasmic membrane. Because of the absence of any topographical relationship between hepatitis and cirrhosis, the presence of lymphocytes in the neighbourhood of the ductules suggested an indirect relationship between both processes, perhaps an autoimmune response initiated by Mallory's bodies.
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PMID:[The hepatocyte in acute alcoholic hepatitis. Histoenzymological and ultrastructural analysis (author's transl)]. 3 Oct 27

The incidence and phenotype of preneoplastic and neoplastic liver lesions appearing in LEC rats after recovery from severe hereditary hepatitis were studied in comparison with the liver lesions appearing in chemical liver carcinogenesis. The livers of 168 rats (90 male, 78 female) were stained for seven histochemical markers at different time periods from the 20th week to the 122nd week of life. Glucose-6-phosphatase (G6Pase), adenosine triphosphatase (ATPase) and non-specific esterase (ES) were used as negative markers. Gamma-glutamyltransferase (GGT), glutathione S-transferase placental form (GSTP), esterase isozyme L-1 (L1) and alpha-fetoprotein (AFP) were used as positive markers. The study on the incidence of liver lesions in the LEC rats revealed sequential development of liver foci, nodules and hepatocellular carcinomas (HCCs) similar to those seen in chemically induced liver carcinogenesis. These lesions appeared earlier and more frequently in male LEC rats than in female ones, suggesting the importance of hormonal environment in spontaneous HCC development. The histochemical analysis of spontaneous liver lesions in LEC rats showed that GSTP was the most reliable positive marker as previously reported in chemical liver carcinogenesis. There was no essential difference in the expression of the markers in spontaneous and chemically induced liver lesions except for L1, which is considered to be related to xenobiotic metabolism. The results of this study suggest that both spontaneous and chemically induced liver cancer may develop by passing through phenotypically similar preneoplastic processes. In addition, the LEC rat uniquely showed chronic liver damage (hepatocyte death and regeneration) at the promotion stage of carcinogenesis. Such a natural history of HCC development in LEC rats is similar to that of human HCC which is frequently associated with chronic liver damage. Thus, the LEC rat provides a useful model for studying the process and underlying mechanisms of human liver cancer development.
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PMID:Phenotype of preneoplastic and neoplastic liver lesions during spontaneous liver carcinogenesis of LEC rats. 169 69

Chronic infection of woodchucks with woodchuck hepatitis virus (WHV) was associated with the development of hepatitis, foci of altered hepatocytes and hepatocellular adenomas and carcinomas. The cytomorphological and cytochemical analysis permitted the identification of three different types of focal lesions; namely, glycogen-storage foci, mixed-cell foci and intermediate-cell foci, each showing a characteristic pattern. The cells of the glycogen-storage foci had clear to acidophilic cytoplasm, and were overloaded with glycogen. They showed a marked elevation in the activity of glucose-6-phosphate dehydrogenase (G6PDH) and malate dehydrogenase (MDH), increased activity of succinate dehydrogenase (SDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and glycerol-3-phosphate dehydrogenase (G3PDH), reduction in the activity of glycogen phosphorylase (PHO), glucose-6-phosphatase (G6Pase), adenosine triphosphatase (ATPase) and adenyl cyclase (ADC), and unchanged activity of glycogen synthase (SYN) and gamma-glutamyl transferase (GGT). The mixed-cell foci mainly consisted of basophilic cells poor in glycogen, but were intermingled with cells containing glycogen. These foci were characterized by a marked decrease in activity of PHO, SYN, G6Pase, G6PDH, ATPase and ADC, and increased activity of GGT, SDH, MDH and GAPDH. The intermediate-cell foci consisted of cells with both basophilic and glycogenotic cytoplasmic compartments, and showed a similar enzyme histochemical profile to the mixed-cell foci, with slight differences in the degree of elevation or reduction of some enzymes. The phenotypic similarities and the close spatial relationship between the foci of altered hepatocytes, and the hepatocellular adenomas and carcinomas in WHV-infected woodchucks, suggest that these lesions are preneoplastic. The focal morphological and metabolic aberrations emerging during hepatocarcinogenesis in WHV-infected woodchuck, are in principle similar to those identified in the course of chemical hepatocarcinogenesis in various species. The focal metabolic aberrations apparently represent a general biological response of the liver parenchyma to oncogenic agents and are closely linked to neoplastic transformation of the hepatocytes.
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PMID:Phenotypic patterns of preneoplastic and neoplastic hepatic lesions in woodchucks infected with woodchuck hepatitis virus. 215 41

A decrease in sodium, potassium and anion (HCO3)-activated erythrocyte ATPases is noted in patients with acute viral hepatitides A and B, chronic persisting hepatitis, liver cirrhosis, chronic cholecystitis and in HBs-antigen carriers, the reduction of HCO8-ATPase being more noticeable. A degree of expression of the above changes depends on the severity of a pathological process in the liver. The most serious changes are noted in liver cirrhosis. In this disease calcium ATPase activity is also on a decrease. Erythrocyte ATPase activity is lowered in chronic cholecystitis to a lesser degree. In patients with chronic persisting hepatitis and liver cirrhosis erythrocyte ATPase activity slightly increases, however it remains significantly lowered as compared to the control level. The determination of erythrocyte ATPase activity can be used for assessment of the status of patients with acute and chronic liver diseases.
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PMID:[Comparative characteristics of adenosine triphosphatase activity in the erythrocytes of patients with acute and chronic liver diseases, chronic cholecystitis and in HBs antigen carriers]. 295 84

Serum samples from 94 patients with primary biliary cirrhosis (PBC) and 17 patients with chronic cholestatic hepatitis (CCH) were tested in the fluorometric immunoassay (FIAX) against the nonorgan-specific ATPase-associated antigen (M2) and against submitochondrial from beef heart and rat liver, to evaluate the specificity and sensitivity of the M2 antigen for the diagnosis of PBC. As controls serum samples from 42 patients with other antimitochondrial antibody (AMA) specificity (against M1, M3, M5, and M6) as well as samples from 417 patients with various other hepatic and non-hepatic disorders were used. Serum samples from 91 of the 94 PBC patients (97%) and all 17 with CCH reacted with the M2 antigen. However, when SMP from rat liver and beef heart were tested in parallel in the FIAX, AMA could be detected in all PBC serum samples. None of the 42 patients with different types of AMA had reactions with the M2 antigen but all had reactions with SMP from rat-liver or beef-heart mitochondria or both. Among the other 417 patients with hepatic and non-hepatic disorders only 4(1%), all with collagen diseases, had anti-M2 antibodies.
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PMID:ATPase-associated antigen (M2): marker antigen for serological diagnosis of primary biliary cirrhosis. 618 86

In patients with pancreatic head cancer and virus hepatitis the lowest values of alpha glycerophosphate dehydrogenase and adenosine triphosphatase in the peripheric blood lymphocytes were determined. The dynamic study of these values in patients with pathology of liver and biliary ducts permits to estimate the disease severity course and equally with other clinico-laboratory data may have prognostic significance.
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PMID:[The cytochemical determination of alpha-glycerophosphate dehydrogenase and adenosine triphosphatase in the peripheral blood lymphocytes of patients with hepatobiliary system pathology]. 760 37

The potential effects of cytokines on hepatocellular transport functions remain undefined. Interleukin-6 (IL-6) is a cytokine that is produced in sepsis, hepatitis, and other inflammatory conditions often associated with cholestasis. Using cultured rat hepatocytes, we have investigated the effects of IL-6 on hepatocellular bile salt uptake. Because hepatocyte Na(+)-K(+)-adenosinetriphosphatase (ATPase) produces the electrochemical gradient that drives sodium-dependent bile salt contransport, we also examined the effects of IL-6 on Na(+)-K(+)-ATPase activity. Hepatocytes cultured for 20 h in media containing IL-6 exhibited a dose-dependent noncompetitive inhibition of [3H]taurocholate uptake, which was maximal at an IL-6 dose of 100 U/ml. IL-6 treatment had no effect on hepatocyte sodium-independent taurocholate uptake. Northern blotting of RNA from cultured hepatocytes revealed that IL-6 had no effect on steady-state RNA levels of the Na(+)-taurocholate transporter (Ntcp). Hepatocytes incubated with IL-6 for 20 h, however, exhibited a 55% decrease in hepatocyte Na(+)-K(+)-ATPase activity. This effect also was dose dependent, with maximal inhibition occurring at an IL-6 dose of 100 U/ml. Similar treatment with IL-6 did not influence hepatocyte Mg(2+)-ATPase activity. The inhibition of Na(+)-K(+)-ATPase activity induced by IL-6 provides a putative mechanism for the observed inhibition of sodium-dependent taurocholate uptake. Since modulation of bile salt transport and Na(+)-K(+)-ATPase activity occurred at IL-6 concentrations comparable to the serum levels observed in patients with severe inflammatory states, these findings have potential pathophysiological relevance for the cholestasis of sepsis and other inflammatory disorders.
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PMID:Interleukin-6 inhibits hepatocyte taurocholate uptake and sodium-potassium-adenosinetriphosphatase activity. 781 Jun 56

LEC rats develop an autosomal recessive hepatitis and subsequently liver cancer associated with copper accumulation in the liver similar to that of Wilson's disease. Using 71 backcross [(WKAH x LEC) x LEC] rats, linkage analysis of the hepatitis with the WD gene for Wilson's disease revealed identical segregation and no recombination event between these two genes. This result indicates that the WD gene is a prime candidate for the hts gene responsible for the hepatitis of LEC rats, and suggests that the hepatitis of LEC rats may be caused by a defect in a copper-transporting ATPase expressed in the liver.
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PMID:The WD gene for Wilson's disease links to the hepatitis of LEC rats. 792 21

The effect of feeding mycotoxins, i.e. aflatoxin B1 (1.25 ppm from 3 to 38 days of age) and ochratoxin A (0.5 ppm from 3 to 38 days of age) along with inclusion body hepatitis virus (IBHV) inoculation (at 10 days of age) singly and in combination was studied in broiler chicks. Birds in combined treatment groups, i.e. aflatoxin fed and virus inoculated and ochratoxin fed and virus inoculated, showed more changes in activities of phosphatases (AKPase, ATPase, G-6-Pase and ACPase) in liver and kidney tissues than their respective individual treatment groups with a few exceptions. Reduction in the activities of oxido-reductases in liver and kidney tissues were almost comparable in different treatment groups. The increase in muco-polysaccharides reaction was more marked in both the combined treatment groups than the single treatment groups. Intensity of lipid reaction was more in ochratoxin virus combination group than either alone.
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PMID:Histochemical/histoenzymic studies in broiler chicks fed aflatoxin, ochratoxin and inoculated with inclusion body hepatitis virus singly and in concurrence. 802 44

Activation of lipid peroxidation (LPP) processes in the hepatocytes of animals suffering from toxic hepatitis leads to disorders of membrane function and causes disorders of transports processes (activity of adenosine triphosphatase, active sodium transport) in them. Administration of prostaglandin E2 (PGE2) as a potent antioxidant simultaneously with casein hydrolysate to animals with experimental pathology intensifies the effect of the nitrous preparation and promotes normalization of the studied processes (LPP, adenosine triphosphatase activity, active sodium transport). Thus, through its action on LPP and the transport systems, PGE2 influences the effect of casein hydrolysate.
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PMID:[Biochemical mechanisms of the effect of prostaglandin E2 on the effect of parenteral nitrogenous nutrition]. 818 94


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