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)

The glycoproteins (GP) of 329 patients with liver diseases and 60 clinically healthy subjects were complexly studied: sialic acid, orozomucoid, haptoglobin, ceruloplasmin, cholinesterase, hexosamine and fucose. Modern laparoscopic, bioscopic, histochemical and histomorphological methods were used in making the diagnosis and determination of the disease phase; The liver diseases are characterized by quantitative and qualitative differences in the character of the GP changes in serum. GP are mostly changed in acute viral hepatitis, cirrhosis, extrahepatic cholestasis and liver tumours, less in chronic aggressive hepatitis and no change in chronic persistent hepatitis and steatosis. The complex GP study is of significance in the characteristic of the activity of the pathological process, in the specification of the liver function as well as for the prognosis of a certain disease.
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PMID:[Complex study of glycoproteins in liver disease]. 710 92

Forty-three women who had viral hepatitis one or more years ago and 35 healthy women who were age and parity matched were given an oral contraceptive containing 0.05mg ethinyl estradiol and 0.5mg levonorgestrel for six consecutive months. Liver function tests (serum bilirubin, SGOT, SGPT and serum alkaline phosphatase) and serum proteins (total, albumin, globulins, ceruloplasmin, haptoglobin and alpha-1 antitrypsin) were measured before beginning treatment and after three and six months of use. Past hepatitis women experienced increased unconjugated bilirubin, SGOT, SGPT and alkaline phosphatase levels throughout the six months while the control women showed less pronounced changes during the first three months with tendency to reversion to normal during the subsequent three months; the group X time of test interactions were significantly different between the two groups. Serum haptoglobin decreased significantly in both groups but the past-hepatitis group showed a more persistent change with time. Changes also occurred in serum albumin, alpha-1 and beta globulins, ceruloplasmin but without group effect or group X time interactions.
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PMID:Effects of oral contraception on liver function tests and serum proteins in women with past viral hepatitis. 712 36

Urinary copper excretion was found to be increased in patients with cholestasis, hepatitis and cirrhosis, but the penicillamine-induced increment was normal. Wilson's disease patients had increased copper excretion before and after penicillamine, especially in untreated cases. Hepatic copper concentrations correlated with urinary copper excretion in cholestasis and treated Wilson's disease, but not in hepatitis or cirrhosis. In treated Wilson's disease, measurement of urinary copper excretion should be valuable in estimating the degree of removal of copper from the body during therapy. Urinary copper clearances were raised in various liver conditions, maximally in untreated Wilson's disease. It is suggested that only part of the serum non-caeruloplasmin copper is available for excretion into urine.
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PMID:Urinary copper excretion and hepatic copper concentrations in liver disease. 721 19

The study was aimed at the assessment of the immune system function of a large group of patients with early phase of acute viral type B hepatitis, who were subsequently follow-up in order to select those developing chronic forms of the infection. It was assumed that re-assessment of their initial immunological status with regard to further evolution of the infection would show some factors predictive of chronic active hepatitis development. Chosen immunological parameters: circulating blood lymphocyte sets and subsets, immunoglobulin concentrations, presence of non-specific immune complexes and concentrations of randomly chosen acute phase proteins (ceruloplasmin, transferrin, haptoglobin, alpha-acid glycoprotein, C3 and C4 complement components) were evaluated in 104 acute viral type B hepatitis patients, aged 18-50, on the days 8, 10, 15, 30, 40, 60, 80 and 130 of the illness. After mean of 744 days, 56 patients reported to final follow-up examination, 15 of whom presented with symptoms of chronic sequelae of acute HBV infection (elimination phase of chronic aggressive hepatitis, chronic persistent hepatitis, or integration phase of HBV infection). Behaviour of cellular immunity parameters, immunoglobulin concentrations, presence of immune complexes or non-specific antibodies, however varied in individual patients, showed no correlation predictive of chronic sequelae of the infection. Significant differences between patients who subsequently developed chronic active or chronic persistent hepatitis were found, however, with regard to all the acute phase proteins tested, most prominent in case of C3 and C4 complement components, haptoglobin, transferrin and ceruloplasmin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Behaviour of chosen acute phase proteins in acute viral type B hepatitis as a predictive factor of further evolution of the infection. 751 Apr 72

Wilson's disease is an hereditary recessive autosomal disorder which affects around five people per million inhabitants. The primary defect is localized in the liver and the disease is manifested by the accumulation of copper in tissues. The diminution of ceruloplasmin, which until a few years ago was mistakenly thought to be the pathogenetic cause of Wilson's disease, is an epiphenomenon of the underlying metabolic defect characterized by defective copper biliary excretion. There are four stages in the natural history of the disease: 1) an asymptomatic stage of hepatic copper accumulation; 2) dismission and redistribution of copper leading to hepatocellular necrosis and hemolysis; 3) extrahepatic accumulation of copper leading to the onset of cirrhosis and neurological damage; 4) stage of homeostasis following treatment but with possible irreversible neurological damage. Treatment of Wilson's disease takes the form of pharmacological, dietary and surgical therapy. Through the formation of copper and protein metal complexes D-penicillamine impoverishes copper deposits causing the reduction or disappearance of hepatic and neurological symptoms; a small percentage of patients treated develops a nephrotic syndrome requiring the compulsory suspension of the drug. In this case a valid alternative is triethylenetetramine dichlorohydrate (TETA) which provokes increased blood copper during copper diuresis. The response to pharmacological treatment is better the earlier treatment is started and the more regular its administration. Dietary intake of copper must be reduced in parallel avoiding foods with a high copper content. Liver transplant obviously leads to the "resolution" of the underlying metabolic problem in patients who develop fulminating hepatitis with hypercupremia and hemolysis and, of course, in cases of uncompensated cirrhosis which do not respond to chelating therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Wilson's disease: physiopathology, therapeutic approach and case report]. 784 48

Zn deficiency is hypothesized to produce poor resistance to injury involving oxidative stress. This could occur by impairing Zn antioxidant function(s) or by indirectly limiting adaptive protective mechanisms such as a rise in acute-phase proteins. The present study examined rats fed diets adequate or moderately low in Zn (4 or 25 micrograms/g diet) for 9 d. The lower intake produced a mild Zn deficiency based on body weight, plasma Zn and plasma alkaline phosphatase (EC 3.1.3.1) activity. Galactosamine injection, an oxidative stress, produced much more liver injury in the mildly Zn-deficient rats. However, injury was strongly inhibited in rats from each dietary group by an acute-phase response due to turpentine-induced leg inflammation. Mild Zn deficiency did not prevent a rise in levels of the acute-phase protein caeruloplasmin (EC 1.16.3.1), but did limit the usual inflammation-induced rise in hepatic levels of metallothionein, a Zn protein with possible antioxidant function. In conclusion, high degrees of galactosamine-induced hepatitis were associated with mild Zn deficiency, but the liver injury was blocked by prior stimulation of an acute-phase response, regardless of Zn status.
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PMID:Effects of mild zinc deficiency, plus or minus an acute-phase response, on galactosamine-induced hepatitis in rats. 798 91

To explain the pathogenesis of excessive copper accumulation in Long-Evans Cinnamon (LEC) rats, regarded as one of the animal models for hepatic-type Wilson's disease, we measured copper contents in liver tissue and bile, serum total copper concentration, and ceruloplamin oxidase activity in LEC rats before and after the onset of spontaneous hepatitis. The copper contents in liver tissue of both 11-wk-old and 18-mo-old LEC rats were about 60 times the amounts in age-matched Wistar and Long-Evans Agouti rats. The biliary copper excretion in 11-wk-old LEC rats was significantly lower than that of the Long-Evans Agouti and Wistar rats that were the same age (27.9 and 41.4%, respectively). In 18-mo-old LEC rats, biliary copper excretion was lower than that in the Long-Evans Agouti rats that were the same age, but the finding was statistically not significant. Serum copper and ceruloplasmin levels were markedly reduced in LEC rats of both ages. These findings suggest that LEC rats have similar defects of biliary copper excretion as observed in patients with Wilson's disease.
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PMID:Impaired hepatic copper homeostasis in Long-Evans Cinnamon rats: reduced biliary excretion of copper. 806 44

The LEC rat is an inbred mutant strain with spontaneous hepatitis isolated from Long-Evans rats. Since approximately 40% of LEC rats die of fulminant hepatitis, the rat serves an animal model for studying the pathogenesis and treatment of human fulminant hepatitis. The remaining 60% of LEC rats survive and develop chronic (prolonged) hepatitis and subsequently develop liver cancer. Therefore, the LEC rat serves an important animal model for studying the significance of chronic hepatitis in the development of human liver cancer, which often develops in association with chronic hepatitis. The LEC rat can also be used as an animal model of Wilson's disease, since recent studies have disclosed high copper accumulation in the liver and low ceruloplasmin concentration in the serum of this mutant rat.
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PMID:The LEC rat: a model for human hepatitis, liver cancer, and much more. 829 9

Copper (Cu) accumulating bound to metallothionein (MT) in the liver of LEC (Long-Evans with cinnamon-like coat color) rats due to a hereditary metabolic disorder is assumed to lead to acute hepatitis with severe jaundice. The metal was shown to be present in the liver in a form not bound to MT at the beginning of hepatitis after first delivery and lactation. Following this change in the distribution of Cu from MT-bound to non-MT bound form in the liver, changes in the concentrations and distributions of Cu, zinc (Zn) and iron in the plasma and kidneys of LEC rats were also observed. Cu plasma distribution on a gel filtration column by HPLC-ICP revealed that the holo-form of ceruloplasmin (Cp) was present before hepatitis and increased with its development, indicating the availability of Cu for Cp by hepatitis. Cu-binding proteins migrating at the same retention times as those of hepatic Cu-MT and Cu,Zn-superoxide dismutase (SOD) were detected in plasma during hepatitis. Albumin was largely present in the form of nonmercaptoalbumin, reflecting that the bloodstream was under oxidative stress. A sudden increase in the concentration of Cu in the kidneys occurred with hepatitis, and the metal came to be distributed more to high molecular weight proteins with its development.
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PMID:Changes in copper distribution in the plasma and kidneys of LEC rats following acute hepatitis. 830 90

Galactosamine model of toxic hepatitis in rats which, as to its morphobiochemical picture, is considered adequate to human hepatitis was used to study the role of disturbances of the functional state of antioxidant and monooxygenase systems as well as humoral area of the systems of immune protection in pathogenesis of the given disease. It is shown that most components of enzymatic and nonenzymatic antioxidant system (superoxide dismutase, catalase, glutathione peroxidase, restored glutathione, phospholipids) are considerably inhibited by the toxin effect. At the same time content of ceruloplasmin is increased in the blood plasma. Considerable disturbances are also observed in the humoral chain of the immune system (content of immunoglobulins and circulating immune complexes varies) and in the processes of microsomal oxidation.
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PMID:[Status of the antioxidant, monooxygenase and humoral immune system of the body in d-galactosamine hepatitis]. 875 5


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