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)

A possible mechanism of the protective effect of Triton WR1339 during chronic CC14-hepatitis was considered. Supposing that the improvement of the process was due to the intensification of the lysosome heterophage function the authors studied the intensity of the C14-albumin uptake by the liver and its subcellular distribution in the liver of rats in the administration of the detergent to the animals with chronic CCI4-hepatitis, Preliminary administration of the detergent failed to influence the intensity of C14-albumin uptake; subsequent administration of triton WR1339 to rats with toxic hepatitis decrease the protein uptake which reached the values in intact rats. In chronic hepatitis C14-albumin was concentrated in the lysosome fraction. Administration of trition WR1339 to CCI4-treated animals was not accompanied by any coincidence in the peaks of labeled protein and lysosome enzymes. The selective participation of lysosomes of the Kupffer cells providing a more rapid restoration of the liver in chronic hepatitis is discussed.
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PMID:[Effect of a lysosome triton WR 1339 load on distribution of C14-albumin in the livers of rats with chronic hepatitis]. 95 40

A sensitive radioimmunoassay for cholylglycine, chenodeoxycholylglycine, deoxycholylglycine, and sulfolithocholylglycine was established using antibodies obtained from rabbits injected with albumin conjugates of these bile acids. Glycine-conjugated bile acid levels were measured in sera from 25 control subjects and 110 patients who had hepatic disease (alcoholic cirrhosis, hepatitis, cholestasis, and hepatic malignancy). Sulfolithocholylglycine was elevated in the sera of all 110 patients with hepatic disease. Cholylglucine was within normal range in only three. Chenodeoxycholylglycine was elevated in most sera of patients who had hepatitis, cholestasis, or hepatic malignancy. It was normal in most sera of patients who had alcoholic cirrhosis, suggesting that chenodeoxycholic acid may be subject to further biotransformations in these patients. Deoxycholylglycine was elevated in a minority of patients, none of whom had cholestasis. The data suggest that serum bile acids, particularly sulfolithocholylglycine, are a highly sensitive index for hepatic dysfunction.
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PMID:Levels of immunoreactive glycine-conjugated bile acids in health and hepatobiliary disease. 98 91

Measurement of blood volume is an important clinical tool in establishing a diagnosis as in polycythemia vera, in assessing the true significance of a low blood count in a patient with splenomegaly, and in evaluating a bleeding patient. In theory, blood volume measurements should be of great value in treating acute blood loss, but this is often too time-consuming to be practicable. The main value of blood volume studies so far has been in clinical research where it is essential for correct interpretation of the peripheral blood measurements. Estimates using the hematocrit (packed cell volume) could be misleading since this measurement does not take into account total blood volume and changes in the plasma volume. A variety of isotopes that tag the red blood cell have been used to measure total blood volume and red cell mass. Most commonly used at present is autologous 51-Cr labeled red cells, thus eliminating the risk of hepatitis in transfusion to the subjects. Radio labeled albumin and other plasma proteins were used to measure plasma volume. A large molecular protein is ideal to eliminate overestimation from extravascular diffusion of labeled material for accurate determination of plasma volume. Physiologic changes in the newborn, in pregnant women, during exercise, bed rest, and altitude in the nonpathologic state are discussed. Studies in the normal subject's adaptation in different physiologic conditions have revealed a variety of factors that regulate blood volume.
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PMID:Physiological changes in blood volume. 109 3

Substitutes for whole blood include blood fractions such as plasma, serum albumin and other fluids of various kinds which are not derived from blood but are used as plasma volume expanders; these, include the usual crystaloid intravenous solutions. Since in comparison to blood far more of these later solutions are given intravenously, a thorough knowledge of plasma volume expanders is essential. The first use of such expanders in human patients was by Hogan in 1915. He used colloidal gelatin and noted an improvement in blood pressure in shock. In 1945, Gronwall and Ingelman advocated the use of dextran in shock. The reguirements for an acceptable plasma substitute are: a satisfactory colloidal osmotic pressure, constand composition at reasonable cost, a viscosity suitable for intravenous administration, stability in prolonged storage at variable temperatures, and sterilization by autoclaving. Such substances must be either fully excreted or metabolized, and must cause no early or late tissue damage. They must be non-antigenic and pyrogen free. They must cause no change in the blood such as haemolysis, R.B.C. agglutination, increased sedimentation rate and no impairment of haemostasis. The presently available plasma expanders include blood derivatives (plasma, albumin), modified protein (gelatin, oxypolygelatin), polymerized carbohydrates (dextran) and plastics (polyvinyl pyrrolidone-PVP). All these substances expand plasma volume, decrease haematocrit and plasma proteins, increase sedimentation rate and blood pressure. Dextran, PVP and geletin do not alter hepatic function. Dextran and gelatin have no deleterious effects on renal function. Features of the clinically used plasma expanders are: 1. Fresh Frozen Plasma Fresh frozen plasma contains all clotting factors except platelets. The risk of the transmission of hepatitis is present as it is with whole blood. 2. Plasma Protein Fractions Plasma protein fractions are free of hepatitis virus, but may cause arteriolar dilatation and hypotension. 3. Serum Albumin Serum albumin is a concentrated blood protein fraction. It is salt poor, stable and does not transmit the virus of hepatitis. Since it has a high oncotic pressure it is necessary to give significant quantities of clear fluids with it. It is expensive, scarce, and dilutes the clotting factors. It is, however, a first choice for emergency treatment of shock; 4. Dextran The dextrans may be of medium or low molecular weight. They are inexpensive and readily available, and do not transmit the virus of hepatitis. In large amounts they cause a coagulation defect and may be antigenic. Continued.
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PMID:Blood substitutes. 110 2

Among 211 patients undergoing gastroduodenoscopy five had been carriers of Australia antigen. The same instrument had been used on all, and follow-up examination was carried out two and four months after the gastroscopy. Twelve patients died during the follow-up period of their original disease. Two additional patients became Australia-antigen positive. One of these had liver cirrhosis. In the other, surgery with multiple infusions of albumin had been carried out after gastroscopy and could have been the cause of the Australia-antigen transmission. No proven case of hepatitis transmission occurred in this group of patients.
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PMID:[Is there a risk of transmitting hepatitis by gastroduodenoscopy?]. 111 11

Four patients are described in whom anicteric hepatitis appeared to be related to the use of nitrofurantoin. All the patients had increased serum transaminase levels, hypergammaglobulinaemia, and liver biopsies suggestive of chronic active hepatitis. Three patients showed cirrhotic features in the biopsy and two had circulating albumin-IgG-complexes ('tailing-albumin'). The serum transaminases became normal within weeks after withdrawal of the drug whereas the hypergammaglobulinaemia and the liver biopsy findings persisted essentially unchanged during two to six months of observation. One patient was re-challenged with nitrofurantoin, which resulted in recurrence of elevated serum transaminases after nine weeks medication.
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PMID:Anicteric liver damage during nitrofurantoin medication. 115 46

On routine hospital admission, 23,714 patients received a 28-test serum metabolic profile. The 33 most common diseases (4,132 patients) of liver, pancreas, and gallbladder (LPG) had unique chemical templates averaging 15 significant serum deviations. Each LPG disease differed from all others by elevations of both leucine-aminopeptidase (LAP) and alkaline phosphatase (AP) levels. LAP level was low or normal and serum glutamic oxaloacetic transaminase (SGOT) and AP levels were elevated in 43 non-LPG diseases. Patients with acute and chronic pancreatitis had elevated amylase levels. The four nonmalignant diseases of the gallbladder were associated with normal levels of amylase and lactic dehydrogenase (LDH); except for silent cholelithiasis, each showed elevated total bilirubin (BIL) levels. Patients with solitary or scattered lesions of the liver had normal bilirubin levels (2,115 patients), and those with diffuse interstitial or parencymal disease had elevated BIL levels. Cancer patients had elevated LDH and alpha1 globulin (A1G) levels, but low albumin levels. The importance of comprehensive liver profiles in the treatment of psychoses is emphasized by significant liver damage in a number of these patients. A1G was normal and LDH was elevated in patients having mononucleosis, hepatitis, lupus erythematosus, alcoholism, and alcoholic cirrhosis.
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PMID:Serum chemistry templates of disease in liver, pancreas, and gallbladder. 116 26

The morphological and functional alterations of the smooth endoplasmic reticulum of the liver cell related to biliary stasis have brought attention to drug biotransformation during cholestasis. The metabolism of meprobamate, pentobarbital and tolbutamide was assessed in subjects with intrahepatic recurrent cholestasis (3), cholestatic hepatitis (6), extrahepatic biliary obstruction (7) and normal controls (16). In the patients with recurrent intrahepatic cholestasis no differences in drug metabolism were noted as compared to the control group. In cholestatic hepatitis the plasma half-lives of meprobamate (828 +/- 422 min.) and pentobarbital (39+-65) were significantly longer than in in controls (444 +/- 37 and 25.4 +/- 1.1 respectively). Tolbutamide plasma half-life appeared unchanged. The most striking variations were observed in the patients with extrahepatic biliary obstruction. In such cases while meprobamate half-life was unchanged, pentobarbital half-life was significantly prolonged (31.2 +/- 2.5) and the in vitro metabolism of the drug, using liver preparations, was decreased to less than 50% of the control value. In contrast the metabolism of tolbutamide was accelerated as evidenced by a significant decrease of plasma half-life (165 +/- 48 min. versus 384 +/- 76 of the controls) and an enhanced urinary excretion of the drug's metabolites. However the metabolism of tolbutamide in vitro did not show any difference between normal and cholestatic liver. Whatever the mechanism of the peculiar behaviour of tolbutamide in extrahepatic biliary obstruction it seems to be related to the increased bile dalt concentration during cholestasis. In fact the low values of plasma half-life increase significantly either relieving the biliary obstruction or producing a bile salt depletion with cholestyramine. Preliminary results in vitro suggest the bile salt could displace tolbutamide from albumin binding thus increasing the amount of free drug available for biotransformation by the liver. In conclusion cholestasis may affect drug metabolism depending on the degree of biliary stasis, liver cell injury and the type of drug tested. The mechanism could be that of an impaired biotransformation in the smooth endoplasmic reticulum or could involve extrahepatic factors.
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PMID:Alteration of drug metabolism during cholestasis in man. 120 63

Synthesis rates of albumin and fibrinogen were determined in six patients with acute virus hepatitis and in nine control patients using the 14C carbonate method of McFarlane. Five patients were restudied several weeks after complete recovery. The following results were obtained. (1) The mean albumin and fibrinogen synthesis rates in the control group were 238.8 and 23.5 mg/kg/day, respectively. (2) In two patients with mild courses of hepatitis and in one patient studied during the early phase of a rapid and fatal course the albumin synthesis rate during the acute disease did not differ from controls whereas fibrinogen synthesis rate was slightly increased. (3) Three patients with severe hepatitis showed a definite decrease in albumin and fibrinogen synthesis rates, the lowest value being 76 mg/kg/day for albumin and 6.3 mg/kg/day for fibrinogen. (4) The decrease in plasma protein synthesis correlated neither with serum transaminase or bilirubin levels nor with plasma albumin or fibrinogen concentrations during the acute phase. (5) The two patients with the lowest albumin and fibrinogen synthesis rates also showed a definite decrease of the prothrombin index during the acute phase. Both patients presented very prolonged courses of the disease. (6) In all patients studied twice, plasma protein synthesis rates were normal after recovery.
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PMID:Synthesis rates of albumin and fibrinogen during and after acute hepatitis. 120 13

A collection of 1,985 lots of normal serum albumin (NSA) and 1,361 lots of plasma protein fraction (PPF) prepared between 1958 and 1974 were tested for the presence of hepatitis B surface antigen (HBsAg). Twenty-one percent of NSA lots and 71 per cent of PPF lots were HBsAg-positive by radioimmunoassay. There was considerable variation in frequency of HBsAg-positive lots among the 17 different manufacturers of NSA and the six manufacturers of PPF. In general, those lots prepared from volunteer donor plasma and placental material demonstrated lower rates of HBsAg-positivity than those prepared from commercial donor plasma. A striking decrease in the prevalence of HBsAg-positive lots of both NSA and PPF occurred during the period 1971 to 1973, coincident with the onset of routine screening of all plasma for HBsAg. Although NSA and PPF can be HBsAg-positive, they probably do not transmit type B hepatitis. Serologic tests for HBsAg and antibody to HBsAg revealed that albumin products prepared from infectious, icterogenic plasma were infectious prior to pasteurization, but that they no longer transmitted type B hepatitis after heat treatment at 60 C for ten hours.
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PMID:Hepatitis B virus and hepatitis B surface antigen in human albumin products. 125 15


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