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)

In order to assess the specificity of transferrin molecular changes, we compared concentrations of subfractions and total transferrin in cirrhotic patients, in patients having non-alcoholic hepatitis, in patients with liver cancer, and in controls. The study was carried out in 79 patients divided into four groups: 20 patients with biopsy-proven cirrhosis of alcoholic origin, 20 patients with non-alcoholic hepatitis, 19 patients with liver cancer and 20 controls. Subfractions of serum transferrin were separated by isoelectric focusing followed by direct immunofixation. Fractions pI 5.7 percentages (expressed as percentages of one fraction over total transferrin) were significantly higher in the cirrhotic group than in the control group (p less than 0.01). Fraction pI 5.9 percentages were significantly higher in the cirrhotic group than in the hepatitis or control groups (p less than 0.05), or liver cancer group (p less than 0.01). A quantitative increase of fraction pI 5.7 was found in the cirrhotic patients. However, in this study, this parameter did not discriminate between patients with parenchymal liver diseases of alcoholic or other origin. Therefore, the value of determining fraction pI 5.7 as a marker of chronic alcohol consumption seems questionable. The elevation of fraction pI 5.9 constantly found in the cirrhotic patients could not be explained and needs further investigations.
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PMID:A study of the microheterogeneity of transferrin in cirrhotic patients. 405 85

Plasma derivatives can be separated into those with either a low or a high risk of transmitting viral hepatitis. Low-risk products, with few exceptions, will remain low-risk irrespective of the plasma from which they are manufactured because they are heated at 60 degrees C for 10 hours (Albumin, Plasma Protein Fraction) or because they contain protective antibodies (Immune Globulin). This would appear to be the case not only for hepatitis B but also for non-A, non-B hepatitis. The risk of hepatitis B associated with plasma derivatives is reduced but not eliminated by HBsAg screening of donors. Further decreasing the risk of hepatitis B associated with AHF or Factor IX lots, as well as newer products like AT-III, alpha-1 antitrypsin, Fibronectin, C-1 Inactivator, and Factor XIII, may be accomplished either by the combination of stabilization and heating or by assuring that these products contain an excess of anti-HBS. For highly-purified products with little residual immunoglobulin it may be necessary to add anti-HBs. The addition of antibodies against non-A, non-B hepatitis agents when they are identified, could prevent transmission of both forms of viral hepatitis by plasma derivatives. Methods to stabilize and heat high-risk plasma derivatives to inactivate hepatitis viruses have the potential to remove both hepatitis B and non-A, non-B hepatitis infectivity.
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PMID:Plasma derivatives and viral hepatitis. 681 45

Serum monoamine oxidase (MAO) was separated electrophoretically into three bands. These bands were termed as Fraction I, II and III in that order from anode to cathode. Elevation of serum MAO activity in Fraction I was observed in patients with organ fibrosis particularly in liver cirrhosis and acromegaly. On the other hand, elevation of MAO activity in Fraction II was observed in patients with massive hepatic necrosis. MAO activities partially purified from aortic vessel and from rat liver mitochondria had electrophoretically in the same position as Fraction I and II respectively. Both of Fraction I and aortic extract were inhibited by aminoacetonitrile but not by pargyline. On the contrary, both of Fraction II and mitochondria were inhibited by pargyline but not by aminoacetonitrile. These findings suggested that the elevation of serum MAO in patients with organ fibrosis correlates with the enhancement of connective tissue metabolism and the increment of serum MAO in fulminant hepatitis correlates with the breakaway of MAO from damaged liver mitochondria.
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PMID:[Monamine oxidase (MAO)]. 760 74

Fractionation of alkaline phosphatase isoenzymes and isoforms by isoelectric focusing is a simple procedure that resolves up to 17 fractions having alkaline phosphatase activity. The fractions are stable at 4 degrees C, and undergo only slight changes during repeated freeze-thaw cycles. Pretreatment with phospholipase-C or sialidase changes the isoelectric focusing patterns of alkaline phosphatase in serum; we recommend they not be used owing to the loss of information. We found that the alkaline phosphatase fractions provide diagnostic information in addition to that given by the common liver-function tests in patients with chronic liver diseases. Primary biliary cirrhosis and primary sclerosing cholangitis showed similar biochemical changes, but they are very different from alcoholic cirrhosis based on the common liver-function tests and the alkaline phosphatase isoform patterns obtained by isoelectric focusing. Analysis of the laboratory data using neural networks has some limited use in distinguishing chronic and chronic-active hepatitis of any cause. We have confirmed the tissue assignments made by Griffiths (Prog Clin Biochem 1989; 8:63-74) for the alkaline phosphatase fractions in liver as obtained by isoelectric focusing: Fractions 1a and 1b show a strong correlation with biliary diseases, and fractions 2, 3, and 4 show consistent increases in patients with primary disorders of hepatocytes; these fractions have good sensitivity for hepatocyte injury, but their specificity is limited. Fraction 10 may be a marker of activated T-lymphocytes; it was abnormal in most of our patients suggesting that it is a sensitive but non-specific test. Analysis of alkaline phosphatase by isoelectric focusing deserves further evaluation, because it may facilitate the diagnosis of certain chronic liver disorders and could be a supplement to the biopsy.
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PMID:Isoforms of alkaline phosphatase determined by isoelectric focusing in patients with chronic liver disorders. 889 23

In contrast to the well known chlorpromazine-induced cholestatic hepatitis, we report the case of a schizophrenic patient who presents a cytolytic hepatitis, without any prior hepatic disease. Mr G. was first hospitalized for depressive symptomatology. A pseudo-nevrotic schizophrenia was diagnosed. Pretherapeutic clinical and biological data were normal. A treatment with chlorpromazine 400 mg/day was given. At day 8, the patient was still anxious and began to be agitated. An increase to 500 mg/day of chlorpromazine posology and an addition of haloperidol 200 mg/day was implemented. At day 10, the following clinical symptoms appeared: 38.6 degrees C fever; headache; myalgia; epigastralgia and hypocondrium pain. Biological hepatitis disturbances (ALAT, 984 U/L; ASAT, 414 U/L) and hypereosinophilia with normal white cell count were found. Clinical and biological investigations were normal. Blood-culture, A, B, C hepatitis, HIV and CMV serologies were negative. Neuroleptic treatment was discontinued. Evolution to normality of the disturbances and biological data suggested a cytolytic hepatitis. Mr G... remained treated with flupentixol without side-effects. Phenothiazine-induced cholestatis is frequent, mild, and recovers spontaneously. The biological mechanism is supposed to be immunologic. Prevalence of biological hepatic disturbances is 10 to 20% with chlorpromazine in long-term treatment. More often, symptomatology is the same; jaundice, pruritus, abdominal pain, fever. Although pharmacological data suggest for a cytotoxic activity of phenothiazines, cytolytic hepatitis is poorly described. Maximum range of transaminase blood level reported in previous studies is about 400 U/l. This level is not clearly correlated with hepatic cell lysis. Few cases of hepatic necrosis have been reported. In all cases, preexistent hepatic injuries were observed. Chlorpromazine-induced cytolytic hepatitis is uncommon and cholestatic hepatitis mild. Biological hepatic parameters investigations remain necessary during neuroleptic treatment.
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PMID:[Cytolytic hepatitis during treatment with phenothiazines: apropos of a case]. 903 96