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)

Frozen, unfixed sections of human liver biopsies from patients with acute, subchronic, and chronic hepatitis or fibrotic liver disease were studied in indirect immunofluorescence with specific antisera to type I and type III procollagen. In early stages of both hepatitis and fibrotic liver disease, intralobular type III collagen synthesis is increased. Maximum values are reached years after the onset of disease. Intralobular procollagen I content is not increased in the acute stage, but rises only later. An increase of procollagen I seems to herald irreversible liver changes. This approach allows for exact localization and semiquantitative analysis of the synthesis of type I and type III collagen, and adds a new parameter to the diagnostic approaches in liver diseases.
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PMID:The diagnostic application of specific antiprocollagen sera. II. Analysis of liver biopsies. 34 27

Serum type IV collagen fragment (7S collagen domain) was measured in 30 controls and 152 liver disease patients with a radioimmunoassay using a polyclonal antibody to human placenta 7S collagen. The serum concentrations of 7S collagen (mean +/- SD) were 4.2 +/- 0.9 ng/mL in controls, 5.1 +/- 2.0 ng/mL in acute hepatitis, 6.5 +/- 2.5 ng/mL in chronic inactive hepatitis, 9.5 +/- 3.8 ng/mL in chronic active hepatitis, 14.4 +/- 7.5 ng/mL in liver cirrhosis, and 14.4 +/- 6.9 ng/mL in hepatocellular carcinoma. In acute hepatitis, 7S collagen was slightly increased, whereas type III procollagen N-peptide and prolyl hydroxylase were markedly increased. In chronic liver disease, 7S collagen concentrations increased with the severity of the disease, and also reflected the degree of fibrosis. The serum 7S collagen concentrations were significantly correlated with those of type III procollagen N-peptide and prolyl hydroxylase in all subjects. These results suggest that serum 7S collagen concentration is a useful diagnostic aid for determining hepatic collagen metabolism in liver diseases.
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PMID:Clinical significance of serum 7S collagen in various liver diseases. 133 51

As serum markers for hepatitis fibrosis, prolyl hydroxylase (PH), type III procollagen peptide (PIIIP), type IV collagen, mesenchymal metalloproteinase (MMP), tissue inhibitor of metalloproteinase (TIMP) and laminin are reliable for clinical application. PH, PIIIP, MMP, TIMP and LM are regarded as the marker of ongoing hepatic fibrosis. Type IV collagen and LM are indicative for the extent of hepatic fibrosis.
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PMID:[Hepatic fibrosis and its serum markers]. 133 65

The authors examined the aminoterminal type III procollagen peptide level of serums and killer-cell activity peripheric blood lymphocytes with 75 patients suffering from ethanol originated liver diseases as well as control samples from 40 healthy volunteers. Determination of type III procollagen peptide (Fab) took place by the RIA method. The cytotoxic activity of killer-cells was tested against human red blood cells. Both in fatty liver and chronic alcoholic hepatitis the level of type III procollagen peptide increased, while in liver cirrhosis the same level reached a value three times of the normal. At the same time in cirrhosis hepatitis an increased killer-cell activity could be observed. Type III procollagen peptide values were also analysed in view of the cytotoxic capacity of killer-cells. At first ill, then healthy control individuals were divided into three groups according killer-cell activity values. Results have shown that in the group with a high level killer-cell activity average type III procollagen peptide values were significantly greater as compared to those of the medium or low level activity groups. These results might indicate a relation between a conditional antibody-dependent cellular cytotoxicity reaction and increasing collagen synthesis.
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PMID:[Serum aminoterminal type III procollagen peptide level and killer cell activity in patients with alcoholic liver diseases]. 195 78

Serum levels of the aminoterminal propeptide of type III procollagen (PIIINP) and hyaluronan were analysed before and during the acute, recovery and chronic phases of non-A, non-B (NANB) posttransfusion hepatitis (PTH) in 13 patients. All patients were discovered during a prospective study on NANB PTH in patients undergoing open-heart surgery. 7/13 (54%) patients resolved their hepatitis within 6 months after onset, whereas 6/13 (46%) went on to chronic hepatitis. In 5 of these 6 patients a liver biopsy during the chronic phase of the hepatitis showed chronic active hepatitis in 2 and chronic persistent hepatitis in 3. During the acute NANB PTH phase the mean serum PIINP level rose significantly as compared to prehepatitis levels and to levels in a reference group not developing hepatitis. Neither PIIINP levels nor hyaluronan levels, however, could differentiate patients with resolving from patients with nonresolving hepatitis. These markers should, however, be further evaluated as potential markers for development of fibrosis/cirrhosis during chronic hepatitis.
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PMID:Serum levels of the aminoterminal propeptide of type III procollagen and hyaluronan during resolving and nonresolving posttransfusion non-A, non-B hepatitis. 210 89

An assay of serum antigens related to the aminoterminal propeptide of type III procollagen has been suggested for monitoring fibrotic processes in the liver. These antigens were measured here in 61 alcoholics who were divided into four groups on the basis of liver histology: normal light microscopy, fatty liver, alcoholic cirrhosis with hepatitis, and inactive cirrhosis. All the subjects having alcoholic hepatitis with cirrhosis had elevated values in the assay, whereas some of those with either fatty liver or inactive cirrhosis still had normal values. It was, therefore, not possible on the basis of this method alone to distinguish fatty liver from cirrhosis or alcoholic hepatitis, although very high values were suggestive of alcoholic hepatitis. In a follow-up study, the aminopropeptide value decreased slowly during recovery from alcoholic hepatitis and increased rapidly after a new drinking bout. The antigens detected by the assay are heterogeneous in human serum. The proportions of the three main peptide forms varied during recovery from alcoholic hepatitis, the authentic propeptide being the main one at the acute stage, but almost disappearing later. The usefulness of the assay could probably be improved if distinct assays were available for the different antigen forms.
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PMID:Aminoterminal propeptide of type III procollagen in serum in alcoholic liver disease. 660 26

A brief description of the structure of collagen and the special features of each type of collagen, followed by a summary of its metabolism, serve as an introduction to the major pathological processes involving the collagen molecule; mutations, inflammatory syndrome bone diseases, basement membrane diseases. The measurement of hydroxyproline isomers in urine is the basic biochemical test for diseases involving the collagen molecule. 4-hydroxyproline is increased in bone disease of Paget and in cancerous metastases of bone, 3-hydroxyproline is increased in case of polycystic kidney. It is possible, but not very useful, to measure serum 4-hydroxyproline. Of more interest, is the radio-immunological measurement of the N-terminal extension of the type III procollagen molecule, which can differentiate ordinary hepatitis from cirrhogenous hepatitis. New and useful information can be gained from tissue biopsy: the proportion of the various types of collagen, the measurement of their hydroxylation and the activity of the enzymes acting on their biosynthesis.
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PMID:[Techniques for studying collagen in medical practice]. 676 Jul 52

In early hepatic fibrosis, increased amounts of type III collagen are deposited. Persistently high serum concentrations of aminoterminal type III procollagen propeptide (PIIIP) correlate with the activity of the fibrogenic process. Another index for the detection of fibrosis, the PGA index, combines the prothrombin time, gamma-glutamyl transpeptidase activity, and serum apolipoprotein A1 concentration (the latter falls with progressive fibrosis). We compared PIIIP measurements and PGA index in patients with various histological forms of alcoholic liver disease (104), primary biliary cirrhosis (38), and chronic B virus hepatitis (27), and in healthy age-matched controls (30). The ability of each test to identify correctly patients with fibrosis or cirrhosis was assessed with receiver operating curves. The PGA index was much higher in all groups of patients with alcoholic liver disease than in controls (p < 0.0001). PIIIP concentrations were also substantially higher than in controls (p < 0.05 for fatty liver, p < 0.0001 for all other groups), especially in the group with alcoholic hepatitis and cirrhosis. For the detection of cirrhosis the PGA was 91% sensitive and 81% specific and the PIIIP concentration was 94% sensitive and 81% specific. The two tests combined had 85% sensitivity, but 93% specificity. Among patients with primary biliary cirrhosis, both PGA index and PIIIP concentration correlated well with the severity of the disease, determined by the Mayo score (r = 0.72 and 0.66 respectively). The combined tests were 96% sensitive for the detection of fibrosis. All patients with chronic B virus hepatitis had raised PGA and PIIIP values in comparison with controls (p < 0.0001) but there were no differences between subgroups. Substantially raised PIIIP concentrations thus identify the subgroup of alcoholic patients with both hepatitis and cirrhosis. The combination of PGA index and PIIIP concentration may be useful for targeting treatment with antifibrotic drugs and to reduce the need for liver biopsy.
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PMID:Comparison of serum procollagen III peptide concentrations and PGA index for assessment of hepatic fibrosis. 790 68

Twenty-three out of 40 patients affected by chronic HCV hepatitis responded (i.e. aminotransferases returned to normal) after 6-month treatment with 6 MU tiw of recombinant alpha-interferon 2a (IFN); in 11 (Group 1), the remission was maintained for a mean observation time of 33.15 months (range 20-50) after withdrawal of therapy; 12 (Group 2) relapsing after IFN withdrawal, were treated again obtaining in 10 a second response. Seventeen did not respond (Group 3). Serum markers of connective tissue metabolism (laminin and aminoterminal peptide of type III procollagen -NPIIIP-) were assayed in all patients before treatment and every 6th month, to evaluate long-term effects of IFN therapy. In non-responders, NPIIIP after treatment was not different from baseline, while laminin significantly increased at 6 and 12 months; in responders, NPIIIP decreased significantly after therapy, maintaining values lower than baseline on long-term observation. Laminin decreased significantly six months after the end of therapy and remained lower than baseline in all sustained responders. In this group, the drop in laminin was progressive, whereas in Group 2, laminin showed only a slight decrease on long-term control. Our data show that these serum markers persistently decrease in sustained responders to IFN, while in relapsed cases, prolonged therapy is needed to obtain minor effects on laminin; on the contrary, in non-responders, NPIIIP remains unchanged and laminin significantly increases, suggesting a persistence of active fibrogenesis.
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PMID:Long-term variations of serum laminin and procollagen III peptide in chronic HCV hepatitis after alpha-interferon therapy. 874 68

An 81-year-old male patient developed hepatic fibrosis with ascites and esophageal varices 4 years after oral administration of UFT(R) as postoperative adjuvant therapy for lung cancer. Although serum transaminase levels remained normal during follow-up periods, ascites developed 3 years after the treatment, and disappeared rapidly after the cessation of UFT(R), but recurred by accidental readministration of UFT(R). Serum markers for hepatitis viruses, various auto antibodies and a history of alcoholic abuse were all negative. Liver biopsy showed mild to moderate hepatic fibrosis without hepatocellular necrosis. Serum levels of N-terminal propeptide of type III procollagen, 7S fragment of type IV collagen and hyaluronic acid were elevated at diagnosis and decreased after the discontinuation of UFT(R). Esophageal varices were also improved. These findings suggest that hepatic fibrosis can be induced by oral administration of UFT(R) and that serum fibrogenesis/fibrosis markers are useful for early diagnosis of UFT(R)-induced hepatic fibrosis.
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PMID:A case with hepatic fibrosis showing ascites and esophageal varices induced by oral UFT(R) administration. 1181 56


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