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    Lesioni litiche costali e neoformazioni epatiche multiple in un caso di pseudotumore infiammatorio

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    Inflammatory pseudotumor is a rare disease, that is regarded as a benign reactive inflammatory process, although its etiology and pathogenesis are still unknown. The liver is one of the organs most frequently involved, but inflammatory pseudotumors have been reported in many other sites in the body. Inflammatory pseudotumor of the liver presents as a solitary or, less frequently, multiple space-occupying lesion, which the common imaging techniques do not clearly distinguish from primitive or metastatic hepatic malignancies. Biopsy of the lesion is therefore necessary for diagnosis. The case of inflammatory pseudotumor described here presented with radiologic features of multiple solid space-occupying lesions in the liver, associated with multiple osteolytic lesions in the ribs. Such an association, very suggestive of malignancy, has not yet been reported for inflammatory pseudotumors. Optimum management of this disease has not yet been standardized. The majority of patients are treated by hepatic resection, although spontaneous regression has also been described. In our case, rapid improvement of both hepatic and costal lesions was observed, although the patient did not receive any specific treatment

    Effects on fibrogenesis markers of rheumatoid arthritis therapy with methotrexate

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    Objective: To evaluate the level of 2 serum markers of hepatic fibrogenesis, aminoterminal peptide of type III procollagen (NPIIIP) and laminin P1 fragment (Lam), in patients with rheumatoid arthritis at baseline and after one year of low dose methotrexate (MTX) therapy. Methods: Serum levels of NPIIIP and Lam were measured in 20 patients, 17 women and 3 men, mean age 48.83 +- 9.25 yrs before and after MTX treatment and compared to levels from 20 sex and age matched, healthy controls. Results: The baseline values of NPIIIP was higher in patients than in controls; it normalized after MTX treatment. The Lam level did not differ between patients and controls; moreover, it did not change after treatment. Conclusion: Low dose MTX therapy does not increase serum indicator levels of hepatic fibrogenesis

    Serum laminin P1 in chronic viral hepatitis: Correlations with liver histological activity and diagnostic value

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    Laminin is a major basement membrane-associated, non-collagenous glycoprotein of the extracellular matrix and is deposited in the space of Disse during sinusoidal capillarisation. Laminin P1, a pepsin-resistant fragment originating from the central portion of the cross-shaped laminin molecule, is detectable in serum and has been related to liver fibrosis and portal hypertension. In this study we investigated the behaviour of serum laminin P1, measured by radioimmunoassay, in a homogeneous group of 95 patients suffering from chronic viral hepatitis, types C or B, in order to determine the relationships between serum laminin P1 and each of the main histological aspects of the disease process (i.e. portal-periportal activity, lobular activity and fibrosis), which were assigned numerical scores. Moreover, we computed, at several cut-off levels, the sensitivity, specificity and positive and negative predictive values of laminin P1 in detecting both necroinflammatory activity and fibrosis in the liver. The results show that serum laminin P1 levels parallel the severity of liver disease, the highest laminin concentrations being observed in cirrhotic patients. They suggest also that serum laminin P1 should be considered a marker of the liver disease process as a whole, rather than a marker exclusively linked to fibrosis. Nevertheless, the usefulness of serum laminin P1 measurement, as investigated in this study, seems too limited to be recommended for routine clinical practice

    Decreased activity of liver glutathione peroxidase in human hepatocellular carcinoma

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    Glutathione peroxidase (GSH-Px) activity, one of the scavenger enzymes of oxygen active radicals, has been measured in hepatocellular carcinoma (HCC) of 17 patients and the values compared with the activity of adjacent tumor-free tissue and with those of 30 histologically normal livers. The results demonstrate a reduced GSH-Px activity in neoplastic tissue (21.19 vs 33.74 U/g prot.; P less than 0.001). However, the adjacent tumor-free liver also had a reduced activity when compared with normal tissue (23.15 vs 33.74 U/g prot.; P less than 0.01), but this value did not differ from that of HCC tissue. These data suggest that HCC might develop in a GSH-Px-deficient condition

    Role of iron load on fibrogenesis in chronic hepatitis C

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    BACKGROUND/AIMS: In chronic viral hepatitis, an enhanced iron load is related to lower response to interferon. Furthermore, iron, through the production of oxygen radicals, may stimulate hepatocyte necrosis and the activation of cells responsible for synthesis and deposition of extracellular matrix. We investigated the relationship between iron load, evaluated by serum assays, and liver fibrogenesis in chronic active viral hepatitis. METHODOLOGY: Serum iron, ferritin, transferrin saturation and serum markers of hepatic fibrogenesis (Laminin and the amino-terminal peptide of procollagen III-NPIIIP-) were assayed in 102 patients (47 females, 55 males, mean age 42.48 years) affected by chronic hepatitis C virus and in 81 healthy controls (47 males, 34 females). In hepatitis C virus patients (studied before alpha-interferon treatment) a semiquantitative score for portal inflammation, necrosis and fibrosis was applied to liver biopsy. RESULTS: Serum indices of iron load were higher in hepatitis C virus patients than in controls, and were higher in cirrhotic than in chronic hepatitis cases. Ferritin and serum iron were positively correlated with NPIIIP and laminin; moreover cases with ferritin levels over the normal limit for sex and age had higher levels of NPIIIP and laminin than cases with normal or poor iron status. CONCLUSIONS: Our data suggest that even a mild increase of iron load stimulates hepatic fibrogenesis, probably adding oxygen free radical injury to the damage of viral infection
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