Biomedical subjects
Publications and source records attributed to V Di Marco.
Twenty-three children, aged 3 to 15 years, with chronic delta hepatitis have been followed for 5 to 12 years to evaluate long-term outcome. Although 83% of patients had chronic active hepatitis when first seen, with cirrhosis in 26%, the clinical and biochemical features of the disease remained reasonably stable during observation; liver histologic findings, obtained in 14 patients, worsened in only two.
In this open, pilot study, interferon (IFN) alpha-2b seemed effective in the treatment of hepatitis C virus (HCV) infection in patients with beta-thalassaemia. In seven of nine patients who completed the study alanine aminotransferase activities returned to normal, and a completely stable response 24 months after treatment was seen in five. Liver biopsy specimen showed a clear reduction in portal, periportal, and lobular necroinflammation in all five cases. Three patients stopped treatment early because of side effects.
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Alpha-interferon (IFN) has been used to treat hepatitis B virus carriers with chronic hepatitis Delta virus superinfection. Although the drug inhibits hepatitis Delta virus replication during administration, long-term clearance of the virus has not been obtained in most patients. The effectiveness of alpha-interferon on chronic HDV infection is therefore questionable. No data are available on acute infection. We report the case of a young, immunocompetent HBsAg carrier in whom hepatitis Delta virus superinfection occurred while he was receiving alpha-interferon in order to reduce high level HBV replication, and followed a peculiar course.
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Virus-specific T-cell responses are believed to be involved in the pathogenesis of liver cell injury secondary to hepatitis B virus infection. In this study, liver biopsy specimens from patients with chronic hepatitis B virus infection were analyzed for expression of two major pathways of adhesion used by cytotoxic T cells to interact with target cells. The lymphocyte function-associated antigen 3 was found preferentially expressed on hepatocytes of patients with active hepatitis B virus replication, whereas the expression of the intercellular adhesion molecule 1 on hepatocytes seemed more closely related with inflammatory activity. Adhesion molecules were also highly expressed on T lymphocytes found in areas of piecemeal and spotty necrosis, indicating the presence of antigen-specific "memory" T cells at the site of hepatocellular injury. This study suggests that the expression of the lymphocyte function-associated antigen 3 on hepatocytes may be important for viral elimination. The coordinate expression of the intercellular adhesion molecule 1 may regulate inflammatory response and enhance viral antigen presentation to T cells. Conversely, the absence of hepatocyte adhesion molecules might be a favorable factor for viral persistence.
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Hepatitis B virus deoxyribonucleic acid (HBV-DNA) was studied by Southern blot analysis in liver biopsy specimens from 75 HBsAg-positive patients with chronic liver disease living in southern Italy. Twenty-seven of the patients were hepatitis delta virus (HDV) superinfected. Intrahepatic HBV-DNA was detected in 54 (72%) patients, 32 (59%) of them with replicative forms. The presence of replicative forms was directly related to liver HBcAg and inversely related to liver HDAg, as shown by multivariate analysis. However, 14 patients with intrahepatic HBV-DNA non-replicative pattern and about half of HDV-infected patients were liver HBcAg and/or serum HBV-DNA positive, mostly in low amounts. Histological inflammatory activity was strongly related to liver HBcAg expression regardless of HDV superinfection, as confirmed by multivariate analysis. Our results confirm previous studies about the concordance between intrahepatic HBV-DNA replicative pattern and liver HBcAg expression and about inhibition by HDV of high-level HBV replication. However, they suggest that low-level HBV replication may have an important role in causing liver damage also among HDV-infected patients, in a population where the spreading of HBV and HDV is a naturally occurring event.
To define the prevalence of Hepatitis C Virus (HCV) infection in patients with chronic hepatitis or cirrhosis of any aetiology, we tested a group of 372 consecutive subjects with biopsy-proven chronic liver disease (CLD) for anti-HCV antibodies, excluding active drug-addicts and alcoholics. Our results show that in Southern Italy HCV infection is widespread among subjects with cryptogenic chronic liver disease, as well as in liver diseases with features of autoimmunity (71.7% and 66.7% anti-HCV positive, respectively). Anti-HCV is infrequent among non drug-addicted HBsAg positive subjects (4.7%), and bears no relation to hepatitis D superinfection. Subjects with CLD and a history of parenteral exposure are almost always anti-HCV positive (89.2%). Patients with HBV-related CLD and previous drug-addicts are on the average younger than other disease groups, irrespective of their HCV status. Among subjects whose CLD is related to parenteral exposure, cryptogenic or autoimmune no increase in the rate of anti-HCV positivity seems to bear a parallel relationship to age. No known risk factor for parenteral transmission, other than use of blood or blood products and previous drug-addiction, can be clearly related to HCV infection. No trend to familiar clustering of HCV-induced liver disease is apparent. Liver disease severity, as assessed by transaminase levels and liver histology, does not correlate to anti-HCV status.
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Thirty-five patients with chronic viral hepatitis (B, D or non A, non B), treated with alpha interferon were evaluated by a highly sensitive enzyme immunoassay for the presence of alpha interferon neutralizing antibodies before and after three months of treatment. Although 4 subjects (11.4%) became immunized against alpha interferon, treatment with the drug was successful in inhibiting viral replication in 3 of them. We conclude that the appearance of anti alpha interferon antibodies does not affect the effectiveness of the drug, and is therefore not worth monitoring.
An in vitro study was conducted into the speed of glycolysis is human erythrocytes. Incubation with Buflomedil does not change the speed of glycolysis.
Variations in erythrocyte ATP content were studied after the oral administration of 600 mg Buflomedil a day for seven days in ten vasculopathy patients. In all patients the drug increased erythrocyte ATP.
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Previous workers found that Buflomedil Hydrochloride increases erythrocyte potential energy and consequently improves membrane plasticity. It was therefore decided to check whether the same molecule was capable of exerting an effect in certain congenital or acquired disease conditions affecting the red cell when increased fragility and early haemolysis are certainly in part by changes in the membrane skeleton and thus to reduced deformability. Sickle cell anaemia is one of these diseases. The surprising, lasting and almost total "protective" action of buflomedil hydrochloride observed in the sickling test is reported. Some explanations are suggested for this effect.