Biomedical subjects

A Cecere

Publications and source records attributed to A Cecere.

7 recordsLinked to original sources

PubMed1997

Eosinophilia triggered by beta-interferon therapy for chronic hepatitis C.

The authors describe a case of eosinophilia occurring in an atopic patient suffering from chronic active hepatitis C following a 2-week course with beta-interferon. Since the most common causes of eosinophilia were ruled out by laboratory and instrumental investigations, the authors suggest a possible role of beta-interferon in triggering eosinophilia, in light of current beliefs about the factors modulating eosinophil growth, differentiation and survival. In particular, it has been supposed that the inhibitory effect of beta-interferon on gamma-interferon production could have triggered a preferential expansion of Th2 type T-helper cells whose particular profile of cytokine secretion has been shown to play a crucial role in the development of eosinophilia. To the authors' knowledge, this is the first report of eosinophilia induced by beta-interferon therapy for chronic hepatitis C.

Chronic Disease↗

PubMed1997

[Hepatitis C and systemic diseases].

In 1989 HCV was demonstrated to be the leading cause of non-A, non-B hepatitis. Not only HCV is able to determine chronic hepatitis in most patients, often leading to hepatocellular carcinoma, but it has also been shown to be strictly associated with a number of immunologically-mediated diseases. This review focuses on the reported associations between HCV and other diseases and the role that HCV might play in their pathogenesis.

Hepacivirus↗

PubMed1997

Serum levels of soluble intercellular adhesion molecule 1 (sICAM-1) as a potential marker of disease activity and remission in patients with chronic hepatitis C.

AIM: To assess whether serum levels of sICAM-1 can be correlated with clinical parameters associated with liver inflammation in chronic hepatitis C patients before and after IFN-alpha treatment and whether in patients who respond to this treatment sICAM-1 levels correlate with relapse or sustained response. METHODS: 34 patients diagnosed with chronic active hepatitis C were administered IFN-alpha at a dose of 9 mU per week for 12 months. In all patients sICAM-1 levels were measured by ELISA before treatment and after 6 and 12 months of therapy. In addition, sICAM-1 levels were measured in all patients who responded to IFN-alpha at 6-month intervals after stopping treatment, for a total 2-year follow-up. RESULTS: In all patients, a significant correlation between sICAM-1 levels and the degree of hepatic involvement at biopsy was observed before starting the treatment. sICAM-1 levels remained elevated throughout the study in all patients who did not respond to IFN-alpha therapy, whereas they showed a significant decrease in all patients exhibiting normal ALT levels following IFN-alpha administration. Moreover, a slow but steady decrease in sICAM-1 serum concentrations to values overlapping those of control subjects was observed in sustained responders after a 2-year follow-up; in contrast, all the patients who relapsed showed a further increase in sICAM-1 levels. CONCLUSIONS: These observations suggest that measurement of sICAM-1 serum levels in chronic hepatitis C patients may be useful for monitoring liver inflammation, especially considering that ALT values may only reflect hepatocellular necrosis while invasive procedures, such as follow-up-liver biopsies, are often not well accepted by patients. Further studies will be necessary to assess whether sICAM-1 levels may be used in helping decide the optimal dose and duration of IFN-alpha treatment.

Adult↗

PubMed1996

Case report of a monoclonal gammopathy in a patient with chronic hepatitis: effects of beta-IFN treatment.

A sixty-one-year-old woman, with cirrhosis, presented with a monoclonal gammopathy of uncertain significance (MGSU). Often in a condition of cirrhosis is present a benign M component hypergammaglobulinemia. The electrophoresis and the immunophoresis showed a dense papraprotein in the gamma-region, an IgG with K light chain, an uncertain Bence-Jones proteinuria, a medullary plasmacytosis (9%), and a following growth of paraprotein were present. Lymphoblastic plasma cell were absent. Treatment with beta-IFN 6 MU for a period of six months and 3 MU for a further period of three months proved ineffective for hepatic disease, but produced a quantitative reduction in gamma-G globulin, the Bence-Jones proteinuria was absent, a reduction in M component and in medullary plasmacytosis. Electrophoresis showed a polyclonal evolution of the gammopathy. Suspension of treatment was followed by de novo rise of monoclonal immunoglobulin. The authors report the use of beta-IFN in the therapy of multiple myeloma.

Antiviral Agents↗

PubMed1996

[Hepatitis C].

HCV carriers are supposed to me 100,000,000 worldwide. 5-15% of subjects are infected via haemotransfusion and another significant amount via intravenous drugs; nevertheless in the major part of subjects the via of transmission remains unclear. HCV causes long-term infectious in the host because of its high frequency of mutations. Mutations origin multiple mutants, called quasi-species, who have distinct immunological features and can so easily escape host immune response. Chronic HCV infection leads to cirrhosis in 5-10 years and to a possible hepatocarcinoma in 15-20 years. Nevertheless, it remains unclear why some patients undergo a slight clinical course, while others experience an aggressive one (exitus in less than 5 years). Alpha-interferon (alpha-IFN) is at date the only drug of proven efficacy in HCV chronic hepatitis, even if HCV eradication is a rare event. The goal to obtain is to standardize doses and duration of the treatment.

Adult↗

PubMed1987

Tissue CEA as prognostic indicator in a series of 44 cases of colorectal cancer.

The role of tissue CEA determination as a complementary test in the staging of colorectal cancer and monitoring of the marker in the follow-up of patients, is stressed. In a group of 44 colorectal cancer patients, tissue CEA was determined by the immunoperoxidase assay in the apical and cytoplasmic portion of tumor cells, stroma, glandular lumen, and cytoplasm of superficial and deep cells. A correlation has been observed between spread and stage of tumor and CEA localization at the level of the stroma and cytoplasm of deep cells. It has been also evidenced that in all cases where CEA was present in the stroma and cytoplasm of deep cells, high serum levels of the marker were detected.

Biomarkers, Tumor↗

PubMedDate not supplied

[Primary biliary cirrhosis].

PURPOSE: To discuss exhaustively: clinical, serological and pathologic aspects of primary biliary cirrhosis (CBP); recent advantages in the knowledge of the disease's pathogenesis, therapeutical approaches that still appear less preferable than liver transplantation. DESIGN: We reviewed the most important recent studios on CBP. RESULTS: More than 90% of patients have antimitochondrial antibodies, so that CBP can be considered an autoimmune disease. Inciting agents could be either PDC E2-like or MHC molecules. An autoaggressive mechanism against biliary ducts could be the following: the neo-antigen on the surface of biliary tract cells could be the target for the immunological damage; anti PDC-E2 antimitochondrial antibodies could be secondary to the cellular damage and to the release of mitochondrial enzymes. CONCLUSIONS: In primary biliary cirrhosis, several circumstances (specificity of biliary-ductal destruction, lymphocyte infiltration of portal tract, abnormal expression of HLA-DR on surface of biliary epithelium cells) suggest that the epithelial cells of intrahepatic biliary ducts are the target of a severe and isolated immune response. The identification of the E2-like PDC antigen is a significant achievement in the knowledge of the pathogenetic process. On this basis, it is now to investigate possible genetic markers of risk and to clarify the role of T cells in the immunopathogenesis of the illness. The only effective treatment for CBP is liver transplantation.

Autoimmune Diseases↗