1,721,034 research outputs found
Management of Delta Hepatitis 45 Years after the Discovery of HDV
Full text linkIn 1977 the viral Delta agent was discovered and subsequently characterized as the hepatitis Delta virus (HDV). HDV infection is associated with HBV infection since the defective HDV needs HBV to infect and replicate in the liver. Even if not a frequent cause of chronic liver disease, HDV infection is responsible for an aggressive progression of hepatitis towards advanced liver disease. At present, no FDA approved treatment exists for this specific form of hepatitis. Interferon alfa has been recommended as off-label therapy by major scientific societies (AASLD, EASL and APASL) and has proved effective in about one quarter of patients. In recent years, new therapeutic approaches have been studied, and EMA has approved a new drug (bulevirtide) for Delta hepatitis. In this review, we encompass the 45-year journey of managing Delta hepatitis and address the most recent developments in treating this severe and aggressive liver disease
Proctosigmoidite ulcerosa refrattaria e recidivante alla terapia topica trattata con beclometasone dipropionato orale
No full textIl caso clinico riportato dimostra la possibilita' di utilizzare, con efficacia mantenuta nel tempo, il beclometasone dipropionato orale nella proctosigmoidite ulcerosa non responsiva e recidivante alla terapia topica rettale
Combination antiviral therapy with ribavirin and interferon alfa in interferon alfa relapsers and non-responders: Italian experience
No full textBackground/Aims: A sustained biochemical and virologic response to standard interferon therapy for chronic hepatitis C is seen in no more than 25% of patients, and the efficacy of re-treatment or of higher doses in non-responders and relapsers has not been established. A more effective therapy for interferon alfa-resistant hepatitis C is needed. Methods: A study of ribavirin plus interferon alfa combination therapy was conducted in 30 patients with chronic hepatitis C resistant to a previous standard course of interferon alfa (14 interferon non-responders, 16 interferon relapsers). Patients were randomly assigned to receive either ribavirin, 800 mg daily, and interferon alfa, 3 MU thrice weekly (n=15), or interferon alfa alone, 3 MU thrice weekly (n=15), for 6 months. Results: At the end of treatment, normal alanine aminotransferase levels were observed in eight patients in the combination therapy group: one (14%) interferon non-responder and seven (87%) interferon relapsers (p=0.01). Six months post-therapy, sustained normalization of alanine aminotransferase was achieved in seven (87%) interferon alfa relapsers, but not in any of the interferon alfa non-responders (p=0.001). In the group of patients treated with interferon alfa alone, sustained normalization of alanine aminotransferase was observed in one interferon relapser only. Serum HCV RNA became negative in eight patients receiving combination therapy - two (28%) interferon non-responders and six (75%) interferon relapsers. Six months later, circulating HCV RNA remained negative in seven patients: one (14%) interferon non-responder and six (75%) interferon relapsers (p=0.04). Sustained clearance of HCV RNA was not observed in patients re-treated with interferon alone. The sustained response to combination therapy was accompanied by reduced hepatic necroinflammatory activity on liver biopsy. Hepatitis C virus genotype was not significantly associated with response to combination therapy. Side effects were mild and well tolerated. Conclusions: Our experience indicates that combination therapy of ribavirin plus interferon alfa induces sustained biochemical, virologic, and histologic responses in most patients who are interferon relapsers
Prospective study on the prevalence of HCV infection in consecutive adult inpatients in a hospital division of Internal Medicine in Tuscany
No full textThe role of gut microbiota in chronic liver diseases
No full textSeveral studies have shown an association between gut microbiota composition changes and different types and stages of chronic liver diseases. Consistent findings seem to indicate a potential role of intestinal dysbiosis in the pathogenesis of liver damage. However, conclusive answers are still lacking to two fundamental questions: (1) Do changes in gut microbiota contribute to liver disease development, or are they simply a consequence of the disease? (2) May altering gut microbiota prevent the onset or influence the outcome of liver diseases? In the present chapter, the authors analyze the available data and highlight the significant contributions in the field of two primary chronic liver conditions: metabolic liver disease and primary sclerosing cholangitis. © 2021 Copyrigh
Comment on “Autoimmune hepatitis developing after coronavirus disease 2019 (COVID-19) vaccine: causality or casualty?”
No full textSerum IgM antibodies to hepatitis C virus in acute and chronic hepatitis C
No full textA standardized commercially available immunoassay is not available for detection of IgM antibodies against hepatitis C virus antigens (IgM anti-HCV). Therefore, different ''in-house'' enzyme immunoassays have been assessed. These assays vary greatly in sensitivity, but specificity seems satisfactory in all of them. A typical IgM antibody response to HCV antigens is usually found in nearly all patients with acute hepatitis C. This antibody response rarely precedes the appearance of IgG anti-HCV, and it persists for a few months at high titer. Low titers of IgM anti-HCV are detectable in 50-80% of cases with chronic hepatitis C. IgM anti-HCV reactivity is typically found during acute exacerbation of chronic hepatitis C. Furthermore, many patients with chronic active hepatitis C without acute exacerbation also have IgM anti-HCV. In these patients a correlation exists between the titer of IgM anti-HCV and the biochemical parameters of liver disease. When alpha interferon therapy induces a sustained remission of liver disease activity, positivity for IgM anti-HCV disappears in more than 70% of cases. In contrast, patients who do not respond to therapy rarely loose IgM anti-HCV. In conclusion, serum IgM antibodies to HCV antigens are reliable markers of active HCV-induced liver disease both in acute and in chronic HCV infection
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