1 / 27

Vito Di Marco Gastroenterology Hepatology Department Di.Bi.M.I.S. University of Palermo Italy

Causes of liver damage in thalassemia patients. . . IRON OVERLOAD. VIRUS INFECTION. Clinical course of chronic virus related liver disease. . Acute Hepatitis. Resolution. . . 20 - 30 Years. Chronic Hepatitis. Stabilisation. Cirrhosis. Compensated Cirrhosis. . . . . . . . Decompensated Cirrhosis(Dea

onslow
Download Presentation

Vito Di Marco Gastroenterology Hepatology Department Di.Bi.M.I.S. University of Palermo Italy

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

    4. Hepatitis virus infections in thalassemic patients: the key issues How many patients have chronic virus infection? What are invasive and non-invasive methods for the diagnosis of chronic hepatitis or cirrhosis? What are the risks of developing severe liver disease? Development of cirrhosis Development of hepatocellular carcinoma (HCC) What are the therapies for patients with chronic virus hepatitis?

    5. Hepatitis virus infection in thalassemic patients Hepatitis B Virus (HBV) infection HBV infection is present in less than 5% of adult subjects. Anti-hepatitis B vaccination has ruled out the risk of new virus B infections. Hepatitis Virus C (HCV) infection Hepatitis C virus is the most common viral infection. Worldwide 20%-80% of thalassemics are seropositive for anti-HCV antibodies HCV chronic infection is more common in thalassemics transfused before 1990.

    8. Viral genotypes in thalassemic patients with HCV chronic hepatitis

    11. Rates of cirrhosis in 3 groups of thalassemic patients who underwent liver biopsy.

    12. Which non-invasive markers can replace liver biopsy to evaluate fibrosis? a. Serologic markers Routine laboratory tests (indirect markers) Fibrogenesis markers (direct markers) b. Imaging techniques Ultrasonography Transient elastography (Fibroscan) Transient elastography-MRI

    13. Transient Elastography by Fibroscan®

    15. Causes of death in a cohort of 406 patients with thalassemia major followed for 16 years (1993-2009)

    16. Antiviral therapy for HCV chronic hepatitis (AASLD & EASL Guidelines)

    17. Milestones in Therapy of HCV

    18. Alfa-interferon monotherapy in thalassemic patients with chronic C hepatitis.

    19. Viral genotypes and Sustained Virological Response (SVR) to alpha Interferon

    20. Early Virological Response (EVR) as predictor of SVR . (Data of 23 thalassemics with chronic hepatitis C treated with alpha-interferon)

    21. Combination therapy with alpha-interferon and ribavirin in thalassemic patients with chronic C hepatitis.

    22. Combination therapy with Peg-Interferon and ribavirin in thalassemic patients with chronic C hepatitis.

    23. Changes in transfusion requirement and chelation regimen

    24. Conclusions (I) HCV infection is common in thalassemic patients. Half of subjects with chronic HCV infection develop chronic hepatitis. Adult patients with active HCV infection have frequently a moderate or severe liver fibrosis and 20% of them have a cirrhosis.

    26. Conclusions (III) Death related to liver cirrhosis or to hepatocellular carcinoma is rare in thalassemic patients without HCV infection Development of hepatocellular carcinoma is associated with the presence of cirrhosis and active HCV infection.

    27. Conclusion (IV) Patients with HCV hepatitis or cirrhosis should be treated with peg-interferon plus ribavirin. The sustained virological response is more common in patients without cirrhosis, infected with genotypes 2 or 3, with early suppression of viral load on therapy. In thalassemic patients treated with interferon and ribavirin the blood transfusions can increase because of ribavirin-associated haemolysis. Combination antiviral therapy can increase the number of patients cured by virus C and can reduce the risk of liver related death.

More Related