Resolution of chronic delta hepatitis after 12 years of interferon alfa therapy. Gastroenterology 117:1229-1233
Liver Diseases Section, Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USa. Gastroenterology
(Impact Factor: 16.72).
12/1999; 117(5):1229-33. DOI: 10.1016/S0016-5085(99)70409-9
Chronic delta hepatitis is an uncommon but severe form of chronic viral hepatitis for which there is currently no satisfactory therapy. A patient with chronic delta hepatitis was treated with interferon alfa, 5 million units daily for 12 years. Serial serum samples were tested for routine liver tests and selected samples for quantitative levels of hepatitis B surface antigen (HBsAg) and hepatitis delta virus RNA. Liver biopsies were performed before, during, and after an initial 1-year course of therapy and again after 3 and 10 years of continuous therapy. With initiation of interferon therapy, serum aminotransferase levels decreased to normal range, became abnormal again when the dose was reduced, and increased to pretreatment levels when therapy was stopped. With reinstitution and prolonged therapy, aminotransferase levels became persistently normal; after several years, both hepatitis delta virus RNA and serum HBsAg became undetectable. Liver biopsy, which initially revealed cirrhosis, showed gradual improvement in inflammatory and fibrosis scores and, after 10 years, no abnormalities or fibrosis. Therapy was stopped, and the patient remained free of evidence of infection. In conclusion, long-term therapy with interferon alfa in high doses led to resolution of chronic delta hepatitis, disappearance of hepatitis delta and B virus markers, and improvement in fibrosis.
- "This could be a concept for the treatment of hepatitis delta. However, time to achieve HBsAg loss on IFN therapy can be as long as 12 years as demonstrated by Lau et al in a similar case report . "
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ABSTRACT: Chronic hepatitis B virus (HBV) infection can result in liver cirrhosis, hepatic decompensation, and hepatocellular carcinoma (HCC). However, the natural course of the disease is highly dynamic and not every patient requires therapy. The challenges for optimal management are who to treat, which therapeutic regimen to use, and when to begin or stop treatment. Constant monitoring is mandatory to predict the natural course and guide treatment decisions. Surrogate markers for baseline and on treatment decisions are needed. Besides HBV DNA, hepatitis B surface antigen levels also proved to be useful to help judge the natural course and guide treatment. High levels of HBsAg are suggestive of low fibrosis and immune tolerance in hepatitis B e antigen (HBeAg) positive patients; whereas low levels of HBsAg indicate a lower risk for HCC and inactive carrier state in HBeAg negative patients. Data also support the possible use of HBsAg levels as an on-treatment response marker. So far, the best evidence exists for treatment with interferon (IFN)-α where lack of HBsAg decline after 12 weeks is associated with non-response. Thus, stopping rules after 12 weeks therapy could be established for HBeAg positive as well as for HBeAg negative patients. However, the positive predictive value for achieving sustained response is still vague. The value of HBsAg monitoring is less clear during treatment with nucleos(t)ide analogues (NA) but it can be a useful marker for new concepts such as stopping NA or add-on IFN strategies. Currently, several studies are underway to validate HBsAg in these settings.
Annals of Gastroenterology 03/2014; 27(2):105-112.
Available from: Prakash Ramachandran
- "However, the wound healing response is a dynamic process and has the potential to resolve without scarring. Removal of the injury stimulus has been shown to improve liver fibrosis in alcoholic liver disease , viral hepatitis [3-5], biliary obstruction  and autoimmune hepatitis . Current treatments for liver fibrosis are directed towards suppression or removal of inflammatory stimuli that drives the development of fibrosis. "
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ABSTRACT: Liver cirrhosis is a major cause of morbidity and mortality worldwide and has very limited therapeutic options. Regardless of the aetiology, hepatic fibrosis is a characteristic feature of chronic liver disease. Our knowledge regarding the pathogenesis of this scarring has grown exponentially in the past 25 years. It has now clear that this is a highly dynamic process and the long-held dogma that it is irreversible and relentlessly progressive is now being challenged. In this review, we will summarise the key pathogenic mechanisms at play and will focus on the evidence demonstrating that liver fibrosis is reversible in humans and animal models. In particular, we will examine the role of hepatic stellate cells, MMPs, TIMPs and macrophages in this process. Finally, we will discuss some of the studies aimed to therapeutically target the resolution of fibrosis and their potential for translation into a badly-needed treatment modality in the clinical setting.
Annals of hepatology: official journal of the Mexican Association of Hepatology 06/2012; 8(4):283-91. DOI:10.1186/1755-1536-5-S1-S26 · 2.07 Impact Factor
Available from: Ulrike Protzer
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