April 15, 2016, Barcelona, Spain: New research presented today shows that interferon alpha (IFNa) based therapies are effective in suppressing disease progression in a severe form of chronic viral hepatitis, Hepatitis delta.
The study, presented at The International Liver CongressTM 2016 in Barcelona, Spain, demonstrated that 35% of patients with Hepatitis delta who responded to IFNa based therapies achieved sustained suppression of the virus and had favourable outcomes compared to those untreated or treated with nucleos(t)ide analogues (NUCs are a treatment option in Hepatitis B).
Hepatitis delta infections can only occur in those who are infected with Hepatitis B.1 This dual infection is a very severe form of viral hepatitis and can result in a more serious disease and worse outcome.2 According to the EASL guidelines, pegylated interferon is the only treatment effective against Hepatitis delta.3
"There has been significant debate over whether there are long-term benefits to patients with Hepatitis delta receiving antiviral treatment," said Anika Wranke, Fellow of Hannover Medical School, Germany and lead author of the study. "Our study demonstrates that the long-term outcomes for patients with severe Hepatitis delta, who have limited treatment options, could be improved with a widely available medication."
The German study authors selected 136 individuals with chronic Hepatitis delta who were followed for at least six months and conducted follow-up for a median of five years. Clinical endpoints, which included; ascites (fluid accumulation causing abdominal swelling), encephalitis (a serious condition that causes inflammation in the brain), esophageal bleeding (enlarged veins that bleed in the esophagus), liver cancer (hepatocellular carcinoma), liver transplant or death, were present in 40% of patients at baseline. According to study results, clinical endpoints were less frequent in patients who received IFNa-based therapies compared to those treated with NUCs or given no treatment at all. Out of the 52 patients treated with IFNa based therapies in the study, 18 (35%) achieved sustained suppression of Hepatitis delta.
"This study is evidence of the great progress being made in finding effective treatment strategies for Hepatitis delta sufferers", says Professor Tom Hemming Karlsen, EASL Vice-Secretary. "Additional research must be conducted to enhance antiviral treatment for this serious disease."
About The International Liver Congress™
This annual congress is the biggest event in the EASL calendar, attracting scientific and medical experts from around the world to learn about the latest in liver research. Attending specialists present, share, debate and conclude on the latest science and research in hepatology, working to enhance the treatment and management of liver disease in clinical practice. This year, the congress is expected to attract approximately 10,000 delegates from all corners of the globe. The International Liver Congress™ takes place from April 13 - 17, 2016, at the Fira Barcelona Gran Via, Barcelona, Spain.
Since EASL's foundation in 1966, this not-for-profit organisation has grown to over 4,000 members from all over the world, including many of the leading hepatologists in Europe and beyond. EASL is the leading liver association in Europe, having evolved into a major European Association with international influence, with an impressive track record in promoting research in liver disease, supporting wider education and promoting changes in European liver policy.
For more information, please contact the ILC Press Office at:
Telephone: +44 (0)7841 009 252
Onsite location reference
Viral Hepatitis B and D, Hall 6.0
Friday 15 April, 16:00 - 18:00
Presenter: Anika Wranke, Germany
Abstract: PS053, Does antiviral treatment affect the clinical long-term outcome of Hepatitis delta?
Author disclosures of interest
1 World Health Organization. Hepatitis D. Available from: http://www.
2 World Health Organization. What is hepatitis? Available from: http://www.
3 EASL. EASL Clinical practice guidelines. Available from: http://www.