2.5 million people in Africa need urgent hepatitis B treatment

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Around 2.5 million people with hepatitis B in sub-Saharan Africa already have cirrhosis and need immediate antiviral treatment, a systematic review of published studies reports this month in the journal Liver International.

Approximately 60 million people in sub-Saharan Africa are living with hepatitis B, according to the World Health Organization (WHO), around 6% of the continent’s population. Around one-third of all people with hepatitis B live in Africa.

WHO recommends lifelong antiviral treatment for everyone with cirrhosis caused by hepatitis B but the number of people in need of urgent treatment in sub-Saharan Africa has been unclear until now.

A systematic review of 17 studies carried out by the University of Bern, Switzerland, found a pooled prevalence of cirrhosis of 12.7% in cohorts of patients attending tertiary facilities and 4.1% in cohorts in primary care.

The researchers say their analysis indicates that around 2.5 million people with cirrhosis caused by hepatitis B are in urgent need of antiviral treatment. Only 150,000 people with hepatitis B had been diagnosed in the region by 2015, according to WHO, so major efforts are needed to diagnose and treat hepatitis B in sub-Saharan Africa, the researchers conclude.

High hepatitis C cure rate achieved in New York prisons

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Hepatitis C treatment in prisons can result in a high cure rate but people released from prison during treatment are less likely to be cured due to challenges in medication supply, continuity of care, follow-up and viral load testing, researchers report from New York in the journal Open Forum Infectious Diseases.

Direct-acting antiviral treatment for hepatitis C is now offered to prisoners in many European countries and a growing number of states in the United States. Prison health care can offer the opportunity to test for hepatitis C on entry and to complete a course of direct-acting antiviral treatment.

Prisons have been identified as one of the key settings for microelimination of hepatitis C – intensified screening and treatment to eliminate hepatitis C in a population with a high prevalence of hepatitis C. In the United States, it has been estimated that around one-third of people with hepatitis C have spent at least part of a year in a correctional facility.

Justin Chan and colleagues in New York City Health Services’ Correctional Health Department looked at the outcomes of people who started hepatitis C treatment in prison or who entered prison during a course of treatment. Direct-acting antiviral treatment in New York City prisons is offered to anyone who will be in prison long enough to complete a course of treatment and to people with advanced liver disease.

They identified 269 people who started or continued hepatitis C treatment in prisoners between January 2014 and October 2017.

Of the 269 people treated, 195 had a post-treatment viral load test and of these 88% were cured. People who completed treatment in prison were nearly three times more likely to be cured compared to people who were released on treatment.

Post-treatment viral load follow-up was less likely for people who started treatment in prison, either because they were released from prison before this point or because the opportunity for viral load testing was missed while they were in prison. Correctional Health Services has now established transition clinics for people released into the community to enable healthcare follow-up and improved its systems for checking viral load follow-up among people who remain in prison.

The findings also show the importance of diagnosing hepatitis C early in a prison stay and starting treatment promptly after diagnosis, as well as the value of treating with a shorter-course regimen wherever appropriate.

London comes together to treat hepatitis C during lockdown

In London during the spring COVID-19 lockdown of 2020, healthcare teams, peer workers, hotel staff and others came together to make the most of the ‘Everyone In’ policy, which aimed to house people sleeping rough in temporary accommodation to prevent the spread of COVID-19. Taking this opportunity to engage people while they were housed for an extended period, partners from across London delivered a hepatitis C testing operation in hotels, hostels and on the streets.

Over 1000 people were tested for blood-borne viruses over the course of 98 testing events held between May and August 2020, including for hepatitis C, HIV and hepatitis B.

More than one in ten (11%) of those who were tested for hepatitis C were found to have antibodies for the virus, indicating a past or active infection, and 7% of all those tested for hepatitis C were identified as having an active infection.

By November 2020, 43 people had commenced hepatitis C treatment, demonstrating the importance of continued hepatitis C testing outreach for the homeless population if London is to eliminate this disease by 2025, as NHS England has aimed to do.

The results of this initiative have been published in the London Joint Working Group's report Hepatitis C testing and treatment interventions for the homeless population in London during the Covid-19 pandemic: Outcomes and learning.

Experimental treatments for NASH at the Liver Meeting

Non-alcoholic steatohepatitis (NASH) refers to liver inflammation and fibrosis caused by non-alcoholic fatty liver disease (NAFLD). Left untreated, NASH may lead to the development of cirrhosis and hepatocellular carcinoma. NASH is often accompanied by obesity and other metabolic disorders such as type 2 diabetes and dyslipidemia.

A meta-analysis of studies carried out in Europe shows that around one in 20 people have advanced fibrosis due to NAFLD or NASH, and NASH is the fastest-growing reason for a liver transplant in the United States.

There is no approved form of treatment for NASH. Numerous pharmaceutical companies are working to develop treatments targeting a variety of metabolic pathways.

Several companies reported results of phase 2 efficacy studies of experimental NASH treatments at the AASLD Liver Meeting in November.


Efruxifermin reduced liver fat and improved liver inflammation and fibrosis in the majority of people with NASH who received it in a phase 2a trial but nausea and vomiting led 10% of people who received the drug to drop out of the trial, Professor Stephen Harrison of the University of Oxford reported at the conference.

Efruxifermin is designed to treat NASH by regulating levels of FGF-21. FGF-21 is involved in the regulation of numerous metabolic pathways governing glucose and lipid levels. Levels of FGF-21 are elevated in people with NAFLD, type 2 diabetes and obesity. Efruxifermin is an analogue of FGF-21, designed to normalise FGF-21 levels.

The phase 2a study randomised 80 people to one of three doses of efruxifermin or placebo for 16 weeks.

Liver fat declined significantly at all doses compared to the placebo group. Liver fat reduced substantially in more patients in the 50mg and the 70mg groups compared to the 28mg group. Participants in the 70mg group were more likely to experience a normalisation in liver fat content (< 5%).

Forty-eight per cent of responders in the efruxifermin arms achieved resolution of NASH and there was no difference between dosing groups.

As with several other drugs being investigated for NASH treatment, gastrointestinal side effects were common in people who received efruxifermin and 10% of people receiving the drug stopped due to nausea and vomiting.

A phase 2b/3 clinical trial of efruxifermin in NASH patients is due to begin recruiting in early 2021, drug developer Akero Therapeutics said in a press release.


Semaglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist that mimics the action of natural GLP-1, which increases insulin secretion and plays a role in appetite regulation and glucose and lipid metabolism. Several studies of semaglutide as a treatment for NASH were presented at the Liver Meeting.

A phase 2 study of semaglutide alone as NASH treatment randomised 230 people to receive one of three doses or placebo.

People who received semaglutide were significantly more likely to experience NASH resolution. A slightly higher number also had improvement in liver fibrosis. Improvements in metabolic markers were also observed more frequently compared with placebo.

In another phase II study, Dr Naim Alkhouri of Arizona Liver Health and colleagues compared regimens of semaglutide alone or in combination with Gilead Science's firsocostat, cilofexor or both.

All groups lost weight, with percentage loss ranging from -7% to -10%. Liver fat decreased more in all the combination groups, with the greatest loss in the triple therapy arm.

Liver stiffness declined in all groups, with the greatest improvement seen in the triple therapy arm. Enhanced liver fibrosis (ELF) score, a composite index of fibrosis biomarkers, showed similar improvement across all treatment groups.


Lanifibranor is a PPAR agonist. It activates all three types of PPAR and is dosed orally, once a day.

PPARs regulate the expression of genes and are involved in the regulation of numerous metabolic and inflammatory pathways. PPARs appear to play a role in the development of NAFLD and NASH and levels of PPARs are reduced in people with NASH.

Various PPAR agonists are being tested in clinical trials. Lanifibranor is the only PPAR agonist which activates all forms of PPAR.

The NATIVE phase 2b study randomised 247 people with biopsy-confirmed NASH to either 800mg or 1200mg of lanifibranor or placebo for 24 weeks.

The study used a new outcome measure, changes in steatosis-activity-fibrosis (SAF) score. SAF score is calculated differently from NAFLD Activity Score, using only liver tissue inflammation and ballooning of hepatocytes to assess the severity of disease. After 24 weeks of treatment, participants in the lanifibranor 1200mg group were significantly more likely to experience a 2-point reduction in SAF score compared to the placebo group.

Lanifibranor 1200mg also resulted in improvement of fibrosis by one stage and no worsening of NASH in 42% compared to 24% in the placebo group and resolution of NASH and improvement of fibrosis in 31%, compared to 7% in the placebo group.

Lanifibranor will enter phase 3 studies in 2021.


Cotadutide, an experimental therapy that alters glucose and lipid metabolism, led to weight loss and improvements in metabolic, cardiovascular and liver fibrosis biomarkers in overweight people with diabetes and fatty liver disease, but nausea was a common side effect, another study reported at the conference.

The phase 2b study included 834 people who were overweight or obese and had type 2 diabetes treated with metformin. Participants were randomly assigned to receive one of three doses of cotadutide (100, 200 or 300mcg) via once-daily subcutaneous injection, daily injections of the diabetes drug liraglutide (a GLP-1 agonist) or a placebo.

After 54 weeks of treatment, people assigned to all three doses of cotadutide and liraglutide lost significantly more weight than those in the placebo arm. Those in the high-dose cotadutide group saw a weight reduction of 5%, which is considered clinically beneficial.

All three doses of cotadutide and liraglutide reduced NAFLD fibrosis scores, but the difference was only significant for the high-dose group.

Nausea, vomiting and diarrhoea were common side effects. More than one in five people (22%) taking the high dose of cotadutide stopped treatment due to adverse events, as did 13% taking the low dose and 15% taking the intermediate dose.

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