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Ahead of its Non-Alcoholic Fatty Liver Disease (NAFLD) Summit in Seville, Spain, this week, the European Association for the Study of the Liver (EASL) has called for action by policy makers to combat rising levels of obesity in Europe.

More than half of adults and one third of children in Europe are classified as overweight or obese, with the highest proportion coming from lower socio-economic groups where NAFLD is prevalent.

NAFLD is the accumulation of excess fat in the liver and is now the most common cause of liver disease in western countries due to the rapid rise in levels of obesity and type 2 diabetes. It is a major European health burden resulting in liver cirrhosis and liver cancer, as well as big increases in cardiovascular disease and non-liver cancers.

Lack of physical activity and excess calorie intake leads to weight gain and fat deposition, which plays a major role in the development and progression of NAFLD.

“We have reached a tipping point with obesity and NAFLD and swift action is urgently needed by policy makers to reverse the growing epidemic. Obesity is the normal response to an abnormal environment and can only be tackled by addressing the multiple physical, social and economic obesogenic drivers in society,” said Philip Newsome, Secretary General of EASL.

EASL is calling for:

• public health policies to restrict advertising and marketing to children of sugar-sweetened beverages (SSBs) and industrially processed foods high in saturated fat, sugar and salt.
• the introduction of taxes to discourage the consumption of SSBs and legislation to ensure that the food industry improves labelling and the composition of processed foods.

EASL says that research indicates that governmental measures aimed at increasing the cost of SSBs can reduce consumption by 20 to 50%. It is estimated that a 20% levy on SSBs would prevent 3.7 million cases of obesity and 25,498 cases of BMI-related disease over the next 10 years.

“It is clear that many of the causes of NAFLD – sedentary behaviour, excessive energy intake and a poor diet are avoidable. If we are to reduce the incidence of obesity and NAFLD we need to have a significant re-think about the regulations regarding the sale and marketing of sugar products,” concluded Professor Newsome.

Obesity without non-alcoholic fatty liver disease (NAFLD) does not raise the risk of cancer, but people with NAFLD who are also obese are almost twice as likely to be diagnosed with cancer as non-obese people of the same age who did not have NAFLD, US researchers report in the Journal of Hepatology.

Excess body weight has been identified as a risk factor for cancer in numerous large epidemiological studies. But the mechanism by which excess weight leads to the development of cancer is unclear, and some studies have shown that different patterns of fat distribution affect cancer risk.

NAFLD develops as a result of metabolic disorders including type 2 diabetes, insulin resistance and elevated lipids, as well as obesity. These conditions lead to the accumulation of fat in the liver. Eventually the build-up of fat may lead to inflammation and scarring of the liver and, in a small minority of people with NAFLD, to the development of liver cancer.

Cancer is one of the most frequent causes of death in people with NAFLD. The study was designed to establish which cancers occur most frequently in people with NAFLD, and the extent to which cancer risk is determined by obesity or NAFLD.

NAFLD raised the risk of liver cancer and uterine cancer and also the risk of gastrointestinal tract cancers – stomach, pancreatic and colon cancer. The risk of developing colon cancer was especially elevated in men.

The investigators say that their results should be used in counselling people with NAFLD about their cancer risk.

People with HIV and hepatitis C co-infection who had fatty liver disease were twice as likely to die during a five-year follow-up period as their counterparts without fatty liver disease, French researchers report in Hepatology.

The researchers say that using non-invasive measures of fatty liver disease can help doctors identify people at higher risk of death and they urge investigation of other cohorts of people with HIV and hepatitis C to validate the fatty liver index.

Accumulation of fat in liver cells – hepatic steatosis – is caused by metabolic disorders, by insulin resistance and systemic inflammation. Hepatitis C causes insulin resistance and both hepatitis C and HIV cause inflammation.

The Fatty Liver Index is calculated using body mass index, waist circumference, triglycerides and gamma glutamyl transferase (GGT). A score below 30 rules out hepatic steatosis and a score above 60 confirms hepatic steatosis.

The French study looked at 983 people recruited to the HEPAVIH cohort between 2005 and 2008.

People with a fatty liver index above 60 at baseline were twice as likely to die during the follow-up period after controlling for other risk factors.

The investigators say that theirs is the first study to show that an elevated fatty liver index is associated with an increased risk of death, independent of other risk factors, in people with HIV and hepatitis C co-infection.

Persistence of very low-level hepatitis C infection after a sustained virologic response (SVR) to hepatitis C treatment is an extremely rare event and is not associated with any liver damage, Spanish researchers report in Nature Scientific Reports this month.

Although SVR is agreed by liver experts to signify that hepatitis C virus (HCV) infection has been cured, several research groups have reported persistence of HCV RNA (viral genetic material measured by viral load tests) for up to nine years without rebound, and subsequent disappearance of HCV. Other studies, following cohorts of people cured of hepatitis C, have reported isolated cases of late viral rebound up to 18 months after achieving SVR.

Viral rebound after SVR is rare, but it is unclear how rare it is and whether persistence of low-level infection is associated with continuing liver damage.

Furthermore, it is unclear if a compromised immune system – as in advanced HIV disease – might encourage low-level viral persistence.

Spanish scientists investigated the frequency of viral persistence in people with HIV who received treatment for hepatitis C between 2015 and 2018 at hospitals in Andalusia. Among 123 people with SVR, HCV RNA was detected in only one person. The participant tested positive for HCV RNA in peripheral blood mononuclear cells (PBMCs) but not in serum at baseline. In this person, the viral levels in PBMCs steadily declined at each visit and became undetectable at the fourth visit.

The investigators conclude that viral persistence after achieving SVR is a very rare event, but evaluation of people who have achieved SVR using ultrasensitive tests may be warranted before organ and blood donation, and for women who wish to have children after being cured of hepatitis C.

Successful treatment of hepatitis C virus (HCV) may lead to a reduction in immune activation related to leakage of bacteria from the gut in people with HIV/HCV co-infection, according to a study presented at the 10th International AIDS Society Conference on HIV Science in Mexico City in July.

Research has shown that chronic inflammation contributes to a host of conditions – including cardiovascular disease and cancer – in people living with HIV, even if they are on effective antiretroviral therapy that maintains viral suppression.

HCV also plays a role in chronic inflammation, which may help explain why it increases the risk of other health conditions beyond liver disease.

The study, carried out in the US, looked at markers of inflammation that are known to be involved in the development of cardiovascular disease. The researchers found that levels of these inflammatory markers declined significantly after hepatitis C was cured, and that greater reduction in inflammatory markers was strongly correlated with greater improvement in liver fibrosis, as measured by laboratory markers (APRI score and FIB-4 score).

Public Health England estimates that approximately 95,000 people with hepatitis C remain undiagnosed in England – but also estimates that the total population of people living with hepatitis C has fallen by approximately 40,000 since 2015, largely due to successful treatment.

With organisations across London coming together to eliminate hepatitis C in the capital, the London Joint Working Group on Substance Use and Hepatitis C is calling on drugs services, outreach testing services and hospitals to review and improve their data sharing processes.

The new report, Joining the Dots: Linking pathways to hepatitis C diagnosis and treatment, highlights that, with people being diagnosed with hepatitis C at various different locations such as at a drugs service, prison, GP practice, or outreach service, it is crucial these organisations have systems that can process and share patient information efficiently. Effective data sharing is essential to ensure that people receive timely care and so that progress towards eliminating hepatitis C can be checked.

This issue is likely to be relevant in many settings outside the United Kingdom. Data protection rules will differ in other countries, but the lessons learned by services in the UK may prove helpful to others in thinking about how and why to implement data sharing.

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