A revolutionary new drug made from body fat could transform the treatment of sepsis, the deadly condition that kills over 40,000 Britons a year.
The experimental treatment uses a hormone called resistin, found in human fat cells.
Tests at the University of California found mice with sepsis had a 100 per cent survival rate when given the hormone.
Sepsis currently kills up to one in three victims – many within a few hours of symptoms first appearing.
A revolutionary new drug made from body fat could transform the treatment of sepsis, the deadly condition that kills over 40,000 Britons a year (file photo)
But injecting resistin seems to stop the lethal condition in its tracks, scientists said.
Top British experts welcomed the breakthrough.
Professor William Harnett, a specialist in immunology at Strathclyde University, said: ‘This is an exciting finding.
‘It’s a noteworthy development in the drive to find new treatments for sepsis.’
Sepsis kills more people in the UK than breast, bowel and prostate cancer combined.
The UK Sepsis Trust estimates there are 150,000 cases a year and claims at least 12,000 lives a year could be saved if doctors, nurses and paramedics were better trained to spot the vital early signs.
BAFTA award winning actor Jason Watkins, who starred in the BBC spoof W1A and ITV’s The Lost Honour of Christopher Jefferies, lost his two-year-old daughter Maude to the lethal condition in 2011.
Many victims fall ill when germs get into the body through wounds in the skin, dental abscesses or infections in the ears, lungs or urinary tract.
This can trigger a massive over-reaction by the immune system.
William Mead from Cornwall, died aged 12 months in 2014 from sepsis. His death followed a catalogue of errors, misdiagnoses and missed opportunities by doctors and NHS helpline staff
It floods the body with cytokines, chemicals that cause blood vessels to widen, leading to a dramatic reduction in blood pressure.
Widespread inflammation also blocks oxygen supplies to the heart, lungs, liver and kidneys – triggering organ failure.
Doctors treat it with large doses of antibiotics to beat the bacteria and fluids to bolster blood pressure.
But speed is vital to stop this potentially fatal chain reaction.
In December 2014, 12-year-old William Mead died from sepsis after a string of NHS failings.
Health Secretary Jeremy Hunt apologised to William’s parents after GPs, out-of-hours services and a 111 call handler failed to spot he had sepsis caused by an underlying chest infection and pneumonia
Health Secretary Jeremy Hunt apologised to the boy’s parents after GPs, out-of-hours services and a 111 call handler failed to spot he had sepsis caused by an underlying chest infection and pneumonia.
Scientists already knew resistin was found in much higher levels in obese people because it is secreted by fat cells.
Some earlier studies pointed to better survival rates among obese patients struck down by sepsis, although others found no such link.
During laboratory tests, researchers noticed that resistin was able to block a molecule called TLR4.
Normally, this molecule alerts the immune system to a foreign invader so it can launch cells to attack it.
But in sepsis TLR4 becomes massively overstimulated and triggers a catastrophic over-reaction by the immune system.
Resistin ‘binds’ to TLR4 and stops this happening.
Scientists looked at mice with sepsis who had raised levels of resistin in their blood and found none died, according to a report in the Proceedings of the National Academy of Sciences.
Professor Meera Nair, who led the research at the University of California in Riverside, said: ‘Resistin is protective in sepsis.
‘And because our bodies make it naturally, there is no fear of it being rejected.
‘If it can stop the excessive immune system reaction, it can stop sepsis.’
Researchers have developed an experimental drug – called Retn N-pep(Correct) – which contains resistin and can be injected into sepsis patients to try and halt the life-threatening reaction.
They are planning clinical trials next year to test the drug’s effectiveness on humans.
Professor Harnett said: ‘This is an intriguing development because resistin was previously thought to actually contribute to sepsis.
‘But researchers have used state-of-the-art experimental procedures to suggest a new approach.’