An arthritis drug that could delay the progression of type 1 diabetes has been hailed “life changing”. A study by University College London (UCL) has raised hopes after the rheumatoid arthritis drug abatacept appeared to preserve the pancreas’ ability to produce insulin.
Type 1 diabetes occurs when a person’s body attacks the cells that produce the blood glucose lowering hormone insulin. As a result they need to inject insulin to control the amount of glucose circulating in their body.
A third of the patients taking part in a two-year trial experienced no progression to their condition while on the medication, leaving the team optimistic it could be available in as little as three years.
The rheumatoid arthritis drug abatacept was found to benefit a third of type 1 diabetes patients whose insulin production was impaired.
“We’ve found something new and if it holds up with further tests it’s a new paradigm that could potentially be really important,” said study author Professor Lucy Walker.
Impact of diabetes
Nearly 4 million people in the UK had been diagnosed with diabetes in 2019. The majority (90%) had type 2, 8% had type 1, while the remaining 2% were diagnosed with rarer forms of the condition.
In Australia, more than 1.3 million Australians live with diabetes. As in the UK, the majority (87%) live with type 2 diabetes, 9% have type 1 diabetes, 3% gestational diabetes and less than 1% live with a rarer form of the condition.
Poorly-controlled diabetes can lead to serious complications like nerve damage, heart attacks and blindness.
Studying the arthritis drug and the preserving of insulin producing cells
Abatacept suppresses an aspect of the immune system called T cells, which mistakenly attack insulin-producing cells in the pancreas.
In 1999, the UCL scientists identified signals that controlled “follicular helper T cell” behaviour, later discovering these cells appear in high numbers in those with type 1 diabetes.
Abatacept is known to suppress the excessive immune response that occurs in conditions like rheumatoid arthritis.
Off the back of their results, the UCL scientists hope the drug will delay the progression of type 1 diabetes by even longer than the two years it was investigated for. Trials must be carried out to confirm this, they added.
The team also believe patients at any stage of the condition could benefit, however, only those who were newly diagnosed were enrolled on to the trial.
Abatacept is not thought to be effective in type 2 diabetes, which comes about when the insulin that is released does not work properly, causing blood-glucose levels to keep rising.
For unclear reasons, abatacept was found to be effective in a third of the type 1 diabetes participants only.
Blood samples analysed via artificial intelligence reportedly allowed the scientists to uncover the T-cell make-up of the different patients, enabling them to gauge how effective the drug may be.
“Early tests in people with type 1 diabetes have found the drug is not suitable for routine use because the response is very variable; some people benefit a lot, while others not at all,” said Professor Walker.
‘Huge step forward’ in diabetes treatment
“Being able to tell in advance who is likely to respond may reignite interest in this therapy for those with diabetes.”
The scientists are reportedly in discussion with the pharmaceutical giant AstraZeneca about conducting a larger clinical trial. They hope abatacept will be available for patients in three to five years.
Elizabeth Robertson, from Diabetes UK – which funded the research, said: “We could rapidly see this treatment licensed and this could be life changing [for] many of the 10,000 children and adults diagnosed with type 1 diabetes in the UK each year.
“This would be a huge leap forward in how we treat the condition and in changing lives.”
Dr Janaka Karalliedde from Guy’s and St Thomas’ Hospital in London agreed, adding there are always “non responders” among patients.
By identifying markers that suggest an individual will respond, those who stand to benefit most can be targeted, he added.