The UK wide collaboration which we have helped to fund, led by the University of Exeter, Royal Devon & Exeter NHS Foundation Trust and the Wellcome Sanger Institute, has shown that a genetic variant carried by 40% of the population explains why some patients develop antibodies against the anti-TNF drugs, infliximab and adalimumab, which means they stop working. 

The researchers now want to undertake a further trial to confirm that if people with Crohn’s were genetically tested before starting treatment, whether it would reduce the rate of treatment failure by making sure they were given the most effective medication. They want to find the right drug for the right patient the first time.  

Infliximab and adalimumab are used to treat patients with moderate to severe Crohn’s and Colitis when other treatments have not worked. Also known as biological medicines, these drugs work by blocking TNF, a protein which leads to gut inflammation. 

Unfortunately, these drugs don’t always work as the immune system can recognise them as a potential threat rather than a medicine. This leads to the production of antibodies, which means the drugs aren’t as effective and can stop working. 

Published in Gastroenterology, the Personalised anti-TNF therapy in Crohn’s Disease study (PANTS) looked at the clinical data and genetics of 1,240 people with Crohn’s who were starting anti-TNF treatment at 120 UK hospitals. The researchers identified a genetic marker HLA-DQA1*05, carried by 40 per cent of the European population that doubles the risk of developing antibodies against infliximab and adalimumab. 

The PANTS study uses IBD BioResource to recruit people. 

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