This study day, jointly run by The Academy for Paediatric Gastroenterology and Coeliac UK and hosted by UCL Institute of Child Health in London, took place on 20th November 2014. Alex Gazzola went along to report on some of the highlights from the day’s speakers.
Sarah Sleet, Coeliac UK’s Chief Executive welcomed delegates – mainly dietitians and paediatricians – and introduced speakers, but not before announcing that the charity would be running a major diagnosis campaign in 2015, in order to address the half a million British people still living with coeliac disease (CD) and unaware they have it.
Dr Jenny Epstein
Kicking off, consultant paediatric gastroenterologist Dr Jenny Epstein spoke on the genetics and epidemiology of CD.
Only half of the genes associated with CD are known. “We would have to screen around 200,000 people to establish the rest,” she said.
However, genes are only half the picture at best: environmental aspects are key. Over twenty years on from the end of the event, and despite the hypothesis that it was caused by changing weaning advice, we have yet to fully explain the Swedish paediatric epidemic of CD from the mid-eighties to the mid-nineties, she said.
Possibilities effecting the development of the disease include the quality and quantity of gluten we consume, the microbiome, gastrointestinal infection, infant feeding and breastfeeding. These factors need to be studied more.
Dr Epstein made an important point regarding those living with CD but undiagnosed – that it has not been established whether their quality of life would improve on a gluten-free diet (GFD).
Paediatric dietitian Natalie Yerlett
Paediatric dietitian Natalie Yerlett spoke on the GFD. The safety of oats formed a major part of her talk, and many of the studies and issues raised were covered in our previous article, Oats and the Gluten-Free Diet. She advised that if reintroducing GF oats into the diet of a coeliac patient whose serology had normalised a year after diagnosis, it was important that this was very gradual, as follow-on symptoms may be due to the increase in fibre which oats bring to the diet, rather than a sign of intolerance to the gluten-like protein avenin in oats.
Clinical psychologist Dr Lisa Barkely
In an insightful talk, clinical psychologist Dr Lisa Barkely addressed quality-of-life issues and GFD adherence in the young – and their perceptions of their disease.
Young children do not understand the concept of ‘forever’ in relation to illness. Chickenpox, for example, will come and go, and be a temporary part of their identity. Getting their heads around the permanency of CD is a hurdle for them, and indeed their families. Older children, whose identities are more formed, may find it harder to ‘incorporate’ CD if diagnosed a little later.
There is a tendency in the very young to view illness as a consequence of being naughty. At around eight, children perceive CD to be more about ‘germs’. It’s only when they get to ten, eleven or twelve that they begin to understand gluten as the cause of their illness.
What is it like for a child to have CD? The illness can be largely invisible: coeliac children will look like non-coeliac children. But this comes with a downside: peers asking “What’s the matter with you? You look fine to me!” – and children may not be able to respond well if they are at an age where they don’t fully understand it themselves.
Social situations can be a minefield if children wish to be discreet. Stay away from them? Go forward and risk being ‘unmasked’? Lie and/or cheat? None of these options is good, but eating is such a part of our social fabric that ‘discretionary disclosure’ – keeping a disease secret with the exception of close confidantes – cannot be applied. Food is a part of family life, school life and social life. Every interaction with food poses a potential challenge. Trained in being hypervigilant all their lives, CD is never far from children’s minds. The interest of others can be perceived as caring, but alternatively it can be perceived as intrusive.
Children fear being stigmatised, and may feel that they are, even when they are not. When “beautifully compliant seven-year-olds morph into disengaged, disobedient teens” family life can be thrown into turmoil: food is so key to it that teens can use it as a “big stick” to hit parents with. They may cheat. They may understand the long-term risks of gluten consumption as they do the risks with smoking, but may not care about a time decades into the future.
The temptation when this happens is to become one more person – clinician, medic, teacher, parent – who will tell the teen what to do, which they already live with daily. They will disengage at directions. Try to understand, argued Barkely. It may feel like a personal slight or failure when a teen does not take your advice to avoid gluten, but the reality is this: chances are they are not doing it to annoy anyone; they are doing it to make the disease less prominent in their young lives.
Ask them what benefit they perceive from sticking to the GFD: don’t tell them what the benefit will be. Guide, rather than instruct. “Do this, don’t do that” will not help; nudging, listening, summarising, will.
Dr Peter Gillett
Dr Peter Gillett took delegates through the history of diagnosis in paediatric patients, and brought us up to date with current guidelines, which we covered in our article New Joint BSPGHAN / Coeliac UK Guidelines for Coeliac Diagnosis in Children. He reminded us that these were guidelines – not dictats.
Dr Marios Hadjivassiliou
This was followed by Dr Marios Hadjivassiliou on the neurological symptoms of CD – a very similar talk to that which he gave at Coeliac UK’s 2014 annual research conference, which we also covered, called Understanding the Patient.
Consultant paediatric gastroenterologist Professor Luisa Mearin
Consultant paediatric gastroenterologist Professor Luisa Mearin of Leiden University Medical Centre, Netherlands, presented the detailed results of the PreventCD study, in which she had collaborated along with other experts across Europe, and which made widespread news just weeks earlier in many media outlets, after being published in the New England Journal of Medicine.
The project, which was started in spring 2007, was set up to test the hypothesis that CD may be prevented in genetically high-risk babies (HLA-DQ2 or HLA-DQ8 positive, with a first-degree relative diagnosed with CD) by introducing small quantities of gluten into the diet at 4-6 months, preferably along with breastfeeding.
475 babies were randomly assigned 100mg gluten daily; 469 received placebo. All were closely followed until their third birthdays. 44 diagnoses of CD were made in the gluten group; 36 in the placebo group. This representated a cumulative incidence of 5.2%, with 5.9% in the gluten group and 4.5% in the placebo group – but this was not statistically significant. Aspects which were not related to the results or development of CD included the country of origin of the children, parental CD status, rotavirus vaccination, gastrointestinal or respiratory infection, or the mean daily gluten intake after the intervention was completed.
“Also breastfeeding was not related to the development of CD, and that was a surprise for us,” acknowledged Mearin. “We had expected it to be protective, but it was not the case.”
So what was related to the incidence of CD? Being a girl, rather than a boy, is one answer – and this difference begins early. The HLA profile is important too. Cumulatively, having two ‘doses’ of HLA and being female, means the risk is at its highest.
The disappointing conclusion was that early introduction of small quantities of gluten did not reduce the risk of CD at the age of 3 years in genetically predisposed children from high-risk families, and that the results did not support the protective effect the researchers had hoped to find, and that breastfeeding doesn’t protect against the development of CD in young children.
Professor Simon Murch, Professor of Paediatrics at Warwick Medical School
The final talk was from Professor Simon Murch, Professor of Paediatrics at Warwick Medical School. He addressed non-coeliac gluten sensitivity (NCGS) in paediatrics, and its existance in a broader sense.
In terms of non-coeliac reactions to wheat, non-IgE-mediated allergic reactions are much more common in children than IgE-mediated, but are very easily missed and difficult to diagnose. The morphine content of wheat and milk is not often discussed, but ‘toxic’ gliadomorphins alter animal behaviour and the activation of neurones in the lymbic system and these are deeply under-studied [they have been implicated in autism, albeit controversially, and in part form the basis for the gluten-free, casein-free diet].
Murch pointed to a study which found that for at least some individuals with IBS (either constipation- or diarrhoea-dominant) a mast cell reaction triggered by food antigens could induce muscular contractions. More recently it has been established that extraintestinal manifestations in children with gastrointestinal food allergy occur. Accordingly, he outlined his suspicion that a good proportion of those with NCGS could in fact have non-IgE-mediated wheat allergy.
But that isn’t the full story, by any means. At the mucosal level in NCGS, there is an increase in intraepithelial lymphocytes, which has also been recorded in IBS. Murch stated that he believed that “something is going on of an immunological nature that is not a part of adaptive immunity and that is not related to the HLA-linked coeliac response”.
Supporting this hypothesis, he provided unusual evidence that innate immune responses to gliadin peptides are universal throughout the animal kingdom. It is well known that a significant proportion of Irish setters have non-HLA-related gluten sensitivity – in essence, a canine NCGS – and only two insects can consume wheat – and they pre-digest it via enzymes in their saliva.
Is gluten inherently toxic in the gut outside of coeliac disease? Yes. If you take gut epithelial cells and challenge them with gliadin they are activated: gliadin effects the innate immune system of us all, and whether or not that induces any clinical response will depend on other factors, in particular the ability to degrade gliadin in the gut, and to detoxify the products of gliadin.
What we currently lack are the tools to distinguish NCGS and non-IgE WA and diagnose either by blood or other tests, said Murch, before reassuring gluten consumers that if they are well, he does not believe elimination of gluten is necessary.
For upcoming courses at the APG, see their website.
Coeliac Disease: What you need to know by Alex Gazzola, is available on Amazon.
First published November 2014.
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