The UK is currently facing an epidemic in paediatric allergies. We have the highest prevalence of childhood asthma in the world and the rate of sensitisation to peanut has trebled in the past six years, currently affecting just under 2 per cent of children.1,2
In the UK, 40 per cent of all children have an allergy. Nearly one in three has asthma, one in four suffers from rhinitis, one in five has eczema and one in 10 is allergic or intolerant to a particular food.
This article, using a typical case study, aims to empower primary care clinicians with the knowledge to diagnose and treat common paediatric conditions in the primary care setting.
Jack is a six-month-old baby who was born at term following an uncomplicated pregnancy and delivery.
His mother has hayfever and his father has asthma.
Jack developed eczema at two weeks of age, primarily affecting his cheeks and the flexural aspects of his upper and lower limbs. In the first 20 weeks of life, his weight dropped significantly. He was an itchy, possety, colicky baby who frequently had constipation. He had very poor sleep. His parents requested a referral to a paediatrician.
GPs will frequently encounter infants with eczema and 80 per cent of these children will have mild to moderate disease. However, 20 per cent will have moderate to severe infantile eczema that adversely affects the quality of life of both child and parents. Jack is in the 2 per cent with most severe eczema.
Eczema and the allergic march
Eczema is fundamentally a genetic condition in which mutations in the filaggrin gene have been described.
This gene encodes for a protein that maintains the skin barrier function of keeping moisture in and allergens out.
When the integrity of the skin barrier is compromised due to mutations in the filaggrin gene, the resulting inflamed, eczematous skin allows moisture to escape and allows allergens to penetrate the skin and present themselves to the immune system, leading to sensitisation and the development of specific IgE antibodies.
Indeed, this has led to the well-documented concept of the 'allergic march'.3 This is a phenomenon where children tend to progress from one allergic condition to another, most commonly from eczema and food allergy to asthma and rhinitis with inhalant allergy.4
Associated food allergy
It is important to note that around 50 per cent of children with severe eczema may also have an associated food allergy, which may exacerbate the eczema and contribute towards an enteropathy and indeed may also be associated with a severe immediate allergic reaction.
Most IgE-mediated food allergies are caused by one of nine foods: milk; egg; soy; wheat; tree nuts; peanut; fish; shellfish and sesame. It is very important when taking a history from parents to ask whether they have noticed an immediate hypersensitivity reaction or a worsening of their child's eczema when exposed to each of these foods.
If so, confirmation of sensitisation and possible allergy can be made by obtaining blood for serum-specific IgE antibody levels, but these need to be interpreted cautiously as there may also be false positive results.
Positive predictive values for diagnosing allergy to each of the major food allergens have been published. Skin prick tests can also be used and are slightly more sensitive in detecting food allergy with fewer false positive results than serum-specific IgE.
We test infants with moderate to severe eczema whose eczema develops in the first six months of life and/or there is a history of a type-1 reaction, failure to thrive or GI symptoms. In addition, even if the skin prick test and specific IgE is negative, asking parents to keep a food diary can be very useful.
Parents may identify certain foods that exacerbate their child's eczema. If they note a worsening of the eczema after the child eats a particular food, proceed to an elimination diet of the proposed food allergen for two to six weeks (the gold standard test) to look for significant improvement of the eczema followed by a worsening of it on re-introduction of the food.
These foods can be slowly re-introduced into the child's diet (on confirmation of a negative specific IgE level) after the child reaches its first birthday.
This is particularly true for dairy, although emerging data suggest that a significant proportion of children grow out of their dairy allergy at five years of age and hence periodically re-visiting whether the child has grown out of their allergies is important. Equally, if a child is on any exclusion diet, they ought to be assessed by a dietician.
Aside from food, there are several known triggers that exacerbate atopic eczema. One must also be mindful of synthetic clothing, detergents, contact allergens, inhalane allergens and the physical environment.5
Another very important concept in the treatment of eczema is that of infection. Colonisation with Staphylococcus aureus can be found in 70 per cent of children with eczema.
The presence of this organism is increased to 90 per cent in acutely inflamed, eczematous skin where the organism may be causing a secondary bacterial infection. If left untreated, this may produce enterotoxins that will further exacerbate and propagate the inflammatory response.
The NICE atopic eczema guidelines support the use of skin swabs with the commencement of appropriate antibiotic treatment to eradicate the organism cultured when there is evidence of recurrent infection or a suspicion of antibiotic resistance and not for mere colonisation alone.5 It must also be borne in mind that infection with other organisms can cause a worsening of the eczema and these should be treated promptly.
Jack had raised serum-specific IgE antibody levels to dairy and was commenced on a dairy-free diet. Due to his severe weight loss an amino-acid based formula was commenced.
He was reviewed by a dietician who ensured he received adequate amounts of calcium in his diet. His parents were advised to moisturise his skin six to eight times a day using emollients. They were prescribed soap substitutes and bath oils.
A non-sedating antihistamine was also started to relieve some of his pruritus and reduce skin inflammation. Swabs were taken from infected skin lesions, which demonstrated Staph aureus infection. This was treated with a week-long course of oral antibiotics.
Moderate potency topical steroids were also started for two weeks. Jack's eczema and GI symptoms began to improve after a week and his weight also improved substantially.
As a toddler, Jack went on to develop a constant runny nose, cough and wheeze at night. It is important to remember that highly atopic children like Jack may develop rhinitis at a much younger age.
Inspection of the nasal mucosa and treatment of the rhinitis as well as any concomitant asthma is paramount, as optimal treatment of rhinitis will reduce hospitalisation and improve quality of life.6
- Dr Sohi is a consultant paediatrician at The Royal Free Hampstead NHS Trust
1. Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee. Lancet 1998; 351(9111): 1225-32.
2. Grundy J, Matthews S, Bateman B, Dean T, Arshad SH. Rising prevalence of allergy to peanut in children: Data from 2 sequential cohorts. J Allergy Clin Immunol 2002; 110(5): 784-9.
3. Barnetson RS, Rogers M. Childhood atopic eczema. BMJ 2002; 324(7350): 1376-9.
4. Scadding G. Allergic rhinitis in children. Paediatr Child Health 2008; 18(7): 323-9.
5. Atopic Eczema in Children. NICE Clinical Guideline. 2007
6. Corren J, Manning BE, Thompson SF, Hennessy S, Strom BL. Rhinitis therapy and the prevention of hospital care for asthma: a case control study. J Allergy Clin Immunol 2004; 113: 415-9.