The GP and infantile atopic dermatitis, by Dr. J. Robert

T6, 08/08/2014 - 12:45
Dr Robert

 Atopic dermatitis or eczema is a condition that specialists consider mild, but which gives rise to so many different interpretations, prohibitions, excesses, consultations and conflicting opinions that, in recent years, necessary centers have been set up for listening to patients and providing advice and information in France. Multidisciplinary support is provided in these atopy centers, often by bringing together groups of parents and/or children which in turn creates a dynamic.


But, beyond the issue of prescription, what can a doctor actually say and do in his office when faced with a small child showing the first signs of or with fully established eczema that is set to get worse? The doctor must be able to:

  • answer all the parents’ usual questions (the same that have been asked for the past 50 years);
  • explain to a child over the age of 3 how to apply the ointment, how to avoid scratching and where to apply the anti-inflammatory drug;
  • understand the pathophysiology of the illness, which remains shrouded in mystery. This report offers a number of guidelines that should be found useful by doctors, who can then use them to find their own answers.


“Where does it come from, doctor?”

Although a pertinent question, the answer can prove disappointing. You need to explain that we are not sure of the exact cause and that, for the time being, knowing the cause changes nothing in terms of treatment. You can explain that it is an immunological illness related to our defense system involving sensitizing antibodies and cells. That others in the family may also have this sensitization to molecules found naturally in the environment (hay fever, asthma, oral allergy syndrome, etc.). It is also an illness affected by our genetic background, not only in terms of the transmission of an atopic predisposition, but also the onset of a dry skin condition called xerosis. The word “xerosis” should be pronounced, because patients will find this “xer” stem in numerous emollients. You can say that much genetic research is being carried out into how AD damages the epidermal barrier. And this intrinsic lack of cohesion in the epidermisstratum corneum is made worse by use of detergents, which makes it easier for allergens to penetrate the skin and promotes the activation of the immune response responsible for inflammation. You can go back to the notion of “blotting paper” type skin, whereas emollient treatment tends to recreate a “protective film” barrier type skin. Avoid trying to develop the notion of filaggrin mutations or those involving the components of the stratum corneum, SPRR3, etc., which is bound to be a flop!

If, however, you do want to explain the role played by filaggrin, you can say it is a protein produced by epidermal cells (keratinocytes) to keep the outer layers of the skin hydrated. Filaggrin deficiency can be qualitative (several gene mutations are described), and this concerns about 30% of individuals (various ethnicities), however it is always quantitative since chronic inflammation affects filaggrin production. Use these explanations to motivate the family to continue the first-line twice-daily treatment with the emollient.


  • AD is caused by numerous factors, and you do not need to know the cause in order to treat your child.
  • The words “xerosis” and “skin barrier” must be pronounced.
  • The notion of filaggrin may be addressed in an academic setting!


“Are there aggravating factors?”

These must be sought in each young patient. The number one culprit for adults is “stress,” a nociceptive stimulus, but in babies it is worth remembering that the main source of stress is the eczema itself. Parents always agree on this point!

The condition can also be exacerbated by:

  • heat: child too well wrapped-up, baths that are too hot. The ideal temperature for a bath is 33° and for the bedroom 19°;
  • woolen clothing in contact with bare skin;
  • detergents and fragrance;
  • poorly-rinsed laundry (overloaded washing machine);
  • all immunity stimulants (infections, vaccines, etc.).

Message :

  • The main source of stress for an atopic infant is the eczema itself, which causes pruritus and insomnia.

“What if it is caused by an allergy?”

This question is never asked without cause. There is an implication: It’s up to you, doctor, to find the allergen and tell us what it is, then we can remove it and our child will be cured! Go in peace, Madam... it’s biblical.

Explain that although in 80% of cases the atopic predisposition is inherited from the family, AD is not linked with a specific allergen like hay fever. But the more the eczema is neglected, the more sensitive children become to the molecules found naturally in the environment, which will then become “allergens” for them.


  • There is an atopic predisposition, which makes subsequent sensitization more likely.
  • “The” eczema gene does not exist.

Is the eczema caused by a food allergy?

There is one well-established fact: it is in populations of infants suffering from AD that we find the most food allergies (around 10%) compared to a normal population (around 4%). Furthermore, those with eczema are good IgE producers (in 80% of cases) and allergenic multitests for IgE (Trophatop®, CLA®, etc.) will come back positive. In the overwhelming majority of cases, it will be an asymptomatic sensitization, not a clinical allergy. The skill for the doctor will then lie in explaining the difference between sensitization (presence of antibodies, in this case 80%) and an allergy (presence of an illness, in this case 10%). To avoid such a cryptic debate, you should not therefore ever prescribe this kind of biological test. They are not sufficiently specific and often lead to elimination diets, which can have non-negligible consequences in this period of growth and development. An infant may however become allergic to milk protein (CMPA). In this case, the AD will not be isolated and may be accompanied by “IgE-dependent” signs synchronous with the diet: acute urticaria, vomiting, bloody diarrhea, shock. A more torpid form will be characterized by chronic enteropathy, a break in the weight curve and sadness. When a food allergy is associated with eczema, the AD is not therefore “naked.” In the example of CMPA, milk absolutely must be eliminated, of course, and a hydrolyzed milk prescribed (EH milk), but this will not cure the AD and so the topical treatment must be continued.

Before prescribing a diet, you must prove the allergy exists (skin tests and tests for specific IgEs that are oriented and concordant with the clinical picture). In enteropathic forms, the check-up will take place in a hospital environment (elimination/reintroduction test, sometimes TPO test, endoscopy, etc.). Food will never be excluded just “to see,” without a valid argument.

Atopic dermatitis in infants

What is the relationship between eczema and asthma?

There is a risk as atopy progresses of developing other illnesses such as asthma or hay fever (called the “atopic march”). In this case, the child becomes allergic to aeroallergens (mites, pollen, animal hair, etc.). You must therefore ask the family of children suffering from AD about their environment, and ask that their bedroom be kept at a temperature of 18° / 20° and aired morning and evening, which reduces the mite load. You must mention asthma:

  • if the child coughs often, especially at night, when exercising or at the slightest cold;
  • if the child is quickly out of breath when exercising, laughing or crying;
  • if the child wheezes when breathing in or out.

AD can therefore coexist with a respiratory or digestive allergic illness, but it is not mandatory. In any case, the skin illness is never caused by an isolated allergen. In a European multicenter study in which we participated (ETAC study), conducted on more than 800 babies monitored for 3 years, 80% of infants with severe eczema became asthmatic.


  • Severe eczema is often a marker of a subsequent respiratory multiple sensitization.
  • Genetics aside, severe eczema can be the result of therapeutic negligence.

“Are corticosteroids dangerous?”

Corticophobia exists.

AD can be easily diagnosed, prescriptions are relatively consensual and... that is not enough. Very few mild chronic infant illnesses are accompanied by so many taboos, beliefs and doctor-shopping. In addition, comments such as “your doctor is hopeless, he’s treating you without knowing what caused it!” are common. You need to return to the basics: baths at 33° with detergent-free soaps, bedroom at 19° aired morning and evening, oiling of skin with ointment in the winter and with cream in the summer. You must also, and above all, take the time to fight corticophobia.           

A recent survey in February 2012 conducted by Pierre Fabre Laboratories gathered 4,000 responses from mothers of children aged under 11. More than a quarter of those surveyed had a child with an allergic illness and 13%, i.e. 525 children, were infected with AD (Fig.3). One of the questions concerned the use of topical corticosteroids during acute episodes: in total, 28% of mothers refuse to use such a product, and when eczema is considered severe 18% do not use it! Corticophobia was still going strong in 2012.

How should you cope with a refusal to treat?

Above all, avoid lecturing and preaching, you will only get the opposite reaction from the one you hope for, and it will do more harm than good—as L. Boutry says, a scientific message at odds with parents’ opinions can have a negative effect. You must first pinpoint the parents’ fears (often made worse by guilt: “my child has eczema because of me and, what’s more, to relieve him, I’m applying a dangerous cream to his skin”). Then you must above all reassure them, because today, after half a century of use, we are safe in the knowledge that, when used properly, topical corticosteroids are not harmful for children. They should be applied in compliance with certain rules, which must be written on the prescription. All are not absolute, but a certain consensus exists among pediatrics on the following:

Apply the cortisone cream (or ointment) only on inflammatory areas, once a day, until the lesions disappear. The amount of topical corticosteroid used must decrease as the lesions fade. Weaning is therefore natural and gradual.

Eczema progresses in flare-ups, so immediately apply more on relapse since there is no “resistance” to treatment.

Give an idea of the doses to be used to avoid disapproval from the entourage or pharmacist: “Use approximately one 30g tube for the first 8 or 15 days, then one tube per month for 3 months.”

You might be interested to know that in hospital consultation I have already applied 2 tubes of topical corticosteroids on D1 to a child under an expandable Tubifast® tubular bandage.


Corticophobia begins with pharmacist/doctor “corticonervousness.”

Another anti-inflammatory drug is available: Tacrolimus, or Protopic®. It can be prescribed only after 2 years, by dermatologists and pediatricians.

Another anti-inflammatory drug is available: Tacrolimus, or Protopic®. It can be prescribed only after 2 years, by dermatologists and pediatricians.

  • Over the past 50 years, ideas have come in the form of dictatorship and unchecked liberalism. This (somewhat muddled) fermentation came from allergists who, out of respect for the precautionary principle, advocated late diversification. An even more rigid attitude was adopted for foods strongly associated with allergies, such as eggs, fish and peanuts. The sanction was immediate in European countries: food allergies doubled in 10 years. One example: in England, the restrictive measures on peanut were recommended for breastfeeding mothers and children. Result: the peanut allergy has increased from 0.6 to 1.8% in 10 years according to a study carried out on 1,072 mothers and their children!
  • It is currently recommended to start introducing each new food during windows of opportunity or favorable periods after the 4th month, between the 17th and 24th week of life. One new food at a time. This common-sense attitude promotes tolerance to food...

Food is still the number one topic brought up by parents at pediatric consultations. This is because “providing nourishment” has a more emotional dimension than “giving something to eat.” When babies experience minor disorders (regurgitation, crying in the first months, soft stools with no impact on weight), the finger is too often pointed at the cow, our placid ruminant. But additional arguments are needed to change the milk. Do not forget that the cow, too, can be a mother!

“Can my child be cured?”

Talk about the usual progression:

It is normally characterized by flare-ups, which can be triggered by any kind of aggression (stimulus) whether physical (sweating), immunological (infection) or psychological (pressure, etc.). Conversely, other stimuli can promote healing: a change in location, in climate, in treatment, in diet, etc. The most common AD progression profile is therefore an improvement in 80% of cases at least before the age of 6.


Addressing children

Three main points should be developed at each consultation. If the patient is a baby, speak to the mother, in the case of children, involve them.

Explain the concepts of inflammation and skin dryness

Skin is dry in a diffuse manner and inflammatory in specific areas, often in skin folds. To educate your patients and their family, you can use metaphorical images such as fire for inflammation and the cement in a wall for the skin barrier. The aim being to motivate children to moisturize their skin on a daily basis. Shouting: “Apply your cream!” is doomed to failure if you do not explain why. An emollient is required for xerosis and a topical corticosteroid for red patches on the cheeks and in skin folds. Folds are bastions that must be conquered immediately on relapse.

Show how to apply cream and ointment

At the very first consultation, you must apply the topical treatment yourself:

  • Apply the emollient in a fun way using the “white ladybug” idea (rapidly dot the cream in various places then homogenize by massaging them together).
  • Apply the topical corticosteroid on the inflammatory areas. Count in front of the mother how many adult finger pads (FP) are needed to cover all the lesions. Note the number down (e.g. 7 FP) on the prescription. The next day, the mother will use this same amount, which will then decrease daily as the inflammation decreases. After that, do not oblige the parents to continue with this obsessive counting!

Promote alternatives to scratching

What could be more normal, and even enjoyable, than scratching when pruritus takes over. This is true, but very rapidly the action becomes painful, aggravates lesions and causes secondary infections. Possible solutions include:

  • cold (gel packs, sprays of thermal water stored in the fridge);
  • contact with soft materials (massage wheels, smooth cold pebbles);
  • diverting attention (handling a foam ball, stroking a teddy bear), etc.

Associating children with their illness from a very early age seems to help raise their awareness of the necessary treatment and pathological mechanisms. You need to identify the side effects (emotional and/or physical pain, treatment constraints, lassitude) and help children adopt the right approach to treatment to improve their self-image and quality of life.

Do not hesitate to call the patient back, AD consultations are, as we know, very time-consuming.


  • AD is a visible illness, and children who feel good about themselves will have a more positive attitude.
  • Consultations take time and must be repeated. It is a matter of helping the child to live well with it.


AD or atopic eczema is a difficultly-determined disease combining a genetic predisposition and the influence of environmental factors. The end of the 20th century was marked by a multitude of publications looking to prove it was caused by an allergy, in particular a food allergy, with many changes in opinion. We all know that infants with eczema, as good producers of IgE, are more sensitive to the molecules in their environment. This sensitization is not always a sign of disease, and even less so the cause of eczema, but it can sometimes be an aggravating factor.

At the beginning of this century, however, studies on AD finally refocused on the skin. We are rediscovering the fact that eczema is a skin illness involving a deterioration in the quality of the stratum corneum. The primum movens probably lies here. The most important fight for parents is that of protecting the skin barrier. The practitioner must help parents and children overcome their lassitude, fight corticophobia, which is the main cause of treatment failure, and search for aggravating factors. Treating AD involves much more than a prescription. Medical practitioners, often short of time, can also seek help by sending children/parents (or adults) to atopy schools. Their number has grown over the past five years, and they deliver a multidisciplinary education.

“Education can do anything, it makes bears dance” GW. Leibniz



Eigenmann PA, Dermatite atopique et allergie alimentaire. Rev Fr Allergol 2012 ; 52 : 175-176

Henino A, Marty JP, Nicolas JF. Pénétration des allergènes protéiques par voie cutanée. Rev Fr Allergol Clin Immunol  2005 ; 45:50-53.

F. Bérard. Bases physiopathologiques de la dermatite atopique. Ann Dermatol Vénéréol  2005 ; 132 :1S123-54.

Robert J. Vivre mieux avec les Allergies de l’Enfant. Odile Jacob ;  2012 (1 vol. 233p)

Scheinmann P. La marche de l’allergie : que reste-t-il de l’histoire dite naturelle de l’allergie ? Rev Fr Allergol Immunol Clin ; 2006, 46 : 402-407

Simon M. La dermatite atopique est-elle toujours associée à une altération de la barrière épidermique ? Rev Fr Allergol ; 2013, 53 : 125-128

Stadler JF, Barbarot S. Atopic dermatitis school: therapeutic education of atopic patients. Rev Prat 2006; 56(3): 273-276

Taieb A. Atopic dermatitis pathophysiology update. Bull Acad Nati Med 2012; 196: 621-629



lieu de discussion :

Plaquette pédagogique téléchargeable sur 

GET dermatologie :