Endogenous factors - Atopy
Atopy is an inherited predisposition which causes a tendency to suffer from one or more of the following “atopic diseases”: allergic asthma, allergic rhino-conjunctivitis and atopic dermatitis. The diagnosis of “atopy” is not based on one single distinctive clinical feature or laboratory test, but rather results from a combination of patient and family history and clinical findings. These features include:
- Family and patient history with regard to eczema, allergic rhinitis and allergic asthma
- Patient history with regard to milk crust, sweat-induced pruritus, intolerance of certain cloth fabrics or metals, photophobia
- Present or past clinical findings such as xerosis cutis, ear fissures/ eczema, dyshidrosis or dyshidrotic hand eczema, pityriasis alba, atopic winter feet, nipple eczema, angular cheilitis
- Atopic stigmata such as palmar hyperlinearity, Hertoghe’s sign, “dirty neck”, keratosis pilaris
- White dermographism, acrocyanosis
- Laboratory tests such as total IgE, phadiatop
As mentioned above, atopy may lead to the eczematous disease “atopic dermatitis”. It may also facilitate the development of irritant contact dermatitis.
Genetics of atopic dermatitis
The risk for AD is doubled in children whose father or mother have a history of atopy and it is more than 50% if both parents have at least one atopic disease. Interestingly AD is rather associated with maternal than paternal atopy. Several genes are suspected to be linked to AD such as 5q31-33 with a cluster of cytokine genes.
Immunology of atopic dermatitis
The best funded explanation for the increase of AD is the so called “hygiene hypothesis”, which assumes that atopic diseases are prevented by infections in early childhood contracted e.g. through contact with other siblings or playing outside. This theory is supported by the already known potential risk factors for AD like small family size, increased income and use of antibiotics or migration to urban environments. Also immunological findings sustain the “hygiene hypothesis“. Allergic responses are pushed by the T helper-cell type (TH) 2 immune response. On the other hand infections are induced by TH 1 immune responses. TH 1 responses antagonise the development of TH 2 cells. This could be the explanation why a decreased number of infections during early childhood could boost the TH 2 allergic responses.
Triggering factors of atopic dermatitis
Although the predisposition for atopic dermatitis is genetically determined, several trigger factors may influence the outbreak of skin changes. These trigger factors include:
- Respiratory allergy. In affected individuals, respiratory allergy to house dust mites, pollen and animal epithelia may cause an outbreak or worsening of skin changes if they come into contact with the allergen
- Food allergies. Food allergy is more frequent in infants and children with atopic dermatitis. In affected individuals, common allergens such as cow milk, eggs, fish, soy or peanuts may cause an outbreak or worsening of skin changes if they come into contact with the allergen.
- Microbial agents. Staphylococcus aureus colonises more than 90% of AD skin lesions. Proteins of Staphylococcus aureus may function as foreign antigens, their exotoxins operating as superantigens and thus exacerbate AD.
- Dry skin induced e.g. by long bathing, cold dry climate, insufficient use of emollients may lead to exacerbation of eczema.
- Itching and subsequent scratching
- Sweating induced by e.g. impermeable clothing, hot work places or stress may lead to worsening of skin changes.
- Chemical/physical irritants like smoking or clothes also may lead to exacerbations.
- Psychological stress