Atopy

Atopy (Greek ἀτοπία - placelessness, out of place, special, unusual) or atopic syndrome is a predisposition toward developing certain allergic hypersensitivity reactions. Atopy may have a hereditary component, although contact with the allergen must occur before the hypersensitivity reaction can develop.

Terminology
The term "atopy" was coined by Coca and Cooke in 1923.

There is some controversy over the proper use of the terminology.

Many physicians and scientists use the term "atopy" for any IgE-mediated reaction (even those appropriate and proportional), but many pediatricians reserve the word "atopy" for a genetically mediated predisposition to an excessive IgE reaction.

Presentation
Atopy (atopic syndrome) is a disease characterized by a tendency to be “hyperallergic”. A patient with atopy typically presents with one or more of the following: eczema (atopic dermatitis), allergic rhinitis (hayfever), allergic conjunctivitis, or allergic asthma. Patients with atopy also have a tendency to have food allergies.

Causes
Atopic reactions are caused by localized hypersensitivity reaction to an allergen. Atopy appears to show a strong hereditary component. One study concludes that the risk of developing atopic dermatitis (3%) or atopy in general (7%) "increases by a factor of two with each first-degree family member already suffering from atopy".

Environmental factors are also thought to play a role in the development of atopy, and the 'hygiene hypothesis' is one of the paradigms available to date that may explain the steep rise in the incidence of atopic diseases. This hypothesis proposes that excess 'cleanliness' in an infant's or child's environment can lead to a decline in the number of infectious stimuli that are necessary for the proper development of the immune system. The decrease in exposure to infectious stimuli may result in an imbalance between the infectious-response elements and the allergic-response elements within the immune system.

Some studies also suggest that the maternal diet during pregnancy may be a causal factor in atopic diseases (including asthma) in offspring, suggesting antioxidants, certain lipids, and a Mediterranean diet may help to prevent atopic diseases.

The multicenter PARSIFAL study in 2006, involving 6630 children age 5 to 13 in 5 European countries, suggested that restrictive use of antibiotics and antipyretics are associated with a reduced risk of allergic disease in children.

Signs and symptoms
Patients with atopy usually develop what is referred to as the “allergic triad” of symptoms, i.e., eczema (atopic dermatitis), hayfever (allergic rhinitis), and allergy-induced asthma (allergic asthma). They also have a tendency to have food allergies, and other symptoms characterized by their hyperallergic state. For example, eosinophilic esophagitis is found associated with atopic allergies.

The individual components of atopy are all caused at least in part by allergy (type I hypersensitivity reactions). Therefore, atopic responses appear after the body is exposed to various allergens, for example pollen, dander, dust mites, certain foods, or chemical/physical irritants.

Although atopy has various definitions, in general, it is defined by the presence of elevated levels of total and allergen-specific IgE in the serum of patient, leading to positive skin-prick tests to common allergens.

Atopic syndrome can be fatal for those that experience serious allergic reactions, such as anaphylaxis, brought on by reactions to food or environment.

Genetic predisposition
There is a strong genetic predisposition toward atopic allergies, especially on the maternal side. Because of the strong familial evidence, investigators have tried to map susceptibility genes for atopy. These have been reviewed, but, in essence, genes for atopy tend to be involved in allergic responses or other components of the immune system.

Staphylococcus aureus colonization
Patients with atopic eczema often improve with the administration of antibiotics or bleach baths (half a cup of bleach per tubful of water) to control bacterial colonization on the skin. Filaggrin mutations are associated with atopic eczema, and may contribute to the excessive dryness of the skin and the loss of the barrier function of normal skin. It may be possible that the filaggrin mutations and the loss of the normal skin barrier expose crevices that make it possible for Staphylococcus aureus to colonize the skin. Atopic eczema is often associated with genetic defects in genes that control allergic responses. Thus, some investigators have proposed that atopic eczema is an allergic response to increased Staphylococcus aureus colonization of the skin. A hallmark indicator of atopic eczema is a positive “wheal-and-flare” reaction to a skin test of S. Aureus antigens. In addition, several studies have documented that an IgE-mediated response to S. aureus is present in patients with atopic eczema. The unmistakable improvement in atopic eczema observed with antibiotic administration or bleach baths helps correlate the hypothesis that Staphylococcus aureus colonization is critical to the appearance of atopic eczema.

Symptoms
Some symptoms, from an atopy questionnaire :
 * Cracks in the skin under the earlobe
 * Eczema
 * In elbow flexures and/or hollow of the knees
 * Nipple eczema
 * Neurodermatitis
 * Subtype Dyshidrosis
 * Keratosis pilaris
 * Perlèche
 * Conjunctivitis
 * Chronic or seasonal rhinitis

Treatments
Corticosteroids: For years, there was no treatment for atopic eczema. Atopy was believed to be allergic in origin due to the patients’ extremely high serum IgE levels, but standard therapies at the time did not help. Oral prednisone was sometimes prescribed for severe cases. Wet wraps (covering the patients with gauze like a mummy) were sometimes used in hospitals to control itching. However, a true medical miracle occurred in the 1950s with the discovery that corticosteroids could be used topically in creams or ointments for atopic eczema and other conditions. Thus, the use of topical steroids avoided many of the undesirable side-effects of systemic administration of corticosteroids. Topical steroids control the itching and the rash that accompanies atopic eczema. Side-effects of topical steroid use are plentiful, and the patient is advised to use topical steroids in moderation and only as needed.

Immune modulators: Pimecrolimus and tacrolimus creams and ointments became available in the 1980s, and are sometimes prescribed for atopic eczema. They act by interfering with T cells, but have been linked to the development of cancer.

Avoiding dry skin: Dry skin is a common feature of patients with atopic eczema (see also eczema for information), and can exacerbate atopic eczema.

Avoiding allergens and irritants: See eczema for information.