The word eczema comes from the ancient Greek meaning; "to boil over". It is used to describe a pattern of inflammatory responses. Clinically, acute eczema is associated with marked erythema, superficial papules & vesicles that easily excoriate and lead to crusts. Chronic eczema is composed of rather faint erythema, thickening, and scaling.
Eczema accounts for a large proportion of skin diseases and is a common reason to see an Allergist or dermatologist.
A range of external triggers may induce the condition & internal factors acting singly or in combination.
The terms Eczema and Dermatitis are used interchangeably. Dermatitis tends to be used more to imply an external trigger.
Classification of Eczematous Skin Diseases
Atopic Dermatitis: Allergic mechanisms play a major role in this disease and it will be discussed at length later. This usually starts off as an Immediate Type 1 Hypersensitivity Reaction. Haematogenous reaction is also possible.
Allergic Contact Dermatitis: This is eczema provoked by local contact with allergen (eg, Nickel and Poison Ivy). This is a delayed Type 4 Hypersensitivity Reaction.
Photoallergic Dermatitis: This is caused by local contact with an allergen followed by exposure to Ultra Violet radiation. Hematogenous induction is also possible.
Irritant Contact Dermatitis: Provoked by local irritants, like detergents and water on the hands in a chef or cleaner. This condition is more common in people with atopic dermatitis.
Seborrheic Dermatitis: This is a very common skin condition characterized by redness and scaling. It occurs in the areas of the skin, where the sebaceous glands are most active, such as the face, scalp, and the presternal area. It is more common in men. Pityrosporum ovale is thought to be the cause of this disorder.
Atopic dermatitis is a chronic relapsing, pruritic dermatitis that usually occurs in individuals with a personal or family history of atopy. It is estimated that 65% of patients develop atopic dermatitis in the first year of life and 90% before the age of 5. Onset after 30 years of age is so unusual that the diagnosis should be questioned. Most patients improve with age.
Prevalence: Population studies suggest that the prevalence of AD has been steadily increasing since World War II, and in most countries it now affects more than 10% of the children at some point. In some countries it is as high as 25%.
Modified criteria for diagnosis of atopic dermatitis in infants (Adapted from Seymour JL, et al)
Three major features:
Family history of atopic disease
Typical facial or extensor eczematous or lichenified dermatitis
Evidence of pruritus
Three minor features:
Xerosis, ichthyosis, hyper linear palms
Post auricular fissures
Chronic scalp scaling
Provocation factors in atopic dermatitis
A number of different triggers of atopic dermatitis are well established. The relative importance of these triggers will depend on whether the patient first sees an Allergist or a Dermatologist.
The Eczema – Food Allergy Story
The role of food allergy in atopic dermatitis has been the source of more controversy than perhaps any other skin disorder. The disagreement oftentimes is one of semantics. The fact that some patients with atopic dermatitis respond adversely to some foods at some time in the history of their disease cannot be denied. The fact that exacerbations of atopic dermatitis can be caused by multiple and varied "triggers" confounds the objective evaluation of any single trigger. One should not allow rationality to succumb to emotions.
Positive skin prick test to foods only mirrors serum food specific IgE responses to food antigen, it does not equal clinical food allergy. Hugh Sampson demonstrated this when he demonstrated that, in his select population, only one-third of patients with positive skin prick test result correlated with positive food challenge result.
Positive skin prick test or RAST have been reported in 51% to 96% of patients with AD. Unfortunately, the positive predictive value of skin prick tests is less than 50%, but the negative predictive value is more than 90%. So a negative skin prick test almost certainly excludes a food allergy.
Double-blind placebo-controlled food challenges (DBPCFCs) must be considered the most reliable technique for confirming the diagnosis of food allergy (the "gold standard").
From many studies utilizing DBPCFCs, 33% to 66% of patients with AD tested developed a reaction when challenged. DBPCFC has been reported to produce skin reactions in 84% to 96% of patients tested. These reactions, however, develop within minutes up to 2 hours after challenge and last only 30 to 120 minutes. It is believed that this reaction causes histamine release from mast cells, which is the stimulus for the itch in Eczema.
In Dr Hugh Sampsons (tertiary) hospital referral population, 80% of the children evaluated were found to be food allergic. It is also found in several paediatric studies, that the more severe the atopic dermatitis, the more likely food will be a clinically relevant trigger.
Fortunately, food hypersensitivity in young patients is not always a life-long affliction. One study reported that food sensitivity persisted in 67% of children 7 to 16 years of age with severe AD and was always associated with aeroallergen sensitivity. Hugh Sampson reports that the development of tolerance to peanuts, nuts, and seafood almost never occurs, whereas children sensitive to soy, milk, eggs, and wheat frequently outgrew their clinical reactivity after several years of allergen avoidance.
Based on all the studies it can be concluded that in patients with persistent, generalized, moderately severe to severe AD, food allergy should always be excluded.
Irritant triggers in AD
The most consistent perturbations of atopic dermatitis are irritants. The skin response to irritants is increased in atopic individuals with or without apparent dermatitis. Occupational substances have particular clinical and social relevance.
Intolerance to wool is in part based on its irritating effect on the skin (other part related to the dust mites which it harbours).
Cigarette smoke may also elicit irritating eczema on the eyelids in atopic dermatitis.
It is speculated that an altered composition of the epidermal lipids, an enhanced release of histamine, or a latent, subclinical inflammatory reaction in the skin may play a role in the enhanced vulnerability of the atopic skin.
Both systemic and local infections can trigger the eczematous response in atopic dermatitis. Staphylococcus aureus has been studied extensively as a possible trigger factor as it is detected in the skin in more than 90% of all atopic dermatitis patients. Exotoxins are detectable in two thirds of all cultures containing s. aureus, which have been generated from skin swabs in AD. They may function as superantigens, which are capable of stimulating the release of potent inflammatory agents.
It is well established, in clinical experience, that atopic dermatitis can be improved, in many cases by systemic antibiotics. This may be associated with the reduction of superantigens on the skin.
In addition to s. aureus, the saprophyte Pityrosporum ovaleis thought to elicit a specific immune response and thus provoke eczema on the face and neck of atopic dermatitis patients.
Environmental and contact allergen
Hypersensitivity to house dust mite antigen is found in 5% of all people in Western nations whereas it is found in up to 90% of adolescents or adults suffering from atopic eczema. Exacerbations of atopic dermatitis caused by dust mites are presumed to be related to both inhalation and skin contact. Several clinical studies have reported improvement of the skin condition after a reduction in the level of house dust mites.
In addition to mites, sensitisation to pollen or animal dander may be associated with eczematous skin reactions. Therefore, contact with animals should be avoided even if the patients do not suffer from respiratory symptoms.
Most studies indicate that the frequency of sensitisation to contact allergens in ingredients of common preparations (e.g., vehicles, preservatives, fragrances, antibiotics, steroids) appear to be higher than normal. Thus, classical patch testing should not be neglected in patients with atopic dermatitis because it may reveal important cofactors in the development of eczematous skin lesions in these patients.
Hormonal and emotional factors
Fluctuations in severity of atopic dermatitis are frequently observed in women. This points to hormonal influences with menstruation, pregnancy, birth and menopause as possible trigger factors.
Many studies emphasize the importance of psychological factors, such as personality traits or psychological stress, in the worsening and maintenance of skin symptoms. Stressful life events may be associated with an increas in itching which leads to scratching and, by this mechanism, to a deterioration of the skin condition. Neuropeptides and increased number of nerve fibres, which have close contact with mast cells may be possible links between the nervous system and the skin in atopic dermatitis.
Diagnosis of AD
Simplified Diagnostic criteria of Atopic Dermatitis (According to the UK Working Partys diagnostic criteria for Atopic Dermatitis)
Itchy skin condition (obligatory)
Plus three more of the following
History of flexural involvement
History of asthma / hay fever
History of generalized dry skin
Onset of rash under the age of 2 years
Visible flexural dermatitis
Treatment of Atopic Dermatitis
Avoid all allergic triggers (foods, dust mites, pets, pollens, and contact allergens)
Skin Hydration – Plenty of Emollients several times per day
Anti-inflammatory – Topical steroid creams & ointments Antimicrobial- Oral Antibiotics & sometimes antifungals Antihistamines – Value disputed. Older, sedating antihistamines preferred by some because of sedating effects.
Newer Approaches to therapy
Tacrolimus is an immunosuppressive macrolide like cyclosporin, which has potent T cell suppressive effects as well. Topical tacrolimus has shown promise in AD.
Specific desensitisation (immunotherapy) to airbourne allergens has been shown to be of benefit in several open studies