Atopic dermatitis/Eczema (AD) is an inflammatory skin condition in which number of factors including aberrant immune regulator and epidermal barrier dysfunction, seem to contributes to its pathogenesis.

Definition:

While at new level the clinical diagnosis of AD is relatively simple and straight forward, it has not always been entirely clear how wide those clinical parameters showed be. The first major advance in this area came with the widely quoted “Hanifin & Rajka “ Criteria, which were based entirely on elements of the history and on clinical examination.

These criteria are often still offered as the diagnostic key to selection of patients in studies. These have been subsequent attempts at refinement which work reasonable well, at least in epidemiological and research settings.

Prevalence

Although the methods used vary considerably from study to study, making direct, accurate, comparisons difficult, most authorities accept that the prevalence of AD is rising and is much greater in those countries that are more “developed”. There are certain studies which indicate that the prevalence of AD is significantly higher in first generation baby’s born in developed countries than in their parents generation strongly suggesting that environmental factors play a role in expression of the disease. Similar support comes from a well respected Punjabi research group who found that children which AD appeared to come much more commonly from urban rather than rural areas.

Genetics

That genetics play a major role in ad is without questions. Observations such as that linking atopic with the high affinity IgE receptor appeared to support a multi genetic basis for atopic diseases but interestingly. There seems to overlap between some of those identified for AD and those for psoriases’ more recently, however another vitally important genetic story began to unfurl among filaggrin which leads nicely on to the epidermal  at barrier in AD .

Epidermal Barrier

The unequivocal establishment of a primary, in born abnormality of barrier function in some AD patents, especially those with severe disease and early onset or persistence in to adulthood has given everyone pause for thoughts. Thus the beginnings of clinical research programs aimed at primary Prevention of AD by the use of emollients is Clearly some thing to keep an eye on.

Immune Dysfunction

It is self evident that Immune system is involved in pathophysiology of AD. The disorder is characterized histologically by a lymphocytic predominance in the inflammatory infiltrate with  majority being T-cells. There is also an abnormally high level of circulating IgF. prick tests and RASTS to common allergens including aeroallergens such as pollens, cats, dogs and however dust mite. Frequently yield a degree of sensitivity through specific IgE. Patients usually have low basal If levels and persistence  of th-2 dominant responses. IgE is thought to be involved as ago between and presenter of antigenic Stimulation, bound as it is to the langerhans cell surface via the high affinity IgE receptor, but is also capable of being a direct target for antibodies as well as being auto reactive  and forming immune complexes with other proteins.

Role of staphylococcal is also present as individuals with Ad are frequently colonized by bacterium and is addition to direct effects that infection may have on the skin and on immune responses. It is clear that S. Aureus may also provide an additional “Kicks to T cell activation becomes keretinocytes exposed to staphylococcal enterotoxin B- stimulated mononuclear cells show significantly enhanced allrgen presentation.

Therapy

·        An accurate diagnosis &  proper assessment.

·        Education & information

·        Emollients

·        Topical anti-inflammatory therapy

·        First line-topical corticosteroids.

·        Second line – topical calcineurin inhibitors

·        Photo and photo chemotherapy.

Systematic therapies known to be effective in severe AD include Azathioprine and cyclosporine.