Atopic eczema causes

The symptoms of many chronic diseases, such as rheumatoid arthritis, multiple sclerosis, asthma and chronic obstructive pulmonary disease (COPD) are caused in large part by an excessive and chronic inflammatory response and are therefore potential human diseases for drugs which inhibit the SSAO/VAP-1 activity. Notably, it has been recently shown that patients suffering from either atopic eczema or psoriasis, both chronic inflammatory skin disorders, demonstrate an increase in SSAO/VAP-1 positive vessels in their skin compared to skin from healthy controls [47,48]. 

There is little evidence to support the use of coal tar in treating atopic eczema and it would therefore be inappropriate. In addition, hypersensitivity reactions may be caused by the use of coal tar. 

Staphylococcus aureus is the most common cause of bacterial infected eczema as 90% of atopic eczema patches are colonised by this organism. 

Certain pitfalls were encountered in the surveillance program whereby elevated PNP levels were observed but did not relate to poor spray techniques. These pitfalls are best illustrated by two case studies. The first was a 28-year-old sprayman, whose persistently elevated PNP levels could not be explained on the basis of a careless technique. It was not until the operator himself was examined and the extensive atopic eczema identified that the cause became apparent. There were deep fissures on the dorsum of his hands and in the interdigital clefts. Later, when his skin condition improved, lower concentrations of urinary PNP were observed, suggesting that the mechanism of this exposure was a breakdown of the natural protection provided by the intact skin barrier. 

Topical monoethyl fumarate caused contact dermatitis in a patient with atopic eczema and a generalized, partly pustulous, exanthema in a patient with psoriasis (10). The authors suggested that the mechanism was non-immunological contact urticaria. 

A defect in the capability of the enzyme 5-6-desaturase to convert linoleic acid to y-linolenic acid is known to occur in patients with atopic dermatitis (9). Patients with atopic eczema have a dietary deficiency in metabolites of linoleic y-linolenic acid, dihomo-y-linolenic acid, arachidonic acid, adrenic acid, and docosapentaenoic acid caused by a reduced rate of activity in the 5-6-desturase enzyme (8). Galli et al. compared blood samples from babies born to parents who suffered from atopic eczema. Results showed... 

Atopic eczema is a chronic fluctuating inflammatory condition of the skin with no known cause, although there is often a genetic link and a family history of allergic sensitivity. 

Eczema is caused by environmental influences affecting genetically predisposed individuals [146(111), 147(111)]. It is the most frequent inflammatory skin disease in childhood. Prevalence estimates for eczema ranged between 1.1 and 3.1% in the early literature, however, in newer studies these figures reach 25% based upon questionnaires, and 12.9% based upon dermatological examinations. There is evidence that the IgE-associated subgroup of eczema, atopic eczema, has increased in frequency over the past decades. 

A slightly dry skin may be treated with an extra fat containing hydrophUic cream. Patients with a very dry skin use cutaneous preparatirms with a high amount of hpophUic components. Lipophilic creams are suitable for the treatment of the chronic state of atopic eczema. Hydrophobic ointments or saturated hydrocarbons are not indicated because they have an occlusive effect, which causes heat accumulation and enhances itching. 

Other reports indicate that aqueous cream may cause local skin irritations such as stinging, burning, itching and redness, when it is used as a leave-on emollient, particularly in children with atopic eczema. The reactions, which are not generally serious, often occm within 20 min but can occur later. However, patients and those who care for them should be warned of this risk dming an eczema treatment consultation [15 ]. 

Johnson (73 -) conducted an interesting experiment in which he proved that in a number of skin conditions simple protective applications are quite effective, and that the use of topical corticosteroids is superfluous. Especially those conditions which are characterized by dryness, scaling and cracking of the skin, and in which environmental aspects are likely to be involved, responded well. These were xeroderma, winter (asteatotic) eczema and atopic eczema with dryness and cracking. Simple preparations are especially recommended by this author in skin conditions the cause of which is clearly traumatic in the sense that everyday activities associated with work, the home and leisure, unavoidably have a traumatic component. 

One in 10 persons, 22 million people, in the United States have allergies. Ten million of these suffer from the nasal discomfort of "hay fever" and six million from die more serious asthma. Substantial numbers of people in the United States die of allergic reactions to insect stings (more than 30 per year) or to injections of penicillin (300 per year in 1970). Foods, drugs, pollens, mold spores, mites in house dust, and even heat or cold can evoke serious allergic reactions. Among these eczema (atopic dermatitis) is very common. A major cause of allergic reactions has been... 

Eczema—inflammation of the skin, usually causing itching and sometimes accompanied by crusting, scaling, or blisters. A type of eczema often made worse by allergen exposure is termed atopic dermatitis. ... 

It has become conventional to apply the term eczema to conditions with an endogenous cause in atopic individuals and dermatitis to reactions to external agents. 

Eczema vaccinatum. Serious skin rashes caused by widespread infection of the skin in people with skin conditions such as eczema or atopic dermatitis. 

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