Naslov
Current state on atopic dermatitis management and skin care

Autori
Lipozenčić, Jasna

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, stručni

Izvornik
Strokovno srečanje z mednarodno udeležbo / Miljković, Jovan - Maribor : Univerzitetna knjižnica Maribor, 2005

Skup
III Dermatološki dnevi

Mjesto i datum
Maribor, Slovenija, 2005

Vrsta sudjelovanja
Predavanje

Vrsta recenzije
Nije recenziran

Ključne riječi
Atopic dermatitis; atopic eczema; management; skin care

Sažetak
AD is a chronic inflammatory skin disease due to genetic predisposition, characterized by pruritus, typical age-specific clinical picture, and frequently associated with other atopic diseases such as asthma and/or allergic rhinitis. The prevalence of AD is rather high, mostly involving children.There are probably several reasons for the increased incidence of AD, including higher exposure to air pollution, smaller families with less exposure to infections, more pets, higher maternal age, and a wider range of foods. There is clearly also an important hereditary component of atopic eczema. Atopy is a condition caused by multiple gene defects. Thirty genes responsible for expression of AD have been demonstrated. Several chromosomal regions contain pathophysiologically relevant candidate genes, especially on chromosome 5q31-33.Atopic constitution is more frequently transmitted by maternal inheritance. Various environmental factors influence clinical expression of AD, e.g., allergens, irritants, climatic and geographical conditions, body structure, psychological stress, secondary infections, etc. AD is frequently associated with immunodeficiency (selective IgA and IgM). Numerous factors are implicated in the onset of the disease. Hyperimmunoglobulinemia E is characteristic of atopic diseases, however, AD is also a consequence of immune response type IV. Elevated level of IgE, eosinophilia, activated macrophages with an increased secretion of the granulocyte-macrophage colony-stimulating factor (GM-CSF), prostaglandin E2 (PGE2), interleukin 10 (IL-10), IL-4 and IL-5 (by Th2 cells), decreased secretion of IFN-γ (by Th1), and enhanced spontaneous basophile release of histamine have been demonstrated in atopic skin. A correlation of elevated eosinophilic protein (ECP), soluble E-selectin with eosinophilia has been reported.Besides genetic there are other factors such as the environmental influence which consists of the climate itself, air pollution, airborne allergens (plant, animal allergens) and psychological and emotional factors which play an important role in the course of the disease. Environmental factors: irritants, alimentary allergens, aeroallergens, microbial factors, fungal infections, viruses are included in etiopathogenesis of atopic dermatitis.Atopic dermatitis is a multifaceted disease. The clinical picture, morphology and distribution of the skin lesion, varies greatly depending on the age of patient, the ethnic group he or she belongs to, the course and duration of the disease, aggravating factors and possible complications such as superinfection. It manifestation range from very mild to severe disease. There are currently no single laboratory tests for the diagnosis of AD, there has been substantial progress in the past decade toward understanding the basis of the immune response in allergic diseases such as atopic dermatitis. Laboratory tests are chosen according to history data and physical examination. In vivo tests in the diagnosis of immediate hypersensitivity are prick test, scratch test (scarification test) and intradermal tests. Despite the dilution, the allergen concentration is 100-1000-fold higher than prick testing and the risk of systemic allergic reaction is greater. Intradermal tests are recommended only if skin prick test are negative. Standard series with common aeroallergens and food allergens are employed. Patch test or epicutaneous test is used to determine delayed (type IV) hypersensitivity. In Atopy patch test aeroallergens, rarely food allergens, are used for path testing.Successful management of atopic dermatitis requires a different approach involving skin care, identification and elimination of flare factors, and anti-inflammatory treatment. Local therapy Skin care preparation should be applied over the skin within three minutes (3-minute rule) of bathing, otherwise bathing will lead to skin drying instead of desirable skin hydration. Skin infections with Staphylococcus aureus are rather common in AD patients, manifesting as madidations of skin lesions, pustules and crusts. Therefore, therapy with oral antibiotics, mostly erythromycin, azithromycin and cephalosporin preparations, is quite frequently justified. In case of localized pyodermal lesions, local antibiotics, mostly mupirocin, is applied. The yeast Pityrosporum ovale is efficiently eliminated by use of a ketoconazole shampoo, or with miconazole alone or in combination with hydrocortisone. Antihistaminics are widely used in acute flares against itch. Systemic corticosterods, such as oral prednisone, may require in the treatment of severe chronic AD. The dramatic clinical improvement that may occur with systemic corticosteroids may be also associated with an equally dramatic rebound flaring of atopic dermatitis after discontinuation of systemic corticosteroids. Ultraviolet light.Natural sunlight is frequently beneficial to patients with AD. However, if the sunlight occurs in the setting of high heat and humidity, thereby triggering sweating and pruritus, it may be deleterious to patients. Heliomarinotherapy (sun and sea therapy) is also useful. UVB or combined UVAB exposure is efficacious in AD patients. High daily doses of UVA1 (340-400 nm) are even more efficacious. Photocemotherapy with oral photosensitizer methoxypsoralen (Meladinin tablets) followed by the UVA exposure (PUVA therapy) may be indicated in patients with severe, widespread AD with failure of topical steroid therapy or significant corticosteroid side-effects. Topical application of 0.3% 8-MOP ointment (PUVA cream therapy) could be used to treat palmo-plantar AD lesions. Cyclosporine is potent immunosuppressive drug that acts primary on T cells by suppressing cytokine transcription. Severe AD patients, refractory to topical corticosteroid therapy, can benefit from treatment with oral cyclosporine (5 mg/kg/per day). Discontinuation of treatment frequently results in rapid relapse of skin disease. Interferons.INF-γ is known to suppress IgE responses and downregulate TH2 proliferation and function. Extracorporeal photopheresis consists of passage of psoralen-treated leukocytes through an extracorporal UVA light system. It could be used in severe, resistant to therapy AD patients. Allergen immunotherapy.Available evidence of the effectiveness of immunotherapy with aeroallergens in the treatment of AD is mixed. Immunotherapy with aeroallergens in many studies has not be proven to be efficacious in the treatment of AD. Chinese herbal therapy had significantly reduced skin disease, reduced pruritus, and improved sleep. The beneficial response of the therapy is temporary and effectiveness may wear off despite continued treatment. Other Systemic immunosuppressants such as methotrexate, azathioprine, mycophenolate mofetil are indicated in the management of resistant forms of AD. Thalidomide (25-200 mg/day) is efficacious in resistant cases of AD, even in children. Phosphodiesterase inhibitors are agents intended for generalized forms of the disease. AD develops as a consequence of complex etiology and pathogenesis. The severity and extent of skin lesions, and deviation in laboratory parameters, especially immunologic ones, may greatly differ from patient to patient. A consensus will have to be established in the near future on the new criteria defining AD, on the model of those set 25 years ago by Hanifin and Rajka. The ever growing prevalence of the disease worldwide underlines the role of prevention, timely recognition, and optimal treatment of the many patients with AD.

Izvorni jezik
Engleski

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