PubMed Health⌕ Search

Biomedical subjects

Wiesław Gliński

Publications and source records attributed to Wiesław Gliński.

3 recordsLinked to original sources

[Diagnostic, prophylactic and therapeutic guidelines in patients with atopic dermatitis. Position paper by the task force of the National Specialists on Dermatology, Venereology and Allergology].

Treatment modalities of patients with atopic dermatitis (AD) are dependent on patient age, on the intensity of both skin symptoms and subjective signs of the disease i.e. itch and sleep disturbances, on the body surface involved with lesions, as well as on the type of sensitizing allergens. The characteristic of these allergens is crucial to start prophylaxis and to make decision about specific immunotherapy. In asymptomatic period of the disease the most important factor is to prevent dryness of the skin using emollients, which reconstruct integrity and continuity of stratum corneum. This procedure prevents penetration of air-borne allergens across damaged skin barrier into the skin. In mild AD cases, pimecrolimus (mainly in children) and corticosteroids of the lowest potency alternatively with their basis should be recommended. In moderate intensity AD either topical treatment with calcineurin inhibitors i.e. tacrolimus and pimecrolimus or topical corticosteroids from 4-5 group of American classification should be applied. In addition, PUVA/UVB phototherapy may be beneficial, as well as immunotherapy with specific airborne allergen/s. Coexisting bacterial skin infections should be treated with systemic antibiotics (macrolides, quinolones, and cephalosporins), viral herpes infection systemically using acyclovir for 5-7 days, and fungal infections applying ketoconazole orally, accompanied by topical treatment with miconazole or other antimycotics. Severe AD is an indication for the systemic use of cyclosporin A (rather than corticosteroids), and antibiotics as mentioned above. Prolonged 3-5 year specific immunotherapy is significant concern for selected cases. Sensitive skin areas such as face, orbicular skin, flexures should be treated with pimecrolimus and tacrolimus rather than with corticosteroids, however, topical corticosteroids are recommended on involved skin of the trunk and the extremities besides of flexures. While the improvement of severe AD is reached, the treatment modalities for benign and mild AD should be observed. In all AD patients with active skin lesions antihistaminic drugs of 2nd generation reactive with H1 receptor are a gold standard (or short treatment with these drugs of 1st generation to achieve a sedative effect, followed by the 2nd generation drug), as well as tranquilizers as the combined treatment. There is no reason for the use of anti-leukotriene drugs.

Adolescent↗

[Latent sources of contact allergy].

In individuals sensitized to many contact allergens in the course of 4th immunological mechanism, in whom allergic contact dermatitis develops at the site of exposure to haptens, disseminated eczematous skin lesions might be provoked by latent source of hapten, which penetrates to the body omitting the skin. The most frequent clinical situations include: allergy to drugs, food additives, inhaled chemicals originated from plants, allergic reactions to metal endoprostheses used in orthopaedics and/or dentistry, and all conditions facilitating penetration of hapten directly to the blood through damaged skin (erosions, ulcers, etc.) and/or under occlusive dressings.

Dermatitis, Contact↗

[Allergic contact dermatitis].

Clinical definition of eczema is based on the presence of multiform erythematous, papular and vesicular lesions which are followed by marked desquamation. When the underlying mechanism is allergic, skin lesions are mediated by inflammatory Th1 lymphocytes recognizing hapten determinants, i.e. IVth allergic mechanism in allergic contact dermatitis. This mechanism is responsible also for allergy to bacterial proteins in nummular eczema, or to fungal and bacterial proteins, atopens and nickel in dyshidrotic eczema. Eczematous lesions can develop after damage to the skin barrier by toxic chemical or irritating substances, as non-allergic irritation eczema. These substances non-specifically stimulate the Langerhans cells and keratinocytes to produce numerous cytokines inducing expression of adhesion molecules on the endothelial cells. This is responsible for non-specific mobilization of Th1 cells to the skin. A model example is dermatitis induced by mercury salts and/or sodium lauryl sulfate. Intermediate position between allergic and non-allergic eczema is occupied by atopic dermatitis/eczema. In addition to classical IgE-dependent mechanism leading to degranulation of mast cells, there is generation of specific population of Th2 lymphocytes recognizing food and air-borne atopens. This reaction is responsible for skin inflammation in the late-phase response, in which allergic process started by Th2 cells switches to non-specific migration of Th1 cells attracted by cytokines released from eosinophils, keratinocytes and Th2 lymphocytes.

Cytokines↗