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Biomedical subjects

R Niedner

Publications and source records attributed to R Niedner.

At least 19 recordsLinked to original sources
PubMed2003

[Topical corticosteroids versus topical inhibitors of calcineurin].

Topical corticosteroids (TCC) have significantly shaped dermatological therapy for five decades. A few months ago the TCC were joined by competition, the topical inhibitors of calcineurin (TIC), wrongly termed topical immunomodulators. The present paper reviews the pharmacological effects and clinical efficacy of TIC, compares the risks, benefits and costs of those two groups of topical drugs and develops a position on the use of TIC. While TIC have ushered in a new era of topical anti-inflammatory therapy, the age of TCC is far from over.

Acute Disease↗
PubMed2001

[Diagnosis of eczema. Can you recognize what your patient's symptom?].

The term eczema is applied to specific non-infectious inflammatory reactions of the skin, and covers a number of etiologically highly heterogeneous conditions which, however, demonstrate common features in terms of clinical presentation and pathogenesis. Eczematous disorders account for approximately 20% of the dermatological disturbances. They include allergic, contact and irritant contact dermatitis, atopic dermatitis, seborrheic dermatitis, nummular-microbial and dyshidrotic eczema, and stasis eczema. They have a high individual and socio-economic impact, and are dependent on individual predisposition.

Dermatitis, Atopic↗
PubMed2001

[Dermatological local therapy. How to control eczema].

The success of a topical treatment of eczema depends not only on the active agent employed, but also to a large extent on the choice of a suitable base. In the overview, therefore, not only the physical effects of the various galenic preparations (solution, shaking mixture, cream, etc.) are considered, but also the pharmacological and clinical effects of the topical corticoids and alternatives, such as, for example, bufexamac, dyes, coal tar, capsaicin, as also radiation treatment with UV-A in combination with psoralens.

Administration, Topical↗
PubMed1997

Cytotoxicity and sensitization of povidone-iodine and other frequently used anti-infective agents.

Povidone-iodine is an antiseptic widely used in dermatology. In vitro experiments showed a certain cytotoxicity, yet it is not easy to transfer these toxicological data to in vivo circumstances. In vivo investigations in animals and in humans could exclude cytotoxic effects of povidone-iodine, measured by the wound healing process. Only when administered in combination with detergents was an obvious cytotoxicity seen in wounds but not on the intact skin. In comparison to the frequently used antibiotic neomycin, the sensitization rate of povidone-iodine is very low.

Animals↗
PubMed1993

Phorbol-12-myristate-13-acetate-treated human keratinocytes express B7-like molecules that serve a costimulatory role in T-cell activation.

In previous studies, Phorbol-12-myristate-13-acetate (PMA)-treated human keratinocytes (PMA-HNK) were shown to induce T-cell proliferation via a major histocompatibility complex (MHC)- and antigen (Ag)-independent mechanism, that was mediated in part by PMA-induced intercellular adhesion molecule (ICAM)-1 on HNK. Recently, the interaction of the B7 Ag on antigen-presenting cells with its ligand CD28 on T cells has been shown to deliver activation signals distinct from the interaction of MHC/Ag with the T-cell receptor. These findings led us to assess whether B7-dependent signals play a role in T-cell proliferation induced by PMA-HNK. We first examined B7 expression on HNK by staining with three different monoclonal antibodies (MoAbs). When analyzed by fluorescence-activated cell sorter, untreated HNK stained only faintly. By contrast, PMA induced a dose-dependent upregulation of B7 staining. This staining identifies a molecule closely related to B7 because it was blocked by purified recombinant B7 immunoglobulin. Upregulation of B7 staining was first observed 16 h after PMA treatment and persisted for at least 48 h; it was protein kinase C dependent and required de novo protein synthesis. Anti-B7 MoAbs reduced specifically the capacity of PMA-HNK to trigger proliferation of allogeneic peripheral blood mononuclear cells and T cells. The combination of anti-B7 and anti-ICAM-1 MoAbs further reduced this response. We conclude that PMA upregulates on HNK the expression of a B7-like molecule that contributes in concert with ICAM-1 to the capacity of PMA-HNK to induce proliferation of allogeneic T cells.

Animals↗
PubMed1992

High-dose UVA1 therapy in the treatment of patients with atopic dermatitis.

BACKGROUND: Besides glucocorticosteroids, there is currently no known effective therapy for patients with acute atopic dermatitis. OBJECTIVE: The therapeutic effectiveness of high-dose UVA1 irradiation in the management of patients with acute exacerbation of atopic dermatitis was examined. METHODS: Patients in the high-dose UVA1 group (n = 15) were irradiated with 130 joules/cm2 UVA1; the control group (n = 10) was treated with UVA-UVB therapy in a minimal erythema dose-dependent manner (total number of treatments 15). RESULTS: High-dose UVA1 irradiation was found to induce a significant clinical improvement of atopic dermatitis (p less than 0.001). In comparison with UVA-UVB therapy, significant differences in favor of high-dose UVA1 were observed (p less than 0.01). High-dose UVA1, but not UVA-UVB treatment, significantly reduced the elevated serum level of eosinophil cationic protein in patients with atopic dermatitis (p less than 0.003). CONCLUSION: These studies indicate that high-dose UVA1 irradiation may represent a novel phototherapeutic modality for the treatment of patients with an acute exacerbation of atopic dermatitis.

Adult↗
PubMed1991

Factor XIII-deficiency in the blood of venous leg ulcer patients.

Pericapillary fibrin cuffs are probably involved in the pathogenesis of venous leg ulcers. Factor XIII (Fibrin stabilizing factor) is of importance in wound healing. Its activity, which may affect ulceration, was found to be significantly reduced in the blood of venous leg ulcer patients and in post-phlebitic patients, compared with healthy controls.

Chronic Disease↗
PubMed1990

Pericapillary fibrin cuff: a histological sign of venous leg ulceration.

The incidence of pericapillary fibrin cuffs was investigated in 49 biopsies of venous leg ulcers and 67 biopsies of leg ulcers of non-venous etiology. Pericapillary fibrin cuffs were seen in 28 biopsies (57.1%) of venous leg ulcers, but only in 11 biopsies (16.4%) of non-venous leg ulcers. In the venous leg ulcers pericapillary fibrin cuffs occurred predominantly near the ulcer surface and around dilated capillaries. Dilation of the capillaries and inflammation probably contribute more to the pathogenesis of pericapillary fibrin cuffs than venous hypertension.

Capillaries↗