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B Wedi

Publications and source records attributed to B Wedi.

At least 19 recordsLinked to original sources
PubMed2006

[Current position of the role of allergic and non-allergic food hypersensitivity in urticaria].

Foods are usually the first suspect as the cause of urticaria. However, a causal relationship is found only in special subtypes of urticaria. IgE-mediated food allergy should be clearly separated from non-allergic hypersensitivity (pseudoallergic reactions). The former may play a role in acute urticaria, particularly in patients with atopic dermatitis. The responsible food proteins vary with age. IgE-mediated sensitization can apply to food-dependent exercise-induced urticaria/anaphylaxis but more often the combination of food intake (irrespective of which type) plus exercise results in symptoms. In chronic urticaria, IgE-mediated sensitization to food is normally irrelevant while pseudoallergic reactions to food additives and perhaps also to biogenic amines may be involved. Another urticaria subtype that may be caused by food is contact urticaria which is mostly found in the context of occupational food handling. Very rarely anisakiasis and nickel may cause food-induced urticaria. Aspirin is able not only to exacerbate and aggravate urticaria but can also enhance food-dependent urticaria.

Diagnosis, Differential↗
PubMed2006

EAACI/GA2LEN/EDF guideline: management of urticaria.

This guideline is the result of a consensus reached during a panel discussion at the second International Consensus Meeting on Urticara, Urticaria 2004, a joint initiative of the EAACI Dermatology Section and GA2LEN. Urticaria has a profound impact on the quality of life, and effective treatment is therefore required. The recommended first line treatment are nonsedating H1 antihistamines. They have proven to be effective in double-blind controlled studies, but dosages increased up to fourfold over the recommended doses may be necessary. However, for different urticaria subtypes and in view of individual variation in the course of the disease and response to treatment, additional or alternative therapies may be required. Immunosuppressive drugs like cyclosporin A and corticosteroids are not recommended for long-term treatment due to unavoidable severe adverse effects. This guideline was, in addition, accepted by the European Dermatology Forum (EDF) and formally approved by the European Union of Medical Specialists (UEMS).

Anti-Allergic Agents↗
PubMed2006

EAACI/GA2LEN/EDF guideline: definition, classification and diagnosis of urticaria.

This guideline is the result of a consensus reached during a panel discussion at the 2nd International Consensus Meeting on Urticaria, Urticaria 2004, a joint initiative of the European Academy of Allergology and Clinical Immunology Dermatology Section and the European Union (EU)-funded network of excellence, GA2LEN. It covers the definition and classification of urticaria, taking into account the recent progress in identifying causes, eliciting factors and pathomechanisms of this disease. We have outlined useful diagnostic approaches for different subtypes of urticaria. This guideline was, in addition, accepted by the European Dermatology Forum (EDF) and was formally approved by the European Union of Medical Specialists (UEMS).

Allergens↗
PubMed2006

Circulating levels of brain-derived neurotrophic factor correlate with disease severity in the intrinsic type of atopic dermatitis.

BACKGROUND: Recent studies have shed light on the complex regulation of genetic, environmental, immunologic and pharmacologic factors, which contribute to the development of atopic dermatitis (AD). However, it is still unclear to which extent neuroimmune mediators have a role in AD. AIMS OF THE STUDY: To assess peripheral neurotrophin levels and their correlation with scoring atopic dermatitis (SCORAD) scores in both the intrinsic and extrinsic types of AD compared with patients with psoriasis and nonatopic healthy subjects. METHODS: Levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were assessed in peripheral blood with enzyme-linked immunosorbent assay. Based on IgE-mediated sensitization, AD was divided into the extrinsic and intrinsic type. Severity of AD was assessed with SCORAD score and with psoriasis area and severity index (PASI) in patients with psoriasis. RESULTS: Brain-derived neurotrophic factor and NGF were detectable in all the subjects studied. However, the levels of both neurotrophins were significantly higher in patients with extrinsic and intrinsic types of AD compared with patients with psoriasis and nonatopic healthy subjects (NGF: P < 0.001, BDNF: P < 0.001). NGF and BDNF levels were similar in the intrinsic and extrinsic type of AD. There was a significant correlation between BDNF and SCORAD score only in patients with the intrinsic type of AD (r = 0.57, P < 0.05). CONCLUSIONS: This study shows for the first time that NGF and BDNF are increased in both, the extrinsic type and the intrinsic type of AD. This finding points to a similar pathophysiologic background implicating a neuroimmune network in both variants of this chronic inflammatory skin disease. Future studies are needed to show the direct mechanisms of neurotrophin action in chronic inflammatory skin.

Adult↗
PubMed2004

[New therapeutic strategies for the different subtypes of urticaria].

Urticaria is one of the most common skin diseases. It is divided into several categories including acute and chronic urticaria as well as physical urticaria and special subtypes such as cholinergic and autoimmune urticaria. The causes of urticaria are multiple. In more than 80%, urticaria is triggered by an inflammatory focus, a subclinical infection or autoimmune actions. In addition, non-specific pharmacological or toxin-mediated release of inflammatory mediators from basophils or mast cells can also trigger urticaria. These new aspects in the pathophysiology of urticaria suggest new and promising therapeutic strategies. The first line treatment of urticaria still consists of non-sedating H1-antihistamines. Since urticaria has a profound impact on quality of life, effective treatment is very important. We consider new therapeutic options based on our long-term experience in treating patients with urticaria.

Administration, Oral↗
PubMed2004

[Chronic urticaria in childhood].

Chronic urticaria in children occurs more often than it might be supposed, but its management is not part of the usual daily routine. While acute urticaria in children can be treated symptomatically without further investigations, chronic urticaria requires a search for trigger factors. Autoimmune urticaria can occasionally be documented in children. The treatment of chronic urticaria depends on the suspected trigger, always keeping in mind that medications may need to be adjusted to meet pediatric requirements.

Age Factors↗
PubMed2004

[Specific immunotherapy. Hyposensitization with allergens].

Successful allergen-specific immunotherapy (SIT) induces complex immunologic chan-ges resulting in reduced allergic inflammatory reactions. SIT has long-term effects in mild forms of inhalant allergies and is effective even when standard pharmacotherapy fails. Moreover, the risk to develop additional allergic sensitizations and the development of asthma is significantly reduced in children with allergic rhinitis. SIT is the treatment of choice in patients with systemic reactions to hymenoptera venoms. Although the exact effector mechanisms of SIT still have to be clarified, the most probable effect is a modulation of regulatory T cells associated with a switch of allergen-specific B-cells towards IgG4 production. The critical point to insure efficacy and safety is the selection of patients and allergens, task best performed by a specialist trained in allergology. Further details are available in the position papers of the German allergy societies - DGAI(Deutsche Gesellschaft fiir Allergologie und Klinische Immunologie) and ADA (Arzte-verband Deutscher Allergologen) - which can be found at www.dgaki.de.

Adolescent↗
PubMed2002

[Acute, chronic or physical urticaria. What causes the hives?].

Urticaria is characterized by strongly pruritic wheals and in some cases, angioedema. On the basis of a careful case history, the type of urticaria presenting can usually be determined. In the case of the acute form, no complicated diagnostic work-up is necessary. Treatment is symptomatic: the use of ASA should be avoided, while an acute infection requires treatment. When there is recurrent angioedema, chronic urticaria and physical forms, a multitude of triggering factors must be considered. In many cases, symptoms may persist for years. Symptomatic treatment with antihistaminics is often inadequate, but long-term treatment with glucocorticoids should be avoided on account of their side effects. For this reason, further diagnostic work-up is usually necessary and, where indicated, treatment should be initiated by a dermatologist with specialist training in allergology.

Angioedema↗
PubMed2002

[Hexadactyly of hand and feet in a patient with basal cell nevus syndrome].

A 35-year-old male patient with hexadactyly on the right hand and both feet presented with multiple basal cell carcinomas of the skin. The results of further investigations led to the diagnosis of basal cell nevus syndrome (BCNS). The basal cell nevus syndrome (Gorlin-Goltz syndrome) characterized by multiple basal cell carcinomas, odontogenic cysts, skeletal abnormalities and associated neoplasms belongs to the group of genodermatoses. Reviewing the current literature we discuss aspects of the pathogenesis of the basal cell nevus syndrome as well as diagnosis criteria and treatment options.

Acitretin↗
PubMed2001

Pathophysiological role of leukotrienes in dermatological diseases: potential therapeutic implications.

In vitro and in vivo data have demonstrated that leukotrienes play a key role not only in allergic airway diseases but also in inflammatory reactions of the skin. Antileukotriene drugs, i.e. leukotriene receptor antagonists and synthesis inhibitors, are a new class of anti-inflammatory drugs that have shown clinical efficacy in the management of asthma, allergic rhinitis and inflammatory bowel disease. To address the question of the validity and applicability of published evidence of the use of antileukotriene drugs in dermatological diseases, we reviewed data concerning the pathophysiological effect of leukotrienes in the skin and in skin diseases, and the experience with antileukotriene treatment that has been published. In vivo and in vitro data suggest that antileukotriene treatment may have efficacy in atopic dermatitis, different types of urticaria or psoriasis and other skin diseases such as bullous skin diseases, collagenoses, Sjogren-Larsson syndrome or Kawasaki disease. Nevertheless, published evidence is very limited and before any conclusions can be drawn, additional basic research needs to be performed with regard to the role of different leukotrienes and leukotriene receptors in skin diseases. On the basis of these data, randomised and placebo-controlled clinical trials with leukotriene antagonists and synthesis inhibitors should be performed. Moreover, future studies investigating the additive benefit of antileukotriene drugs are warranted, e.g. in combination with antihistamines, corticosteroids or other anti-inflammatory drugs.

Animals↗
PubMed2000

Chronic urticaria serum induces histamine release, leukotriene production, and basophil CD63 surface expression--inhibitory effects ofanti-inflammatory drugs.

BACKGROUND: A role of potential histamine-releasing autoantibodies against the high-affinity IgE receptor on the surface of basophils and mast cells is discussed in the pathogenesis of chronic urticaria. This so-called autoimmune urticaria may be diagnosed by a positive intracutaneous autologous serum skin test, which is found in about 30% of patients with chronic urticaria. OBJECTIVE: Our purpose was, first, to compare the effect of complement-inactivated sera of 20 patients with chronic urticaria and positive autologous serum skin tests, 20 patients with chronic urticaria and negative skin tests, and 20 control subjects without chronic urticaria (10 atopic and 10 nonatopic subjects) and, second, to analyze the effect of anti-inflammatory drugs on the serum activity. METHODS: The following assay systems were used: release of histamine in whole blood samples, surface expression of the activation marker CD63 on basophils, and sulfidoleukotriene de novo production in leukocyte suspensions. Whole blood, basophils, and leukocyte suspensions were obtained from a nonatopic and an atopic donor. RESULTS: Sera of patients with autologous serum skin test positive chronic urticaria resulted not only in significantly increased histamine release compared with skin test-negative chronic urticaria sera but also in a significant higher induction of basophil CD63 surface expression and sulfidoleukotriene de novo production. However, serum activity was neither characteristic for chronic urticaria nor for chronic urticaria with a positive autologous serum skin test. Preincubation with dapsone, chloroquine, and lidocaine dose dependently resulted in a significant reduction of all histamine release, CD63 expression, and sulfidoleukotriene production. In addition, mizolastine was able to inhibit serum-induced sulfidoleukotriene production. CONCLUSION: Further studies investigating the in vivo effect of these drugs will have to clarify their role in the management of the subset of patients with chronic urticaria demonstrating serum-induced inflammatory effects.

Anti-Inflammatory Agents↗
PubMed1999

Eosinophil apoptosis is mediated by stimulators of cellular oxidative metabolisms and inhibited by antioxidants: involvement of a thiol-sensitive redox regulation in eosinophil cell death.

The mechanisms for induction of eosinophil apoptosis remain uncertain. The role of oxidative stress has not been investigated. The present study was undertaken to determine the role of reactive oxygen species (ROS) and selective antioxidants in eosinophil apoptosis. Eosinophils were cultured with sodium arsenite (SA) known to induce intracellular oxidative metabolites. There was a significant increase in the rate of eosinophil apoptosis with low concentrations of arsenite, whereas high concentrations showed rates of apoptosis similar to control medium. Investigating the role of intracellular oxidants by flow cytometry, we found that while inducing apoptosis, SA more than anti-Fas resulted in a significant dose-dependent production of intracellular H(2)O(2). In contrast, the extracellular release of superoxide decreased after stimulation with SA or anti-Fas as assessed by lucigenin-dependent chemiluminescence. Coincubation experiments demonstrated that arsenite-induced apoptosis can be nearly completely prevented by selective antioxidants such as glutathione (GSH) and N-acetyl-cysteine (NAC), but not dimethyl sulfoxide (DMSO) or taurine (TAUR). Moreover, GSH and NAC significantly reduced eosinophil apoptosis mediated by a monoclonal antibody directed to Fas antigen. Next it was shown that GSH and NAC, but not DMSO or TAUR, were able to significantly delay spontaneous apoptosis in unstimulated eosinophils. Taken together, these data point to an important role of oxygen-dependent mechanisms in the regulation of eosinophil survival and apoptosis. We propose that eosinophil apoptosis may be related to the ability of the cell to maintain an appropriate oxidant-antioxidant balance.

Acetylcysteine↗
PubMed1999

Helicobacter pylori infection and skin diseases.

There is increasing evidence for systemic effects of gastric H. pylori infection which may result in extragastrointestinal disorders. This review summarizes the available medical literature up to September 1999, identified through a MEDLINE research including own studies, regarding H. pylori and skin diseases. Due to current knowledge best evidence for a potential link of H. pylori infection exists for chronic urticaria although the data are still conflicting. Thus, the search for H. pylori should be included in the diagnostic management of chronic urticaria. With regard to other skin diseases such as rosacea, hereditary or acquired angioedema due to C1-esterase inhibitor deficiency, systemic sclerosis, Schönlein-Henoch purpura, Sjögren's syndrome, sweet's syndrome, and atopic dermatitis only single of few cases have been reported so far. Thus, we clearly need further randomized, double-blind and placebo-controlled studies including adequate diagnostic schedules, sufficient eradication treatment protocols, confirmation of eradication, and adequate control groups to establish a role of H. pylori in skin diseases. Caution must be taken not to accuse H. pylori as the infectious agent responsible for every disease, particularly since H. pylori infection is very common. Although from an epidemiological and morphological view the skin diseases to which H. pylori has been linked seem to be completely different it is striking that in most of them an autoimmune pathogenesis is suspected or considerable vascular impairment can be found.

Helicobacter Infections↗