Urticaria

Urticaria is a very common skin disease which was already described in the ancient world. Questions still remain about its pathogenesis and management remain open. Compared to other common skin diseases, the published evidence is rather low. The clinical symptoms with pruritic transient wheals and/or angioedema are caused by mediators (particularly histamine) released by activated mast cells and basophils. The mechanism of target cell activation has not been clarified in detail for most urticaria subtypes. Different urticaria subtypes should be distinguished. Spontaneous forms are more common than inducible forms. Chronic urticaria and urticaria in certain age groups (children, pregnancy) can be difficult to manage. Therefore, international consensus resulting in the regular update of urticaria guidelines can be very helpful. Currently, these updated guidelines include a three‐step treatment algorithm for chronic spontaneous urticaria. Only the first step of this algorithm, second generation H1‐antihistamine in standard dose, utilized approved drugs. However after omalizumab was established as a third line choice in the guideline algorithm, it has approved in many countries for chronic spontaneous urticaria without response to H1‐antihistamines. The exact mechanism of action of omalizumab in urticaria has not been fully elucidated. Unrevealing this mechanism might result in a deeper understanding of urticaria pathogenesis and the development of further therapeutic strategies.     

Urticaria

Urticaria is often classified as acute, chronic, or physical based on duration of symptoms and the presence or absence of inducing stimuli. Urticarial vasculitis, contact urticaria, and special syndromes are also included under the broad heading of urticaria. Recent advances in our understanding of the pathogenesis of chronic urticaria include the finding of autoantibodies to mast cell receptors in nearly half of patients with chronic idiopathic urticaria. These patients may have more severe disease and require more aggressive therapies. Extensive laboratory evaluation for patients with chronic urticaria is typically unrevealing and there are no compelling data that associate urticaria with chronic infections or malignancy. Pharmacologic therapy consists primarily of the appropriate use of first- and second-generation histamine H1 receptor antihistamines. Additional therapy may include leukotriene receptor antagonists, corticosteroids, and immunomodulatory agents for severe, unremitting disease. Despite our greater understanding of the pathogenesis of urticaria, the condition remains a frustrating entity for many patients, particularly those with chronic urticaria.     

Urticaria

Urticaria and angioedema are common and, if chronic, often persist for years with significant impact on quality of life and occupational ability. To achieve a better understanding of disease etiology and pathogenesis and to compare clinical trials, there is a clear need for cross‐specialty and international agreement of the nomenclature and diagnostic classification of urticaria and angioedema. At least in part this has been achieved by two recently published European guidelines. After the urticaria subtype is defined, potential triggers should be sought including persistent bacterial infections (Helicobacter pylori, streptococci, staphylococci, Yersinia, parasites) pseudoallergic reactions (acetylsalicylic acid, rarely food additives) and/or autoreactive mechanisms (autologous serum test). Identified trigger factors should be avoided or eradicated, as this is the most successful therapeutic approach. Treatment of most urticaria subtypes is difficult and besides H1 antihistamines neither standardized nor evidence‐based. Low‐sedating H1 antihistamines represent the mainstay of treatment, as they have a better therapeutic index and pharmacodynamic properties than older agents. In severe cases their dose has to be increased which is off‐label use. The evidence base for treatment alternatives is totally insufficient and the risk‐benefit profile of each off‐label used drug should be carefully considered.     

Urticaria

The clinical features of acute and chronic urticaria and angio-oedema are described including the physical urticarias, hereditary angio-oedema and urticarial vasculitis. An approach to treatment is discussed.     

Demonstration von Urticaria pigmentosa und Urticaria menstrualis gonorrhoica

Ohne Zusammenfassung     

Urticaria perstans

Archives of Dermatological Research -     

色素性荨麻疹

患儿男,3岁。 主诉:全身出现色素性斑疹、斑丘疹,伴轻度瘙痒2年余。 现病史:患儿于1岁时躯干部开始出现棕褐色斑疹、斑丘疹,黄豆至蚕豆大,伴轻度瘙痒,搔抓或摩擦皮肤后局部可出现皮肤发红或风团,偶有水疱、血疱,皮疹消退后遗留色素沉着斑。患儿发病以来无恶心、呕吐、腹痛、腹泻、关节肿痛等不适。对皮疹未予以特殊诊治,皮疹呈进行性增多,并逐渐扩展至四肢、颜面部。 个人史:患儿系足月顺产,母乳喂养,平素体健,无特殊不良嗜好。