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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Solar urticaria is a relatively rare dermatosis. In reported cases, skin lesions appeared soon after sunlight irradiation, usually within a few minutes, and consisted of a wheal localized to the exposed area with a surrounding flare. The case presented herein is quite different from the others in its clinical manifestation. The time required for the formation of the wheal was far longer and there was neither surrounding flare nor pseudopodia. Also, the degree of local edema was directly proportional to the length of exposure time, up to three hours. A diagnosis of solar urticaria had not previously been made in this patient because he did not show wheal formation except after unusually long exposure.
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PMID:Solar urticaria. Report of an unusual case. 46 99

Since the majority of itching skin diseases are inflammatory or allergic, it has been assumed that release or activation of inflammatory mediators, stimulating the itch receptors, play an essential role in the pathophysiology of itch. In this review some of the possible mediators are discussed. Histamine induces itch upon intradermal injection, but urticaria is the only itching dermatosis which is significantly relieved by antihistamines. Serotonin is much weaker than histamine in provoking itch upon intradermal injection. Serotonin acting in synergism with prostaglandins may cause itch in polycythaemia vera. Neuropeptides release histamine from skin mast cells, but it remains to be determined whether neurogenic peptides are responsible for clinical pruritus. Prostaglandins enhance pruritus induced by intradermal histamine (and serotonin) but are weak pruritogens per se. Lymphocytes are present in many itching skin diseases and it could be assumed that lymphokines are involved in the pathogenesis of itch. Supporting this theory is the finding that ciclosporin A, an inhibitor of lymphokine production, reduces itch in atopic dermatitis. Central mechanisms are essentially unknown, but there are indications that opioid peptides might be involved in the central transmission of itch.
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PMID:Peripheral and central mediators of itch. 157 79

Of a total of 3731 patients investigated between 1974 and 1990, 1844 (49.4%) had an occupational skin disease. Of them 142 (7.7%) had an occupational skin disease caused by epoxy compounds--135 patients (95%) had allergic contact dermatitis, five had irritant contact dermatitis, and two had contact urticaria. Apart from dermatoses, two patients had IgE-mediated asthma from exposure to DGEBA epoxy resins. Thus epoxy compounds are one of the main causes of occupational allergic contact dermatoses and can be considered potential causes of occupational asthma. The most frequent causes were epoxy resin compounds, which together induced 93% (132 cases) of all epoxy compound dermatoses. The three most common causative products were epoxy paints and their raw materials (31%, 41 cases), epoxy resin compounds used in electrical insulation (29%, 38 cases) and epoxy glues (18%, 24 cases). Fewer cases were caused by products containing epoxy acrylate and EPTMAC. The present study found that, in addition to contact allergy to DGEBA epoxy resins, contact allergy to epoxy hardeners, non-DGEBA resins and reactive diluents is common. Polyamine hardeners, most frequently MDA, DETA and TETA, rarely IPDA, tris-DMP, EDA, TMD and XDA, were the second commonest causes of contact allergy induced by epoxy resin compounds, after DGEBA epoxy resins. Cycloaliphatic epoxy resins and other non-DGEBA epoxy resins, including heterocyclic dimethyl hydantoin, phenol novolak and brominated epoxy resins, were the third commonest causes, and reactive diluents the fourth commonest cause of allergic dermatitis due to epoxy resin compounds. Most patients sensitized to reactive diluents were allergic to PGE, ortho-CGE, HDDGE and BDDGE, whereas fewer patients were sensitized to AGE, NPGDGE and BGE. Cross-sensitization between reactive diluents was common. Cardura E 10 and Epoxide 8 provoked no reactions. The present study also indicated that DGEBA epoxy resins with a high average MW ought to be regarded as potential sensitizers, and organic solvents probably promote sensitization to DGEBA, even if the amount of DGEBA is low in the causative products. When contact dermatitis induced by epoxy compounds is suspected, an accurate diagnosis is made with the use of detailed data on the patient's exposure and extensive patch testing, including tests with the patient's own products. No chemical can be used alone to screen for sensitization to all different contact allergens of epoxy compounds.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Occupational skin diseases from epoxy compounds. Epoxy resin compounds, epoxy acrylates and 2,3-epoxypropyl trimethyl ammonium chloride. 183 96

Atopic dermatitis is a genetically determined eczematous skin disease strongly influenced by environmental conditions called flare factors. Allergic reactions are one such flare factor. These reactions include contact urticaria, allergic contact dermatitis, and late phase reactions. Contact urticaria could induce eczema by eliciting scratching. A late phase reaction may be involved in eczema produced by prolonged epicutaneous applications of antigens in individuals with immediate sensitivity to these antigens. Mechanisms of allergic contact dermatitis might also elicit dermatitis. Environmental allergens may include mold, dust, mite, pollens, foods, danders and bacteria.
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PMID:Flare factors and atopic dermatitis: the role of allergy. 207 89

A retrospective survey during a 2-year period disclosed 18 patients with acute febrile neutrophilic dermatosis (Sweet's syndrome). An associated lympho- or myeloproliferative malignancy was found in 6 patients. Attacks of Sweet's syndrome preceded the diagnosis of neoplasia in 4 patients (3 months to 6 years). Some differences in symptoms and signs were found in the group of patients with associated malignancy compared with the group without, that is, male predominance, mucosal symptoms, anemia, and frequent recurrence of skin symptoms. The onset of Sweet's syndrome indicates an acute infectious disease, and the patients are frequently referred to departments of internal medicine and infectious diseases. In addition, the skin lesions may mimic those which often accompany a generalized infection (erythema multiforme, erythema nodosum, vasculitis, pustular eruptions and urticaria). Since Sweet's syndrome may precede the possibly associated malignant disease, the initial diagnosis of the syndrome is important and should be made with confidence with increasing awareness of the characteristic symptoms.
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PMID:Acute febrile neutrophilic dermatosis--a marker of malignancy? 256 9

Urticaria is a rather common, often vexing skin disease, characterized by evanescent, pruritic, erythematous wheals, and sometimes by giant hives (angioedema). The cause of chronic urticaria remains unknown in 75 to 80 percent of the cases. Its pathogenesis is related to the activation of tissue mast cells by many immunologic or non-immunologic mechanisms, resulting in a release of biologically active products. The therapeutic possibilities in practice are discussed. Non-sedative antihistaminic drugs of the H1 type (Terfenadine, Astemizole, Loratidine and Cetirizine) are the main stay in the treatment of urticaria. In case of failure the sedative non-selective antihistaminics from the old generation are used. Particular emphasis is given the possibilities to combining various antiallergic drugs. The combination of a H1 and H1 antihistamine can be effective in individual patients.
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PMID:[Therapy of acute and chronic urticaria and of Quincke's edema]. 256 13

The authors present a new classification for photodermatosis in five groups: 1. Primary toxic photodermatosis that means lesions produced in all human beings by non-ionized radiation. 2. Photodermatosis induced by drugs, with two subgroups--phototoxic and photoalergic--according to the mechanism of action of the drug. 3. Idiopathic photodermatosis in which the photonic effects are known but the chromophores are unknown; four conditions are included here polymorphous actinic eruption, solar urticaria, actinic reticuloid and hidroa vacciniforme. 4. Miscelanea group which includes several conditions of unknown mechanism which are not included in the other groups, such as: actinic cheilitis, actinic poikiloderma, actinic ceratoses, epitheliomas, melanomas and others. 5. Conditions precipitated or aggravated by solar radiation with two sub-groups: hereditary (xeroderma pigmentosum, Hartnup's syndrome and other) and acquired (lupus erythematosus, pellagra and other). In group 1, the authors propose the designation of actinic elastotic dermatosis to unify different conditions described by several authors such as: diffuse elastosis, citrein skin, cutis rhomboidalis, and others.
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PMID:[A new classification of photodermatoses]. 266 86

The abundance of mast cells in human dermis, together with their ability to release a variety of vasoactive and pro-inflammatory mediators following cross-linkage of their cell-surface receptors for IgE, enables these cells to provide an effective defence mechanism within this organ. A similar defensive function is attributed to mast cells of other human organs such as intestine and lung which are in contact with the external environment and therefore susceptible to infiltration by foreign allergens and micro-organisms. However, mast cells of the skin apparently differ from those present in lung and intestine in being activated for histamine release by a variety of endogenous neuropeptides which stimulate the rapid release of histamine in the virtual absence of eicosanoids. This would provide a mechanism of neurogenic control of a variety of homeostatic functions such as blood flow, angiogenesis and fibroblast proliferation. Such processes would aid in the remodelling of tissue during wound healing, and increased numbers of mast cells have been noted around healing wounds of rat skin and areas of developing fibrosis. Neuropeptides modulate the activity of a variety of immuno-competent leucocytes including macrophages, monocytes and lymphocytes. The findings that skin mast cells are activated by neuropeptides suggest that these cells may also be included amongst those involved in neuro-immune interactions. Activation of skin mast cells by non-immunological stimuli may contribute to the aetiology of some forms of skin disease. Patients with chronic idiopathic urticaria appear to have enhanced vascular responsiveness to intradermal injections of the histamine liberator codeine suggesting that this disease may involve hyper-responsiveness of their mast cells to endogenous non-immunological stimuli. The findings of large increases in histamine accompanied by small increases in PGD2 in venous effluent of thermally challenged limbs of patients with cold- or heat-induced urticaria may suggest that their mast cells had been activated by a non-immunological stimulus. However, the interpretation of results gained using such relatively complex in-vivo systems are difficult, as the cellular origin of the detected mediators is by no means clear. However, it is hoped that in the future the alliance of newly developed in-vitro techniques to investigate mast cell function together with in-vivo methods to investigate their interaction with elements in their tissue environment will greatly increase our understanding of the role of the human skin mast cell in health and disease.
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PMID:The human skin mast cell. 266 2

We report the first case of acral localized acquired cutis laxa. The skin laxity was preceded by swelling of the fingers and toes and by the appearance of papular urticaria. Dapsone therapy was effective in controlling the swelling. Examination of skin biopsy specimens showed fragmentation and almost total loss of elastic fibers in the areas of cutis laxa. Electron microscopy showed no abnormalities in elastic structure and function in unaffected skin. In addition, electron microscopic examination of an urticarial lesion showed a neutrophilic dermatosis with polymorphonuclear leukocytes attached to the surface of either normal elastic fibers or fibers showing early degenerative changes. These findings suggest that there is no primary defect in the elastic fibers and that the polymorphonuclear leukocytes play a significant role in the destruction of the elastic fibers and the subsequent development of cutis laxa in this case.
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PMID:Acral localized acquired cutis laxa. 274 70

The urticaria is a common skin disease, characterized by evanescent, pruritic, erythematous and oedematous wheals and sometimes by giant hives (angio-edema). Its pathogenesis is related to the activation of tissue mast cells by many immunologic or non-immunologic mechanisms, resulting in a release of biologically active products. The cause of chronic urticaria remains unknown in 75 to 80% of the cases. This form is rare in childhood. More of 50% of children with acute urticaria are atopic with preexisting dermatitis of pollinosis. A papular urticaria (prurigo strophulus), an urticaria pigmentosa, and, in case of angioedema, the hereditary form due to functional inactivity of the C1-inhibitor must be excluded. The therapeutic possibilities in the praxis are briefly discussed.
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PMID:[Urticaria and Quincke's edema]. 279 39


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