Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of reactions to insect bites both local (erythema, pemphigus, oedema, itching) and systemic (urticaria, angioedema, anaphylactic shock) in Borgomanero (NO) National Health Clinic 54 was assessed. The high incidence of medical treatments for this pathology encountered reflects the fact that in the summer and in a rural area a great many people are exposed to this type of emergency. The importance of careful diagnosis (anamnesis, skin allergy tests, RAST is emphasised as a means of identifying cases at allergic risk and providing the appropriate immunotherapy.
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PMID:[Reactions caused by Hymenoptera: a first aid problem]. 340 56

Captopril, an oral active dipeptidylcarboxypeptidase inhibitor with antihypertensive properties, has been reported to have the following cutaneous side effects: macular and papular skin eruptions, urticaria, angioedema, mouth ulcers, pemphigus, and pityriasis rosea-like eruptions. Here, to the best of our knowledge, is the first case in which a pityriasis rosea-like eruption evolved into a lichenoid drug eruption. Also discussed is the remarkable similarity in the side effects of captopril, gold compounds, d-penicillamine, and organic mercurials.
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PMID:Lichenoid eruption produced by captopril. 621 69

The pathogenetic mechanisms underlying common, and less common but severe, adverse cutaneous drug reactions are reviewed. Pharmacogenetic variability may account for a susceptibility to serious drug reactions to sulphonamides and anticonvulsants, as well as to lupus erythematosus (LE)-like syndrome. Exanthematous drug reactions may have an immunological basis. Cell mediated cutaneous drug reactions, including lichenoid reactions, LE-like syndrome, fixed drug eruption, erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis, will inevitably involve elements of the skin immune system. Graft-versus-host disease provides a useful model for aspects of these drug-induced disorders. Urticaria, angioedema, anaphylaxis and anaphylactoid reactions may involve Type I immunoglobulin (Ig)-mediated or Type III hypersensitivity, or may be caused by pharmacological, non-allergic means. Drug-induced vasculitis, serum sickness and the Arthus phenomenon are manifestations of the immune complex disease. Drug-induced pemphigus may involve immune dysregulation, but several thiol-containing drugs are able to cause antibody-independent acantholysis directly.
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PMID:Mechanisms of drug eruptions: Part I. 748 37

We investigated skin diseases associated with mucocutaneous Candida infection by analyzing the clinical records of 44695 in-patients of the department of dermatology of Kiel. For more than eighty skin diseases the relative risk (RR) was calculated by age-and sex-adjusting methods. 1996 patients demonstrated a mucocutaneous candidosis, 14.8% of them being hospitalized because of extensive Candida infection. In patients with dermatomyositis, bullous pemphigus, tinea inguinalis, and condylomata acuminata a Candida infection was observed more than threefold than expected. Furthermore, patients with urticaria, folliculitis, and bullous pemphigoid demonstrated candidosis more than twice as often as control patients. In addition, patients with erysipelas, acne, psoriasis, and atopic dermatitis showed a candidosis significantly more often (RR between 1.3 and 1.6). Some internistic maladies were investigated, too. In patients presenting with diabetes mellitus, heart-insufficiency, hypertension, chronic tonsillitis, and urinary tract infection a mucocutaneous Candida infection was significantly increased.
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PMID:[Mucocutaneous candidiasis in patients with skin diseases]. 763 Mar 73

The possibility of a causal influence of emotional stress, especially of stressful life events, on the course of various skin diseases has long been postulated. Clinical wisdom and experience, as well as many anecdotal observations and uncontrolled case series, support this opinion. We reviewed the available evidence on the role of stressful life events in triggering or exacerbating skin diseases. The role of stressful events in vitiligo, lichen planus, acne, pemphigus and seborrhoeic dermatitis was either controversial or insufficiently explored. The role of stressful events in psoriasis, alopecia areata, atopic dermatitis and urticaria was apparently clearer. However, only a few studies met acceptable methodological standards for stress measurement. Also, few studies considered common potential confounding factors (e.g. age, duration of illness, familial factors), and no study controlled adequately for the influence of other crucial factors (e.g. discontinuation of treatment, seasonal effects). Adding that the large majority of studies were retrospective, it seems wise to conclude that only preliminary evidence has been published so far on the role of stressful life events in bringing on or worsening any dermatological disease. Further research is mandatory, either in the form of prospective studies or, more feasibly, of well-designed case-control studies with adequate statistical power. Future studies should also pay more attention to protective as well as vulnerability factors in stressful events. Further, it would be important to investigate other sources of psychological stress, such as chronic stress and everyday stress. Measuring stress appraisal, although difficult, would also be important.
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PMID:Stressful life events and skin diseases: disentangling evidence from myth. 1184 50

Photosensitive disorders may be classified as those entirely caused by solar exposure and the photoaggravated disorders. Those in the former category include polymorphic light eruption, juvenile spring eruption, actinic prurigo, hydroa vacciniforme, solar urticaria, also chronic actinic dermatitis. Genodermatoses whose expression mainly depends on UV or light exposure include the DNA repair deficient disorders, some disorders of cornification, the Smith-Lemli-Opitz syndrome and porphyria. Examples of photoaggravated diseases include lupus erythematosus, erythema multiforme, atopic eczema, psoriasis, viral exanthemata, pemphigus, dermatitis herpetiformis and rosacea. Drugs and chemicals may interact with UV to induce photosensitivity. In many of these diseases the action spectrum is known or may be determined by phototesting. Recognition of the reaction patterns associated with the photodermatoses greatly assists clinical classification of the photodermatoses.
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PMID:Diseases associated with photosensitivity. 1174 94

Over a 6-year period seven adult horses of different breeds and genders developed multifocal, exudative, oozing dermatitis characterized histologically by epidermal spongiotic vesicles and perivascular eosinophilic, neutrophilic and mixed mononuclear inflammation. Three horses were pruritic. Systemic disease was not noted. Two horses had a history of recurrent urticaria (hives) and one horse had nodules or welt-type lesions that progressed to exudative, oozing lesions. Interepithelial immunoglobulin (Ig)G was detected by avidin-biotin complex-peroxidase staining, but the pattern of staining was more consistent with epithelial oedema than specific IgG deposition associated with pemphigus. The exudative oozing lesions developed under circumstances suggesting that dermal oedema progressed to intracellular and intercellular epidermal oedema, which in turn progressed to the spongiotic vesicular epidermal lesions.
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PMID:Spongiotic vesicular dermatitis as a cutaneous reaction pattern in seven horses. 1190 55

Alpha1 antitrypsin (AAT) deficiency is an autosomic codominant inherited disorder characterized by inefficient or non-functional serum AAT. The principal clinical manifestations are panlobular emphysema and cirrhoses. Among cutaneous aspects, about 30 cases of panniculitis have been reported in the literature, likewise rare clinical cases: pemphigus herpetiformis, Muir Torre syndrome, urticaria and angioedema, cutis laxa and Marshall syndrome, lupus erythematosus, psoriasis, vasculitis. Probably because of it's high frequency, numerous others diseases have been reported described in association. Acting on several factors of inflammation, AAT deficiency seems product or modify the expression of some, notably cutaneous diseases.
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PMID:[Alpha-1-antitrypsin deficiency. Role in skin disorders]. 1266 63

The pathogenesis of equine urticaria is not well understood. In man, urticaria has been associated with immunological and nonimmunological mechanisms leading to the release of various mediators by mast cells. Skin biopsies of 32 horses with a history of urticaria were stained with toluidine blue, a double-labelling method for chymase and tryptase, and immunohistochemistry for immunoglobulin (Ig)E. These horses were compared with horses with pemphigus foliaceus, insect bite hypersensitivity and control horses with healthy skin. Neither formalin fixation time nor biopsy site influenced the staining methods. No chymase-positive cells were found. In all groups of horses, cells staining with toluidine blue and for tryptase and IgE were found in the epidermis and hair follicle papilla and significantly more positively staining cells were observed in the subepidermal dermis compared with the deep dermis. Horses with urticaria had significantly more IgE-bearing cells in the subepidermal dermis than control horses. However, horses with urticaria had significantly fewer toluidine-blue-stained mast cells in both subepidermal and deep dermis compared with the insect bite hypersensitivity and pemphigus foliaceus groups. This study suggests that IgE-mediated reactions play a role in the pathogenesis of urticaria.
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PMID:Immunoglobulin E-bearing cells and mast cells in skin biopsies of horses with urticaria. 1584 39

The skin is a common target of cellular and/or antibody mediated pathological immune responses. Pemphigoids, pemphigus vulgaris and dermatitis herpetiformis are bullous disease due to autoantibodies targeting specific proteins of the skin. The pemphigoid autoantigens are the BP180 and the BP230 antigens, two components of the epithelial basement membrane zone. Additional antigenic targets reported in a portion of patients are laminin 5, the alpha6 subunit of the hemidesmosomal integrin alpha6beta4 and a glycoprotein termed p200. The epidermal and mucosal epithelial cells detachment (acantholysis) characteristic of pemphigus vulgaris is induced by autoantibodies directed against the desmoglein 3 and 1. The desmogleins are desmosomal cadherins, which play a major role in the cell-to-cell adhesion. Dermatitis herpetiformis is regarded as cutaneous phenotype of coeliac disease. A novel autoimmune hypothesis of coeliac disease links wheat gliadin and tissue transglutaminase (TG2) in the gut, which leads to T cell response and IgA autoantibody formation. In dermatitis herpetiformis skin the target for IgA deposition seems to be epidermal TG3. Urticaria is a complex syndrome caused by both immune and non-immune mechanisms. In a subsets of patients with chronic urticaria mast cell degranulation is induced by autoantibodies directed against the a-subunit of the high-affinity IgE receptor, and/or the IgE.
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PMID:New insights into the autoantibody-mediated mechanisms of autoimmune bullous diseases and urticaria. 1646 21


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