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)

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.
J Dermatol Sci 1990 Sep
PMID:Flare factors and atopic dermatitis: the role of allergy. 207 89

This study comprises 40 patients with skin disorders from current or previous occupational exposure to epoxy resin compounds (ERC) during 1984-1988. ERCs were the 3rd most common cause (32 of 264 cases: 12.1%) of currently relevant allergic contact dermatitis: 23 cases from epoxy resins based on the diglycidyl ether of bisphenol A (DGEBA-ERs), 5 from reactive diluents, 1 from amine hardeners (DETA), and 3 from epoxy acrylates. 2 cases (0.8%) of irritant contact dermatitis were due to ERCs. Methyl hexahydrophthalic anhydride (MHHPA, an epoxy hardener) caused 1 case of contact urticaria. Previously relevant occupational allergic contact dermatitis from DGEBA-ERs was detected in 5 cases. On patch testing, ERC allergens gave the following positive reactions: epoxy resin of the standard series in 35 cases (4.0% of 870 tested), epoxy reactive diluents in 10 (7.1% of 140), cycloaliphatic epoxy resins in 4 (11.1% of 36), epoxy acrylates in 4 (4.5% of 88), and amine compounds commonly used as epoxy hardeners in 17. Despite extensive patch test series, testing with patients' own ERCs remains important.
Contact Dermatitis 1990 Sep
PMID:Occupational dermatoses from epoxy resin compounds. 214 18

The histopathology of systemic allergic contact dermatitis is usually characterized by spongiosis. A number of other much less common to rare histological findings have also been reported, including erythema multiforme-like eruption, vasculitis, urticaria, and miscellaneous groups.
Semin Dermatol 1990 Sep
PMID:Histopathology of exogenous and systemic contact eczema. 220 24

Twenty-seven patients were referred for evaluation of anaphylaxis after induction of general anesthesia (GA) in which thiobarbiturates, muscle relaxants, or antibiotics were administered intravenously. Skin testing by the prick and intracutaneous methods was performed with dilutions of the thiobarbiturates and muscle relaxants; beta-lactam reagents were used in patients who had also received these drugs. No skin test reactivity was noted in 16 normal subjects. Skin tests were positive in 13 patients (thiobarbiturates in five, muscle relaxants in six, and antibiotics in two patients). Two patients were dermatographic and yielded indeterminate skin test results. Eleven of the 27 patients subsequently had GA; all patients received a premedication regimen of prednisone and diphenhydramine. Of three patients with negative skin tests, one experienced an arrhythmia, but no other signs attributable to anaphylaxis were noted. One patient with dermatographism had GA without a reaction. Positive skin tests implicated an agent that was avoided in seven patients; one of these patients experienced delayed urticaria/angioedema after the completion of GA. Thus, no patients developed anaphylaxis during subsequent GA for which agents producing positive skin tests were avoided, and a premedication regimen was used.
J Allergy Clin Immunol 1990 Sep
PMID:Anaphylaxis during induction of general anesthesia: subsequent evaluation and management. 207 81

Ketotifen is an orally active prophylactic agent for the management of bronchial asthma and allergic disorders. Accumulated evidence indicates that after 6 to 12 weeks of administration, ketotifen significantly reduces respiratory symptoms and the need for concomitant antiasthmatic drugs in about 70% and 50%, respectively, of patients with mild to moderate bronchial asthma. However, absolute improvement in lung function is generally slight. Ketotifen also has pronounced antihistaminic and antianaphylactic properties which result in moderate to marked symptom improvement in the majority of patients with atopic dermatitis, seasonal or perennial rhinitis, allergic conjunctivitis, chronic or acute urticaria or food allergy. Comparative trials with established agents--notably sodium cromoglycate (cromolyn sodium) in asthma and histamine H1-antagonists in allergic disorders--indicate that ketotifen has comparable clinical utility. Unlike inhaled sodium cromoglycate, ketotifen ameliorates the symptoms of asthma, rhinitis and dermatitis when present together in atopic patients. Patient acceptance of ketotifen is good, although sedation can be troublesome in older children and adults for the initial 2 weeks of treatment. Weight gain is another notable effect in a small percentage of patients. Thus, ketotifen appears to be a useful agent for the management of allergic disorders and bronchial asthma, particularly in patients for whom oral therapy is preferred. Although a lengthy run-in period is needed in the treatment of asthma, in those patients who respond, continued reduction in the frequency and severity of symptoms and in the use of additional antiasthmatic drugs can be anticipated.
Drugs 1990 Sep
PMID:Ketotifen. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in asthma and allergic disorders. 222 22

Prostaglandin (PG) D2 and histamine concentrations have been measured in blood draining cold-challenged forearm skin in patients with cold urticaria. Local venous concentrations of both histamine and PGD2 rose in four patients who developed a whealing response. Plasma histamine concentration increased from a mean resting value of 0.24 +/- 0.09 (SD) ng/ml to peak values of 16.9 to 96.6 ng/ml. Resting concentrations of PGD2 were below the limit of detection (5 pg/ml) in three patients and 62 and 27 pg/ml in the fourth. Peak plasma PGD2 concentration after challenge ranged from 166 to 279 pg/ml. Time course of histamine and PGD2 release was similar with peak concentrations at 6 and 10 minutes, respectively. The maximum clinical response occurred between 10 and 20 minutes after challenge. Our findings demonstrate that PGD2 is produced in association with mast cell degranulation in man, but the amount, relative to histamine, is low. Despite its high potency in production of inflammatory effects, PGD2 probably has only minor direct effects in cold urticaria, although it may act to potentiate other mediators.
J Allergy Clin Immunol 1986 Sep
PMID:Prostaglandin D2 and histamine release in cold urticaria. 242 56

Twelve patients with a history of aspirin-induced urticaria and/or angioedema were studied before and after the provocation of symptoms with aspirin. The resting plasma histamine levels in these patients (0.95 +/- 0.25 ng/mL) were significantly higher than in 30 control subjects (0.21 +/- 0.02 ng/mL) (P less than .0005) and nine patients with non-aspirin-sensitive urticaria (0.27 +/- 0.06 ng/mL) (P less than .01). The plasma histamine levels fell significantly at the time of adverse reactions to aspirin (P less than .01). The high resting histamine levels, like the high venous prostaglandin F2 alpha levels that we have previously reported in the same group of patients and the high plasma histamine levels we have found in aspirin-sensitive asthmatics suggest an abnormality of mediator release in aspirin-sensitive patients.
Ann Allergy 1987 Sep
PMID:Plasma level of histamine in aspirin-sensitive urticaria. 244 44

Little is known about the molecular mechanisms or inflammatory mediators involved in delayed pressure urticaria (DPU). Pressure sufficient to provoke lesions was applied to the back of six patients with DPU. The levels of products of arachidonic acid transformation in skin exudate from the pressure challenged skin were estimated immediately after pressure was removed and 6 h later when lesions were present. These were compared to levels estimated in a similar way from unchallenged skin in these patients. Levels of leukotriene C4/D4/E4, prostaglandin E2, 12-hydroxyeicosatetraenoic acid and leukotriene B4 were not raised in lesional skin. Our results suggest that arachidonic acid metabolism is not stimulated in DPU.
Br J Dermatol 1989 Sep
PMID:Arachidonic acid transformation is not stimulated in delayed pressure urticaria. 250 40

Urticaria, angioedema, and arthritis are cardinal features of hypocomplementemic urticarial vasculitis syndrome (HUVS). Considered to be an immune complex-mediated disorder, HUVS has been differentiated from systemic lupus erythematosus (SLE), based on its clinical manifestations and the C1q precipitin (C1q-p) reaction, which is manifested as gel precipitation of C1q by a small percentage of HUVS IgG molecules. This phenomenon has been attributed to an Fc region abnormality, and the responsible IgG molecules are said to possess C1q-p activity. We purified IgG from 4 HUVS patients and confirmed that HUVS IgG contains C1q binding activity. F(ab')2 fragments from these patients also bound to C1q, as measured by 2 different C1q binding methods at physiologic ionic strength; HUVS IgG Fc fragments did not bind to C1q. Preincubation of HUVS F(ab')2 fragments with antibody to human F(ab')2 prevented subsequent binding to C1q. We conclude that IgG antibodies to C1q are present in HUVS serum, and it is likely that these antibodies are C1q-p. Because the clinical manifestations of HUVS and the presence of anti-C1q antibodies have been described in patients with SLE, our findings support the concept that HUVS is an autoimmune syndrome related to SLE.
Arthritis Rheum 1989 Sep
PMID:Serum IgG antibodies to C1q in hypocomplementemic urticarial vasculitis syndrome. 252 53

Of 1346 patients with suspected contact dermatitis examined in Toronto, 10 bakers and 10 food handlers were found to have occupational contact dermatitis. Although not dissimilar in age, years in the trade, or length of illness, men were significantly overrepresented in the population of bakers (100% vs 40%, p less than 0.05). One baker had occupational asthma related to rye flour. Compared with the bakers, significantly more of the food handlers had allergic contact dermatitis (70% vs 20%, p less than 0.05). In addition to food components, cinnamates and rubber were found to be causes of allergic response. One food handler had contact urticaria caused by shellfish. The standard screening tests, combined with the use of contactants specific to occupational history, yielded a definitive determination of the existence of a contact allergy in our subjects.
J Am Acad Dermatol 1989 Sep
PMID:Occupational dermatitis in food handlers and bakers. 252 71


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