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)

This study describes the probably eleventh case, mentioned in literature, of acquired heat contact uticaria in an otherwise healthy young woman. With regard to true contact induction heat contact urticaria clearly differs from the more common cholinergic uticaria. On the other hand, heat contact urticaria is completely analogous to cold uticaria because of the exposure area, reversible blocking by unphysiological prolonged heating of the skin, sensitivity to antihistamines and resistance to corticosteroids. In this case, whealing of the skin occurred on exposure to heating of 39 degrees C for 5 min. With a temperature of 44-46 degrees C, The shortest time for wheal induction was 3-5 sec. At 70 degrees C, the shortest time for maximal reaction was only a split second. An "optimal temperature" for wheal induction could not be determined. Local anaesthesia with 2% Xylocain caused a considerable blocking of wheals. Histamine and cholinergic drugs showed normal skin reactions after intradermal injection. Antihistamines administered parenterally or perorally were highly effective. Corticosteroids, however, given systemically in high doses proved to be ineffective. During our observations, a spontaneous remission appeared with a clinical symptom-free state; on unphysiological high temperature stimulus, however, contact uticaria could still be demonstrated. The pathogenetic uniformity of sporadic heat contact urticaria and problems of therapeutical controls are discussed.
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PMID:[Clinical and experimental observations on idiopathic urticaria due to the contact with heat]. 0 89

Urticaria is a problem often as vexing to the physician as to the patient. The approach to the patient with hives first demands a search for the etiology, whether endogenous and triggered by emotions or occult systemic disease, exogenous and triggered by allergy to inhaled or ingested antigens, or physical and due to abnormal sensitivity to heat, cold, light, or pressure. Often a fruitless search, the diagnostic evaluation must be accompanied by appropriate symptomatic therapy requiring familiarity with the antihistamines and their relative advantages in the various forms of urticaria. Elimination diets are of diagnostic as well as therapeutic value: pencillin-free, yeast-free, and salicylate-free diets are particularly useful. Therapeutic trials of tetracycline, nystatin and griseofulvin may be helpful, while corticosteroids and specific desensitization are rarely of value.
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PMID:Urticaria. 0 33

A 33-year-old female patient with acquired cold urticaria, together with her 8-year-old healthy daughter, was subjected to a brief period of cold exposure. The effect of this treatment upon a number of key factors of the plasma coagulation, kallikrein and complement systems was investigated. Cold air provocation caused increased fibrinolysis, together with a measurable consumption of the protease inhibitors alpha1-antitrypsin (alpha1AT), alpha2-macroglobulin (alpha2M) and C1Inactivator (C1INA). Kaolin activation of the patient's plasma elaborated exceptionally high levels of esterolytic activity, both before and after cold exposure, indicating pre-enzyme lability. Both subjects had abnormally high serum ratios alpha2M/alpha AT. Impressive leucocytosis was observed in the symptomless child.
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PMID:Enzyme activation and inhibition induced by cold provocation in a patient with cold urticaria. 4 15

Six patients with cold urticaria were found to possess elevated plasma histamine levels after cold challenge by placing one hand in ice water for 4 minutes. A single patient became hypotensive during the procedure and had a level of 260 ng/ml. histamine in the venous effluent from his hand. No elevation of plasma serotonin or bradykinin was observed. Two patients with cholinergic urticaria possessed elevated plasma histamine levels during and after vigorous exercise for 10 minutes; these patients also gave a positive test for vibration-induced angioedema. A single patient with cholinergic urticaria possessed elevated baseline serotonin levels and elevated levels during and after exercise but no elevation of plasma histamine or bradykinin. The results suggest that histamine is the major mediator of urticaria and hypotension in cold urticaria. Histamine also appears to be released coincident with the development of urticaria in some patients with cholinergic urticaria, while elevated serotonin levels in a single atypical patient suggest that a subpopulation of patients with cholinergic urticaria possess a different pathogenesis.
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PMID:In vivo studies of mediator release in cold urticaria and cholinergic urticaria. 4 22

Patients with idiopathic acquired cold-induced urticaria were evaluated for the release of the preformed mast-cell mediators of immediate-type hypersensitivity during a study in which one arm was immersed in ice water while the other arm remained as a control. Blood specimens were obtained from each arm serially over a one-hour interval, and serum speciments were assessed for histamine, eosinophil chemotactic factor of anaphylaxis, and complement components. Levels of histamine and eosinophil chemotactic factor rose in the arm subjected to cold immersion for three minutes, with peak values occurring between two and five minutes and returning to base line by 30 minutes. No changes occurred in the control arm or in the immersed arm of normal subjects. Assessment of the classical and alternative complement pathways showed no abnormalities. This initial observation of release of eosinophil chemotactic factor of anaphylaxis in vivo along with histamine assigns the mast cell a central role in cold urticaria.
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PMID:Cold urticaria: release into the circulation of histamine and eosinophil chemotactic factor of anaphylaxis during cold challenge. 5 69

The interrelations between cold sensitivity and release of histamine and other mediators in five patients with cold urticaria undergoing cold tolerance treatment were studied. Tolerance to cold was produced in all patients by repeated cold exposure. In four patients tolerance was maintained by once daily exposures. In the fifth patient 4-hourly exposures were necessary. Cold sensitivity was associated with histamine release in venous blood draining urticated skin. No prostaglandin activity was detected, and low concentrations of kinin activity were found in blood draining the normal and exposed skin of healthy subjects as well as in patients with cold urticaria. After induction of tolerance, no histamine release occurred on challenge by cold. Relapse of sensitivity was associated with reappearance of histamine release on challenge. The conclusion that tolerance is due to depletion of histamine stores in skin after repeated cold exposure was supported by diminished wealing in response to injection of a histamine liberator (compound 48/80) in cold-tolerant skin.
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PMID:Induced tolerance in cold urticaria caused by cold-evoked histamine release. 5 49

The hypothesis that deficiencies of plasma protease inhibitors might play a role in the pathogenesis of chronic urticaria was evaluated. Plasma levels were measured in patients with urticaria and a matched control group for alpha1-antitrypsin, alpha2-macroglobulin, total trypsin-inhibiting capacity, kallikrein-inhibiting capacity, and the complement factors C1 esterase inhibitor, C3, and C4. A total of 92 patients with chronic urticaria or more than three months' duration was studied. Patients with acquired cold urticaria had significantly decreased levels of alpha1-antitrypsin and total antitrypsin activity. In patients with acquired angioneurotic edema, alpha1-antitrypsin levels and antichymotrypsin activities were lowered, with less significant decreases in anti-trypsin and antikallikrein activities. Levels of C1 esterase inhibitor , C3, and C4 were normal in all groups. There was no correlation between the increased sensitivity to intracutaneously administered kallikrein injection and deficiencies of of protease inhibitors.
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PMID:Protease inhibitors in plasma of patients with chronic urticaria. 6 Sep 15

Thirteen patients with cold urticaria were studied to assess the effect of the systemic drug doxantrazole, which has actions resembling disodium cromoglycate, on cold evoked histamine release. The patients, all of whom developed an immediate local whealing response after cooling of the forearm, demonstrated release of histamine into venous blood draining that forearm. Following doxantrazole treatment, significant suppression of histamine release occurred. In some but not all patients this was accompanied by diminution of urtication in response to cooling. A double-blind study was carried out in 3 subjects, all of whom showed diminished cold-stimulated histamine release after doxantrazole. Two of these showed clinical improvement. Doxantrazole had no effect on erythema due to intradermal histamine, but did suppress the erythematous reaction to intradermal injection of compound 48/80. Our results suggest that doxantrazole or related anti-allergic agents might be useful in the treatment of cold urticaria.
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PMID:Cold urticaria: inhibition of cold-induced histamine release by doxantrazole. 8 Dec 44

Five patients with delayed cold urticaria are described. The urticarial skin response was present between 24 and 72 hours after ice challenge. In two of the patients the cold sensitivity was of clinical relevance. Some of the patients displayed low alpha1-antitrypsin and increased C4 levels in their serum. Our findings may justify the introduction of cold provocation as a routine procedure in the investigation of a patient with chronic urticaria.
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PMID:Delayed cold urticaria. 8 39

A-20-year-old male Army paratrooper presented with a history of inducible urticaria associated with exercise as well as cold exposure. Upon evaluation, he not only had a positive ice cube test, but also had a positive mecholyl skin test with numberous satellite lesions and generalized punctate urticaria following exercise challenge. Thus, he appeared to have combined cold and cholinergic urticaria. When mediator release was examined during cold and exercise challenge, histamine release was observed in each instance; a rapid rise and fall of plasma histamine was seen after cold challenge, while a lag phase followed by sustained elevation of plasma histamine was associated with exercise challenge. This represents the fourth reported case of combined cold and cholinergic urticaria and is the first in whom mediator release was assessed. The time-course of histamine release was characteristic of each disorder.
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PMID:Evaluation of a patient with cold and cholinergic urticaria. 8 66


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