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

Histamine release in cold urticaria was studied before and after therapy with cyproheptadine to determine whether any effect upon histamine release could be distinguished from end-organ receptor-site blockade. Patients were asymptomatic while taking cyproheptadine, their ice cube test reverted to normal, and only one of six patients had any swelling upon ice-water submersion of one hand for 5 min. Histamine-release curves were obtained following ice-water submersion before and after cyproheptadine therapy. All patients had significant histamine release and in five of six patients there was no evident difference in the magnitude of histamine release before or after therapy. A single patient did have diminished histamine release after therapy, but could not be restudied to be sure this was not a spurious result. Our data demonstrated that cyproheptadine is extremely effective in ameliorating the symptoms and signs of cold urticaria and that its principal effect is that of an H1 receptor antagonist, thereby blocking the effects of histamine. These data further suggest that a sufficient dose of any standard antihistamine should be similarly effective and that patients who do not tolerate cyproheptadine or do not appear to respond to it should be tried on other antihistamines of the H1 type.
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PMID:The role of cyproheptadine in the treatment of cold urticaria. 610 2

Experiments in the skin and synovialis have thrown new light on the allergic-inflammatory reactions. The inflammatory effect of histamine is thus due to stimulation of two different types of receptors in the vessels, i.e. histaminergic H1 and H2 receptors. Both types of receptors are of importance for the immediate cutaneous response to allergens and histamine. Treatment with a combination of H1 antagonists (classical antihistamines) and the H2 antagonist cimetidine will thus cause a much stronger inhibition of the urticarial reactions than treatment with the H1 and H2 antagonist alone. It is therefore probable that a combination therapy could have an advantage over the traditional treatment with classical antihistamines in urticaria and other histamine-mediated skin diseases. Histamine might also be of importance for the swelling of the joints in inflammatory diseases such as rheumatoid arthritis, and clinical trials with H1 and H2 antagonists are in progress.
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PMID:H2 antihistamines (cimetidine) and allergic-inflammatory reactions. 616 Jul 81

Urticaria represents a wide variety of conditions characterized by urticarial papules, wheals, and angioedema. The number of potential causes of urticaria is legion, but a diligent search by careful history and examination is indicated. Laboratory testing depends upon the specific situation, but routine screening examinations are not cost effective. Histamine from mast cells plays an important role in urticaria. Multiple factors, such as aspirin and other nonsteroidal anti-inflammatory agents, direct histamine-releasing agents (including benzoates), tartrazine and other azo dyes, and perhaps blockers of beta 2-adrenergic activity and H2 receptors, adversely influence histamine release either directly or indirectly. Vasodilation is also detrimental. Treatment of both acute and chronic urticaria necessitates removal of the patient from aggravating factors as well as the cause of the outbreak (if one can be found), along with effective antihistaminic agents and perhaps beta 2-adrenergic agonists. Treatment of specific entities within the urticarial group is briefly outlined in this article.
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PMID:Treatment of urticaria. 617 11

Four patients suffering from cold urticaria were treated with ketotifen and oxatomide for one week each. Histamine liberation was measured after the exposure to cold before and after the treatment. A significant inhibition was demonstrated for either product, much more so, however, for oxatomide. This inhibition was associated with a pronounced improvement of complaints.
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PMID:[Effect of ketotifen and oxatomide on histamine liberation due to exposure in cold urticaria]. 619 11

Histamine release from human peripheral leukocytes was studied in patients with urticaria, pollinosis, and psoriasis and compared with the release in normal healthy donors using anti-IgE or the calcium-ionophore A 23187 as stimuli in the presence of three calcium mineral solutions (Frubiase Calcium). It was observed that among 35 donors 29 revealed a calcium dependent inhibition of histamine release. The inhibition was also evident when calcium mineral solution was added to an ongoing histamine release. The membrane biochemical effects of calcium mediated inhibition are currently under investigation.
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PMID:Effect of calcium mineral solutions on the histamine release from human peripheral leukocytes. 620 Jan 23

Histamine is a potent mediator of immediate hypersensitivity reactions, and is stored primarily in mast cells and basophils. It exerts its pharmacologic effects through interactions with H1 and H2 cell surface receptors, which promote changes in vascular permeability, levels of cyclic nucleotides, neutrophil and eosinophil chemokinesis and chemotaxis, gastrointestinal secretion, and smooth muscle contraction. H1 and H2 antihistamines have been utilized to interfere with these responses and have proven clinically useful in the treatment of some types of rhinoconjunctivitis, urticaria, and peptic ulcer disease. Several types of biochemical assays have been developed to assess histamine release from mast cells and basophils as well as to measure blood, urine, and tissue levels of histamine. The guinea pig ileum bioassay, fluorometric assay, and radioenzyme assay, each with certain modifications and limitations, have provided useful information concerning the function of histamine in health and disease.
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PMID:Histamine. 620 Dec 53

Use of differential effects of agonists and antagonists has provided an experimental basis for subdivision of histamine receptors into H1 and H2. This has enabled classification of the responses to histamine in a wide range of organs and tissues. In human skin the vascular and sensory effects of histamine have been studied, and the influence of histamine on epidermal cell growth has been evaluated in vitro. The direct vasodilator and vascular permeability actions of histamine appear to involve both H1 and H2 receptors. However, the axon reflex flare due to histamine appears to be predominantly an H1 effect. Histamine itch involves H1 receptors. These findings have prompted clinical evaluation of combined therapy with H1 and H2 antagonists in patients with urticaria. Initial results have been encouraging in patients with factitious urticaria. Histamine exerts an inhibitory action on epidermopoiesis in vitro in a number of mammalian epidermal cell outgrowth systems including human explants. The pathophysiological relevance of this effect, which involves epidermal H2 receptors and which may be cyclic AMP dependent, is unknown.
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PMID:Histamine receptors in human skin: indirect evidence. 713 77

An 11-yr-old girl presented with a history of urticaria induced by warm or cool showers, exercise, and emotional stimuli. During evaluation she repeatedly developed generalized punctate urticaria, pruritus, palpitations, and headaches after warm baths or exercise, and she had a positive methacholine skin test. She developed similar lesions and pruritus after local application of sterile water, tap water, ethanol, normal saline, or 3% saline. The diagnosis of combined aquagenic and cholinergic urticaria was made and presented a unique opportunity to study and compare mediator release and clinical symptoms in both conditions. The patient was submerged in bath water at either 37 degree or 41 degree C to induce either aquagenic or cholinergic urticaria, respectively. Histamine was released into the systemic circulation in both conditions in a similar time course; however, systemic symptoms occurred only after the 41 degree C bath. After failure to induce tolerance to the 41 degree C bath water, hydroxyzine therapy was instituted. One week later she was rechallenged; few symptoms appeared, and a rise in serum histamine was not detected as had been shown in previous challenges. The data suggest that in our patient, hydroxyzine may have contributed to the inhibition of both histamine release and the appearance of symptoms during hot bath challenging.
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PMID:Evaluation of a patient with both aquagenic and cholinergic urticaria. 731 13

Four patients with cold urticaria and six control subjects were studied. Gastric acid output was measured for 1 hr before and 1 hr after the immersion of both hands in ice cold water. The mean acid output fell in the control group by 16.3%. Acid output in the cold urticaria patients rose in each case following the cold challenge. In three cases it rose by a mean of 52.6% and in one case by 1707%. Histamine is released locally and systemically during the reaction of cold urticaria. This is the most likely cause of the increase in gastric acid secretion.
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PMID:Gastric acid secretion in cold urticaria. 738 40

Primary cold urticaria (PCU) characterized by the association of urticaria, angioedema, and sometimes a shock-like reaction after cold exposure, is usually considered to be linked with histamine and prostaglandin D2 release by mast cells. To determine the involvement of cytokines, we studied the release of tumor necrosis factor-alpha (TNF-alpha) in the blood of the efferent vein after immersion of the hand in chilled water. Five patients with PCU were compared with a control population (three patients with nonphysical urticaria and three healthy subjects). Among patients with PCU who underwent the cold immersion test, two exhibited a shock-like reaction with a large urticarial plaque (patients 1 and 2), one had only a mild cutaneous reaction, and two had no reaction. Patient 1 was reevaluated after 6 months of treatment with H1 and H2 antihistamines: he did not respond to this challenge. All controls were strictly negative. Histamine was released within the first minute after the challenge in the three patients with PCU, but at a higher level for the two patients who had a systemic reaction. TNF-alpha was undetectable in the blood of the patient with only a mild cutaneous reaction, whereas TNF-alpha release was observed for the two patients with a systemic reaction, 2 and 6 minutes after the end of the cold immersion test. The two other patients and the control subjects released neither histamine nor TNF-alpha. In parallel, pathologic and immunohistochemical (with a rabbit anti-TNF-alpha antibody) studies were performed on skin biopsy specimens collected 10 minutes after ice-cube test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tumor necrosis factor-alpha release during systemic reaction in cold urticaria. 750 21


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