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)

Cetirizine, an H1 antihistamine, has properties in addition to H1 blockade that may be useful in the treatment of seasonal rhinitis and urticaria. For example, cetirizine has been shown to block the influx of eosinophils into the site of antigen-stimulated skin blisters. Studies with other antihistamines suggest that this is not a universal property of this type of drug. Pretreatment with cetirizine also has been found to block the augmented sensitivity to methacholine that occurs 24 hours after antigen provocation of the nasal mucosa. This reduction takes place despite the absence of an effect on eosinophil influx into this area, and suggests another action of cetirizine. Our study of allergic rhinitis patients examined the effect of cetirizine on early response to nasal challenge with antigen. Cetirizine, although it did not block the release into nasal secretions of histamine, significantly reduced sneezing and decreased levels of albumin and TAME-esterase activity, which are indicators of vascular permeability. Cetirizine also blocked the generation of leukotriene C4. In vitro studies have shown that cetirizine does not block the release of leukotriene from anti-IgE stimulated mast cells, raising the possibility that cells in the nasal mucosa in addition to mast cells generate leukotrienes.
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PMID:Additional properties of cetirizine, a new H1 antagonist. 168 95

Because urticaria clears spontaneously in most patients, an extensive workup is not advised during the early weeks of an urticarial eruption. Whether and when to perform a screening workup or a more extensive workup depend on the degree of suspicion that the patient is ill, the urgency with which the patient presses for an answer, and the presence or absence of signs or symptoms that might lead the physician to pursue a diagnosis other than chronic idiopathic urticaria. Angioedema may occur with urticaria, and when it does, the prognosis is worse. Whereas urticaria manifests as circumscribed edema involving the superficial dermis, angioedema involves primarily the deep dermis or subcutaneous or deeper layers. Individual urticarial lesions usually disappear within 2 to 4 hours, whereas those of angioedema can persist for 72 hours. The workup for patients with chronic angioedema can be similar to that for patients with urticaria. However, several additional diagnostic possibilities should be pursued in patients with angioedema, such as hereditary angioedema caused by C1-esterase inhibitor deficiency, because anabolic steroids are effective in the treatment of these conditions.
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PMID:Urticaria and angioedema: diagnosis and evaluation. 186 91

Two male patients with hypogonadism and four female patients who received an anti-androgen as contraceptive (cyproteronacetate) and who had recurrent angioedema are described. In one male patient, augmentation of the plasma androgen level resulted in disappearance of symptoms. In the four female patients, recurrent angioedema and urticaria developed after initiation of the anti-androgen treatment. Cessation of cyproteronacetate and a change to another contraceptive resulted in complete resolution of the previously frequent angioedematous attacks. The women are still symptom free after more than 60 patient's months. These cases suggest that an androgen deficit due to either hypogonadism or to anti-androgen treatment may be another cause of angioedema. One of the two male patients was untreated and presented with 40% normal value of C1-INH. Androgen therapy normalized C1-INH concentration in this male patient. Functional C1-INH in the same patient, studied before and after the beginning of androgen therapy, clearly increased when assessed by inhibition of amidolytic activity of C1-esterase. The other male patient with hypogonadism had already been under androgen treatment for 4 years and had C1-INH levels in the normal range. In the female patients, complement profiles were normal before and after cessation of anti-androgen contraception; however, the C1-INH plasma levels were higher after cessation of anti-androgen anticonception. These results indicate an effect of androgen deficit on the level of C1-INH in circulating plasma but do not prove a role of C1-INH in angioedema associated with diminished androgen plasma levels.
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PMID:Recurrent angioedema associated with hypogonadism or anti-androgen therapy. 252 97

Data early obtained on activation of the kallikrein-kinin system in acute forms of pollinosis and urticaria were corroborated in vitro. These experiments exhibited enzymatic activation of Hageman factor and prekallikrein using "liberator", obtained after incubation of the leukocyte fraction enriched with basophils and specific allergen. I ml of the "liberator" containing 10(7) cells activated Hageman factor up to 12-20 mU per min (evaluated by BAEE-esterase activity of the kallikrein developed) as well as kallikrein activity was increased up to 80-130 mU within 1.5-2 hrs of incubation. The Hageman factor was distinctly inactivated after long-term incubation with the "liberator".
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PMID:[The mechanism of activation of kallikrein-kinin system in the plasma of patients with atopic allergic diseases]. 323 45

Plasma aspirin esterase activity and cholinesterase activity were reduced in patients with aspirin sensitive asthma and aspirin sensitive urticaria compared to asthmatic and dermatological controls. Phenylacetate (non specific) esterase activities, were however unaltered in these patients. The reason for the lower activity is uncertain but it does not appear to be due to genetically determined lower cholinesterase or due to the avoidance of aspirin by sensitive patients. A low aspirin esterase activity may be a contributory factor in precipitating these aspirin sensitive reactions.
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PMID:Plasma esterase activity in patients with aspirin-sensitive asthma or urticaria. 344 44

We have used a panel of monoclonal antibodies and enzyme histochemistry in order to characterize further the perivascular mononuclear cell infiltrate found in chronic idiopathic urticaria. Biotinylated anti-mouse immunoglobulin was exposed to avidin-biotin-peroxidase-labeled complex followed by peroxidase development in order to detect binding of monoclonal antibodies. The mean percent staining obtained for 12 patients with chronic urticaria was 47% T-lymphocytes, 22% monocytes (14% by alpha-naphthyl acid esterase), and 11% mast cells. B-lymphocytes were not detectable, and approximately 20% of cells could not be identified. Although patients varied greatly in the ratio of Leu 3a positive helper-inducer T cells to T8 positive cytotoxic-suppressor cells, the average of all patients was not significantly different from the T4/T8 ratio in plasma. Our results suggest that the infiltrate resembles that observed in cellular immune reactions (although no antigen has been identified) and that interaction of T-lymphocytes and/or monocytes with mast cells to cause mediator release appears likely.
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PMID:Studies of the cellular infiltrate of chronic idiopathic urticaria: prominence of T-lymphocytes, monocytes, and mast cells. 349 Nov

Plasma samples from 20 patients with acquired cold urticaria were studied. The C1-esterase inhibitor activity was found to be low, but the total C1-esterase inhibitor concentration was normal. Prekallikrein, plasmin-alpha 2-antiplasmin complex, and kallikrein-like activity were also found to be within normal limits. Cold-promoted activation of coagulation factor VII occurred in 45% of the patient plasmas and resulted in a considerable drop in C1-esterase inhibitor activity.
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PMID:On the role of the C1-esterase inhibitor in cold urticaria. 620 79

The Authors report the results obtained with the histamine radioenzymatic test in the evaluation of the histamine content of granulocytes of 91 subjects, suffering from urticaria and urticaria-angioedema syndrome. The laboratory investigation was also integrated, according to the clinical implications, by other in vitro tests such as: kallikrein, RAST, PRIST, secretory IgA, precipitins assays. In urticaria-angioedema syndrome the quantitative and functional evaluation of C1-esterase inhibitor was also performed, to exclude the heredity of these pathologic forms. Basing on the results obtained, the authors expect that the granulocyte histamine radioenzymatic assay is highly reliable from the diagnostic viewpoint in the urticaria and angioedema forms.
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PMID:[Diagnostic use of a radioenzyme test in urticaria-like disorders and in urticaria-angioedematous syndromes]. 734 23

Mast cells are considered to be the primary effector cells in urticaria but it is possible that lymphocytes contribute to the formation of weals by secreting histamine releasing factors. The aim of this study was to examine the population of mast cells and to quantify the T cell subsets and their activation status in delayed pressure urticaria (DPU), chronic idiopathic urticaria and normal controls. Three biopsies were obtained from each of four patients with chronic idiopathic urticaria but not DPU. Three biopsies were taken from each of 13 patients with DPU, from a combination of unchallenged skin and at 0, 2, 6, 24, 48, and 120 h after weighted steel rods (diameter 1.5 cm) had been applied to the thighs. Three biopsies were similarly obtained from each of four normal controls before an identical pressure challenge and at 6, 24 and 48 h afterwards. The chloracetate esterase stain was used to demonstrate mast cells and an alkaline phosphatase anti-alkaline phosphatase immunohistochemical technique to assess the phenotypic and activation characteristics of the T cell infiltrate. The mast cell count did not differ significantly between unchallenged skin from DPU patients and normal controls. Following a pressure challenge to the DPU patients, the number of stainable mast cells decreased significantly to a level comparable with that in spontaneous weals of chronic idiopathic urticaria. Investigation of T cell subsets showed a preponderance of CD4+ cells over CD8+ cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mast cells and T lymphocytes in chronic urticaria. 760 Mar 77

A multicentre, retrospective study of hereditary deficiency of C1-esterase inhibitor (C1-INH) function, a deficiency which clinically manifests as hereditary angioedema (HAE), was performed in six centres in Germany, Austria and Switzerland. 242 individuals were registered with proven functional or quantitative deficiency of C1-INH who belonged to kindered with disease manifestation in 2 to 6 generations. Considering the total population in the three countries and the number of registered individuals, a frequency of the deficiency of 0.02 x 10(-4) was calculated. As this epidemiological study involved only 6 centres, a 10 to 100 times higher frequency of C1-INH deficiency is estimated to be a more realistic value. Out of the 242 registered individuals 110 were evaluated for type and location of clinical manifestation of the deficiency, the laboratory data and the therapy outcome. 86 (78.2%) of the patients belonged to the "common type" and 24 (21.8%) to the "variant type" of HAE. In 53.9% of the cases first manifestation of the disease was before the age of 20 years. In only 3.9% of the patient population did the disease begin after 40 years of age. A mean time lag of 5,3 years was observed, between the first manifestation and correct diagnosis. Initial diagnosis was correct in only 31.8% of the cases of which dermatologists provided 51.7%. False diagnoses include urticaria (41.3%), allergy (20%), acute abdomen (18.7%), angina (8%), rheumatoid disease (5.3%) and intracranial haemorrhage, CNS tumour, epilepsy, migraine (5.3%). The distribution pattern of HAE resembled that of intolerance reactions and pseudoallergies. Urticarial lesions were not associated with C1-INH deficiency. 24% of the patients had at least one episode of laryngeal edema. 40% of patients were unable to identify a trigger of edema formation. The others indicated as triggers trauma, hormonal changes, mental stress, insect stings and in a few cases food and drugs. Menstruation and oral contraceptives aggravated or made disease manifestations more frequent. In contrast, during pregnancy in many cases clinical manifestations improved and delivery posed no problems. The possibility of HAO is very much suggested by the tailure of edema to respond to classical anti-allergic therapy. Therapy of choice of acute attacks is C1-INH concentrate. No side reactions, antibody formation or virus transmission have been observed. For long term prophylaxis danazol, an attenuated androgen, or tranexamic acid, a protease inhibitor, was chosen. The daily dose of danazol should be kept as low as possible because of its anabolic, anti-estrogenic, anti-gestagenic, and anti-gonadotropic effects. Indeed, adverse reactions were observed in 41.7% of patients receiving danazol. Frequencies of adverse reactions were twice as common in women as in men. Adverse reactions were dose dependent and reversible except for one woman with irreversible deepening of her voice. Measuring C1r is a effective way to assess C1-INH function and monitor therapy.
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PMID:[Hereditary angioedema in the German-speaking region]. 955 33


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