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

A patient with cold urticaria is described in whom weals appeared immediately after an ice cube test for 3 min and persisted for a week as a red, tender swelling. The duration of the oedema was dependent on the intensity of the immediate reaction. If the immediate wealing was blocked by treatment with an oral antihistamine 3 h before the ice cube test, no delayed reaction was seen. Antihistamines given after the immediate wealing had occurred did not influence the delayed reaction. Reactions to intradermally injected histamine, prostaglandin E, kallikrein, serotonin and serum appeared normal.
 ...
PMID:Cold urticaria with persistent weals. 611 41

A functional determination of C1 esterase inhibitor (C1 INH) can be easily performed with an amidolytic assay by monitoring the inactivation of plasma kallikrein. In patients with urticaria as well as in healthy donors kallikrein inactivation, determined as the ratio of kallikrein activity at t60/t15, was found to be 0.47 +/- 0.06; in patients with hereditary angioneurotic edema (HANE). However, it amounted to 0.80 +/- 0.06. There was a good correlation between the inactivation rate of kallikrein and the protein levels of C1 INH (r = -0.93, p less than 0.001). In patients with HANE, levels of plasma kallikrein were slightly decreased (mean = 0.37 +/- 0.11 U/ml, normal mean = 0.47 +/- 0.09 U/ml), but still sufficient for monitoring kallikrein inactivation. In the case of one patient with functionally inactive C1 INH protein, the inactivation of kallikrein was impaired as in the conventional form of the disease.
 ...
PMID:A rapid method for functional determination of C1 esterase inhibitor in plasma. 617 50

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.
 ...
PMID:On the role of the C1-esterase inhibitor in cold urticaria. 620 79

Contrast media reactions may be classified as anaphylactoid, vasomotor, severe or life threatening, and fatal. Anaphylactoid reactions mimic immunoglobulin E-mediated hypersensitivity in that signs may consist of urticaria, angioedema, wheezing, dyspnea, hypotension, or shock. These reactions occur in 2% to 8% of all contrast media infusions. Vasomotor reactions occur in 5% to 8% of patients and consist of nausea, vomiting, flushing, and warmth. Severe reactions during which there is a concern for life occur about once per 1000 procedures. Fatalities have occurred in from 1:3000 procedures for intravenous cholangiography to between 1:10,000 to 1:100,000 procedures for intravenous urography. The pathogenesis of contrast media reactions is unknown, and various mechanisms may be associated with different clinical features. Radiocontrast media infusions can cause rises in plasma histamine and complement activation by either classic or alternate pathways or nonsequentially, yet adverse reactions may or may not occur. Abnormalities in the complement system or an increased conversion of prekallikrein to kallikrein has been demonstrated in some patients who have had anaphylactoid reactions. It is unknown if these mechanisms can explain the pathogenesis of anaphylactoid contrast media reactions. When patients who have had definite anaphylactoid reactions require a repeat procedure, the incidence of reactions ranges from 35% to 60% for intravascular infusion. Pretreatment with prednisone and diphenhydramine has been demonstrated to reduce this reaction rate to 9% in 465 procedures. Prednisone-diphenhydramine and ephedrine have further reduced the reaction rate to 3.1% in 192 procedures. These results are statistically significant (X2 = 5.4996, p = 0.019). Emergency equipment should be available should a severe reaction occur.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Contrast media reactions. 649 Nov 7

Cutaneous and pulmonary reactions to mediators of inflammation were studied in twenty-one patients with cholinergic urticaria, in twenty patients with other types of urticaria, and in seventeen healthy controls. Compared with controls and patients with moderate disease, patients severely affected by cholinergic urticaria or other types of urticaria developed larger weals at sites of injection with histamine (9 X 10(-7) M), but not with compound 48/80 (0.1%), acetylcholine (7 X 10(-5) M), kallikrein (4 X 10(-10) M). On bronchial challenge with acetylcholine (7 X 10(-5) M), pulmonary resistance increased markedly only in severely affected cholinergic urticaria patients. There was no correlation between cutaneous and pulmonary reactivity in individual subjects. Patients with cholinergic urticaria therefore demonstrate features of heightened skin reactivity (shared by patients with other urticarias) and an increased bronchial reactivity (as found in latent asthmatics).
 ...
PMID:Cutaneous and pulmonary reactivity in cholinergic urticaria. 656 2

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.
 ...
PMID:[Diagnostic use of a radioenzyme test in urticaria-like disorders and in urticaria-angioedematous syndromes]. 734 23

We have studied the plasma kallikrein amidolytic activity in healthy control subjects (inactive), patients with chronic urticaria (active) and patients with acute urticaria (active) from their admission to the emergency room (active) to the time after which their clinical symptomatology had disappeared (inactive). We found statistically significant differences (p < 0.01) in the active groups of urticaria patients. This leads us to believe that kallikrein participates in the development of symptomatology in these patients.
 ...
PMID:Plasma kallikrein amidolytic activity in patients with urticaria. 828 44

This review highlights some of the research advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects that were reported primarily in the Journal in 2007. Advances in diagnosis include possible biomarkers for anaphylaxis, improved understanding of the relevance of food-specific serum IgE tests, identification of possibly discriminatory T-cell responses for drug allergy, and an elucidation of irritant responses for vaccine allergy diagnostic skin tests. Mechanistic studies are discerning T-cell and cytokine responses central to eosinophilic gastroenteropathies and food allergy, including the identification of multiple potential therapeutic targets. Regarding treatment, clinical studies of oral immunotherapy and allergen vaccination strategies show promise, whereas several clinical studies raise questions about whether oral allergen avoidance reduces atopic risks and whether probiotics can prevent or treat atopic disease. The importance of skin barrier dysfunction has been highlighted in the pathogenesis of atopic dermatitis (AD), particularly as it relates to allergen sensitization and eczema severity. Research has also continued to identify immunologic defects that contribute to the propensity of patients with AD to have viral and bacterial infections. New therapeutic approaches to AD, urticaria, and angioedema have been reported, including use of sublingual immunotherapy, anti-IgE, and a kallikrein inhibitor.
 ...
PMID:Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects in 2007. 1877 68

Hereditary angioedema (HAE) is an inherited disorder characterized by recurrent, circumscribed, non-pitting, non-pruritic, and rather painful subepithelial swelling of sudden onset, which fades during the course of 48-72 hours, but can persist for up to 1 week. Lesions can be solitary or multiple, and primarily involve the extremities, larynx, face, esophagus, and bowel wall. Patients with HAE experience angioedema because of a defective control of the plasma kinin-forming cascade that is activated through contact with negatively charged endothelial macromolecules leading to binding and auto-activation of coagulation factor XII, activation of prekallikrein to kallikrein by factor XIIa, and cleavage of high-molecular-weight kininogen by kallikrein to release the highly potent vasodilator bradykinin. Three forms of HAE have currently been described. Type I and type II HAE are rare autosomal dominant diseases due to mutations in the C1-inhibitor gene (SERPING1). C1-inhibitor mutations that cause type I HAE occur throughout the gene and result in truncated or misfolded proteins with a deficiency in the levels of antigenic and functional C1-inhibitor. Mutations that cause type II HAE generally involve exon 8 at or adjacent to the active site, resulting in an antigenically intact but dysfunctional mutant protein. In contrast, type III HAE (also called estrogen-dependent HAE) is characterized by normal C1-inhibitor activity. The diagnosis of HAE is suggested by a positive family history, the absence of accompanying pruritus or urticaria, the presence of recurrent gastrointestinal attacks of colic, and episodes of laryngeal edema. Estrogens may exacerbate attacks, and in some patients attacks are precipitated by trauma, inflammation, or psychological stress. For type I and type II HAE, diminished C4 concentrations are highly suggestive for the diagnosis. Further laboratory diagnosis depends on demonstrating a deficiency of C1-inhibitor antigen (type I) in most kindreds, but some kindreds have an antigenically intact but dysfunctional protein (type II) and require a functional assay to establish the diagnosis. There are no particular laboratory findings in type III HAE. Prophylactic administration of either 17alpha-alkylated androgens or synthetic antifibrinolytic agents has proven useful in reducing the frequency or severity of attacks. Plasma-derived C1-inhibitor concentrate, recombinant C1-inhibitor, ecallantide (DX88; a plasma kallikrein inhibitor) and icatibant (a bradykinin B(2) receptor antagonist) have demonstrated significant efficacy in the treatment of acute attacks, whereas the C1-inhibitor concentrate has also provided a significant benefit as long-term prophylaxis. However, these drugs are not licensed in all countries and are not always readily available.
 ...
PMID:Hereditary angioedema in childhood: an approach to management. 2059 9

Swelling is a common chief complaint among patients. Swelling and hives are not typical of hereditary angioedema. Organ transplantation drugs are associated with angiodema and may complicate diagnosis. Our objective was to manage a complex case of angioedema in a setting of rashes and liver transplantation. We present an illustrative case of angioedema, rashes, and intussusception in a setting of a liver transplant and tacrolimus use with a family history of autoimmune disease. Treatment with the kallikrein inhibitor, kalbitor, eliminated angioedema and intussusception, though not permanently. Serial C1 esterase [corrected] inhibitor levels were only suppressed during severe attacks of angioedema. C1q autoantibody was elevated. Although 95% of cases of hereditary angioedema (HAE) have low [corrected] C4 levels, those with C1q immune complexes have autoantibodies leading to low-grade inflammation and eventual consumption of C1 esterase inhibitor levels with C4 unaffected. Rashes associated with angioedema are not urticarial. Physicians should learn to recognize the signs of attacks of HAE.
 ...
PMID:Angioedema in a child with a liver transplant, intussusception, and normal c4 levels. 2061 76


<< Previous 1 2 3 Next >>