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)

Six patients with acquired primary cold urticaria and six normal control subjects were challenged with a 5-minute immersion of an arm in cold water, at 10 degrees C, to induce cold urticaria. Venous blood draining the arm was sampled before and at 5 and 20 minutes after challenge. Prostaglandin D2 levels in the serum increased significantly after cold challenge but did not correlate with the severity of the urticaria. Significant elevations in histamine after cold challenge tended to be higher in the patients with a low threshold to cold reaction. Two markers of platelet activation, platelet factor 4 and beta-thromboglobulin, remained at basal levels 5 minutes and 20 minutes after challenge.
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PMID:Prostaglandin D2 and histamine release in cold urticaria unaccompanied by evidence of platelet activation. 245 77

Five individuals with idiopathic cold urticaria but not normal volunteers released platelet factor 4 (PF4) detected by radioimmunoassay into the circulation after cold challenge. In three patients, a biphasic rise in PF4 was noted with increases at 1 and 10 to 20 min after immersion, whereas in two others only the later rise was detected. Peak levels of PF4 were detected in all five patients 20 min after cold immersion, whereas peak levels of other mediators such as histamine and eosinophil and neutrophil chemotactic activity occurred earlier at 10, 3 to 10, and 5 to 10 min, respectively. The identification of PF4 in the circulation of patients with cold urticaria after cold challenge provides further evidence for the activation of platelets in mast cell-dependent disorders and suggests new potential mechanisms for the expression of cold urticaria.
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PMID:Release of platelet factor 4 into the blood after cold challenge of patients with cold urticaria. 647 Mar 62

Blood platelet significance in inflammation is recognized but poorly characterized in urticaria. It is known that platelets are activated during inflammatory processes and are involved in modulating inflammatory and immune response via various mediator release. The aim of our study was to investigate the functional state of platelets, expressed by release reaction of C-X-C chemokines such as platelet factor 4 (PF-4) and beta-thromboglobulin (beta-TG) in chronic idiopathic urticaria (CIU). Plasma levels of PF-4 and beta-TG, which are established markers of in vivo platelet activation and which play important role in inflammatory processes, were measured by enzyme-linked immunosorbent assay in 19 patients with CIU and in 25 healthy subjects. Mean plasma PF-4 level in CIU patients and control subjects was 5.01 +/- 1.67 and 4.13 +/- 2.05 IU/ml, respectively, whereas that for beta-TG was 29.3 +/- 14.0 and 25.2 +/- 12.6 IU/ml, respectively. In our small study, there have been no significant differences found between the members of the control and CIU group regarding plasma levels of PF-4 and beta-TG. Further studies should be performed to elucidate whether any systemic platelet activation occurs in CIU.
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PMID:Assessment of platelet activity as expressed by plasma levels of platelet factor 4 and beta-thromboglobulin in patients with chronic idiopathic urticaria. 1594 39

Blood platelets participate actively in immune-inflammatory processes. Responding to the variety of stimuli such as cell activation leads to the release of several mediators, including RANTES, platelet factor 4, beta-thromboglobulin, thymus and activation-regulated chemokine (TARC/CCL17), serotonin and arachidonic acid metabolites. It also affects the expression of immunomodulatory and adhesive molecules, including CD154 and P-selectin. Immune-inflammatory processes associated with skin diseases could induce platelet activation, which, in turn, would contribute to acceleration and modulation of these processes. Activated platelets are capable of facilitating leukocyte rolling in the skin and the release of skin inflammation mediators. Changes in platelet function and behaviour may occur in certain types of skin inflammatory conditions and platelets might then be an important effector cell of the skin immune system, contributing to the pathogenesis of some skin inflammatory disorders. The changes in platelet activity and reactivity have been demonstrated to show distinctly different pathogenic mechanisms in cutaneous diseases, such as urticaria, atopic eczema/dermatitis syndrome and psoriasis. Considering the risk of cardiovascular events, some of them seem to be of clinical significance. This contribution is a brief outline of the present knowledge of the platelet function in dermal disorders.
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PMID:Platelet function in cutaneous diseases. 1879 36