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)

In both chronic and dermographic urticaria, superficial perivascular leukocytic infiltrations are seen histologically in lesional skin. We have therefore investigated the role of endothelial adhesion molecule expression in these diseases. E-selectin, P-selectin, ICAM-1 and VCAM-1 expression was examined immunohistologically, and the serum levels of the soluble forms of these adhesion molecules were determined by EIA in patients with chronic urticaria, dermographic urticaria as well as in healthy controls (n = 8 in each group) and subjects with symptomatic allergic rhinitis (n = 7) for comparison. A significant increase (p<0.01) was observed for soluble P-selectin in dermographic urticaria (mean 487+/-44 ng/ml) and chronic urticaria (mean 464+/-74 ng/ml) compared to healthy controls (mean 149+/-15 ng/ml) and rhinitis subjects (mean 177+/-30 ng/ml). In contrast, the other adhesion molecules were not significantly elevated in both urticaria groups. Immunohistologically, a strong expression of P-selectin was found in superficial vessels of lesional and nonlesional skin in dermographic urticaria with only a mild increase of the other adhesion molecules studied, supporting the findings observed with the soluble forms in the patients' sera. Since an alteration of soluble P-selectin was not seen in symptomatic allergic rhinitis, an unspecific effect due to inflammation appears to be unlikely. These results therefore point to a potentially relevant role of the endothelial P-selectin expression in the evolution of urticarial whealing.
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PMID:Enhanced P-selectin expression in chronic and dermographic urticaria. 930 36

Although the etiology of urticaria is mostly unclear, there are a number of recent new insights into the underlying pathomechanisms and causes. Dermal mast cell numbers and endothelial cell adhesion molecule and cytokine expression are also increased in uninvolved skin, while serum P-selectin levels are elevated, suggesting a systemic activation of the cutaneous inflammatory system in urticaria. In all adults, but not children with indolent mastocytosis, we found activating point mutations of c-kit, the mast cell growth factor receptor, in lesional cutaneous mast cells. In acute urticaria, IgE-dependent mechanisms are only rarely involved (0.9%), in contrast to generally held beliefs, whereas acute upper respiratory infections (39.3%) and drug intolerance (9.2%) are more frequent. In chronic urticaria, pseudoallergies to food (73%) and more rarely chronic inflammatory gastrointestinal diseases (11%) play a major role, with avoidance or elimination of the eliciting factors leading to long term remission. On the basis of recent findings, autoantibodies must be viewed mostly as secondary rather than causative in chronic urticaria.
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PMID:[Urticaria. New developments and perspectives]. 1087 66

The levels of interleukin-6 and platelet-derived microparticles (PMPs) were measured in the blood of 137 patients with side effects from platelet concentrate (PC) transfusion with leukocyte removal filtration, P-selectin-expressing platelet and PMPs in stored PC before and after the filtration, and filtered leukocytes positive for P-selectin glycoprotein ligand-1. The side effects, which were observed in 203 transfusions for 84 patients with hematologic disease and 53 patients with nonhematologic disease with no significant difference between the two groups, included urticaria (75.9%), erythema (18.7%), and fever (17.2%), but no anaphylactic reactions. The levels of interleukin-6 and PMP correlated in both groups, and were significantly higher in the hematologic disease group than in the nonhematologic disease group. The level of PMP, but not interleukin-6, was significantly higher for patients testing positive for allergic reaction than for those testing negative. In the stored PC prior to filtration, the level of interleukin-6 was normal. The level of P-selectin-expressing platelets and PMPs was elevated before filtration, but was significantly lower after filtration. Taken together, the results suggest that PMP is involved in the generation of transfusion reactions, and indicate that both platelets and PMP displaying P-selectin bind to P-selectin glycoprotein ligand-1 of leukocytes retained by the leukocyte filter.
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PMID:Platelets expressing P-selectin and platelet-derived microparticles in stored platelet concentrates bind to PSGL-1 on filtrated leukocytes. 1103 May 27

Urticarial reactions are characterized by dermal capillary dilatation and edema, associated with a variably intense mixed inflammatory infiltrate consisting of neutrophils, eosinophils, T-helper lymphocytes, and activated macrophages. Mast cell numbers are moderately increased by a factor of 2.4, in contrast to mastocytosis where numbers are much higher (5-48-fold increase). In urticarial vasculitis there is in addition endothelial damage, leukocytoclasia, and fibrin and complement deposition. The emigration of leukocytes is regulated by vasoactive and chemotactic mediators released firom mast cells, inducing a sequential upregulation of endothelial adhesion molecules (P-selectin, E-selectin, ICAM-1, and VCAM-1), of beta2-integrins on leukocytes, and of cytokines on endothelial, epithelial, and infiltrating cells. In nonlesional skin, there is also an increase of mast cells and an upregulation of endothelial adhesion molecules, probably due to molecules in the circulation of which P-selectin and TNFalpha have so far been demonstrated. Whereas these data provide a molecular basis for the understanding of variations in mast cell-dependent pathology, they underline the fact that they are not diagnostic for different types of urticaria, except for urticarial vasculitis and mastocytosis.
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PMID:Adhesion molecules and cellular infiltrate: histology of urticaria. 1176

P-Selectin expressed on endothelial cells contributes to acute and chronic inflammation by promoting leukocyte tethering/rolling. Despite increasing evidence of P-selectin expression on human umbilical vein endothelial cells in vitro, the regulatory mechanisms of P-selectin expression on dermal endothelial cells in skin diseases are not fully understood. Here, we demonstrate increased expression of P-selectin in dermal vessels of regional skin in urticaria and atopic dermatitis. The present in vitro analyses with human dermal microvascular endothelial cells (HDMECs) revealed that histamine rapidly induced P-selectin expression. Interleukin (IL)-4 and IL-13 induced prolonged expression of surface P-selectin by HDMECs. A combination of tumor necrosis factor-alpha and IL-4 inhibited P-selectin expression. Pretreatment of HDMECs with tumor necrosis factor-alpha followed by incubation with IL-4 markedly increased P-selectin expression. Notably, incubation with substance P alone induced prolonged P-selectin expression. Activation of STAT6 appears to be a key factor in P-selectin expression induced by substance P and IL-4 because treatment with STAT6 decoy oligodeoxynucleotides significantly inhibited P-selectin expression. The present results indicate that novel, complex mechanisms are involved in endothelial P-selectin expression in the skin. STAT6 in dermal endothelial cells appears to be a potent target for controlling cellular infiltrate in allergic and/or neuroinflammatory skin diseases.
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PMID:STAT-6-mediated control of P-selectin by substance P and interleukin-4 in human dermal endothelial cells. 1687 67

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

Plasma levels of platelet-derived microparticles (PDMPs) and soluble P-selectin (sP-selectin) were investigated as markers of platelet activation in 46 atopic dermatitis (AD) patients, 20 non-atopic urticaria patients and 22 healthy controls. The relationships between these markers and the scoring AD (SCORAD) index, blood eosinophil number, serum IgE, and serum lactate dehydrogenase were also investigated in AD patients. Plasma PDMPs and sP-selectin levels were significantly higher in AD patients compared with the other two groups. In multiple regression analysis, the SCORAD index was the most significant factor associated with the platelet activation markers. Among the SCORAD index components, excoriations were most closely related to the markers. The elevated levels of PDMPs and sP-selectin were significantly reduced following skin lesion improvement by drug treatment. Our results show that blood platelets are activated in AD patients upon aggravation of eruption, suggesting that activated platelets may be involved in the pathomechanism of AD.
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PMID:Platelet-derived microparticles and soluble P-selectin as platelet activation markers in patients with atopic dermatitis. 1921 50

Chronic urticaria (CU) is characterized by the occurrence of wheals lasting for more than 6 weeks. The role of platelet activation in the pathophysiology of this condition has not been clearly studied. We undertook a cross-sectional study among 45 patients with CU and 45 age- and gender-matched healthy controls. The severity of the disease was assessed using the urticaria severity score. The autologous plasma skin test (APST) was done in all cases of CU. The platelet count and indices were estimated by an automated haematological laser optical analyzer. Platelet aggregation and soluble P-selectin levels were estimated in all study participants. It was observed that there was a significantly higher mean platelet volume (MPV) and platelet distribution width (PDW) in patients with CU when compared to controls. Platelet aggregation and soluble P-selectin levels were significantly higher in patients with CU, as compared to controls. Urticaria severity score correlated positively with platelet aggregability and soluble P-selectin levels. APST-positive patients had significantly higher platelet aggregation and higher soluble P-selectin levels, when compared to the APST-negative patients, indicating more platelet activation in the autoimmune group. There is significant platelet activation in patients with CU, especially in those with autoreactivity.
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PMID:Platelet activation in chronic urticaria and its correlation with disease severity. 2358 42