Analysis of plasma <scp>d</scp>‐dimer concentration in patients with delayed pressure urticaria

Kasperska−Zając, Alicja; Jasinska, T.

doi:10.1111/j.1468-3083.2010.03699.x

Cited by 7 publications

(7 citation statements)

References 11 publications

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“…In the other cases, the symptoms of urticaria were less severe, and the concentration of D-dimer was within normal limits. The authors suggested that patients with severe delayed pressure urticaria could develop hyperfibrinolysis, associated with increased D-dimer level, possibly due to a systemic inflammatory response (60). Similarly to patients with CU, patients with the multiple drug allergy syndrome had signs of thrombin generation in most cases, as demonstrated by the significant increase in F1 + 2 plasma levels (61).…”

Section: Activation Of Coagulation Cascade In Other Related Diseasesmentioning

confidence: 99%

Chronic urticaria and coagulation: pathophysiological and clinical aspects

Tedeschi

Kolkhir

Asero³

et al. 2014

Allergy

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Chronic urticaria (CU) is a widespread skin disease, characterized by the recurrence of transient wheals and itch for more than 6 weeks. Besides autoimmune mechanisms, coagulation factors, in particular tissue factor and thrombin, might also participate in the disease pathophysiology. Tissue factor expressed by eosinophils can induce activation of blood coagulation generating thrombin which in turn can increase vascular permeability both directly, acting on endothelial cells, and indirectly, inducing degranulation of mast cells with release of histamine, as demonstrated in experimental models. D-dimer, a fibrin degradation product, generated following activation of the coagulation cascade and fibrinolysis, has been found to be increased during urticaria exacerbations; moreover, it has been proposed as a biomarker of severity and resistance to H1-antihistamines in CU patients. The possible role of coagulation in CU is also supported by case reports, case series and a small controlled study showing the efficacy of anticoagulant therapy in this disease. The purpose of this review was to summarize the available data on the possible contribution of coagulation to the pathophysiology of CU focusing on clinical aspects and possible future therapeutic developments.Chronic urticaria (CU) is a widespread skin disease characterized by the recurrence of transient wheals and itch for more than 6 weeks. It is believed that over 50% of CU cases are accompanied by a deep subcutaneous and/or submucosal edema, called angioedema (AE; 1).It is well known that the characteristic symptoms of urticaria appear following the activation of mast cells (MCs) and basophils in the skin by various stimuli. These cells release several biologically active substances, the most important of which is histamine. Histamine induces vasodilation, increases vascular permeability and stimulates sensory nerve endings. These effects lead to the appearance of erythema, wheals and itch (2). It is supposed that other biologically active substances may have similar effects. These include serotonin, C3a and C5a anaphylatoxins, platelet-activating factor (PAF), neuropeptides, and arachidonic acid metabolites (prostaglandin D2, leukotrienes C4, D4 and E4; 3).Activation and degranulation of basophils and MCs may occur by immunological (formation of immune complexes, complement activation, IgE cross-linking), nonimmunological (pseudoallergy, infection, or direct effect of agents on MCs), or mixed mechanisms. The mechanism and cause of urticaria remain unclear in many patients with CU.In recent years, attention was paid to several important aspects of the disease pathogenesis. It is believed that about 30-50% of patients have CU symptoms associated with autoimmune reactions and synthesis of autoantibodies against IgE (4) and/or the FceRI a-subunit on MCs and basophils (autoimmune/autoreactive urticaria; 5). Furthermore, these patients show an increased frequency of HLA DRB1*04 (DR4) as it occurs in other autoimmune diseases (6). The role of coagulation casc...

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Section: Activation Of Coagulation Cascade In Other Related Diseasesmentioning

confidence: 99%

Chronic urticaria and coagulation: pathophysiological and clinical aspects

Tedeschi

Kolkhir

Asero³

et al. 2014

Allergy

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“…During such processes, a tissue factor pathway with generation of thrombin could contribute to oedema, through the increased vascular permeability. 15,[46][47][48][49][50] Whether activation of coagulation ⁄ fibrinolysis is a primary phenomenon involved in the CU pathophysiology or merely a secondary process, enhancing or maintaining urticarial inflammation should be further investigated. It is tempting to speculate that the primary phenomenon is the systemic inflammatory response, followed by secondary activation of coagulation ⁄ fibrinolysis cascade, probably by APR mediators.…”

Section: Is There Any Association Between Coagulation ⁄ Fibrinolysis mentioning

confidence: 99%

“…It is been demonstrated that urticaria is accompanied by activation of the coagulation/fibrinolysis cascade which parallels the disease severity and activity. During such processes, a tissue factor pathway with generation of thrombin could contribute to oedema, through the increased vascular permeability 15,46–50 . Whether activation of coagulation/fibrinolysis is a primary phenomenon involved in the CU pathophysiology or merely a secondary process, enhancing or maintaining urticarial inflammation should be further investigated.…”

Section: Inflammation and Acute‐phase Response (Apr)mentioning

confidence: 99%

Acute‐phase response in chronic urticaria

Kasperska−Zając¹

2011

Acad Dermatol Venereol

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The patterns of acute-phase response (APR) biomarkers differ upon various inflammatory conditions. Little information is available on the systemic inflammatory response in urticaria/angio-oedema. It has been shown that concentrations of circulating APR biomarkers, IL-6 and C-reactive protein (CRP), are elevated more in severe chronic urticaria (CU) than in patients showing milder urticarial symptoms. It is not clear whether the increase of IL-6 and CRP is merely an epiphenomenon or may contribute to the pathogenesis of CU. It is tempting to speculate that mediators of APR may enhance urticarial inflammation. In addition, there is some association between APR and activation of coagulation/fibrinolysis in CU. It is well known that even slight elevation in CRP baseline concentration is enough to produce significant increase in cardiovascular risk. In this light, one should ask whether CU patients, in particular those showing stronger systemic inflammatory response and long-lasting course are more vulnerable to the cardiovascular events. Apart from highly troublesome symptoms and low quality of life, CU may then involve some remote, serious systemic consequences. Taken together, CU can be identified as a mast cell- and basophil-dependent inflammatory disorder of the skin, which is accompanied by APR. Characterization of APR in CU may appear essential for an insight into the activity of this disease and for assessment of the inflammation degree. Moreover, measurement of these biomarkers might be particularly relevant while assessing CU patients demanding an anti-inflammatory or immunosuppressive therapy. This review summarizes information regarding APR in the course of urticaria/angio-oedema.

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“…This process is manifested by increased concentration of biomarkers—IL-6 and C-reactive protein [2–5], together with activation of the coagulation/fibrinolysis cascade [4, 6, 7], but not blood platelets [8, 9]. Unfortunately, these biomarkers may reflect not only the activity and severity of CU [3, 4], but correlate with a systemic response to infections [10].…”

Section: Introductionmentioning

confidence: 99%

Analysis of procalcitonin and CRP concentrations in serum of patients with chronic spontaneous urticaria

et al. 2012

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BackgroundOur previous findings showed the importance of analysing the peripheral markers of acute phase response (APR) activation, C-reactive protein (CRP) and IL-6 in the context of urticaria activity and severity. However, these biomarkers do not reliably differentiate between APR to infectious and the disease severity.AimIn order to investigate a possible association between the immune-inflammatory activation markers CRP and procalcitonin (PCT).MethodsSerum PCT and CRP concentrations were measured in patients with CU of varying severity as well as in healthy subjects.ResultsSerum PCT and CRP concentrations were significantly increased in more severe CU patients when compared to healthy controls and mild CU, and within the CU population there was a significant correlation between concentrations of PCT and CRP. Serum PCT concentrations remained within normal ranges in most CU patients and were only slightly elevated in some severe CU cases.ConclusionsPCT serum concentration may be only slightly elevated in some cases of severe CU. Upregulation of PCT synthesis accompanied by parallel changes in CRP concentration reflects a low-grade systemic inflammatory response in CU. PCT should be considered as a better marker than CRP to distinguish between APR to infection and an active non-specific urticarial inflammation.

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Analysis of plasma d‐dimer concentration in patients with delayed pressure urticaria

Cited by 7 publications

References 11 publications

Chronic urticaria and coagulation: pathophysiological and clinical aspects

Chronic urticaria and coagulation: pathophysiological and clinical aspects

Acute‐phase response in chronic urticaria

Analysis of procalcitonin and CRP concentrations in serum of patients with chronic spontaneous urticaria

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