Coagulation/fibrinolysis and inflammation markers are associated with disease activity in patients with chronic urticaria

Takahagi, Shunsuke; Mihara, Shoji; Iwamoto, Kazumasa; Morioke, Satoshi; Okabe, Takashi; Kameyoshi, Yoshikazu

doi:10.1111/j.1398-9995.2009.02222.x

Cited by 150 publications

(160 citation statements)

References 23 publications

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“…Chronic urticaria is frequently characterized by the presence of elevated levels of plasma markers of thrombin generation and fibrinolysis during severe exacerbations of the disease (37,38,47), which can be due to the expression of TF by activated eosinophils (22). The activation of coagulation and fibrinolysis decreases till complete normalization during remission (47,89). Whether the activation of coagulation/ fibrinolysis has a main role in the pathogenesis of the disease or simply acts as an amplification system has still to be defined.…”

Section: Discussionmentioning

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: Discussionmentioning

confidence: 99%

Chronic urticaria and coagulation: pathophysiological and clinical aspects

Tedeschi

Kolkhir

Asero³

et al. 2014

Allergy

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“…This study showed that there should be possible role of clotting factors in flaring symptoms induced by autologous plasma, because autoantibodies are equally present in serum and plasma [35]. Also, a statistically significant relationship between elevated plasma levels of PF1+2 and D-dimer and the severity of CSU was reported in some studies [36,37].…”

Section: Comorbidities and Possible Triggering Factorsmentioning

confidence: 90%

Comorbidities in Chronic Spontaneous Urticaria

Gönül¹,

Ayvaz²,

Kartal³

2017

A Comprehensive Review of Urticaria and Angioedema

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Chronic spontaneous urticaria (CSU) is a disease that makes people's lives miserable with unknown etiology. In recent years, there have been many studies trying to explain the etiology of CSU, and many of them reported that there are some comorbidities or triggering factors related to CSU. However, it has not been clearly known yet that whether these conditions are true comorbidities associated with CSU or they are coincidentally found at the same time. In this chapter, related comorbidities and conditions have been told.

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“…Although the exact role of the activation of coagulation/ fibrinolysis in the pathogenesis of CSU has still to be defined, the fact that such an activation parallels the activity of the disease [11,47] provides theoretically a rationale to test effects of anticoagulant and antifibrinolytic therapy in patients with severe forms. A small double-blind, placebo-controlled study carried out about 15 years ago first detected the effectiveness of oral anticoagulant therapy in some patients with refractory CSU [48].…”

Section: Anticoagulants/antifibrinolytics In Chronic Spontaneous Urtimentioning

confidence: 99%