Efficacy and safety of desloratadine combined with dipyridamole in the treatment of chronic urticaria

Khalaf, Ahmad Taha; Liu, Xiaoming; Sheng, Wanxiang; Tan, Jian; Abdalla, Ahmed N.

doi:10.1111/j.1468-3083.2007.02511.x

Cited by 32 publications

(28 citation statements)

References 26 publications

(38 reference statements)

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“…Interestingly, D-dimer plasma levels dropped to normal values during CU remission (47). The activation of blood coagulation in patients with CU has been confirmed by other researchers (39,(48)(49)(50). In particular, Wang et al (39) found increased plasma levels of FVIIa (marker of the activation of the TF pathway), thrombin-antithrombin complex (marker of thrombin generation) and D-dimer (marker of fibrin degradation), which are correlated to each other in CU patients.…”

Section: Coagulation Biomarkers In Chronic Urticariasupporting

confidence: 67%

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: Coagulation Biomarkers In Chronic Urticariasupporting

confidence: 67%

Chronic urticaria and coagulation: pathophysiological and clinical aspects

Tedeschi

Kolkhir

Asero³

et al. 2014

Allergy

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“…Finally, in 2006 our group [29] demonstrates the activation of the coagulation cascade, supporting its involvement in chronic urticaria pathophysiology. Coagulation activation stemmed from eosinophil expression of tissue factor has been confirmed by us as well as by other groups [35][36][37][40][41][42] (marker of thrombin generation) and D-dimer (marker of fibrin degradation), which are correlated to each other in CU patients. Thrombin-antithrombin complex and D-dimer plasma levels are also found increased in CU by Fujii et al [40].…”

Section: Pathophysiological Aspectsmentioning

confidence: 58%

“…Furthermore, thrombin triggers mast cell degranulation [31] and may activate protease activated receptor-1 on mast cells [30] in animal models. The activation of blood coagulation in patients with CU has been recently confirmed by other independent researchers [39][40][41], and thus can be added to the mechanisms involved in CU (Fig. 3).…”

Section: Pathophysiological Aspectsmentioning

confidence: 74%

Activation of blood coagulation in chronic urticaria: pathophysiological and clinical implications

et al. 2009

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Chronic urticaria (CU) is a skin disorder characterized by the recurrent eruption of short-lived wheals accompanied by redness and itching for at least 6 weeks. The wheals can be associated with angioedema. CU is considered an autoimmune disease in about 50% of cases with the presence of circulating histamine releasing autoantibodies mainly directed against the high affinity IgE receptor FcepsilonRI on mast cells and basophils or against IgE. In several CU cases regarded as idiopathic; the actual pathophysiological mechanisms are still unknown. Some patients with CU do not respond to antihistamines and require the use of systemic steroids or cyclosporin, which are, however, not always effective. In CU, several investigators have demonstrated the activation of coagulation that is due to the involvement of eosinophils and a tissue factor pathway with generation of thrombin potentially contributing to an increased vascular permeability. CU patients often present with elevation of coagulation and fibrinolysis markers, such as prothrombin fragment F1+2 and D: -dimer, which correlate with the disease severity. Preliminary data indicate that anticoagulant treatment with heparin and warfarin may be effective in reducing the symptoms of this disorder. Taken together, all these findings provide the rationale for proposing clinical trials on the use of anticoagulant drugs as adjuvant treatment in CU patients.

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“…Interestingly, eosinophils might be in turn activated and recruited by mediators, cytokines, chemokines, or other as yet unknown factors released by mast cells [15][16][17][18]. The findings summarized above have been confirmed by several independent groups [19][20][21][22][23][24][25][26]. Thus, it seems likely that coagulation may play a role in the pathogenesis of chronic urticaria.…”

Section: Introductionsupporting

confidence: 59%