Objective: Urticaria is a common disease with unknown reason characterized by recurrent itchy wheals and/or angioedema. Chronic urticaria(CU) is the one which for more than 6 weeks. Chronic spontaneous urticaria(CSU) is a common type of unknown etiology and pathogenesis of chronic urticaria.The pathogenesis of chronic urticaria is still not very clear,may involve infection, allergy, false allergy and its reactivity, etc. Mast cells plays a central role in the onset and its activation and degranulation cause, leukotriene of urticaria, the key to the prognosis and treatment response. Mechanisms indude activation and degranulation of mast cells induced by immunological and non-immunological and idiopathic. Autoimmune mechanisms induding Ig E high affinity Ig E receptor autoimmunity, or Ig E-dependent Antien-antibody complexes and mediated by the complement system and other means. Mast cells in non-immune mechanisms, including direct induction of release agents, small molecular compounds in food-induced allergic reaction, or non-steroidal anti-inflammatory drugs, such as changing the metabolism of arachidonic acid. There is a minority cannot yet articulate its pathogenesis in patients with urticaria, may not even dependent on the activation of mast cells.Studies have found that autologous serum intradermal injection can be induced by 30-60% of patients with chronic urticaria of itchy wheals, A positive ASST may indicate the presence of circulating functional autoantibodies in the serum of some patients. In fact,only part of patients with chronic urticaria can be detected the autoantibodies, It suggest there are some unkown circulation meditors involved the pathogenesis of CSU.Vascular endothelial growth factor(VEGF) is the main pro-angiogenic mediator with relevant vasoactive properties. An increased VEGF has been observed in the circulation of patents with skin disorders, including CU. This might be responsible for the increase of vascular permeability in the skin. Leading to the development of the transitory itchy wheals observed in CU. Endostatin(ES) has been proposed as a new vasoactive mediator due to its direct effect on endothelial cells. Thrombospondin-1(TSP-1) can destabilizes contact between endothelial cells due to its direct effect on the cells. Endostatin(endostatin,ES) with thrombospondin-1(thrombospondin-1,TSP-1) can be affected by vascular endothelial growth factor, play a role in the pathogenesis of chronic urticaria patients; Studies have shown that an increased VEGF has been observed in the CU-The aim of our study is to investigate the circulating levels of ES and TSP-1 in patients with CSU, Explore their roles in the pathogenesis of CSU.Method: 44 cases of chronic spontaneous urticaria patients were in our department, 19 males and 25 famales, aged 12 to 58 years, mean age 34.7 years, duration of 2 months to 4 years. CSU was diagnosed according to the EAACI/GA2LEN/EDF, All patients had tipical clinical manifestations and a history of repeated attacks by a variety of antihistamine treatment and have no significant improvement, and allergen skin test were negative. The control group of 36 patients were performed in normal healthy hospital. The control group 36 cases are normal persons who come to our hospital for physical examination. 16 males and 20 famales aged 16 to 50 years old. Drawn 5ml blood from everyone, stored the frozen serum for batch test. ESã€TSP-1 were detected by enzyme-linked immunoabsorbent assay(ELISA). Measurement data, in line with normal distribution, mean ± standard deviation, homogeneity of variance application if two independent t test, if the missing variance application t ’test.Results: The levels of serum ES, TSP-1 in chronic spontaneous urticaria(ES:107.08±43.86ng/mã€TSP-1:327.8±85.10ng/ml) were significantly higher than that in normal controls(ES: 41.45±24.73ng/ml,TSP-1: 156.01±31.77ng/ml),P﹤0.05 for both.Conclusion: The levels of ESã€TSP-1 are increased in the sera of patients with chronic spontaneous urticaria. Prompt ESã€TSP-1May have played a potential roal in the setting of de disease. |