Zuberbier T, Henz B M, Fiebiger E, Maurer D, Stingl G
Department of Dermatology and Allergy, Charité, Humboldt University, Berlin, Germany.
Allergy. 2000 Oct;55(10):951-4. doi: 10.1034/j.1398-9995.2000.00445.x.
In recent years, a histamine-releasing anti-FcepsilonRIalpha autoantibody has been demonstrated in about one-third of patients with chronic urticaria. However, its clinical significance is still unclear. The objective was to detect a possible correlation between the occurrence of the anti-FcepsilonRIalpha autoantibody and the clinical type or cause of urticaria.
Sera from 66 consecutively seen in- and outpatients with various types of urticaria and five healthy controls were examined for the presence of anti-FcepsilonRIalpha autoantibodies with a sandwich ELISA technique. In addition, basophil histamine release was studied in 13 autoantibody-positive sera.
Anti-FcepsilonRIalpha autoantibodies were found in 17/48 patients with chronic urticaria, in 2/4 with angioedema, in 1/2 with urticarial vasculitis, and in 2/11 with dermographic urticaria. However, no anti-FcepsilonRIalpha autoantibodies were detected in acute, cold, or delayed-pressure urticaria; in urticaria pigmentosa; or in normal controls. Of all chronic urticaria patients, 22 were classified as idiopathic since no underlying cause could be found. Of this group, seven were seropositive for anti-FcepsilonRIalpha. However, anti-FcepsilonRIalpha was also found in patients who went into remission after treatment of identified causes; namely, in one with type I allergy, one with drug intolerance, one with Helicobacter infection, and six with food intolerance. The autoantibody was also detected in 2/4 patients with associated autoimmune diseases. Functional activity was shown in basophil histamine release in 3/4 autoantibody-positive sera of patients with chronic idiopathic urticaria and in 4/6 autoantibody-positive sera of patients who went into remission after the treatment of underlying causes.
These data confirm that anti-FcepsilonRIalpha autoantibodies in urticaria are mostly found in chronic urticaria. Furthermore, their detection independently of the apparent cause of the urticaria suggests that as yet unidentified mechanisms must be operative, possibly related to the chronic inflammatory process and/or individual predispositions that favor their induction.
近年来，在约三分之一的慢性荨麻疹患者中发现了一种可释放组胺的抗FcepsilonRIα自身抗体。然而，其临床意义仍不明确。目的是检测抗FcepsilonRIα自身抗体的出现与荨麻疹的临床类型或病因之间是否存在可能的相关性。
采用夹心ELISA技术检测66例连续就诊的各类荨麻疹门诊和住院患者以及5名健康对照者血清中抗FcepsilonRIα自身抗体的存在情况。此外，对13份自身抗体阳性血清进行了嗜碱性粒细胞组胺释放研究。
在48例慢性荨麻疹患者中有17例检测到抗FcepsilonRIα自身抗体，4例血管性水肿患者中有2例，2例荨麻疹性血管炎患者中有1例，11例皮肤划痕症患者中有2例。然而，在急性、寒冷或迟发性压力性荨麻疹、色素性荨麻疹患者或正常对照者中未检测到抗FcepsilonRIα自身抗体。在所有慢性荨麻疹患者中，22例因未发现潜在病因被归类为特发性。在这组患者中，7例抗FcepsilonRIα血清学呈阳性。然而，在明确病因治疗后病情缓解的患者中也发现了抗FcepsilonRIα，即1例I型过敏患者、1例药物不耐受患者、1例幽门螺杆菌感染患者和6例食物不耐受患者。在4例合并自身免疫性疾病的患者中也检测到了这种自身抗体。在慢性特发性荨麻疹患者的3/4自身抗体阳性血清和潜在病因治疗后病情缓解患者的4/6自身抗体阳性血清中，嗜碱性粒细胞组胺释放显示出功能活性。
这些数据证实，荨麻疹中的抗FcepsilonRIα自身抗体大多见于慢性荨麻疹。此外，无论荨麻疹的明显病因如何都能检测到这些抗体，这表明一定存在尚未明确的机制在起作用，可能与慢性炎症过程和/或有利于其诱导的个体易感性有关。
