Regression of autoimmune thrombocytopenia after eradication of Helicobacter pylori
Regression of autoimmune thrombocytopenia after eradication of Helicobacter pylori
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DOI：
10.1016/s0140-6736(05)60004-9
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发表时间：
1998-09-12
期刊：
影响因子：
168.9
通讯作者：
Gasbarrini, G
中科院分区：
文献类型：
--
作者：
Gasbarrini, A;Franceschi, F;Gasbarrini, G
自身免疫可能通过胃上皮细胞表达的Lewisvt抗原与幽门螺杆菌之间的交叉模拟而在幽门螺杆菌引起的胃粘膜损伤中起作用。抗幽门螺杆菌的单克隆抗体与消化外组织反应，如唾液腺导管细胞和肾小管细胞。多克隆抗幽门螺杆菌抗体在膜性神经病中与肾小球毛细血管壁反应，提示可能的因果关系。幽门螺杆菌根除后过敏性紫癜的治愈也有报道：自身免疫性血小板减少症（AT）是由抗血小板的自身抗体引起的。“细菌感染与这种疾病有关。为了确定AT是否与幽门螺杆菌感染相关，对18例AT患者（13例女性;平均年龄45岁[SD 14]）进行了评价。AT的定义是在排除血小板减少症的其他原因后，存在抗血小板自身抗体并伴有血小板计数减少。当患者的血小板计数低于100 × 10 - 7/mL时，给予患者类固醇。采用I3 C尿素呼气试验检测幽门螺杆菌感染情况。在诊断时给予阿莫西林（1000 mg，每日两次）、克拉霉素（250 mg，每日三次）和泮托拉唑（40 mg，每日两次），持续7天。完成治疗6周后，通过尿素呼气试验评估根除情况。治疗结束后2个月和4个月分别检测血小板抗体和血小板计数，11例患者发现幽门螺杆菌感染。感染患者和未感染患者的性别没有差异;然而，感染患者的平均年龄较低（43 [14] vs 49 [12]岁，p> 0· 05）。感染和未感染患者的血小板计数相似（95 [39] vs 103 [24] × 10 - 6/L，p> 0.05）。11名幽门螺杆菌阳性患者中有8名在治疗后根除了细菌。根除幽门螺杆菌的患者在2个月和4个月时血小板计数显著增加（图）;这8例患者中有6例抗血小板自身抗体消失（p<0.003）。抗血小板和血小板抗体
Autoimmunity may play a part in'determining gastric mucosal damage caused by Helicobacterpylori through a cross mimicry between Lewisvt antigens expressed by gastric epithelial cells and the bacterium.'Monoclonal antibodies against H pylori react with extradigestive tissues, such as ductal cells of the salivary gland and renal tubular cells.'Polyclonal anti-H pylori antibodies react with glomerular capillary walls in membranous neuropathy, suggesting a possible causal relation.'Healing of Schonlein-Henoch purpura after eradication of H pylori has also been reported: Autoimmune thrombocytopenia (AT) is caused by autoantibodies against platelets.'Bacterial infections have been implicated in the disease. To determine whether AT could be associated with H pylori infection, 18 patients (13 female; mean age 45 [SD 14] years) with AT were evaluated. AT was defined by the presence of autoantibodies against platelets with reduction of the platelet count when other causes of thrombocytopenia had been excluded. Patients were given steroids when their platelet counts were below 100 x i O'/mL. H pylori infection was assessed by I3C urea breath test. Amoxicillin (1000 mg twice daily), clarithromycin (250 mg three times daily), and pantoprazole (40 mg twice daily) was given at the time of diagnosis for 7 days. Eradication was assessed after 6 weeks of finishing treatment by urea breath test. Antibodies against platelets and platelet count were assessed 2 and 4 months after treatment was finished.H pylori infection was found in 11 patients. There was no difference in sex between infected and uninfected patients; mean age, however was lower in infected patients (43 [14] vs 49 [12] years, p> 0· 05). Platelet count was similar in infected and uninfected patients (95 [39] vs 103 [24] X 10'/L, p> 0· 05). Eight of the 11 H pylori-positive patients had the bacterium eradicated after treatment. Patients in whom H pylori was eradicated had a significant increase in platelet count a~ er 2 and 4 months (figure); six out of these eight patients had disappearance of autoantibodies against platelets (p< 0· 003). Antibodies against platelets and platelet