Ferraccioli G F, Sorrentino D, De Vita S, Casatta L, Labombarda A, Avellini C, Dolcetti R, Di Luca D, Beltrami C A, Boiocchi M, Bartoli E
Department of Internal Medicine, School of Medicine, Udine, Italy.
Ann Rheum Dis. 1996 May;55(5):311-6. doi: 10.1136/ard.55.5.311.
To determine the prevalence of mucosa associated lymphoid tissue (MALT) in the stomach and of a possible antigen driven proliferation, in patients with Sjögren's syndrome (SS).
Twenty one patients with primary SS and 80 dyspeptic controls underwent upper endoscopy. Lymphoid tissue and Helicobacter pylori were assessed by histopathological analysis. Epstein-Barr virus (EBV) or human herpes virus-6 (HHV-6) genome were studied by polymerase chain reaction (PCR) DNA amplification. Two PCR VDJ procedures were used to detect immunoglobulin heavy chain (IgH) gene rearrangement.
Organised MALT was found in 33.3% of the patients, compared with 21.5% of the controls (NS). H pylori infection was seen in 71% of patients and 63% of controls. Genomic EBV or HHV-6 was found in a minor portion of SS gastric tissues. B cell expansion was detected in nine of the 21 patients. Infectious agents in the stomach might have contributed to B cell clonality only in 55.5% of the cases. No strict relationship was found between lymphoid follicles and clonality.
Lymphoid accumulation in the gastric mucosa is common in Sjögren's syndrome, but full evidence for an antigen driven B cell expansion could not be demonstrated. Only a portion of those with clonal B cell expansion had evidence of an infectious agent. Other unknown infectious agents or factors related to the underlying disease (autoantigen) and its tissue environment may have a further role as possible causes of B clonal expansion in the gastric mucosa.
确定干燥综合征（SS）患者胃黏膜相关淋巴组织（MALT）的患病率以及是否存在可能的抗原驱动性增殖。
对21例原发性SS患者和80例消化不良对照者进行上消化道内镜检查。通过组织病理学分析评估淋巴组织和幽门螺杆菌。采用聚合酶链反应（PCR）DNA扩增技术研究爱泼斯坦-巴尔病毒（EBV）或人疱疹病毒6型（HHV-6）基因组。使用两种PCR VDJ方法检测免疫球蛋白重链（IgH）基因重排。
33.3%的患者发现有组织化的MALT，而对照组为21.5%（无显著性差异）。71%的患者和63%的对照者存在幽门螺杆菌感染。在一小部分SS胃组织中发现了基因组EBV或HHV-6。21例患者中有9例检测到B细胞扩增。胃中的感染因子可能仅在55.5%的病例中导致B细胞克隆性。未发现淋巴滤泡与克隆性之间有严格的关系。
干燥综合征患者胃黏膜中淋巴组织积聚很常见，但无法证明存在抗原驱动的B细胞扩增的确切证据。只有一部分克隆性B细胞扩增患者有感染因子的证据。其他未知的感染因子或与基础疾病（自身抗原）及其组织环境相关的因素可能在胃黏膜B细胞克隆性扩增的可能原因中发挥进一步作用。
