Fiona Stanley Hospital, Perth, Western Australia, Australia.
Department of Clinical Immunology, PathWest Laboratory Medicine, Queen Elizabeth II Medical Centre, Perth, Western Australia, Australia.
PLoS One. 2019 Apr 10;14(4):e0215051. doi: 10.1371/journal.pone.0215051. eCollection 2019.
The aim of this study was to ascertain whether mannose binding lectin deficiency is implicated in coexistent rheumatoid arthritis and bronchiectasis and to determine whether undetectable mannose binding lectin confers poorer long-term survival in coexistent rheumatoid arthritis and bronchiectasis or in rheumatoid arthritis in general.
A retrospective audit was conducted in a rheumatoid arthritis cohort in which mannose binding lectin had been measured by enzyme linked immunosorbent assay from 2007-11. Rheumatoid arthritis patients with physician diagnosed HRCT proven bronchiectasis were recruited during this time and compared to those with uncomplicated rheumatoid arthritis. Survival from disease onset was recorded in October 2018. Kaplan-Meier survival estimates were performed to assess mortality over time in the two groups. Log rank tests were used for equality of survivor functions.
The two groups were demographically comparable. A higher frequency of undetectable mannose binding lectin was observed in coexistent rheumatoid arthritis and bronchiectasis (37.5%) compared to uncomplicated rheumatoid arthritis, (8.9%, P = 0.005). Undetectable mannose binding lectin correlated with a strong trend toward poor survival in rheumatoid arthritis overall (P = 0.057). Cox regression analysis however, showed no difference in the hazard ratio for survival between the two groups when corrected for age, gender, prednisolone use ever, rheumatoid factor status and the full range of MBL concentrations.
In summary, undetectable mannose binding lectin is associated with coexistent rheumatoid arthritis and bronchiectasis and correlates with poor survival in rheumatoid arthritis overall. These findings further implicate immunodeficiency in the genesis of bronchiectasis in rheumatoid arthritis.
本研究旨在确定甘露聚糖结合凝集素（MBL）缺陷是否与同时存在的类风湿关节炎和支气管扩张症有关，并确定不可检测的 MBL 是否会降低同时存在的类风湿关节炎和支气管扩张症或一般类风湿关节炎患者的长期生存。
对 2007 年至 2011 年间通过酶联免疫吸附试验（ELISA）检测 MBL 的类风湿关节炎队列进行了回顾性审计。在此期间，招募了同时患有经医生诊断的 HRCT 证实的支气管扩张症的类风湿关节炎患者，并将其与单纯类风湿关节炎患者进行比较。记录 2018 年 10 月的疾病发病后的生存情况。采用 Kaplan-Meier 生存估计评估两组随时间的死亡率。对数秩检验用于比较两组生存函数的均等性。
两组在人口统计学上具有可比性。同时存在类风湿关节炎和支气管扩张症的患者中，不可检测的 MBL 频率（37.5%）明显高于单纯类风湿关节炎患者（8.9%，P = 0.005）。不可检测的 MBL 与总体类风湿关节炎患者的生存呈强趋势相关（P = 0.057）。然而，Cox 回归分析显示，在校正年龄、性别、泼尼松龙使用情况、类风湿因子状态和 MBL 浓度全范围后，两组的生存风险比无差异。
总之，不可检测的 MBL 与同时存在的类风湿关节炎和支气管扩张症有关，并与总体类风湿关节炎患者的生存不良相关。这些发现进一步表明免疫缺陷在类风湿关节炎支气管扩张症的发生中起作用。
