类风湿关节炎患者血清低氧诱导因子－1α水平与肺间质病变的关系

摘要

目的：探讨类风湿关节炎（ RA）患者血清低氧诱导因子－1α（ HIF－1α）水平与肺间质病变（ ILD）的关系。方法收集RA患者272例，其中合并ILD 68例（ RA－ILD组），未合并ILD 204例（ RA组），并选择年龄、性别相匹配的健康体检者80例（健康对照组）作为对照。采集3组的静脉血，采用ELISΑ方法检测血清HIF－1α、结缔组织生长因子（ CTGF）、转化生长因子－β1（ TGF－β1）水平，并检测两组RA患者的肺功能等相关实验室指标。结果与健康对照组相比，RA组及RA－ILD组血清HIF－1α水平显著升高（P＜0.01），且RA－ILD组血清HIF－1α、CTGF、TGF－β1水平较RA组明显升高（ P＜0.01）。 RA－ILD组肺活量占预计值百分比、用力肺活量占预计值百分比和一氧化碳弥散量占预计值百分比（ DLCO％）较RA组患者明显降低（ P＜0.05，P＜0.01）。 RA患者血清HIF－1α与类风湿因子呈正相关（r＝0.80，P＜0.01），与抗环瓜氨酸抗体呈正相关（r＝0.59，P＜0.01），与DLCO％呈负相关（r＝－0.76，P＜0.01）。结论 HIF－1α参与RA的发病过程，且可能与RA合并ILD的发病相关。%Objective To investigate the correlation of serum hypoxia inducible factors -1α( HIF-1α) level with interstitial lung disease ( ILD) in patients with rheumatoid arthritis ( RA) .Methods Two hundred and seventy -two RA patients were enrolled in the study , of whom 68 cases had associated ILD ( RA-ILD group ) and 204 cases did not (RA group).Eighty subjects scheduled for healthy physical examination and with age and sex matched were enrolled as control ( normal control group ) .Venous blood of the 3 groups was collected and concentrations of serum HIF -1α, connective tissue growth factor (CTGF) and transforming growth factor -β1(TGF-β1) were measured by ELISA.Lung function and related laboratory indicators in patients with RA were detected .Results HIF-1αconcentrations of the RA-ILD and RA groups were significantly higher than that of the normal control group ( P<0.01 ) .Concentrations of HIF -1α, CTGF and TGF-β1 of the RA-ILD group were significantly higher than those of the RA group (P<0.01).Vital capacity, forced vital capacity and carbon monoxide diffusing capacity ( DLCO) of the RA-ILD group were significantly lower than those of the RA group (P<0.05, P<0.01).Serum level of HIF-1αin RA patients was positively correlated with that of rheumatoid factor ( r =0.80, P <0.01) and anti -cyclic citrullinated peptide antibody ( r =0.59, P<0.01), and was negatively correlated with DLCO (r=-0.76, P<0.01).Conclusion HIF-1αparticipates in the pathogenesis of RA , and may be involved in the pathogenesis of RA associated ILD .