接受不同種類生物製劑治療的僵直性脊椎炎病人，其免疫球蛋白A的變化：台灣單一醫學中心回溯性研究

Change in immunoglobulin A level in ankylosing spondylitis patients treated with different biologic DMARDs: a retrospective study in a medical center in Taiwan

目的：本篇回溯性研究主要針對接受不同生物製劑治療的僵直性脊椎炎患者，比較其血中免疫球蛋白A濃度於治療前後的變化，同時也探討血中免疫球蛋白A與發炎指標和疾病活動度的相關性。
方法：根據第十版國際疾病臨床編碼M45.00以及臨床資料庫中的病歷，本研究收納自西元2019年5月至2022年5月共三年期間，於中國醫藥大學附設醫院風濕免疫科診斷為僵直性脊椎炎且接受不同生物製劑治療，包括抗腫瘤壞死因子抑制劑以及介白素17A抑制劑的患者，於使用生物製劑之前與12個月治療後的比較。比較的參數包括疾病活動度（巴斯僵直性脊椎炎疾病活動量表評核分數）和血中發炎指標（包括紅血球沉降速率、C反應蛋白、以及免疫球蛋白A）。
結果：在共收納98位接受不同生物製劑治療之僵直性脊椎炎患者，包括6位使用恩博、50位使用復邁、36位使用欣普尼、及6位使用可善挺生物製劑。使用藥物前，血中免疫球蛋白A濃度與紅血球沉降速率及C反應蛋白皆呈現正相關（分別為r=0.540，p<0.0001；r=0.458，p<0.005），但與巴斯僵直性脊椎炎疾病活動量表分數無顯著相關。接受復邁治療患者之血中免疫球蛋白A濃度的下降程度明顯高於接受欣普尼治療的患者（中位值，55.0［四分位距11.5-141.5］相對於9.0，［四分位距15.5-30.0］，p<0.05）。在接受12個月治療後，血中免疫球蛋白A濃度的下降程度與發炎指標的下降程度皆有顯著的正相關性，包括紅血球沉降速率（r=0.416，p<.001）及C反應蛋白（r=0.448，p<0.01），但在巴斯僵直性脊椎炎疾病活動量表分數的比較並無顯著相關。
結論：本研究結果顯示不同生物製劑的治療，僵直性脊椎炎患者其血中免疫球蛋白A的變化會有所不同。同時也觀察到治療前血中免疫球蛋白A濃度與發炎指標呈正相關性，且於接受12個月治療後，其免疫球蛋白A的下降程度同步於紅血球沉降速率及C反應蛋白的下降程度。

Objective: This retrospective study aimed to analyze the change in immunoglobulin (Ig)A level in ankylosing spondylitis (AS) patients undergoing therapy with biologic disease-modifying antirheumatic drugs (bDMARDs). The association of serum IgA level with inflammatory parameters and disease activity was also examined.
Method: We identified AS patients using the International Classification of Diseases, Tenth Revision- Clinical Modification (ICD-10-CM) code M45.00 in their medical records, as well as those who underwent therapy with tumor necrosis factor (TNF)-αinhibitors or interleukin (IL)-17A inhibitors from the clinical databank of China Medical University Hospital between May 2021 and May 2022. The disease activity of AS was assessed using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) before (at baseline) and after 12 months of therapy with bDMARDs. The erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) level, and serum IgA level were determined using the Westergren method, an immunoturbidimetric method, and the nephelometer method, respectively, at baseline and after 12 months of therapy with bDMARDs.
Results: A total of 98 AS patients were enrolled, including 6 etanercept-treated patients, 50 adalimumabtreated patients, 36 golimumab-treated patients, and 6 secukinumab-treated patients. Among the 98 AS patients, baseline IgA level was positively correlated with baseline ESR (r=0.540, p<0.0001) and baseline CRP level (r=0.458, p<0.005) but not BASDAI. The change in IgA level (ΔIgA) was significantly greater in adalimumab-treated patients than in golimumab-treated patients (median decrease, 55.0, interquartile range, IQR, 11.5–141.5 versus 9.0, 15.5–30.0, p<0.05). After 12 months of bDMARD therapy,ΔIgA was significantly and positively correlated with the decrease of ESR (r=0.416, p<.001) and the decrease of CRP level (r=0.448, p<0.01) but not the decrease of BASDAI.
Conclusion: Our results demonstrated the effect of different bDMARDs on the change in serum IgA level in AS patients. We also observed the positive and significant association of serum IgA level with inflammatory parameters at baseline, as well as the change in IgA level parallel to the decrease of ESR and CRP level after 1 year of therapy with bDMARDs in AS patients.