Analysis of clinical characteristics of anti-SRP antibody positive interstitial pneumonia and comparison with anti-Jo-1 antibody positive interstitial pneumonia_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

ZHU Haijia ^1,2 , YAN Xin ² , YU Min ² , CAO Min ² , DAI Jinghong ² , CAI Hourong ² , XIAO Yonglong ² ,  ZHUANG Yi ²

1. Department of Geriatrics, Pukou District Hospital of Traditional Chinese Medicine, Nanjing, Jiangsu 211800, P. R. China;
2. Department of Respiratory and Critical Care Medicine, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008, P. R. China;

Corresponding author：

ZHUANG Yi, Email: drzy78@163.com

Keywords：

Anti-signal recognition particle antibody; anti-Jo-1antibody; interstitial pneumonia; Clinical characteristics

DOI：

10.7507/1671-6205.202205046

Video：

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Objective To investigate the clinical characteristics of interstitial pneumonia patients with positive anti-signal recognition particle antibody (SRP-IP), and compare those with interstitial pneumonia patients with positive anti-Jo-1 antibody (Jo1-IP). Methods Clinical data of SRP-IP patients admitted to Department of Respiratory and Critical Care Medicine of Drum Tower Hospital affiliated to Nanjing University Medical School from May 2017 to May 2021, including clinical manifestations, laboratory examinations, pulmonary function tests and radiographic types, were retrospectively analyzed. The results were compared with those of Jo1-IP patients admitted during the same period. Results The SRP-IP patients were older than Jo1-IP patients (P=0.044). There were no significant differences in clinical manifestations or pulmonary function tests results between the two groups. The proportion of SRP-IP patients combined with positive anti-EJ antibody (P<0.001) or perinuclear anti-neutrophil cytoplasmic antibody (P=0.028) was significantly higher than that of Jo1-IP patients, while the proportion of SRP-IP patients combined positive anti-Ro-52 antibody was significantly lower than that of Jo1-IP patients (P=0.009). The erythrocyte sedimentation rate (ESR) of SRP-IP patients was faster than that of Jo1-IP patients (P=0.026). The serum IgM level (P=0.039) and peripheral NK cell counts (P=0.013) of SRP-IP patients were significantly lower than those of Jo1-IP patients. The most common chest CT findings in SRP-IP patients were organizing pneumonia and the proportion of usual interstitial pneumonia in SRP-IP patients was higher than that of Jo1-IP patients (P=0.032). The levels of creatine kinase (P=0.010), creatine kinase myocardial brand (P=0.025) and alanine aminotransferase (P=0.045) in interstitial pneumonia patients with high titer (++~+++) SRP antibody were higher than those in interstitial pneumonia patients with low titer (+) SRP antibody. SRP-IP and Jo1-IP patients were mainly treated with glucocorticoids combined with or without immunosuppressants, and there was no significant difference in the choice of treatment between the two groups. The proportion of patients with Jo1-IP evaluated as improved was significantly higher than that of patients with SRP-IP (p=0.005), while the proportion of patients with SRP-IP evaluated as stable was significantly higher than that of patients with Jo1-IP (P=0.035). The mortality of SRP-IP patients within 3 months was significantly higher than that of Jo1-IP patients (P=0.028). Conclusion Compared with Jo1-IP patients, SRP-IP patients are older, have faster ESR, are more likely to be combined with other autoantibodies, have lower serum IgM level and peripheral blood NK cell count, have more UIP imaging manifestations, and have a worse short-term prognosis.

Citation： ZHU Haijia, YAN Xin, YU Min, CAO Min, DAI Jinghong, CAI Hourong, XIAO Yonglong, ZHUANG Yi. Analysis of clinical characteristics of anti-SRP antibody positive interstitial pneumonia and comparison with anti-Jo-1 antibody positive interstitial pneumonia. Chinese Journal of Respiratory and Critical Care Medicine, 2022, 21(9): 643-650. doi: 10.7507/1671-6205.202205046 Copy

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18.	Kao AH, Lacomis D, Lucas M, et al. Anti-signal recognition particle autoantibody in patients with and patients without idiopathic inflammatory myopathy. Arthritis Rheum, 2004, 50(1): 209-215.
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20.	Rams A, Kosalka-Wegiel J, Kuszmiersz P, et al. Characteristics of idiopathic inflammatory myopathies with novel myositis-specific autoantibodies. Adv Clin Exp Med, 2021, 30(12): 1239-1248.
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22.	杨红霞, 田小兰, 江薇, 等. 免疫介导坏死性肌病的临床和病理特征分析. 北京大学学报(医学版), 2019, 51(6): 989-995.
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24.	Hervier B, Perez M, Allenbach Y, et al. Involvement of NK cells and NKp30 pathway in antisynthetase syndrome. J Immunol, 2016, 197(5): 1621-1630.
25.	Galati D, De Martino M, Trotta A, et al. Peripheral depletion of NK cells and imbalance of the Treg/Th17 axis in idiopathic pulmonary fibrosis patients. Cytokine, 2014, 66(2): 119-126.
26.	Xu HJ, Geddes R, Roberts-Thomson PJ. Low molecular weight IgM and CD5 B lymphocytes in rheumatoid arthritis. Ann Rheum Dis, 1994, 53(6): 383-390.
27.	Zhan X, Yan W, Wang Y, et al. Clinical features of anti-synthetase syndrome associated interstitial lung disease: a retrospective cohort in China. BMC Pulm Med, 2021, 21(1): 57.

1. Casal-Dominguez M, Pinal-Fernandez I, Pak K, et al. Performance of the 2017 European Alliance of Associations for Rheumatology/American College of Rheumatology Classification Criteria for Idiopathic Inflammatory Myopathies in Patients with Myositis-Specific Autoantibodies. Arthritis Rheumatol, 2022, 74(3): 508-517.
2. Vincze M, Danko K. Idiopathic inflammatory myopathies. Best Pract Res Clin Rheumatol, 2012, 26(1): 25-45.
3. Targoff IN, Johnson AE, Miller FW. Antibody to signal recognition particle in polymyositis. Arthritis Rheum, 1990, 33(9): 1361-1370.
4. Gunawardena H, Betteridge ZE, Mchugh NJ. Myositis-specific autoantibodies: their clinical and pathogenic significance in disease expression. Rheumatology (Oxford), 2009, 48(6): 607-612.
5. Travis WD, Costabel U, Hansell DM, et al. An official American Thoracic Society/European Respiratory Society statement: Update of the international multidisciplinary classification of the idiopathic interstitial pneumonias. Am J Respir Crit Care Med, 2013, 188(6): 733-748.
6. Hansell DM, Bankier AA, Macmahon H, et al. Fleischner Society: glossary of terms for thoracic imaging. Radiology, 2008, 246(3): 697-722.
7. Lynch DA, Sverzellati N, Travis WD, et al. Diagnostic criteria for idiopathic pulmonary fibrosis: a Fleischner Society White Paper. Lancet Respir Med, 2018, 6(2): 138-153.
8. Khanna D, Mittoo S, Aggarwal R, et al. Connective tissue disease-associated interstitial lung diseases (CTD-ILD) - Report from OMERACT CTD-ILD Working Group. J Rheumatol, 2015, 42(11): 2168-2171.
9. 王迁, 李梦涛. 2018中国结缔组织病相关间质性肺病诊断和治疗专家共识. 中华内科杂志, 2018, 57(8): 558-565.
10. Romisch K, Miller FW, Dobberstein B, et al. Human autoantibodies against the 54 kDa protein of the signal recognition particle block function at multiple stages. Arthritis Res Ther, 2006, 8(2): R39.
11. Satoh M, Tanaka S, Ceribelli A, et al. A comprehensive overview on myositis-specific antibodies: new and old biomarkers in idiopathic inflammatory myopathy. Clin Rev Allergy Immunol, 2017, 52(1): 1-19.
12. Gono T, Kuwana M. Current understanding and recent advances in myositis-specific and -associated autoantibodies detected in patients with dermatomyositis. Expert Rev Clin Immunol, 2020, 16(1): 79-89.
13. Anquetil C, Boyer O, Wesner N, et al. Myositis-specific autoantibodies, a cornerstone in immune-mediated necrotizing myopathy. Autoimmun Rev, 2019, 18(3): 223-230.
14. Pinal-Fernandez I, Casal-Dominguez M, Mammen AL. Immune-mediated necrotizing myopathy. Curr Rheumatol Rep, 2018, 20(4): 21.
15. Suzuki S, Nishikawa A, Kuwana M, et al. Inflammatory myopathy with anti-signal recognition particle antibodies: case series of 100 patients. Orphanet J Rare Dis, 2015, 10: 61.
16. Ge YP, Yang HB, Xiao XY, et al. Interstitial lung disease is not rare in immune-mediated necrotizing myopathy with anti-signal recognition particle antibodies. BMC Pulm Med, 2022, 22(1): 14.
17. Hanaoka H, Kaneko Y, Suzuki S, et al. A unique case of polymyositis with anti-signal recognition particle antibody complicated by subacute interstitial lung disease and subluxing arthropathy, resembling anti-synthetase syndrome. Mod Rheumatol, 2016, 26(6): 979-980.
18. Kao AH, Lacomis D, Lucas M, et al. Anti-signal recognition particle autoantibody in patients with and patients without idiopathic inflammatory myopathy. Arthritis Rheum, 2004, 50(1): 209-215.
19. Malkan A, Cappelen-Smith C, Beran R, et al. Anti-synthetase syndrome associated with anti PL-12 and anti-signal recognition particle antibodies and a necrotizing auto-immune myositis. J Clin Neurosci, 2015, 22(2): 396-398.
20. Rams A, Kosalka-Wegiel J, Kuszmiersz P, et al. Characteristics of idiopathic inflammatory myopathies with novel myositis-specific autoantibodies. Adv Clin Exp Med, 2021, 30(12): 1239-1248.
21. Gupta L, Naveen R, Gaur P, et al. Myositis-specific and myositis-associated autoantibodies in a large Indian cohort of inflammatory myositis. Semin Arthritis Rheum, 2021, 51(1): 113-120.
22. 杨红霞, 田小兰, 江薇, 等. 免疫介导坏死性肌病的临床和病理特征分析. 北京大学学报(医学版), 2019, 51(6): 989-995.
23. Jiang DH, Liang JR, Hodge J, et al. Regulation of pulmonary fibrosis by chemokine receptor CXCR3. J Clin Invest, 2004, 114(2): 291-299.
24. Hervier B, Perez M, Allenbach Y, et al. Involvement of NK cells and NKp30 pathway in antisynthetase syndrome. J Immunol, 2016, 197(5): 1621-1630.
25. Galati D, De Martino M, Trotta A, et al. Peripheral depletion of NK cells and imbalance of the Treg/Th17 axis in idiopathic pulmonary fibrosis patients. Cytokine, 2014, 66(2): 119-126.
26. Xu HJ, Geddes R, Roberts-Thomson PJ. Low molecular weight IgM and CD5 B lymphocytes in rheumatoid arthritis. Ann Rheum Dis, 1994, 53(6): 383-390.
27. Zhan X, Yan W, Wang Y, et al. Clinical features of anti-synthetase syndrome associated interstitial lung disease: a retrospective cohort in China. BMC Pulm Med, 2021, 21(1): 57.

Chinese Journal of Respiratory and Critical Care Medicine

Analysis of clinical characteristics of anti-SRP antibody positive interstitial pneumonia and comparison with anti-Jo-1 antibody positive interstitial pneumonia

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