Ankylosing spondylitis combined with acute promyelocytic leukaemia and disseminated intravascular coagulation: A case report and literature review

doi:10.3969/j.issn.1004-583X.2024.04.008

Abstract

Abstract:

Objective To explore the clinical characteristics, diagnosis and treatment of ankylosing spondylitis (AS) combined with acute promyelocytic leukaemia (APL) and disseminated intravascular coagulation (DIC), and to gain a deeper understanding of the potential relationship and mechanism among the three pathological conditions. Methods We reported a case of AS combined with APL and DIC. Clinical characteristics and treatment course of AS combined with APL and DIC were summarized through this case report and literature review. Results The condition of APL achieved a complete relieve, and consolidation therapy was continuously applied to this patient. The relationship among AS, APL and DIC involved human leukocyte antigen-B27, tumour necrosis factor-α and interleukin-23/17 axis and immune function. Conclusion AS is complicatedly linked with APL and DIC, with the underlying pathogenic mechanisms of gene expressions and immune function. Great efforts are needed in the future to unveil the pathogenesis of AS combined with APL and DIC.

Key words: spondylitis, ankylosing, leukemia, promyelocytic, acute, disseminated intravascular coagulation, human leukocyte antigen-b27, tumour necrosis factor-α, interleukin-23/17

CLC Number:

R593.23

Zhang Xiaoyang, Zang Meirong, Suo Jing, Meng Jianbo, Song Xiaoning, Wang Jinkai. Ankylosing spondylitis combined with acute promyelocytic leukaemia and disseminated intravascular coagulation: A case report and literature review[J]. Clinical Focus, 2024, 39(4): 342-346.

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URL: https://huicui.hebmu.edu.cn/EN/10.3969/j.issn.1004-583X.2024.04.008

https://huicui.hebmu.edu.cn/EN/Y2024/V39/I4/342

References 40

[1]	Zhu W, He X, Cheng K, et al. Ankylosing spondylitis: Etiology, pathogenesis, and treatments[J]. Bone Res, 2019, 7(1):22.
[2]	Landgren AM, Landgren O, Gridley G, et al. Autoimmune disease and subsequent risk of developing alimentary tract cancers among 4.5 million US male veterans[J]. Cancer, 2011, 117(6):1163-1171. doi: 10.1002/cncr.25524 pmid: 21381009
[3]	Kim SH, Lee SH. Updates on ankylosing spondylitis: Pathogenesis and therapeutic agents[J]. J Rheum Dis, 2023, 30(4):220-233.
[4]	Sieper J, Braun J, Rudwaleit M, et al. Ankylosing spondylitis: An overview[J]. Ann Rheum Dis, 2002, 61:8-18.
[5]	Breen KA, Grimwade D, Hunt BJ. The pathogenesis and management of the coagulopathy of acute promyelocytic leukaemia[J]. Br J Haematology, 2012, 156(1):24-36.
[6]	Sureda A, Frade G, Torrado MC, et al. A continuous spectrum of hypercoagulability exists in acute nonlymphoblastic leukemia[J]. Acta Haematol, 1992, 88(2-3):100-104.
[7]	Dally N, Hoffman R, Haddad N, et al. Predictive factors of bleeding and thrombosis during induction therapy in acute promyelocytic leukemia-a single center experience in 34 patients[J]. Thromb Res, 2005, 116(2):109-114. pmid: 15907524
[8]	苏雁华, 王兆钺. 急性早幼粒细胞白血病弥散性血管内凝血发病机制及治疗进展[J]. 国外医学输血及血液学分册, 2005, (6):508-510.
[9]	Chan TM, Luo SF, Yu KH, et al. Risk of cancer in patients with ankylosing spondylitis: A nationwide cohort study in Taiwan[J]. Scand J Rheumatol, 2021, 50(2):132-138. doi: 10.1080/03009742.2020.1804612 pmid: 33464145
[10]	Ranganathan V, Gracey E, Brown MA, et al. Pathogenesis of ankylosing spondylitis-recent advances and future directions[J]. Nat Rev Rheumatol, 2017, 13(6):359-367. doi: 10.1038/nrrheum.2017.56 pmid: 28446810
[11]	Garrido-Mesa J, Brown MA. T cell repertoire profiling and the mechanism by which HLA-B27 causes ankylosing spondylitis[J]. Curr Rheumatol Rep, 2022, 24(12):398-410. doi: 10.1007/s11926-022-01090-6 pmid: 36197645
[12]	Evans DM, Spencer CC, Pointon JJ, et al. Interaction between ERAP1 and HLA-B27 in ankylosing spondylitis implicates peptide handling in the mechanism for HLA-B27 in disease susceptibility[J]. Nat Genet, 2011, 43(8):761-767. doi: 10.1038/ng.873 pmid: 21743469
[13]	Darby SC, Doll R, Gill SK, et al. Long term mortality after a single treatment course with X-rays in patients treated for ankylosing spondylitis[J]. Br J Cancer, 1987, 55(2):179-190.
[14]	Au WY, Hawkins BR, Cheng N, et al. Risk of haematological malignancies in HLA-B27 carriers[J]. Br J Haematol, 2001, 115(2):320-322.
[15]	Wellcome Trust Case Control Consortium, Australo-Anglo-American Spondylitis Consortium (TASC), Burton PR, et al. Association scan of 14, 500 nonsynonymous SNPs in four diseases identifies autoimmunity variants[J]. Nat Genet, 2007, 39(11):1329-1337. doi: 10.1038/ng.2007.17 pmid: 17952073
[16]	Aggarwal S, Ghilardi N, Xie MH, et al. Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17[J]. J Biol Chem, 2003, 278(3):1910-1914. doi: 10.1074/jbc.M207577200 pmid: 12417590
[17]	Liu R, Lauridsen HM, Amezquita RA, et al. IL-17 promotes neutrophil-mediated immunity by activating microvascular pericytes and not endothelium[J]. J Immunol, 2016, 197(6):2400-2408. doi: 10.4049/jimmunol.1600138 pmid: 27534549
[18]	Lubberts E. The IL-23-IL-17 axis in inflammatory arthritis[J]. Nat Rev Rheumatol, 2015, 11(7):415-429. doi: 10.1038/nrrheum.2015.53 pmid: 25907700
[19]	Kaaij MH, Van Tok MN, Blijdorp IC, et al. Transmembrane TNF drives osteoproliferative joint inflammation reminiscent of human spondyloarthritis[J]. J Exp Med, 2020, 217(10):e20200288.
[20]	王医林, 王健, 刘英纯, 等. 强直性脊柱炎患者外周血TNF-α、IL-17、IL-33的表达及与疾病活动程度的相关性研究[J]. 现代生物医学进展, 2017, 17(35):6934-6937.
[21]	李卫, 刘佳, 白家媛, 等. α肿瘤坏死因子的研究进展[J]. 动物医学进展, 2010, 31(12):108-111.
[22]	韩丽娜, 周晋. 血清TNF-α在急性早幼粒细胞白血病中的意义[J]. 哈尔滨医科大学学报, 2005, (1):79-81.
[23]	Sakaguchi S, Ono M, Setoguchi R, et al. Foxp3+ CD25+ CD4+ natural regulatory T cells in dominant self‐tolerance and autoimmune disease[J]. Immunol Rev, 2006, 212(1):8-27.
[24]	Liao HT, Tsai CY. Cytokines and regulatory T cells in ankylosing spondylitis[J]. Bone Joint Res, 2023, 12(2):133-137.
[25]	Wu C, Wang S, Wang F, et al. Increased frequencies of T helper type 17 cells in the peripheral blood of patients with acute myeloid leukaemia[J]. Clin Exp Immunol, 2009, 158(2):199-204. doi: 10.1111/j.1365-2249.2009.04011.x pmid: 19737137
[26]	Szczepanski MJ, Szajnik M, Czystowska M, et al. Increased frequency and suppression by regulatory T Cells in patients with acute myelogenous leukemia[J]. Clin Cancer Res, 2009, 15(10):3325-3332. doi: 10.1158/1078-0432.CCR-08-3010 pmid: 19417016
[27]	Parovichnikova EN, Gal'tseva IV, Vorob'ev IA, et al. Characteristics of T-cell immunity in patients with acute leukemia[J]. Ter Arkh, 2006, 78(7):18-25. pmid: 16944746
[28]	Buggins AG, Milojkovic D, Arno MJ, et al. Microenvironment produced by acute myeloid leukemia cells prevents T cell activation and proliferation by inhibition of NF-κB, c-Myc, and pRb pathways[J]. J Immunol, 2001, 167(10):6021-6030. pmid: 11698483
[29]	Fontenot JD, Rudensky AY. A well adapted regulatory contrivance: Regulatory T cell development and the forkhead family transcription factor Foxp3[J]. Nat Immunol, 2005, 6(4):331-337. doi: 10.1038/ni1179 pmid: 15785758
[30]	黎阳, 李文益. 弥散性血管内凝血病因发病机制及其防治[J]. 中国实用儿科杂志, 2013, 28(9):669-672.
[31]	Penn MS, Topol EJ. Tissue factor, the emerging link between inflammation, thrombosis, and vascular remodeling[J]. Circ Res, 2001, 89(1):1-2. pmid: 11440969
[32]	Zhao S, Ge Y, Li Z, et al. Influence of cytokines on early death and coagulopathy in newly diagnosed patients with acute promyelocytic leukemia[J]. Front Immunol, 2023, 14.
[33]	Cozzolino F, Torcia M, Miliani A, et al. Potential role of interleukin-1 as the trigger for diffuse intravascular coagulation in acute nonlymphoblastic leukemia[J]. Am J Med, 1988, 84(2):240-250. pmid: 3261536
[34]	Griffin J, Rambaldi A, Vellenga E, et al. Secretion of interleukin-1 by acute myeloblastic leukemia cells in vitro induces endothelial cells to secrete colony stimulating factors[J]. Blood, 1987, 70(4):1218-1221. pmid: 3498521
[35]	Degos L, Dombret H, Chomienne C, et al. All-trans-retinoic acid as a differentiating agent in the treatment of acute promyelocytic leukemia [see comments][J]. Blood, 1995, 85(10):2643-2653. pmid: 7742522
[36]	Marchetti M, Falanga A, Giovanelli S, et al. All-trans-retinoic acid increases adhesion to endothelium of the human promyelocytic leukaemia cell line NB4.[J]. Br J Haematol, 1996, 93(2):360-366.
[37]	Bi KH, Jiang GS. Relationship between cytokines and leukocytosis in patients with APL induced by all-trans retinoic acid or arsenic trioxide[J]. Cell Mol Immunol, 2006, 3(6):421-427. pmid: 17257495
[38]	王可, 李慧波, 孙丽丽, 等. 急性早幼粒细胞白血病分化综合征的发生机制、早期诊断及治疗研究进展[J]. 医学研究杂志, 2019, 48(9):188-191.
[39]	中华医学会血液学分会, 中国医师协会血液科医师分会. 中国急性早幼粒细胞白血病诊疗指南(2018年版)[J]. 中华血液学杂志, 2018, 39(3):179-183.
[40]	米汝佳, 蔡兆鹏, 苏鸿君, 等. 肿瘤坏死因子α对强直性脊柱炎患者间充质干细胞成骨分化的影响[J]. 免疫学杂志, 2020, 36(3):254-259.