多发性肌炎/皮肌炎患者相关脏器受累和人类白细胞抗原-G表达水平的临床研究
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摘要
目的特发性炎性肌病(IIM)是一种病因和发病机制均不完全明确的多系统受累的自身免疫性疾病,临床上以多发性肌炎(PM)和皮肌炎(DM)最常见,临床表现多种多样。本文前两部分探讨分析PM/DM的消化道受累和甲状腺功能异常的临床特征,以期提高对PM/DM消化道和甲状腺受累特点的认知。第三部分对人类白细胞抗原-G(HLA-G)在PM/DM患者中表达水平及与疾病活动度相关性进行了初步探索,探讨HLA-G在PM/DM发病机制中的可能作用。
方法第一部分检索并筛选PM/DM合并消化道受累患病率及药物治疗相关文献,并进行meta分析和系统评价。第二部分回顾性总结204例PM/DM患者甲状腺功能异常及合并自身免疫性甲状腺疾病(AITD)特点,比较甲状腺功能异常组与正常组患者临床特征及免疫学特征差异。第三部分采用ELISA、流式细胞术和组织免疫荧光方法检测96例PM/DM患者血清、外周血T淋巴细胞和肌肉组织中HLA-G表达水平,并分析其与PM/DM临床特征和疾病活动度的关系。
结果第一部分：共纳入23篇合格文献,包含1719例PM/DM患者。食道受累患病率为47%(95%CI43.5-50.4%),最常见症状是吞咽困难,发生率为31%(95%CI26.9-35.2%)。PM和DM患者食道受累及吞咽困难发生率无显著差异。食道受累相关吸入性肺炎发生率为8.8%(11.2-13.8%),是PM/DM合并消化道受累患者的主要死因。激素及免疫抑制剂基础上加用静脉注射免疫球蛋白(IVIG)治疗可有效改善激素难治性PM/DM患者食道受累症状。
第二部分：204例/DM患者中甲状腺功能异常者达47.5%,最常见表现为正常甲状腺病态综合征(ESS)(34.3%),其次是甲状腺功能减退(甲减)(8.3%)和甲状腺功能亢进(甲亢)(4.4%)。与正常组相比,ESS组患者死亡率明显升高(P<0.05),且多见合并关节炎、发热及间质性肺疾病(ILD)和血液系统损害,CRP、ESR、Fet升高和HGB降低发生率,TGAb阳性率较正常组明显升高(P值均<0.05)。甲减组患者血浆胆固醇(CH0)升高率,TPOAb、TGAb阳性率显著高于正常组(P值均<0.05)；甲亢组患者血浆CH0水平明显升高(P<0.05)。PM/DM合并AITD发生率为5.4%,最常见类型为桥本甲状腺炎(HT)(4.4%)。
第三部分：血清sHLA-G水平在PM/DM组患者明显高于健康对照者(43.96±70.20U/ml vs.4.22±5.13U/ml;(P<0.001). sHLA-G水平与PM/DM患者MYOACT疾病活动度总体评分呈正相关(r=0.732;P<0.001)。24例多发性肌炎/皮肌炎患者外周血CD4+T细胞和CD8+T细胞中HLA-G+T细胞比例显著高于13例健康对照者(分别为4.45%±3.60%vs.1.65%±1.40%：P==0.002和4.33%±3.41%vs.1.40%±1.64%：P=0.001)。此外,35例PM/DM患者肌肉活检标本中的63%(5/10PM,17/25DM)检测到HLA-G表达,8例健康对照者中均未检测到。
结论第一部分：食道损害是PM/DM的常见并发症,主要表现为吞咽困难,食道受累继发的吸入性肺炎是PM/DM合并食道受累患者主要死因,IVIG联合糖皮质激素及免疫抑制剂对消化道损害治疗有效。第二部分：PM/DM患者甲状腺功能异常发生率高,以ESS最常见,且合并ESS的DM患者死亡率更高。PM/DM合并AITD最常见类型为HT。第三部分：HLA-G在PM/DM患者血清、外周血T淋巴细胞及肌肉组织中均表达增高,并且与疾病活动度相关,为PM/DM发病机制的研究提供了可能的新方向。
Objective Idiopathic inflammatory myopathy (IIM) is a heterogeneous group of systemic autoimmune diseases of unknown pathogenesis, including polymyositis (PM) and dermatomyositis (DM) as two common subtypes. The aims of this study are to investigate the clinical features of PM/DM patients with gastrointestinal involvement and thyroid dysfunction. Then we preliminaryly examined human leukocyte antigen-G (HLA-G) expression in PM/DM and its correlation with disease activity to determine its role in the pathogenesis of the disease.
Methods In the first part of this study, we retrieved and filtered literature about prevalence and drug therapy of PM/DM patients with gastrointestinal involvement, and then conducted a meta-analysis and systematic reviews. In the second part, a retrospective analysis of204PM/DM patients was conducted to find out the clinical and immunological characteristics of PM/DM patients with thyroid dysfunction and autoimmune thyroid disease (AITD). In the third part of the study, HLA-G expression in the serum samples, peripheral blood lymphocytes and muscle biopsies were determined by enzyme-linked immunosorbent assay(ELISA), flow cytometry and immunohistochemistry respectively in96PM/DM patients.
Results In the first part of this study, a total of23articles were included, which included1719patients. The pooled prevalence of esophageal involvement was47%(95%CI43.5-50.4%). Dysphagia was the most frequently reported symptom with a prevalence of31%(95%CI26.9-35.2%). There was no significant difference in the prevalence of esophageal involvement or dysphagia between PM and DM. Aspiration pneumonia secondary to esophageal involvement is the main cause of death in PM/DM patients with esophageal involvement with a prevalence of8.8%(95%CI11.2-13.8%). IVIG therapy showed excellent efficacy in patients with life-threatening steroid-resistant gastrointestinal involvement.
In the second part,47.5%of204PM/DM patients had thyroid dysfunction. The most common subgroup of thyroid dysfunction is euthyroid sick syndrome (ESS)(34.3%), followed by hypothyroidism(8.3%) and hyperthyroidism (4.4%). PM/DM patients with ESS were prone to have higher incidence of arthritis, fever, interstitial lung disease (ILD) and blood system damage, as well as higher levels of C-reactive protein(CRP), erythrocyte sedimentation rate(ESR), ferritin, and lower level of hemoglobin(HGB)(P<0.05). The ESS subgroup showed a higher incidence of deaths(P<0.05). The subgroup with hypothyroidism were with higher levels of cholesterol(CHO), thyroid peroxidase antibodies(TPOAb) and thyroglobulin antibodies(TGAb)(P<0.05). The hyperthyroidism group had a significant higer level of CHO(P<0.05). The incidence of PM/DM associated with AITD was5.4%. The most commonly seen AITD was Hashimoto's thyroiditis(HT)(4.4%).
The third part indicated that Serum sHLA-G levels were significantly higher in PM/DM patients than that observed in the controls (43.96±70.20U/ml vs.4.22±5.13U/ml; P<0.001). Additionally, a positive correlation was observed between sHLA-G levels and the MYOACT-global disease activity score of the PM/DM patients (r=0.732; P<0.001). The expression of HLA-G in peripheral CD4+T lymphocytes (4.45%±3.60%vs.1.65%±1.40%; P=0.002) and CD8+T lymphocytes (4.33%±3.41%vs.1.40%±1.64%; P=0.001) from24PM/DM patients was higher than that in the controls. Furthermore, HLA-G molecules were detected in63%of muscle biopsies from35patients with PM/DM, whereas no control sample expressed HLA-G.
Conclusion The first part of this study revealed that esophageal involvement is a common complication in PM/DM patients, mainly manifested as dysphagia. Aspiration pneumonia secondary to esophageal involvement is the main cause of death in this subtype of PM/DM patients. IVIG combined with glucocorticoids and immunosuppressant is effective against gastrointestinal damage. The second part of our study indicated that thyroid dysfunction is common in PM/DM. ESS was most frequently seen and exhibited a higher incidence of deaths. The most commonly seen AITD associated with PM/DM is HT. The third part of this study demonstrated that HLA-G was higher in PM/DM patients and correlated with disease activity, which allow HLA-G to potentially act as a useful disease activity marker for clinical practice.
方法第一部分检索并筛选PM/DM合并消化道受累患病率及药物治疗相关文献,并进行meta分析和系统评价。第二部分回顾性总结204例PM/DM患者甲状腺功能异常及合并自身免疫性甲状腺疾病(AITD)特点,比较甲状腺功能异常组与正常组患者临床特征及免疫学特征差异。第三部分采用ELISA、流式细胞术和组织免疫荧光方法检测96例PM/DM患者血清、外周血T淋巴细胞和肌肉组织中HLA-G表达水平,并分析其与PM/DM临床特征和疾病活动度的关系。
结果第一部分：共纳入23篇合格文献,包含1719例PM/DM患者。食道受累患病率为47%(95%CI43.5-50.4%),最常见症状是吞咽困难,发生率为31%(95%CI26.9-35.2%)。PM和DM患者食道受累及吞咽困难发生率无显著差异。食道受累相关吸入性肺炎发生率为8.8%(11.2-13.8%),是PM/DM合并消化道受累患者的主要死因。激素及免疫抑制剂基础上加用静脉注射免疫球蛋白(IVIG)治疗可有效改善激素难治性PM/DM患者食道受累症状。
第二部分：204例/DM患者中甲状腺功能异常者达47.5%,最常见表现为正常甲状腺病态综合征(ESS)(34.3%),其次是甲状腺功能减退(甲减)(8.3%)和甲状腺功能亢进(甲亢)(4.4%)。与正常组相比,ESS组患者死亡率明显升高(P<0.05),且多见合并关节炎、发热及间质性肺疾病(ILD)和血液系统损害,CRP、ESR、Fet升高和HGB降低发生率,TGAb阳性率较正常组明显升高(P值均<0.05)。甲减组患者血浆胆固醇(CH0)升高率,TPOAb、TGAb阳性率显著高于正常组(P值均<0.05)；甲亢组患者血浆CH0水平明显升高(P<0.05)。PM/DM合并AITD发生率为5.4%,最常见类型为桥本甲状腺炎(HT)(4.4%)。
第三部分：血清sHLA-G水平在PM/DM组患者明显高于健康对照者(43.96±70.20U/ml vs.4.22±5.13U/ml;(P<0.001). sHLA-G水平与PM/DM患者MYOACT疾病活动度总体评分呈正相关(r=0.732;P<0.001)。24例多发性肌炎/皮肌炎患者外周血CD4+T细胞和CD8+T细胞中HLA-G+T细胞比例显著高于13例健康对照者(分别为4.45%±3.60%vs.1.65%±1.40%：P==0.002和4.33%±3.41%vs.1.40%±1.64%：P=0.001)。此外,35例PM/DM患者肌肉活检标本中的63%(5/10PM,17/25DM)检测到HLA-G表达,8例健康对照者中均未检测到。
结论第一部分：食道损害是PM/DM的常见并发症,主要表现为吞咽困难,食道受累继发的吸入性肺炎是PM/DM合并食道受累患者主要死因,IVIG联合糖皮质激素及免疫抑制剂对消化道损害治疗有效。第二部分：PM/DM患者甲状腺功能异常发生率高,以ESS最常见,且合并ESS的DM患者死亡率更高。PM/DM合并AITD最常见类型为HT。第三部分：HLA-G在PM/DM患者血清、外周血T淋巴细胞及肌肉组织中均表达增高,并且与疾病活动度相关,为PM/DM发病机制的研究提供了可能的新方向。
Objective Idiopathic inflammatory myopathy (IIM) is a heterogeneous group of systemic autoimmune diseases of unknown pathogenesis, including polymyositis (PM) and dermatomyositis (DM) as two common subtypes. The aims of this study are to investigate the clinical features of PM/DM patients with gastrointestinal involvement and thyroid dysfunction. Then we preliminaryly examined human leukocyte antigen-G (HLA-G) expression in PM/DM and its correlation with disease activity to determine its role in the pathogenesis of the disease.
Methods In the first part of this study, we retrieved and filtered literature about prevalence and drug therapy of PM/DM patients with gastrointestinal involvement, and then conducted a meta-analysis and systematic reviews. In the second part, a retrospective analysis of204PM/DM patients was conducted to find out the clinical and immunological characteristics of PM/DM patients with thyroid dysfunction and autoimmune thyroid disease (AITD). In the third part of the study, HLA-G expression in the serum samples, peripheral blood lymphocytes and muscle biopsies were determined by enzyme-linked immunosorbent assay(ELISA), flow cytometry and immunohistochemistry respectively in96PM/DM patients.
Results In the first part of this study, a total of23articles were included, which included1719patients. The pooled prevalence of esophageal involvement was47%(95%CI43.5-50.4%). Dysphagia was the most frequently reported symptom with a prevalence of31%(95%CI26.9-35.2%). There was no significant difference in the prevalence of esophageal involvement or dysphagia between PM and DM. Aspiration pneumonia secondary to esophageal involvement is the main cause of death in PM/DM patients with esophageal involvement with a prevalence of8.8%(95%CI11.2-13.8%). IVIG therapy showed excellent efficacy in patients with life-threatening steroid-resistant gastrointestinal involvement.
In the second part,47.5%of204PM/DM patients had thyroid dysfunction. The most common subgroup of thyroid dysfunction is euthyroid sick syndrome (ESS)(34.3%), followed by hypothyroidism(8.3%) and hyperthyroidism (4.4%). PM/DM patients with ESS were prone to have higher incidence of arthritis, fever, interstitial lung disease (ILD) and blood system damage, as well as higher levels of C-reactive protein(CRP), erythrocyte sedimentation rate(ESR), ferritin, and lower level of hemoglobin(HGB)(P<0.05). The ESS subgroup showed a higher incidence of deaths(P<0.05). The subgroup with hypothyroidism were with higher levels of cholesterol(CHO), thyroid peroxidase antibodies(TPOAb) and thyroglobulin antibodies(TGAb)(P<0.05). The hyperthyroidism group had a significant higer level of CHO(P<0.05). The incidence of PM/DM associated with AITD was5.4%. The most commonly seen AITD was Hashimoto's thyroiditis(HT)(4.4%).
The third part indicated that Serum sHLA-G levels were significantly higher in PM/DM patients than that observed in the controls (43.96±70.20U/ml vs.4.22±5.13U/ml; P<0.001). Additionally, a positive correlation was observed between sHLA-G levels and the MYOACT-global disease activity score of the PM/DM patients (r=0.732; P<0.001). The expression of HLA-G in peripheral CD4+T lymphocytes (4.45%±3.60%vs.1.65%±1.40%; P=0.002) and CD8+T lymphocytes (4.33%±3.41%vs.1.40%±1.64%; P=0.001) from24PM/DM patients was higher than that in the controls. Furthermore, HLA-G molecules were detected in63%of muscle biopsies from35patients with PM/DM, whereas no control sample expressed HLA-G.
Conclusion The first part of this study revealed that esophageal involvement is a common complication in PM/DM patients, mainly manifested as dysphagia. Aspiration pneumonia secondary to esophageal involvement is the main cause of death in this subtype of PM/DM patients. IVIG combined with glucocorticoids and immunosuppressant is effective against gastrointestinal damage. The second part of our study indicated that thyroid dysfunction is common in PM/DM. ESS was most frequently seen and exhibited a higher incidence of deaths. The most commonly seen AITD associated with PM/DM is HT. The third part of this study demonstrated that HLA-G was higher in PM/DM patients and correlated with disease activity, which allow HLA-G to potentially act as a useful disease activity marker for clinical practice.
引文
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[11]廖二元.实用内科学.[M].第2版.北京：人民卫生出版社,2007：1258-1281.
[12]Lukjanowicz M, Bobrowska-Snarska D, Brzosko M. [Coexistence of hypothyroidism with polymyositis or dermatomyositis].[J]. Ann Acad Med Stetin,2006,52 Suppl 2:49-55.
[13]姚海红,李玉慧,张学武,等.皮肌炎合并甲状腺功能异常的临床及免疫学特征分析[J].北京大学学报(医学版),2011,43(2)：4.
[14]Arnaout M A, Nasrallah N S, El-Khateeb M S. Prevalence of abnormal thyroid function tests in connective tissue disease[J]. Scand J Rheumatol,1994,23(3):128-132.
[15]Williams D E, Chopra I J, Orgiazzi J, et al. Acute effects of corticosteroids on thyroid activity in Graves' disease[J]. J Clin Endocrinol Metab,1975,41(2):354-361.
[16]Wartofsky L, Burman K D. Alterations in thyroid function in patients with systemic illness:the "euthyroid sick syndrome"[J]. Endocr Rev,1982,3(2):164-217.
[17]Economidou F, Douka E, Tzanela M, et al. Thyroid function during critical illness[J]. Hormones (Athens),2011,10(2):117-124.
[18]Chen I J, Jan W Y, Lin C W, et al. Interstitial lung disease in polymyositis and dermatomyositis[J]. Clin Rheumatol,2009,28(6):639-646.
[19]Bronner I M, van der Meulen M F, de Visser M, et al. Long-term outcome in polymyositis and dermatomyositis[J]. Ann Rheum Dis,2006,65(11):1456-1461.
[20]Boelen A, Kwakkel J, Fliers E. Beyond low plasma T3:local thyroid hormone metabolism during inflammation and infection[J]. Endocr Rev,2011,32(5):670-693.
[21]Kubota K, Tamura J, Kurabayashi H, et al. Evaluation of increased serum ferritin levels in patients with hyperthyroidism[J]. Clin Investig,1993,72(1):26-29.
[22]Selva-O'Callaghan A, Mijares-Boeckh-Behrens T, Solans-Laque R, et al. Dermatomyositis and Graves' disease[J]. Clin Exp Rheumatol,2001,19(5):595-596.
[23]Biro E, Szekanecz Z, Czirjak L, et al. Association of systemic and thyroid autoimmune diseases[J]. Clin Rheumatol,2006,25(2):240-245.
[24]Selva-O'Callaghan A, Redondo-Benito A, Trallero-Araguas E, et al. Clinical significance of thyroid disease in patients with inflammatory myopathy[J]. Medicine (Baltimore),2007,86(5): 293-298.
[25]Wang H, Tao L, Li H, et al. Dermatomyositis related to autoimmune thyroiditis.[J]. J Eur Acad Dermatol Venereol,2010.
[26]Jenkins R C, Weetman A P. Disease associations with autoimmune thyroid disease[J]. Thyroid, 2002,12(11):977-988.
[27]Paul S, Li L, Kalaga R, et al. Characterization of thyroglobulin-directed and polyreactive catalytic antibodies in autoimmune disease[J]. J Immunol,1997,159(3):1530-1536.
[1]Sultan S M, Ioannou Y, Moss K, et al. Outcome in patients with idiopathic inflammatory myositis:morbidity and mortality[J]. Rheumatology (Oxford),2002,41(1):22-26.
[2]Rider L G, Giannini E H, Brunner H I, et al. International consensus on preliminary definitions of improvement in adult and juvenile myositis[J]. Arthritis Rheum,2004,50(7):2281-2290.
[3]Vincze M, Danko K. Idiopathic inflammatory myopathies[J]. Best Pract Res Clin Rheumatol, 2012,26(1):25-45.
[4]Bohan A, Peter J B. Polymyositis and dermatomyositis (first of two parts)[J]. N Engl J Med, 1975,292(7):344-347.
[5]Rayavarapu S, Coley W, Nagaraju K. An update on pathogenic mechanisms of inflammatory myopathies[J]. Curr Opin Rheumatol,2011,23(6):579-584.
[6]Dalakas M C. Autoimmune muscular pathologies[J]. Neurol Sci,2005,26 Suppl 1:S7-S8.
[7]Bradshaw E M, Orihuela A, Mcardel S L, et al. A local antigen-driven humoral response is present in the inflammatory myopathies[J]. J Immunol,2007,178(1):547-556.
[8]Veit T D, Chies J A. Tolerance versus immune response -- microRNAs as important elements in the regulation of the HLA-G gene expression[J]. Transpl Immunol,2009,20(4):229-231.
[9]Apps R, Gardner L, Moffett A. A critical look at HLA-G[J]. Trends Immunol,2008,29(7): 313-321.
[10]Carosella E D, Moreau P, Lemaoult J, et al. HLA-G:from biology to clinical benefits[J]. Trends Immunol,2008,29(3):125-132.
[11]Hughes A L, Nei M. Evolution of the major histocompatibility complex:independent origin of nonclassical class I genes in different groups of mammals[J]. Mol Biol Evol,1989,6(6):559-579.
[12]Marchal-Bras-Goncalves R, Rouas-Freiss N, Connan F, et al. A soluble HLA-G protein that inhibits natural killer cell-mediated cytotoxicity[J]. Transplant Proc,2001,33(3):2355-2359.
[13]Fournel S, Aguerre-Girr M, Huc X, et al. Cutting edge:soluble HLA-G1 triggers CD95/CD95 ligand-mediated apoptosis in activated CD8+ cells by interacting with CD8[J]. J Immunol,2000, 164(12):6100-6104.
[14]Liang S, Ristich V, Arase H, et al. Modulation of dendritic cell differentiation by HLA-G and ILT4 requires the IL-6--STAT3 signaling pathway[J]. Proc Natl Acad Sci U S A,2008,105(24): 8357-8362.
[15]Du L, Xiao X, Wang C, et al. Human leukocyte antigen-G is closely associated with tumor immune escape in gastric cancer by increasing local regulatory T cells[J]. Cancer Sci,2011,102(7): 1272-1280.
[16]Baricordi O R, Stignani M, Melchiorri L, et al. HLA-G and inflammatory diseases[J]. Inflamm Allergy Drug Targets,2008,7(2):67-74.
[17]Verbruggen L A, Rebmann V, Demanet C, et al. Soluble HLA-G in rheumatoid arthritis[J]. Hum Immunol,2006,67(8):561-567.
[18]Rizzo R, Hviid T V, Govoni M, et al. HLA-G genotype and HLA-G expression in systemic lupus erythematosus:HLA-G as a putative susceptibility gene in systemic lupus erythematosus[J]. Tissue Antigens,2008,71(6):520-529.
[19]Wiendl H, Behrens L, Maier S, et al. Muscle fibers in inflammatory myopathies and cultured myoblasts express the nonclassical major histocompatibility antigen HLA-G[J]. Ann Neurol,2000, 48(4):679-684.
[20]Sultan S M, Allen E, Oddis C V, et al. Reliability and validity of the myositis disease activity assessment tool[J]. Arthritis Rheum,2008,58(11):3593-3599.
[21]Creput C, Le Friec G, Bahri R, et al. Detection of HLA-G in serum and graft biopsy associated with fewer acute rejections following combined liver-kidney transplantation:possible implications for monitoring patients[J]. Hum Immunol,2003,64(11):1033-1038.
[22]Luque J, Torres M I, Aumente M D, et al. Soluble HLA-G in heart transplantation:their relationship to rejection episodes and immunosuppressive therapy[J]. Hum Immunol,2006,67(4-5): 257-263.
[23]Torres M I, Le Discorde M, Lorite P, et al. Expression of HLA-G in inflammatory bowel disease provides a potential way to distinguish between ulcerative colitis and Crohn's disease[J]. Int Immunol, 2004,16(4):579-583.
[24]Aractingi S, Briand N, Le Danff C, et al. HLA-G and NK receptor are expressed in psoriatic skin: a possible pathway for regulating infiltrating T cells?[J]. Am J Pathol,2001,159(1):71-77.
[25]Khosrotehrani K, Le Danff C, Reynaud-Mendel B, et al. HLA-G expression in atopic dermatitis[J]. J Invest Dermatol,2001,117(3):750-752.
[26]Waschbisch A, Sandbrink R, Hartung H P, et al. Evaluation of soluble HLA-G as a biomarker for multiple sclerosis[J]. Neurology,2011,77(6):596-598.
[27]Veit T D, Vianna P, Scheibel I, et al. Association of the HLA-G 14-bp insertion/deletion polymorphism with juvenile idiopathic arthritis and rheumatoid arthritis[J]. Tissue Antigens,2008, 71(5):440-446.
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[35]Ertekin C, Secil Y, Yuceyar N, et al. Oropharyngeal dysphagia in polymyositis/dermatomyositis[J]. Clin Neurol Neurosurg,2004,107(1):32-37.
[36]Oh T H, Brumfield K A, Hoskin T L, et al. Dysphagia in inflammatory myopathy:clinical characteristics, treatment strategies, and outcome in 62 patients[J]. Mayo Clin Proc,2007,82(4): 441-447.
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[1]Mammen A L. Dermatomyositis and polymyositis:Clinical presentation, autoantibodies, and pathogenesis[J]. Ann N Y Acad Sci,2010,1184:134-153.
[2]Bohan A, Peter J B. Polymyositis and dermatomyositis (first of two parts)[J]. N Engl J Med, 1975,292(7):344-347.
[3]Chandrasekhara P K, Jayachandran N V, Thomas J, et al. Systemic lupus erythematosus and dermatomyositis with symptomatic bilateral sacroiliitis:an unusual and interesting association[J]. Mod Rheumatol,2009,19(1):84-86.
[4]Dalakas M C, Hohlfeld R. Polymyositis and dermatomyositis[J]. Lancet,2003,362(9388): 971-982.
[5]Pyne D, Isenberg D A. Autoimmune thyroid disease in systemic lupus erythematosus[J]. Ann Rheum Dis,2002,61(1):70-72.
[6]Antonelli A, Fallahi P, Mosca M, et al. Prevalence of thyroid dysfunctions in systemic lupus erythematosus[J]. Metabolism,2010,59(6):896-900.
[7]Kumar K, Kole A K, Karmakar P S, et al. The spectrum of thyroid disorders in systemic lupus erythematosus[J]. Rheumatol Int,2012,32(1):73-78.
[8]Antonelli A, Ferri C, Fallahi P, et al. Clinical and subclinical autoimmune thyroid disorders in systemic sclerosis[J]. Eur J Endocrinol,2007,156(4):431-437.
[9]Andonopoulos A P, Siambi V, Makri M, et al. Thyroid function and immune profile in rheumatoid arthritis. A controlled study[J]. Clin Rheumatol,1996,15(6):599-603.
[10]Lazurova I, Benhatchi K, Rovensky J, et al. Autoimmune thyroid disease and autoimmune rheumatic disorders:a two-sided analysis[J]. Ann N Y Acad Sci,2009,1173:211-216.
[11]廖二元.实用内科学.[M].第2版.北京：人民卫生出版社,2007：1258-1281.
[12]Lukjanowicz M, Bobrowska-Snarska D, Brzosko M. [Coexistence of hypothyroidism with polymyositis or dermatomyositis].[J]. Ann Acad Med Stetin,2006,52 Suppl 2:49-55.
[13]姚海红,李玉慧,张学武,等.皮肌炎合并甲状腺功能异常的临床及免疫学特征分析[J].北京大学学报(医学版),2011,43(2)：4.
[14]Arnaout M A, Nasrallah N S, El-Khateeb M S. Prevalence of abnormal thyroid function tests in connective tissue disease[J]. Scand J Rheumatol,1994,23(3):128-132.
[15]Williams D E, Chopra I J, Orgiazzi J, et al. Acute effects of corticosteroids on thyroid activity in Graves' disease[J]. J Clin Endocrinol Metab,1975,41(2):354-361.
[16]Wartofsky L, Burman K D. Alterations in thyroid function in patients with systemic illness:the "euthyroid sick syndrome"[J]. Endocr Rev,1982,3(2):164-217.
[17]Economidou F, Douka E, Tzanela M, et al. Thyroid function during critical illness[J]. Hormones (Athens),2011,10(2):117-124.
[18]Chen I J, Jan W Y, Lin C W, et al. Interstitial lung disease in polymyositis and dermatomyositis[J]. Clin Rheumatol,2009,28(6):639-646.
[19]Bronner I M, van der Meulen M F, de Visser M, et al. Long-term outcome in polymyositis and dermatomyositis[J]. Ann Rheum Dis,2006,65(11):1456-1461.
[20]Boelen A, Kwakkel J, Fliers E. Beyond low plasma T3:local thyroid hormone metabolism during inflammation and infection[J]. Endocr Rev,2011,32(5):670-693.
[21]Kubota K, Tamura J, Kurabayashi H, et al. Evaluation of increased serum ferritin levels in patients with hyperthyroidism[J]. Clin Investig,1993,72(1):26-29.
[22]Selva-O'Callaghan A, Mijares-Boeckh-Behrens T, Solans-Laque R, et al. Dermatomyositis and Graves' disease[J]. Clin Exp Rheumatol,2001,19(5):595-596.
[23]Biro E, Szekanecz Z, Czirjak L, et al. Association of systemic and thyroid autoimmune diseases[J]. Clin Rheumatol,2006,25(2):240-245.
[24]Selva-O'Callaghan A, Redondo-Benito A, Trallero-Araguas E, et al. Clinical significance of thyroid disease in patients with inflammatory myopathy[J]. Medicine (Baltimore),2007,86(5): 293-298.
[25]Wang H, Tao L, Li H, et al. Dermatomyositis related to autoimmune thyroiditis.[J]. J Eur Acad Dermatol Venereol,2010.
[26]Jenkins R C, Weetman A P. Disease associations with autoimmune thyroid disease[J]. Thyroid, 2002,12(11):977-988.
[27]Paul S, Li L, Kalaga R, et al. Characterization of thyroglobulin-directed and polyreactive catalytic antibodies in autoimmune disease[J]. J Immunol,1997,159(3):1530-1536.
[1]Sultan S M, Ioannou Y, Moss K, et al. Outcome in patients with idiopathic inflammatory myositis:morbidity and mortality[J]. Rheumatology (Oxford),2002,41(1):22-26.
[2]Rider L G, Giannini E H, Brunner H I, et al. International consensus on preliminary definitions of improvement in adult and juvenile myositis[J]. Arthritis Rheum,2004,50(7):2281-2290.
[3]Vincze M, Danko K. Idiopathic inflammatory myopathies[J]. Best Pract Res Clin Rheumatol, 2012,26(1):25-45.
[4]Bohan A, Peter J B. Polymyositis and dermatomyositis (first of two parts)[J]. N Engl J Med, 1975,292(7):344-347.
[5]Rayavarapu S, Coley W, Nagaraju K. An update on pathogenic mechanisms of inflammatory myopathies[J]. Curr Opin Rheumatol,2011,23(6):579-584.
[6]Dalakas M C. Autoimmune muscular pathologies[J]. Neurol Sci,2005,26 Suppl 1:S7-S8.
[7]Bradshaw E M, Orihuela A, Mcardel S L, et al. A local antigen-driven humoral response is present in the inflammatory myopathies[J]. J Immunol,2007,178(1):547-556.
[8]Veit T D, Chies J A. Tolerance versus immune response -- microRNAs as important elements in the regulation of the HLA-G gene expression[J]. Transpl Immunol,2009,20(4):229-231.
[9]Apps R, Gardner L, Moffett A. A critical look at HLA-G[J]. Trends Immunol,2008,29(7): 313-321.
[10]Carosella E D, Moreau P, Lemaoult J, et al. HLA-G:from biology to clinical benefits[J]. Trends Immunol,2008,29(3):125-132.
[11]Hughes A L, Nei M. Evolution of the major histocompatibility complex:independent origin of nonclassical class I genes in different groups of mammals[J]. Mol Biol Evol,1989,6(6):559-579.
[12]Marchal-Bras-Goncalves R, Rouas-Freiss N, Connan F, et al. A soluble HLA-G protein that inhibits natural killer cell-mediated cytotoxicity[J]. Transplant Proc,2001,33(3):2355-2359.
[13]Fournel S, Aguerre-Girr M, Huc X, et al. Cutting edge:soluble HLA-G1 triggers CD95/CD95 ligand-mediated apoptosis in activated CD8+ cells by interacting with CD8[J]. J Immunol,2000, 164(12):6100-6104.
[14]Liang S, Ristich V, Arase H, et al. Modulation of dendritic cell differentiation by HLA-G and ILT4 requires the IL-6--STAT3 signaling pathway[J]. Proc Natl Acad Sci U S A,2008,105(24): 8357-8362.
[15]Du L, Xiao X, Wang C, et al. Human leukocyte antigen-G is closely associated with tumor immune escape in gastric cancer by increasing local regulatory T cells[J]. Cancer Sci,2011,102(7): 1272-1280.
[16]Baricordi O R, Stignani M, Melchiorri L, et al. HLA-G and inflammatory diseases[J]. Inflamm Allergy Drug Targets,2008,7(2):67-74.
[17]Verbruggen L A, Rebmann V, Demanet C, et al. Soluble HLA-G in rheumatoid arthritis[J]. Hum Immunol,2006,67(8):561-567.
[18]Rizzo R, Hviid T V, Govoni M, et al. HLA-G genotype and HLA-G expression in systemic lupus erythematosus:HLA-G as a putative susceptibility gene in systemic lupus erythematosus[J]. Tissue Antigens,2008,71(6):520-529.
[19]Wiendl H, Behrens L, Maier S, et al. Muscle fibers in inflammatory myopathies and cultured myoblasts express the nonclassical major histocompatibility antigen HLA-G[J]. Ann Neurol,2000, 48(4):679-684.
[20]Sultan S M, Allen E, Oddis C V, et al. Reliability and validity of the myositis disease activity assessment tool[J]. Arthritis Rheum,2008,58(11):3593-3599.
[21]Creput C, Le Friec G, Bahri R, et al. Detection of HLA-G in serum and graft biopsy associated with fewer acute rejections following combined liver-kidney transplantation:possible implications for monitoring patients[J]. Hum Immunol,2003,64(11):1033-1038.
[22]Luque J, Torres M I, Aumente M D, et al. Soluble HLA-G in heart transplantation:their relationship to rejection episodes and immunosuppressive therapy[J]. Hum Immunol,2006,67(4-5): 257-263.
[23]Torres M I, Le Discorde M, Lorite P, et al. Expression of HLA-G in inflammatory bowel disease provides a potential way to distinguish between ulcerative colitis and Crohn's disease[J]. Int Immunol, 2004,16(4):579-583.
[24]Aractingi S, Briand N, Le Danff C, et al. HLA-G and NK receptor are expressed in psoriatic skin: a possible pathway for regulating infiltrating T cells?[J]. Am J Pathol,2001,159(1):71-77.
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