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Results in Journal Clinical Rheumatology: 9,143

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, , Loiane Cristina de Souza, Joaquim Henrique Lorenzetti Branco,
Clinical Rheumatology pp 1-9; doi:10.1007/s10067-021-05738-z

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, Mengru Liu, Erye Zhou, Xin Chang, Michun He, Mingjun Wang,
Clinical Rheumatology pp 1-17; doi:10.1007/s10067-021-05686-8

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Aida Malek Mahdavi, Afshin Khalili, Samin Alihosseini, Mehran Jaberinezhad, Kamal Esalatmanesh, Mehrzad Hajialilo, SeyedMostafa Seyedmardani,
Clinical Rheumatology pp 1-9; doi:10.1007/s10067-021-05758-9

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Siqin Lan, Yuanlin He, Maijudan Tiheiran, Wenya Liu,
Clinical Rheumatology pp 1-6; doi:10.1007/s10067-021-05752-1

Abstract:
Objective The Angiopoietin-like protein 4 (ANGPTL-4) has been proved to be a protein associated with multiple inflammatory responses. Nevertheless, whether it contributes to distinguishing brucella spondylitis (BS) from tuberculous spondylitis (TS) remains an open question. Our study aim is to explore the capability of the ANGPTL-4 to differentiating BS from TS. Materials and method In our study, 53 patients were screened out according to the criteria precisely in Xinjiang Medical University Affiliated of the First Hospital from 1 January, 2016, to 31 December, 2018. Their clinical data were retrospectively reviewed. All of them underwent pathological biopsy and magnetic resonance imaging examination. All the frozen tissue sections were stained for testing ANGPTL-4. Result Among the 53 patients, BS had 26 patients, and TS had 27 patients. There was no significant difference between the baseline (P = 0.682) between the two groups. The positive rate of ANGPTL-4 in TS patients (24/27, 88.89%) was higher than that in BS patients (17/26, 65.83%) (P < 0.05). The incidence of microangiopathy and fibrous connective tissue hyperplasia in patients with BS was distinctly higher than those in the TS (P = 0.001, P = 0.008, respectively). Patients of TS frequently presented more granuloma, caseous necrosis, epithelial-like reaction, interleukin 6 (IL-6), and C-reactive protein (CRP) than those of BS. Conclusion Our study provided novel insights into distinguishing BS from TS using the ANGPTL-4 combining with histopathology, which may become new supporting evidence. Key Points• Brucella spondylitis and tuberculous spondylitis are a significant public health concern and even have prolonged damage, contributing to severe health and economic outcomes in Xinjiang of China.• The granuloma, caseous necrosis, epithelioid reaction, microangiosis, and fibrous connective tissue of pathological tissue might play a critical significance for distinguishing brucella spondylitis from tuberculous spondylitis patients.• ANGPLT-4 may become new supporting evidence identify brucella spondylitis and tuberculous spondylitis which is implicated in inflammation angiogenesis-related disorders.
Cheng-Cheng Hou, Hai-Fen Ma, Jing-Fen Ye, Dan Luo, Hua-Fang Bao,
Clinical Rheumatology pp 1-13; doi:10.1007/s10067-021-05755-y

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Hongchao Li, Huaqun Zhu, Liling Xu, Jimeng Xue, Zhen Zhao, Hua Zhong, ,
Clinical Rheumatology pp 1-10; doi:10.1007/s10067-021-05687-7

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, N. Dennis, S. D. Chakravarty, R. Villacorta, L. Mesana, I. Lin, Y. Wang, M. Shawi, M. Pacou, T. Baker, et al.
Clinical Rheumatology pp 1-10; doi:10.1007/s10067-021-05713-8

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Chao Zhen, Yabo Wang, Haifeng Wang,
Clinical Rheumatology pp 1-8; doi:10.1007/s10067-021-05751-2

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Clinical Rheumatology pp 1-11; doi:10.1007/s10067-021-05739-y

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Wei Lin, Zhifei Xin, , Yang Li, Xiuying Ren, Yashuang Su, Meilu Liu, Shaoying Guo, Liu Yang, Yixuan Liu, et al.
Clinical Rheumatology pp 1-7; doi:10.1007/s10067-021-05749-w

Abstract:
Objective The aim at the current study was to investigate the clinical characteristics and risk factors of Raynaud’s phenomenon (RP) in patients with primary Sjögren’s syndrome (pSS). Methods Retrospective analysis of the medical records of 333 new-onset pSS patients was performed. Demographic, clinical, and serological data were compared between individuals with and without RP. Logistic regression analysis was used to identify risk factors. Results RP was present in 11.41% of the pSS patients. pSS-RP patients were younger (49.74±14.56 years vs. 54.46±13.20 years, p=0.04) and exhibited higher disease activity (11 [5.75–15] vs. 7 [4–12], p=0.03) than those without. The prevalence of lung involvement was significantly higher in pSS patients with RP (60.53% vs. 17.29%; p<0.001). A significantly higher proportion of patients with pSS-RP tested positive about antinuclear (ANA), anti-RNP, and anti-centromere antibodies (ACA) compared to those without (p=0.003, <0.001, and 0.01, respectively). Multivariate analysis identified lung involvement (odds ratio [OR]=8.81, 95% confidence interval [CI] 2.02–38.47; p=0.04), anti-RNP positive status (OR=79.41, 95% CI 12.57–501.78; p<0.0001), as well as ACA (OR=13.17, 95% CI 2.60–66.72; p=0.002) as prognostic factors for pSS-RP. Conclusion The presence of RP defined a subset of pSS with a unique phenotype, manifesting as increased lung involvement and a higher frequency of anti-RNP antibodies and ACA, as well as greater disease activity. These results suggest that RP has clinical and prognostic value of pSS patients. Further prospective studies with a larger number of subjects are warranted to confirm our findings and assess the prognostic and treatment implications of RP in pSS patients. Key Points• Raynaud’s phenomenon (RP) was present in 38 (11.41%) of 333 patients with primary Sjögren’s syndrome (pSS), with patients with RP exhibiting a younger age and higher disease activity.• The presence of RP indicates a subset of pSS with a unique phenotype, with manifestations including increased lung involvement and a higher frequency of anti-RNP antibodies and anti-centromere antibodies.• Patients with pSS and RP need close follow-up and long-term observation (including assessment of microangiopathy), with specific attention paid to the possible development of clinical features of systemic sclerosis.
, Murat Torgutalp, Serdar Baysal, Anil Colaklar, Serdar Sezer, , Caglar Uzun, Tahsin Murat Turgay, Gulay Kinikli, Askin Ates
Clinical Rheumatology pp 1-8; doi:10.1007/s10067-021-05748-x

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, Carlos Sanchez-Piedra, Blanca Garcia-Magallón, Ana Pérez-Gómez, Sara Manrique-Arija, Raquel Martín-Doménech, María Colazo, Cristina Campos, José Campos, Javier del Pino-Montes, et al.
Clinical Rheumatology pp 1-10; doi:10.1007/s10067-021-05742-3

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Daan Fritz, Bart Ferwerda, Matthijs C. Brouwer,
Clinical Rheumatology pp 1-9; doi:10.1007/s10067-021-05684-w

Abstract:
Objective We studied genetic risk factors associated with sarcoidosis within a family with a high prevalence of this disease. Methods We studied 41 members of a family with a high rate of sarcoidosis, including an index patient with treatment-resistant neurosarcoidosis. Whole genome sequencing was performed for six affected family members and variations associated with loss of function were filtered out as candidate genes. Findings were validated by using amplicon sequencing within all 41 family members with DNA available and candidate genes were screened on absence and presence within the sarcoidosis affected and non-affected. Results Family members (n = 61) from 5 generations were available for participation including 13 subjects diagnosed with sarcoidosis (20%). Analyses identified 36 candidate variants within 34 candidate genes. Variations within three of these genes (JAK2, BACH2, and NCF1) previously have been associated with autoimmune diseases. Conclusions We identified 34 genes with a possible role in the etiology of sarcoidosis, including JAK2. Our results may suggest evaluation of JAK inhibitors in treatment-resistant sarcoidosis. Key Points • JAK2 has a potential role in the etiology of sarcoidosis and is a potential therapeutic target. • We identified 33 additional candidate genes of which BACH2 and NCF1 have been previously associated with autoimmune disease.
Yingying Wang, Jian Hong, ,
Clinical Rheumatology pp 1-12; doi:10.1007/s10067-021-05747-y

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, Ethan I. Bent, , Gregory C. Gardner
Clinical Rheumatology pp 1-6; doi:10.1007/s10067-021-05740-5

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, Contributors, Vincenzo Venerito, Serena Bugatti, Chiara Bazzani, Martina Biggioggero, Luca Petricca, Rosario Foti, Alessandra Bortoluzzi, Silvia Balduzzi, et al.
Clinical Rheumatology pp 1-9; doi:10.1007/s10067-021-05734-3

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Siming Dai, Hui Wang, Meng Wang, Yue Zhang, ,
Clinical Rheumatology pp 1-10; doi:10.1007/s10067-021-05726-3

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, , Francisco Javier Godoy-Navarrete, Sara Manrique-Arija, María Carmen Aguilar-Hurtado, Carmen María Romero-Barco, Inmaculada Ureña-Garnica, F. Espildora, María Isabel Padin-Martín, Antonio Fernández-Nebro
Clinical Rheumatology, Volume 40, pp 2527-2527; doi:10.1007/s10067-021-05737-0

M. Fornaro, G. Righetti, A. Abbruzzese, G. Lopalco, F. Cacciapaglia, M. G. Anelli, V. Venerito,
Clinical Rheumatology pp 1-7; doi:10.1007/s10067-021-05728-1

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, Maria Bouzamel, Myriam Mrad-Nakhlé, Ghada Abi Karam, Ihsane Hmamouchi, Redouane Abouqal, Wehbeh Farah
Clinical Rheumatology pp 1-12; doi:10.1007/s10067-021-05735-2

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Byeongzu Ghang, So Hye Nam, Jungsun Lee, Doo-Ho Lim, Soo Min Ahn, Ji Seokchan Hong, Yong-Gil Kim, Bin Yoo, Jinseok Kim,
Clinical Rheumatology, Volume 40, pp 2525-2525; doi:10.1007/s10067-021-05732-5

Ilenia Di Cola, Federico Bruno, Onorina Berardicurti, Riccardo Monti, Alessandro Conforti, Alessandra Di Sibio, Viktoriya Pavlych, Carlo Masciocchi, Antonio Barile, Paola Cipriani, et al.
Clinical Rheumatology pp 1-8; doi:10.1007/s10067-021-05727-2

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Sara E. Sabbagh, for the Johns Hopkins Myositis Center Group, Iago Pinal-Fernandez, Maria Casal-Dominguez, Jemima Albayda, Julie J. Paik, Frederick W. Miller, Lisa G. Rider, Andrew L. Mammen,
Clinical Rheumatology pp 1-6; doi:10.1007/s10067-021-05730-7

Abstract:
We analyzed the prevalence of anti-mitochondrial autoantibodies (AMA) in adult- and juvenile-onset myositis longitudinal cohorts and investigated phenotypic differences in myositis patients with AMA. We screened sera from myositis patients including 619 adult- and 371 juvenile-onset dermatomyositis (DM, JDM), polymyositis (PM, JPM), inclusion body myositis (IBM), or amyopathic DM patients and from healthy controls, including 164 adults and 92 children, for AMA by ELISA. Clinical characteristics were compared between myositis patients with and without AMA. AMA were present in 5% of adult myositis patients (16 of 216 DM, 10 of 222 PM, 4 of 140 IBM, 1 of 19 amyopathic DM), 1% of juvenile myositis patients (3 of 302 JDM, 1 of 25 JPM), and 1% of both adult and juvenile healthy controls. In patients with adult-onset myositis, AMA were associated with persistent muscle weakness, Raynaud’s phenomenon, dysphagia, and cardiomyopathy. Adult myositis patients with AMA may have more severe or treatment refractory disease, as they more frequently received glucocorticoids and intravenous immunoglobulin. In juvenile myositis, children with AMA often had falling episodes and dysphagia, but no other clinical features or medications were significantly associated with AMA. AMA are present in 5% of adult myositis patients and associated with cardiomyopathy, dysphagia, and other signs of severe disease. The prevalence of AMA is not increased in patients with juvenile myositis compared to age-matched healthy controls. Our data suggest that the presence of AMA in adult myositis patients should prompt screening for cardiac and swallowing involvement. Key Points • Approximately 5% of a large North American cohort of adult myositis patients have anti-mitochondrial autoantibodies. • Adults with anti-mitochondrial autoantibodies often have chronic weakness, Raynaud’s, dysphagia, cardiomyopathy, and more severe disease. • Anti-mitochondrial autoantibodies are rare in juvenile myositis and not associated with a specific clinical phenotype.
Antonietta Gigante, Francesco Iannazzo, Luca Navarini, Maria Chiara Sgariglia, Domenico Paolo Emanuele Margiotta, Valentina Vaiarello, Federica Foti, Antonella Afeltra, Rosario Cianci,
Clinical Rheumatology pp 1-6; doi:10.1007/s10067-021-05731-6

Abstract:
Introduction Aims of study were to evaluate the prevalence of metabolic syndrome (MetS) in systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) patients and to evaluate serum level of adipokines in SLE and SSc patients with and without MetS. Methods Fifty SLE patients and 85 SSc patients were enrolled. The diagnosis of MetS was made according to the criteria of the National Cholesterol Education Program (NCEP) Adult Treatment Panel III. Clinical assessment and serum levels of adiponectin and resistin were evaluate in SLE and SSc patients. Results Prevalence of MetS was significantly (p<0.0001) higher in SLE patients than SSc patients (36% vs 10.6%). Median values of resistin were significantly (p<0.001) higher in SLE patients with MetS than SLE patients without MetS [4.01 ng/mL (2.7–4.5) vs 1.92 ng/mL (1.2–3)]. Median values of adiponectin were significantly (p<0.05) lower in SLE patients with MetS than SLE patients without MetS [5.64 ng/mL (4.96–8) vs 8.38 ng/mL (6.54–11.01)]. Systemic Lupus Erythematosus Activity Index [8 (6–12) vs 10 (6–13), p<0.01] and Systemic Damage Index [2 (1–3) vs 2 (0–3), p<0.001] were significantly higher in MetS patients than in patients without MetS. In SSc, the median value of disease severity scale was significantly higher (p<0.05) in MetS patients than in patients without MetS [7 (5–7) vs 5 (3–6)]. Conclusion Prevalence of MetS is higher in SLE patients. In SLE patients, MetS showed an association with adipokine levels and inflammation/activity disease scores. In SSc patients, MetS was associated with severity of disease. Key Points • Prevalence of metabolic syndrome is higher in SLE patients than SSc patients. • Resistin is higher in SLE patients with metabolic syndrome. • Adineponectin is lower in SLE patients with metabolic syndrome. • Disease severity scale is higher in SSc patients with metabolic syndrome.
Tien-Ming Chan, Meng-Jiun Chiou,
Clinical Rheumatology pp 1-8; doi:10.1007/s10067-021-05688-6

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Diana Castillo-Martínez, Zaira Torres, ,
Clinical Rheumatology pp 1-5; doi:10.1007/s10067-021-05724-5

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, Elena Borlandelli, Cecilia Tetta, Marco Miceli, Riccardo Meliconi, Francesco Ursini
Clinical Rheumatology pp 1-2; doi:10.1007/s10067-021-05714-7

, For Ussonar, Karina D. Torralba, Kristal S. Choi, Robert M. Fairchild, Amy Cannella, Lorena Salto, Eugene Y. Kissin, Ralf Thiele, Edward J. Oberle, et al.
Clinical Rheumatology pp 1-10; doi:10.1007/s10067-021-05716-5

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, Kaan Yıldız, Tuncay Küme, Ceyhun Açarı, Hatice Adıgüzel Dundar, Balahan Makay, Mustafa Kır, Erbil Ünsal
Clinical Rheumatology pp 1-8; doi:10.1007/s10067-021-05721-8

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Eleni Pilitsi,
Clinical Rheumatology pp 1-5; doi:10.1007/s10067-021-05725-4

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Shasha Duan, Si Ha, Shujuan Li, Yaxi Wang, Yilu Shi, Haiyue Zhao, Lu Zhang, Xiaoshan Zhang,
Clinical Rheumatology pp 1-9; doi:10.1007/s10067-021-05723-6

Abstract:
Objectives To compare cardiac function and systolic dyssynchrony of fetuses not exposed to and those exposed to maternal autoimmune antibodies using two-dimensional speckle tracking echocardiography (2DSTE). Methods An observational study of 52 fetuses, 18 from mothers with autoimmune antibodies (anti-SSA/Ro60, anti-Ro52 or/and anti-SSB/La) and 34 from healthy mothers without antibodies, was conducted. Maternal baseline characteristics, fetoplacental Doppler parameters, and conventional echocardiographic data were prospectively collected. Systolic global and regional longitudinal strain of left and right ventricle (LV and RV) and the time to peak strain of regional myocardium were measured using 2DSTE. We also calculated the differences in time to peak strain between the LV free wall and RV free wall (two-chamber dyssynchrony, 2C-DYS) and the LV dyssynchrony between the septum and LV free wall (one-chamber dyssynchrony, 1C-DYS). Results There were no significant differences in conventional systolic and diastolic functional parameters for the LV and RV. No effect modification was demonstrated in a myocardial deformation analysis. However, 1C-DYS was significantly more prolonged in the maternal autoimmune disease group (19.50 [8.00 to 29.25] vs. 28.50 [13.50 to 39.25], P = 0.042). Conclusions LV systolic mechanical dyssynchrony in fetuses of mothers with autoimmune antibodies suggests in-utero subclinical damage of the cardiac conduction system. Key points• The left ventricular systolic dyssynchrony was significantly more prolonged in the maternal autoimmune disease (AD) fetuses. • Subclinical damage to the left ventricular conduction system of the fetal heart in maternal AD was observed. • Systolic and diastolic functional of the left and right ventricle were preserved in fetuses exposed to maternal autoimmune disease.
Maliheh Moradzadeh, Mehrdad Aghaei, Zahra Mehrbakhsh, ,
Clinical Rheumatology pp 1-22; doi:10.1007/s10067-021-05698-4

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Benzeeta Pinto, Prateek Deo, Susmita Sharma, Arshi Syal,
Clinical Rheumatology pp 1-14; doi:10.1007/s10067-021-05711-w

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, Yu Qian, Sarah L Mackie, Chengping Wen,
Clinical Rheumatology pp 1-5; doi:10.1007/s10067-021-05718-3

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, , Chrisoula Iliou, Zoi Tziortzioti, Maria I. Argyropoulou, ,
Clinical Rheumatology pp 1-8; doi:10.1007/s10067-021-05712-9

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Yan Ding, Yang Zhou, Hua-Rong Li, Yue-Hua Xiong, Wei Yin,
Clinical Rheumatology pp 1-6; doi:10.1007/s10067-021-05707-6

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