Archives of rheumatology最新文献

Intelligence is the ability of humans to learn from experiences to ascribe conscious weights and unconscious biases to modulate their outputs from given inputs. Transferring this ability to computers is artificial intelligence (AI). The ability of computers to understand data in an intelligent manner is machine learning. When such learning is with images and videos, which involves deeper layers of artificial neural networks, it is described as deep learning. Large language models are the latest development in AI which incorporate self-learning into deep learning through transformers. AI in Rheumatology has immense potential to revolutionize healthcare and research. Machine learning could aid clinical diagnosis and decision-making, and deep learning could extend this to analyze images of radiology or positron emission tomography scans or histopathology images to aid a clinician's diagnosis. Analysis of routinely obtained patient data or continuously collected information from wearables could predict disease flares. Analysis of high-volume genomics, transcriptomics, proteomics, or metabolomics data from patients could help identify novel markers of disease prognosis. AI might identify newer therapeutic targets based on in-silico modelling of omics data. AI could help automate medical administrative work such as inputting information into electronic health records or transcribing clinic notes. AI could help automate patient education and counselling. Beyond the clinic, AI has the potential to aid medical education. The ever-expanding capabilities of AI models bring along with them considerable ethical challenges, particularly related to risks of misuse. Nevertheless, the widespread use of AI in Rheumatology is inevitable and a progress with great potential.

Objectives: The aim of this study was to identify differences and similarities between connective tissue disease (CTD) patients with and without progressive pulmonary fibrosis (PPF) by applying the new guidelines.

Patients and methods: Patient characteristics and disease courses from medical records of 50 CTD-associated Interstitial lung disease (ILD) patients (33 females, 17 males; mean age: 60.1±12.9 years) were longitudinally studied between January 2018 and May 2022. Respiratory involvement in CTD patients was described, and differences in CTD patients who developed PPF compared to those who did not were identified by the 2022 ATS (American Thoracic Society)/ERS (European Respiratory Society)/JRS (Japanese Respiratory Society)/ALAT (Asociación Latinoamericana de Thórax) Guidelines on Idiopathic Pulmonary Fibrosis and Progressive Pulmonary Fibrosis in Adults.

Results: In the majority (74%) of patients, CTD was diagnosed before ILD onset. Nonspecific interstitial pneumonia was the most common high resolution computer tomography pattern, followed by the usual interstitial pneumonia pattern. On pulmonary function test, 38% had a restrictive pattern at baseline. Patients without PPF tended to have worse lung function at baseline and increased macrophage count in bronchoalveolar lavage than patients with PPF.

Conclusion: In patients without PPF, disease progression may be missed, resulting in inadequate management. Interdisciplinary management of patients with CTD with the participation of pulmonologists and precise lung function diagnostics is recommended.

Objectives: This study aimed to compare three-dimensional kinematic of the trunk, pelvis, hip, and knee during the single-leg squat and hip torque in individuals with and without isolated patellofemoral osteoarthritis (PFOA). Patients and methods: This cross-sectional study evaluated trunk, pelvis, hip, and knee kinematics at 30°, 45°, and 60° knee flexion during the single-leg squat using the Vicon motion capture and analysis system, the Nexus System 2.1.1, and 3D Motion Monitor software. Sixteen individuals (8 males, 8 females; mean age: 49.3±6.2 years; range 40 to 61 years) participated in the study, of which eight were PFOA patients and eight were healthy controls. Isometric hip abductor, extensor, and external rotator torques were evaluated using a handheld dynamometer. Results: The PFOA group exhibited greater hip adduction at 30° (p=0.008), 45° (p=0.005), and 60° (p=0.008) knee flexion in the descending phase of the single-leg squat, as well as at 60° (p=0.009) and 45° (p=0.03) knee flexion in the ascending phase. No significant differences were found between groups for other kinematic variables (p>0.05). The PFOA group exhibited lower isometric hip abductor (p=0.02), extensor (p <0.001), and external rotator (p=0.007) torques. Conclusion: Individuals with PFOA exhibited excessive hip adduction that could increase stress on the lateral patellofemoral joint at 30°, 45°, and 60° knee flexion during the single-leg squat and exhibited weakness of the hip abductors, extensors, and external rotators in comparison to healthy controls.

Objectives: This study sought to compare the protective effect of the upper zone of the growth plate and unique cartilage matrix-associated protein (UCMA) with hyaluronic acid (HA) and corticosteroids (CS) in a rat model of osteoarthritis (OA).

Materials and methods: In the experimental animal study, 40 adult male rats were randomly assigned into five groups: control, monosodium iodoacetate (MIA) + vehicle (MIA+V), MIA+HA, MIA+CS, and MIA+UCMA. The OA model was induced by an intra-articular MIA injection to the right knee, and intra-articular injections into the right knee were performed on the treatment groups seven times every three days for 21 days. The knee joints were taken for histopathology and immunohistochemistry (IHC) analyses after the rats were sacrificed. All sections were stained with hematoxylin-eosin, safranin O and fast green FCF, and toluidine blue, and bone morphogenetic protein 2 (BMP-2) and nuclear factor-kappa B (NF-κB) expressions were analyzed with IHC. The Mankin scoring was utilized to determine the histopathological changes in the joint tissues.

Results: Mankin score was significantly higher in the MIA group compared to the control group. Histopathologically, in the UCMA-, HA-, and CS-treated groups, degenerations in the articular cartilage were milder than in the MIA+V group. Mankin score was found to be decreased significantly in the UCMA-, HA-, and CS-treated groups compared to the MIA group. Furthermore, IHC analyses revealed that NF-κB and BMP-2 expressions elevated in the MIA-induced OA model, while they were downregulated after UCMA, HA, and CS treatments.

Conclusion: Our data revealed that UCMA could be used as a potential protective molecule in the prevention and treatment of OA. Furthermore, the protective effect of UCMA was similar to HA and CS, and its possible beneficial roles against OA may be linked to the reduced BMP-2 and NF-κB levels. Further experimental research would make significant contributions to a better understanding of the therapeutic effect of UCMA on degenerative cartilage tissues.

Objectives: The aim of our study was to investigate whether TNFAIP3, PTPN22, and TRAF1-5 single nucleotide polymorphisms (SNPs) are associated with susceptibility, severity, or serological markers in primary Sjögren's syndrome (pSS).

Patients and methods: The cases and controls study was conducted between December 2021 and June 2022. TNFAIP3 rs10499194C/T, rs6920220G/A, and rs2230926T/G, PTPN22 rs2476601C/T and rs33996649G/A, and TRAF1-C5 rs10818488G/A polymorphisms were genotyped in 154 female pSS patients (mean age: 45.2±6.8 years) and 313 female control subjects (mean age: 50.3±7.5 years) using the TaqMan® SNP genotyping assay. An association analysis between TNFAIP3, PTPN22, and TRAF1-C5 SNPs and susceptibility, clinical characteristics, and serological markers of pSS was performed. Interactions between TNFAIP3, PTPN22, and TRAF1-C5 SNPs were also evaluated in patients and controls.

Results: The genotype and allele frequencies showed no association with susceptibility, severity, or serological markers of pSS. Nevertheless, several interactions between TNFAIP3 and TRAF1-C5 or TNFAIP3, PTPN22, and TRAF1-C5 genotypes were associated with susceptibility to pSS (p<0.01).

Conclusion: Individual TNFAIP3, PTPN22, and TRAF1-C5 SNPs are not associated with susceptibility, severity, or serological markers of pSS. However, genetic interactions between TRAF1-C5 and TNFAIP3 or TNFAIP3, PTPN22, and TRAF1-C5 SNPs are risk factors for pSS.

Objectives: This study compared the secukinumab treatment responses and adverse effects in psoriatic arthritis patients who received secukinumab as second-line with those that received secukinumab after two or more tumor necrosis factor-alpha (TNF-α) inhibitors.

Patients and methods: The retrospective study included 68 psoriatic arthritis patients followed up between October 2018 and October 2021. The patients were divided into two groups according to their anti-TNF-α treatment history. Group 1 consisted of 29 patients (11 males, 18 females; mean age: 45.3±13.3 years; range, 21 to 69 years) who had previously received one anti-TNF-α agent, while Group 2 included 39 patients (18 males, 21 females; mean age: 46.4±13.0 years; range, 24 to 70 years) who had been treated with two or more anti-TNF-α agents. Treatment responses of the groups were measured and compared using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Visual Analog Scale (VAS). A posttreatment BASDAI score ≤4 was used as a criterion for remission.

Results: The mean duration of secukinumab treatment was 16.6±12.7 months for Group 1 and 16.0±11.6 months for Group 2 (p=0.84). Both groups responded significantly to secukinumab in terms of BASDAI and VAS scores (p<0.001 and p<0.001, respectively). Group 1 had a greater decline in BASDAI and VAS scores than Group 2 (p=0.045 and p=0.032, respectively). Furthermore, the remission rate was greater in Group 1 compared to Group 2 (58% vs. 34%, p=0.03). The adverse effects of secukinumab treatment were an allergic reaction in Group 1 and one case of ulcerative colitis in Group 2.

Conclusion: Second-line secukinumab treatment resulted in a greater decline in BASDAI and VAS scores. Moreover, secukinumab achieved a significantly higher rate of remission when it was used as second-line therapy after one anti-TNF-α agent.

Objectives: The study aimed to evaluate the correlation between the clinical disease activity of axial spondyloarthropathy (axSpA) and magnetic resonance imaging findings of the sacroiliac joint.

Patients and methods: Thirty-two patients (21 males, 11 females; mean age: 39.3±9.2 years; range, 18 to 55 years) who were diagnosed with axSpA according to the Assessment in Spondyloarthritis International Society classification criteria between November 2015 and August 2017 were included in this cross-sectional study. Visual Analog Scale (VAS), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Ankylosing Spondylitis Disease Activity Score (ASDAS)-erythrocyte sedimentation rate (ESR), and ASDAS-C-reactive protein (CRP) were used as the indicators of clinical activity. Magnetic resonance imaging of the sacroiliac joint was performed and the Spondyloarthritis Research Consortium of Canada (SPARCC) score was evaluated by a radiologist who was blinded to the clinical and laboratory parameters of the patients.

Results: The mean duration of symptom onset was 9.3±7.7 years, and the mean duration of diagnosis was 3.6±2.8 years. Human leukocyte antigen (HLA)-B27 was positive in 16 (50%) patients. There was no correlation between the SPARCC score and VAS, BASDAI, MASES, BASFI, ASDAS-CRP, ASDAS-ESR, ESR, and CRP values (p>0.05). In the HLA-B27 subgroup analyses, a statistically significant correlation was found between HLA-B27-negative patients and SPARCC score (r=0.639, p=0.008).

Conclusion: No relationship was found between other clinical disease parameters and sacroiliac joint imaging findings, except for the relationship between the SPARCC and BASDAI in HLA-B27- negative patients with axSpA.

Objectives: Aim of the study was to perform a systemic review and meta-analysis of the current case-control studies based on the assessment of the left ventricular (LV) systolic function with standard and advanced echocardiographic methods.

Materials and methods: Objectives of the study, methods of statisticalanalysis, literature search strategy, inclusion andexclusion criteria, and outcome measurementswere defined according to Cochrane Collaborationsteps, 13 including recommendations for metaanalysisof observational studies in epidemiology (MOOSE).

Results: A total of 850 papers were collected. Of those, eight papers (10 groups) including 174,442 SLE patients and 45,608,723 controls with heart failure (HF), 20 papers including 1,121 SLE patients and 1,010 controls with an evaluated LV ejection fraction (LVEF), and eight studies (nine groups) including 462 SLE patients and 356 controls with a measured LV global longitudinal strain (LVGLS) met the predefined inclusion criteria. HF rate in SLE patients was 2.39% (4,176 of 174,442 patients with HF), and SLE patients showed a 3.4 times higher risk for HF compared to controls. SLE patients had a lower LVEF compared to controls. LVGLS was more impaired in SLE patients compared to controls, irrespective of two-dimensional or three-dimensional speckle tracking echocardiography.

Conclusion: Heart failure rate in SLE patients is high, and SLE patients showed a 3.4 times higher risk in patients with SLE compared to controls. LV systolic function, as measured by LVEF and LVGLS, is significantly affected in SLE patients, and LVGLS potentially represents a new tool for the early assessment of LV function.