Archives of rheumatology最新文献

Objectives: This study aimed to investigate the potential effect of the mevalonate kinase (MVK) gene polymorphisms on the pathogenesis and clinical findings in ankylosing spondylitis (AS) patients.

Patients and methods: This cross-sectional study was conducted with 103 participants (63 males, 40 females) between January 2013 and January 2014. Of these, 51 (32 males, 19 females; mean age: 37.3±10.2 years; range, 19 to 60 years) were adult AS patients who met the 1984 Modified New York Criteria, and 52 (31 males, 21 females; mean age: 33.8±12 years; range, 19 to 60 years) were healthy volunteers with similar demographics. MVK gene analysis was performed using polymerase chain reaction sequencing by isolating deoxyribonucleic acids from peripheral blood samples. We determined serum immunoglobulin (Ig)D levels using radial immunodiffusion. We performed physical examinations on the AS patients. The Bath Ankylosing Spondylitis Disease Activity Index and the Bath Ankylosing Spondylitis Functional Index forms were filled and erythrocyte sedimentation rate, C-reactive protein, and IgD levels were recorded.

Results: There was no statistically significant difference in the mean age between the groups (p=0.121). The frequency of symptomatic single nucleotide polymorphisms (SNPs), c.769-38 C>T heterozygous, c.769-7 T>G heterozygous, and c.769-38 C>T homozygous were similar between the groups (15/15; p=0.646). Nonsymptomatic SNPs were more common in the patient group, but the difference was not significant (83/58; p>0.05). The rate of having an MVK gene polymorphism was 36 (70.6%) in the AS compared to the 33 (63.4%) in the control group (p>0.05). There were no associations in clinical findings between the AS patients with or without MVK gene polymorphisms. New heterozygous SNPs, I56V A>G, E281D G>D, V80I G>A, and C173Y G>A, were present in four AS patients.

Conclusion: The frequency of MVK gene polymorphisms was higher in AS patients than in healthy controls. But there was no statistically significant difference. We determined no effect of the present polymorphisms on AS clinical and laboratory findings.

Objectives: This study aims to investigate proprotein convertase subtilisin/kexin 9 (PCSK9) in patients with diffuse systemic sclerosis (d-SSc) and its relation to disease activity, severity and subclinical atherosclerosis in such group of patients.

Patients and methods: Between December 2019 and July 2021, a total of 41 patients with d-SSc (17 males, 24 females; mean age: 36.1±1.9 years; range, 19 to 58 years) and 41- age and sex-matched healthy controls (17 males, 24 females; mean age: 40.1±1.7 years; range, 20 to 60 years) were included. Disease activity and skin thickness of the patients were evaluated using the European Scleroderma Study Group (EScSG) score and modified Rodnan skin score (mRSS), respectively. Serum PCSK9 and carotid intima-media thickness (CIMT) were measured using enzyme-linked immunosorbent assay (ELISA) and Duplex ultrasound, respectively.

Results: Serum PCSK9 was higher in patients compared to controls (p=0.003), particularly in those with digital ulcer (DU) and interstitial lung disease (ILD) (p<0.001). The PCSK9 positively correlated with the mean pulmonary artery pressure, EScSG, mRSS, C-reactive protein (p<0.001), erythrocyte sedimentation rate (p<0.05), lipid profile, and mean CIMT (p<0.01). In the multivariate analysis, EScSG, mRSS, lipid profile, and waist circumference were significantly correlated with PCSK9. Serum PCSK9 levels of (182.6 ng/mL) had 77.7% sensitivity and 81.2% specificity for diagnosing DU versus (172.8 ng/mL) 90.1% and 73.5% for ILD (p<0.001).

Conclusion: Serum PCSK9 is upregulated in d-SSc with higher levels in severe disease manifestations such as DU and ILD. It is correlated well with disease activity, more severe disease manifestations, and CIMT. The PCSK9 inhibitors may be a target of therapy in diseases with premature atherosclerosis such as d-SSc regardless of its anti-cholesterol effect, at least in more severe manifestations.

Objectives: This study aimed to compare the prevalence and musculoskeletal ultrasonography (US) findings of rheumatoid arthritis (RA) patients with concomitant fibromyalgia (FM) according to the 1990 American College of Rheumatology (ACR) FM classification criteria or the 2016 ACR FM diagnostic criteria.

Patients and methods: This cross-sectional study included 63 patients (17 males, 46 females; mean age: 48.2±7.1 years; range, 18 to 62 years) with RA. Medical history and laboratory data were obtained from electronic records. Clinical examination, composite disease activity measures, functional status, and the German 7-joint ultrasound score were assessed to evaluate disease activity and synovial inflammation. The patients were divided into three groups: patients who met only the 2016 ACR criteria, patients who met only the 1990 ACR criteria, and patients who met both criteria.

Results: In patients with RA, concomitant FM prevalence was 34.9% according to the 2016 ACR FM diagnostic criteria versus 23.8% according to the 1990 ACR FM classification criteria. Rheumatoid arthritis patients with FM had high tender joint count and disease activity scores, while musculoskeletal US findings were similar. Patients who met only the 2016 ACR FM diagnostic criteria had significantly higher gray-scale US and power Doppler US synovitis scores than patients who satisfied only ACR 1990 FM classification criteria (p=0.03 and p=0.02, respectively).

Conclusion: Synovial inflammation is a prominent sign in RA patients diagnosed with FM according to the 2016 ACR FM diagnostic criteria. The higher disease activity seen in the presence of FM in RA patients is associated with FM rather than synovitis.

Objectives: The aim of this study was to examine the clinical and phenotypic features of pediatric Behçet's disease (PEDBD) in our clinic and present the rates of fulfilling the diagnostic criteria.

Patients and methods: Thirty-four patients (20 males, 14 females; mean age: 16.0±2.1 years; range, 10 to 18 years) diagnosed with PEDBD between January 2010 and December 2019 were retrospectively evaluated. Patients were reclassified according to 1990 International Study Group (ISG) criteria, 2014 International Criteria for Behçet's Disease (ICBD), and PEDBD criteria.

Results: The mean age at diagnosis was 12.6±3.1 years, the median diagnosis delay time was 12.0 (range, 4.5 to 27.0) months, and the mean age at symptom onset was 10.8±2.9 years. The mean follow-up period was 31.9±20.9 months. Oral aphthous ulcer was observed in 33 (97.1%), genital ulcer in 16 (47.0%), ocular involvement in 15 (44.1%), skin lesion in 11 (32.3%), joint involvement in nine (26.4%), both vascular and neurological involvement in six (17.6%) patients. The pathergy test was positive in 11 (37.8%) patients, and human leukocyte antigen (HLA)-B51 was positive in 11 (78.5%) of 14 patients. The rates of patients meeting the criteria for ISG, ICBD, and PEDBD were 52.9%, 82.4%, and 50.0%, respectively.

Conclusion: Pathergy and HLA-B51 can be used as supportive findings in patients who do not meet the diagnostic criteria. However, expert opinion is still the gold standard in diagnosis.

Objectives: The main goal of the study was to investigate how pregabalin (PGB) affects proinflammatory cytokine release in patients with fibromyalgia syndrome (FMS).

Patients and methods: This experimental research study was conducted with 85 female participants (mean age: 49.6±10.1 years; range, 30 to 73 years) between April 2020 and November 2020. Of the participants, 30 were FMS patients using PGB 150 mg/day for at least three months, 30 were FMS patients not using PGB, and 25 were healthy individuals. The detection of FMS was carried out according to the 2010 American College of Rheumatology diagnostic criteria. Levels of proinflammatory cytokines (interleukin [IL]-2, IL-6, IL-12, IL-17, interferon-gamma, and tumor necrosis factor-alpha) were measured by enzyme-linked immunosorbent assay.

Results: Serum concentrations of proinflammatory cytokines were remarkably decreased in FMS patients using PGB (p<0.001) and were higher in patients with FMS not using PGB than in healthy subjects (p<0.001). The highest values of proinflammatory cytokines were found in the group of FMS patients not using PGB (p<0.001).

Conclusion: These results indicate that PGB inhibits the release of proinflammatory cytokines, suggesting that it can be used as an anti-inflammatory agent in inflammatory cases.

Objectives: This study aimed to investigate whether early ocular findings can be demonstrated with optical coherence tomography angiography in patients with Behçet's disease.

Patients and methods: Thirty-seven eyes of 22 patients with Behçet's disease with ocular involvement, 48 eyes of 26 Behçet patients without any ocular involvement, and 44 eyes of 22 healthy controls were included, for a total of 70 patients (39 males, 31 females; mean age: 42.3±11.7 years; range, 18 to 65 years), in the cross-sectional study conducted between September 2019 and April 2020. The parameters analyzed were the foveal avascular zone (FAZ), central macular thickness, total deep capillary plexus vessel density (DCPVD), parafoveal deep capillary plexus vessel density (PaDCPVD), total superficial capillary plexus vessel density (SCPVD), and parafoveal superficial capillary plexus vessel density (PaSCPVD).

Results: Total DCPVD, total SCPVD, PaDCPVD, and PaSCPVD were found to be low in the ocular involvement group compared to the others, and the FAZ area was larger compared to the control group. Capillary plexus densities were positively correlated with the best-corrected visual acuity and negatively correlated with disease duration. No statistically significant difference was found between patients with Behçet without ocular involvement and the control group in terms of the FAZ area, DCPVD, PaDCPVD, SCPVD, and PaSCPVD.

Conclusion: Optical coherence tomography angiography demonstrated decreased vascularity in Behçet patients with ocular involvement; however, it revealed no microvascular differences between patients with Behçet's disease who do not have ocular involvement and the control group.

Objectives: This study aims to investigate skeletal muscle architecture and strength in patients with primary Sjögren syndrome (pSS).

Patients and methods: Between July 01, 2017 and November 30, 2017, 19 pSS patients (19 females; mean age: 54.1±6.6 years; range, 42 to 62 years) and 19 age-, body mass index-, and sex-matched healthy controls (19 females; mean age: 53.2±6.7 years; range 42 to 61 years) were included. Sjögren symptoms were assessed with the European Alliance of Associations for Rheumatology (EULAR) Sjögren's Syndrome Patient Reported Index (ESSPRI). Muscle thickness, pennation angle, and fascicle length were measured at quadriceps femoralis, gastrocnemius and soleus muscles. Isokinetic muscle strength tests were performed at 60 and 180°/sec for knee and at 30 and 120°/sec for ankle. Anxiety and depression evaluated with the Hospital Anxiety and Depression Scale (HADS), fatigue with Multidimensional Assessment of Fatigue scale (MAF), and functionality with Health Assessment Questionnaire (HAQ).

Results: In the pSS group, the mean ESSPRI was 7.70±1.17. The mean scores of depression (10.05±3.09 vs. 4.47±2.29; p<0.0001), anxiety (8.26±4.28 vs. 3.79±2.42; p<0.0001), functionality (0.94±0.78 vs. 0.22±0.26; p<0.0001), and fatigue (37.69±5.47 vs. 17.69±5.26; p<0.0001) were significantly higher in patients with pSS. Only, the pennation angle of vastus medialis in dominant leg was significantly greater in healthy controls (p=0.049). Peak torques/body weight of knee and ankle muscles were found to be similar.

Conclusion: Excluding a minor decrease of the pennation angle at vastus medialis, muscle structure of lower extremity of pSS patients were similar to healthy controls. In addition, isokinetic muscle strength did not significantly differ in patients with pSS compared to healthy controls. In patients with pSS, disease activity and fatigue level were negatively correlated with isokinetic muscle strength measurements.

Objectives: The study aimed to determine the levels of change of the markers related to radiographic progression, such as Dickkopf-1 (DKK-1), sclerostin (SOST), bone morphogenetic protein (BMP)-2 and -4, and interleukin (IL)-17 and -23, in ankylosing spondyloarthritis (AS) during anti-tumor necrosis factor alpha (TNF-α) treatment.

Patients and methods: Fifty-three anti-TNF-α naïve AS patients (34 males, 19 females; median: 38 years; range, 20 to 52 years) refractory to conventional treatments meeting the modified New York criteria or Assessment of SpondyloArthritis International Society classification criteria were enrolled to this cross-sectional, controlled study between October 2015 and January 2017. Fifty healthy volunteers (35 males, 15 females; median: 36 years; range, 18 to 55 years) with similar age and sex characteristics were recruited. Serum DKK-1, BMP-2, BMP-4, SOST, IL-17, and IL-23 levels were measured in both groups. The serum levels of the markers were measured again after about two years (mean follow-up duration of 21.7±6.4 months) in AS patients who started anti-TNF-α treatment. Demographic, clinical characteristics, and laboratory parameters were recorded. The disease activity at the time of inclusion was assessed through the Bath Ankylosing Spondylitis Disease Activity Index.

Results: Serum DKK-1, SOST, IL-17, and IL-23 levels in the AS group before anti-TNF-a treatment were significantly higher compared to the control group (p<0.01 for DKK-1, p<0.001 for others). There was no difference regarding serum BMP-4 levels, whereas BMP-2 levels were significantly higher in the control group (p<0.01). Forty (75.47%) AS patients had serum marker levels measured after anti-TNF-α treatment. No significant change was observed in the serum levels of these 40 patients measured 21.7±6.4 months after the initiation of anti-TNF-α treatment (p>0.05 for all).

Conclusion: In AS patients, there was no change in DKK-1/SOST, BMP, and IL-17/23 cascade with anti-TNF-α treatment. This finding may suggest that these pathways act independently of each other, and their local effects are not influenced by systemic inflammation.

Objectives: This study aims to investigate the prognosis of novel coronavirus disease-2019 (COVID-19) infection in patients with the chronic inflammatory-rheumatic disease and evaluate the effects of immunosuppressive drugs on the prognosis, clinical characteristics, laboratory findings and hospitalization periods of the rheumatic patients with COVID-19 infection.

Patients and methods: Between April 2020 and March 2021, a total of 101 patients (30 males, 71 females; mean age: 48±14.4 years; range, 46 to 48 years) with the rheumatic diseases diagnosed with COVID-19 infection were included. A total of 102 age- and sex-matched patients (35 males, 67 females; mean age: 44±14.4 years; range, 28 to 44 years) who were diagnosed with COVID-19 infection and had no history of rheumatic disease in the same period were included as the control group. Data including demographic characteristics of the patients, presence of any symptoms of COVID-19 disease, laboratory data at the time of diagnosis, and treatments administered were collected.

Results: The rate of hospitalization was higher in 38 (37%) patients without rheumatic diseases than in 31 (31%) patients with rheumatic diseases (p=0.324). The rate of lung infiltration on radiographic examination was higher in patients without rheumatic diseases (40% vs. 49%) (p=0.177). COVID-19 infection symptoms such as anosmia 45 (45%), ageusia 51 (50%), shortness of breath 45(45%), nausea 29 (29%), vomiting 16 (16%), diarrhea 25 (25%) and myalgia-arthralgia 81 (80%) were higher in patients with rheumatic diseases. In terms of laboratory values, lymphocyte count (p=0.031) was statistically higher in patients without rheumatic diseases. Hydroxychloroquine (35%), oseltamivir 10 (10%), antibiotics 27 (26%), acetylsalicylic acid 52 (51%), and supplementary oxygen 25 (25%) treatments which used to cure COVID 19 infection were administered more in patients without rheumatic diseases. The number of treatments administered was higher in patients without rheumatic diseases (p<0.001).

Conclusion: Patients with the chronic inflammatory-rheumatic disease have more symptoms due to COVID-19 infection, but the disease course is not poor and hospitalization rates are lower.