Increased Risk of Thyroid Dysfunction Among Patients With Rheumatoid Arthritis.
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ABSTRACT:
SUBMITTER: Li Q
PROVIDER: S-EPMC6336701 | biostudies-other | 2018
REPOSITORIES: biostudies-other
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Project description:BackgroundRheumatoid arthritis (RA) is one of the most common chronic non-organ-specific autoimmune diseases; meanwhile, autoimmune thyroid disease (AITD) is the most common organ-specific autoimmune disease that can lead to hypo or hyperthyroidism. Although the etiology of both diseases is complex with a combination of genetic and environmental factors, there are overlaps in genes contributing to the pathogenesis of both diseases. Numerous studies found a correlation between thyroid abnormality and RA in different populations, yet some didn't. This study is aimed to evaluate the prevalence of thyroid dysfunction, AITD, and anti-thyroid peroxidase (anti-TPO) positively in Iranian patients with RA.MethodsA total of 250 RA patients and 248 patients with non-inflammatory rheumatologic disease were included in this case-control study. All participants underwent complete clinical and laboratory assessments. Participants were also assessed for thyroid function testing, including anti-TPO antibodies.ResultsThyroid dysfunction was twice as common in RA patients as in controls (OR = 2.16; P-value > 0.001). Overt hypothyroidism was the most common thyroid dysfunction among RA patients (58 out of 84). Anti-TPO positivity was also significantly more common in RA compared with controls (OR = 2.65; P-value > 0.001). The proportion of controls and RA patients with AITD were 9 and 21.5%, respectively. AITD was found 2.8 times more common in RA group than controls (OR = 2.77; P-value > 0.001).ConclusionIt was demonstrated that RA was an independent factor associated with thyroid dysfunction and AITD.
| S-EPMC9590164 | biostudies-literature
Project description:Immune cells are majorly dysregulated in rheumatoid arthritis patients and are a major cause of pathogenesis and progression of this autoimmune condition. As mitochondria are master regulators of metabolism of all cells present in human body, it is of prime importance to study mitochondrial homeostasis in immune cells for identifying any dysfunction contributing to pathogenesis or progression of RA. The objective of our study is to understand the mitochondrial and mitochondrially driven alterations in immune cells of RA patients which may cause them to perform abnormal functions and may have an important contribution in progression of the disease.
2020-06-22 | PXD011934 | Pride
Project description:Rheumatoid arthritis is a systemic autoimmune disease characterized by excess morbidity and mortality from cardiovascular disease. Mechanisms linking rheumatoid arthritis and cardiovascular disease include shared inflammatory mediators, post-translational modifications of peptides/proteins and subsequent immune responses, alterations in the composition and function of lipoproteins, increased oxidative stress, and endothelial dysfunction. Despite a growing understanding of these mechanisms and their complex interplay with conventional cardiovascular risk factors, optimal approaches of risk stratification, prevention, and treatment in the context of rheumatoid arthritis remain unknown. A multifaceted approach to reduce the burden posed by cardiovascular disease requires optimal management of traditional risk factors in addition to those intrinsic to rheumatoid arthritis such as increased disease activity. Treatments for rheumatoid arthritis seem to exert differential effects on cardiovascular risk as well as the mechanisms linking these conditions. More research is needed to establish whether preferential rheumatoid arthritis therapies exist in terms of prevention of cardiovascular disease. Ultimately, understanding the unique mechanisms for cardiovascular disease in rheumatoid arthritis will aid in risk stratification and the identification of novel targets for meaningful reduction of cardiovascular risk in this patient population.
| S-EPMC6889899 | biostudies-literature
Project description:ObjectivesConsidering growing evidence of mucosal involvement in RA induction, this study investigated circulating free secretory component (SC) in patients with either recent-onset RA or with ACPA and musculoskeletal pain.MethodsTwo prospective cohorts were studied: TIRA-2 comprising 452 recent-onset RA patients with 3 years of clinical and radiological follow-up, and TIRx patients (n = 104) with ACPA IgG and musculoskeletal pain followed for 290 weeks (median). Blood donors and three different chronic inflammatory diseases served as controls. Free SC was analysed by sandwich ELISA.ResultsSerum levels of free SC were significantly higher in TIRA-2 patients compared with TIRx and all control groups (P < 0.01). Among TIRx patients who subsequently developed arthritis, free SC levels were higher compared with all control groups (P < 0.05) except ankylosing spondylitis (P = 0.74). In TIRA-2, patients with ACPA had higher baseline levels of free SC compared with ACPA negative patients (P < 0.001). Free SC status at baseline did not predict radiographic joint damage or disease activity over time. In TIRx, elevated free SC at baseline trendwise associated with arthritis development during follow-up (P = 0.066) but this disappeared when adjusting for confounders (P = 0.72). Cigarette smoking was associated with higher levels of free SC in both cohorts.ConclusionSerum free SC levels are increased in recent-onset RA compared with other inflammatory diseases, and associate with ACPA and smoking. Free SC is elevated before arthritis development among ACPA positive patients with musculoskeletal pain, but does not predict arthritis development. These findings support mucosal engagement in RA development.
| S-EPMC7850007 | biostudies-literature
Project description:ImportanceAutoimmune thyroid disease ([AITD] including hypothyroidism and hyperthyroidism) is the most common organ-specific autoimmune disorder and is more prevalent among patients with rheumatoid arthritis (RA). Real-world studies on when and how this increased risk of AITD develops, in association with the time before or after the onset of RA, are lacking.ObjectiveTo estimate the risk of thyroxine-treated AITD among patients with RA at different time points before and after the diagnosis of RA.Design, setting, and participantsA nationwide register-based case-control and cohort study was conducted between January 1, 2006, and June 30, 2013, with a maximum follow-up time of 7 years before and 8 years after diagnosis of RA. The study used the Swedish Rheumatology Quality Register and linkage to other nationwide registers to identify 8090 adults with new-onset RA and a random population-based sample of 80 782 referents matched by age, sex, and residential area. Statistical analysis was performed from July 1, 2015, to June 30, 2017.ExposuresPresence of AITD in the participants in the case-control design and RA in the participants in the cohort design.Main outcomes and measuresPrevalence and relative risk of incident AITD before (odds ratios) and after (hazard ratios) diagnosis of RA compared with the population as reference.ResultsThere were 8090 patients with RA (5529 women and 2561 men; mean [SD] age, 58.3 [15.2] years) and 80?782 population-based participants as reference who were identified. By the time of diagnosis of RA, the prevalence of AITD was 10.3% among the patients with RA (n?=?832) vs 7.1% among the controls (5725 of 80?350) (odds ratio, 1.5; 95% CI, 1.4-1.7). This increased risk of AITD developed during the 5 years (range, 2-5 years) before diagnosis of RA (odds ratio, 1.5; 95% CI, 1.2-1.8) and peaked by the time of diagnosis of RA (range, 0-3 months before diagnosis of RA) (odds ratio, 5.3; 95% CI, 3.7-7.6). From diagnosis of RA and onward, the risk of developing AITD decreased (range, 2-5 years after diagnosis of RA) (hazard ratio, 0.7; 95% CI, 0.5-1.0).Conclusions and relevanceCompared with the general population, Swedish patients with RA appear to have a higher prevalence of thyroxine-treated AITD at diagnosis of RA and an increased incidence of AITD during the 5-year period before diagnosis of RA. After diagnosis of RA, the risk of developing AITD is suggested to decrease below the expected rate. Besides temporal changes in diagnostic intensity, this pattern of risk raises the question whether AITD may influence the pathogenesis of RA (or vice versa) and, conversely, the question whether antirheumatic therapies may prevent AITD.
| S-EPMC6324433 | biostudies-literature
Project description:BackgroundRheumatoid arthritis (RA) is a common rheumatological disease which can involve a variety of different renal manifestations. This may be explained by disease effect itself or by medications used for treatment that may lead to renal dysfunction and its complications.We aimed to identify the prevalence and factors that played a role in renal dysfunction among RA Jordanian patients.Method285 patients with RA visiting outpatient clinic between March 2016 and March 2017 were included in a retrospective study design. Age, gender, comorbidities, duration of the disease, medications and laboratory results were gathered and scoring of RA activity was done.ResultsData gathered from the 285 patients showed a female predominance with 88.4% female and 11.6% male. The average disease duration was 6.7 years. Age, DM, HTN, and serum CRP were associated with worse renal function on univariate analysis. 44 patients (18.8%) presented with microscopic hematuria, 16 (6.9%) with proteinuria and only 5 (2.1%) patients presented with both microscopic hematuria and proteinuria. Patients with eGFR <60 ml/min had longer disease duration with a mean of 11 years (±7.7) in comparison to 6.4 years (±6.1) for those with eGFR>90 ml/min (P = 0.001).ConclusionRenal dysfunction is not common in RA Jordanian population and has variable presentations. Age and the duration of illness play a major role in the progression of CKD if present. Future prospective studies evaluating renal biopsies in RA patients are needed.
| S-EPMC7649584 | biostudies-literature
Project description:Novel biomarkers of rheumatoid arthritis (RA), in addition to antibodies against cyclic citrullinated peptides, are required. Metabolome analysis is a promising approach to identify metabolite biomarkers for clinical diagnosis. We adopted a comprehensive non-targeted metabolomics approach combining capillary electrophoresis time-of-flight mass spectrometry (TOFMS) and liquid chromatography TOFMS. We constructed metabolomics profiling of 286 plasma samples of a Japanese population [92 RA patients, 13 systemic lupus erythematosus (SLE) patients and 181 healthy controls). RA case-control association tests showed that seven metabolites exhibited significantly increased levels in RA samples compared with controls (P < 1.0 × 10-4; UTP, ethanolamine phosphate, ATP, GDP, ADP, 6-aminohexanoic acid and taurine), whereas one exhibited a decreased level (xanthine). The plasma levels of these eight metabolites were not significantly different between seropositive and seronegative RA patients (P > 0.05; n = 68 and 24, respectively). The four nucleotide levels (UTP, ATP, GDP and ADP) were significantly higher in the non-treatment patients in comparison between patients with and without treatment (P < 0.014; n = 57 and 35, respectively). Furthermore, we found that none of the four nucleotide levels showed significant differences in SLE case-control association tests (P > 0.2; 13 patients with SLE and the 181 shared controls) and psoriatic arthritis (PsA) case-control association tests (P > 0.11; 42 patients with PsA and 38 healthy controls), indicating disease specificity in RA. In conclusion, our large-scale metabolome analysis demonstrated the increased plasma nucleotide levels in RA patients, which could be used as potential clinical biomarkers of RA, especially for seronegative RA.
| S-EPMC7846180 | biostudies-literature
Project description:BackgroundAutoimmune thyroid disease (AITD), which is characterized by an increased presence of thyroid autoantibodies (TAbs), such as antibodies against thyroid peroxidase (TPOAbs) and antibodies against thyroglobulin (TgAbs), has been reported to be associated with rheumatoid arthritis (RA) because AITD and RA both involve autoimmunity. However, few data are available on the incidence of TAbs in Chinese RA patients, and studies on the association between TAbs and joint damage as well as synovitis in RA patients remain sparse. Here, we aimed to evaluate the incidence of TAbs in a consecutive Chinese RA cohort and to investigate whether the elevated presence of TAbs is associated with joint damage and synovitis in RA patients.MethodsA total of 125 hospitalized RA patients were consecutively recruited. Clinical data and available synovial tissues were collected at baseline, and TAbs and thyroid function were detected by chemiluminescent immunoassay. Patients who tested positive for TPOAbs or TgAbs were classified as the TAbs-positive group, and patients who tested positive for neither TPOAbs nor TgAbs were recruited as the TAbs-negative group. Disease activity was assessed using DAS28-ESR (the disease activity score in 28 joints and including the erythrocyte sedimentation rate). X-ray assessment of the hand/wrist was performed according to the Sharp/van der Heijde-modified Sharp score (mTSS), and patients with an mTSS score >10 were defined as having radiographic joint damage (RJD). Serial tissue sections were stained immunohistochemically for CD3, CD15, CD20, CD34, CD38, and CD68, and synovitis were assessed according to Krenn's synovitis score.ResultsA total of 44 (35%) patients were positive for either TPOAbs or TgAbs. Importantly, there was a significantly greater percentage of patients with RJD in the TAbs-positive group versus the TAbs-negative group (68% vs. 42%, p = 0.005). Compared with the TAbs-negative group, significantly more CD38-positive plasma cells infiltrated the TAbs-positive synovium, and a higher percentage of patients with high-grade synovitis were observed in the TAbs-positive group (5/8, 63% vs. 5/14, 36%). Moreover, RF positivity and disease activity indicators, including TJC28, DAS28-ESR, and CDAI, were significantly higher in the TAbs-positive group (all p < 0.05). Adjusted logistic regression analysis revealed that positive TAbs (OR 2.999, 95% CI [1.301-6.913]; p = 0.010) and disease duration (OR 1.013, 95% CI [1.006-1.019]; p < 0.001) were independently associated with RJD, and an odds ratio of 2.845 (95% CI [1.062-7.622]) was found for RJD in women with positive TAbs (n = 37) compared with those without TAbs (n = 59) (p = 0.038).ConclusionOur data showed that joint destruction was amplified in RA patients with an elevated presence of TAbs, which supports the importance and necessity of TAbs and thyroid function screening and monitoring in RA patient management in clinical practice.
| S-EPMC5756613 | biostudies-literature
Project description:BackgroundRheumatoid arthritis (RA) preferentially affects women, with the peak incidence coinciding with estrogen decrease in menopause. Estrogen (E2) may therefore have intrinsic immune-regulatory properties that vanish with menopause. Fc sialylation is a crucial factor determining the inflammatory effector function of antibodies. We therefore analyzed whether E2 affects immunoglobulin G (IgG) sialylation.MethodsPostmenopausal (ovariectomized) mice were immunized with ovalbumin and treated with E2 or vehicle. Total and ovalbumin-specific IgG concentrations, sialylation, and Fcγ receptor expression were analyzed. Postmenopausal women with RA receiving hormone replacement therapy, including E2, or no treatment were analyzed for IgG sialylation. Furthermore, effects of E2 on the expression of the sialylation enzyme β-galactoside α2,6-sialyltransferase 1 (St6Gal1) were studied in mouse and human antibody-producing cells.ResultsE2 treatment significantly increased Fc sialylation of total and ovalbumin-specific IgG in postmenopausal mice. Furthermore, E2 led to increased expression of inhibitory Fcγ receptor IIb on bone marrow leukocytes. Treatment with E2 also increased St6Gal1 expression in mouse and human antibody-producing cells, providing a mechanistic explanation for the increase in IgG-Fc sialylation. In postmenopausal women with RA, treatment with E2 significantly increased the Fc sialylation of IgG.ConclusionsE2 induces anti-inflammatory effector functions in IgG by inducing St6Gal1 expression in antibody-producing cells and by increasing Fc sialylation. These observations provide a mechanistic explanation for the increased risk of RA in conditions with low estrogen levels such as menopause.
| S-EPMC5932893 | biostudies-literature
Project description:Rheumatoid arthritis (RA) is associated with cardiovascular disease (CVD), but little is known about its association with another form of vascular disorder, venous thromboembolism (VTE).A retrospective cohort study was conducted using US insurance claims. RA and non-RA patients were matched on age, sex, and index date. Incidence rates (IRs) and rate ratios (RRs) of VTE, defined as the composite of deep vein thrombosis (DVT) or pulmonary embolism (PE), were calculated. Cox proportional hazards models compared VTE risks between RA and non-RA patients, adjusting for VTE risk factors such as CVD, surgery, hospitalization, medications, and acute-phase reactants.Over the mean followup of 2 years, the IR for VTE among RA patients was 6.1 per 1,000 person-years, 2.4 times higher (95% confidence interval [95% CI] 2.1-2.8) than the rate of non-RA patients. The IRs for both DVT (RR 2.2, 95% CI 1.9-2.6) and PE (RR 2.7, 95% CI 2.2-3.5) were higher in RA patients compared with non-RA patients. After adjusting for risk factors of VTE, the VTE risk remained elevated in RA patients (hazard ratio 1.4, 95% CI 1.1-1.7) compared to non-RA patients. The result was similar after further adjustment for elevated acute-phase reactants (hazard ratio 1.5, 95% CI 0.3-6.5). One-third of patients who developed VTE had at least 1 major VTE risk factor 90 days before and after the VTE event.Our results showed an increased risk of developing VTE for RA patients compared with non-RA patients. The risk was attenuated but remained elevated even after adjusting for various risk factors for VTE.
| S-EPMC4090802 | biostudies-literature