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ID PMID Title PublicationDate abstract
29569382 Case of lamotrigine-induced drug adverse reaction under tocilizumab treatment with clinica 2018 Jun The pathological mechanisms and immunological kinetics of drug-induced hypersensitivity syndrome (DIHS), including the relevance of interleukin (IL)-6, remain unclear. We report a case of drug adverse reaction that does not fulfill the diagnostic criteria of DIHS but mimics its characteristic features. Because the patient was under anti-IL-6 therapy at the onset, some symptoms typically seen in DIHS were absent, such as fever and leukocyte count abnormalities. However, the characteristic features of DIHS were clearly observed in the subsequent course, including the repeated recurrence of skin rash, prolonged liver dysfunction and reactivation of herpes viruses. This case suggested that IL-6 role at the onset is not a main factor to determine the subsequent pathomechanism of DIHS and attention should be paid to the preceding therapy for achieving accurate diagnosis.
30009417 Therapeutic Effects of a TANK-Binding Kinase 1 Inhibitor in Germinal Center-Driven Collage 2019 Jan OBJECTIVE: The production of class-switched high-affinity autoantibodies derived from organized germinal centers (GCs) is a hallmark of many autoimmune inflammatory diseases, including rheumatoid arthritis (RA). TANK-binding kinase 1 (TBK-1) is a serine/threonine kinase involved in the maturation of GC follicular helper T (Tfh) cells downstream of inducible costimulator signaling. We undertook this study to assess the therapeutic potential of TBK-1 inhibition using the small-molecule inhibitor WEHI-112 in antibody-dependent models of inflammatory arthritis. METHODS: Using the models of collagen-induced arthritis (CIA), antigen-induced arthritis (AIA), and K/BxN serum-transfer-induced arthritis (STIA), we determined the effectiveness of WEHI-112 at inhibiting clinical and histologic features of arthritis in C57BL/6 and DBA/1 mice. We used immunohistochemistry to characterize GC populations during CIA development, and we used enzyme-linked immunosorbent assays to determine levels of Ig autoantibodies in WEHI-112-treated mice compared to vehicle-treated mice. RESULTS: WEHI-112, a tool compound that is semiselective for TBK-1 but that also has activity against IKKε and JAK2, abolished TBK-1-dependent activation of interferon (IFN) regulatory factor 3 and inhibited type I IFN responses in vitro. In vivo, treatment with WEHI-112 selectively abrogated clinical and histologic features of established, antibody-dependent CIA, but had minimal effects on an antibody-independent model of AIA or on K/BxN STIA. In keeping with these findings, WEHI-112 reduced arthritogenic type II collagen-specific IgG1 and IgG2b antibody production. Furthermore, WEHI-112 altered the GC Tfh cell phenotype and GC B cell function in CIA. CONCLUSION: We report that TBK-1 inhibition using WEHI-112 abrogated antibody-dependent CIA. As WEHI-112 failed to inhibit non-antibody-driven joint inflammation, we conclude that the major effect of this compound was most likely the targeting of TBK-1-mediated mechanisms in the GC reaction. This approach may have therapeutic potential in RA and in other GC-associated autoantibody-driven inflammatory diseases.
30209188 Bmi1 Regulates IκBα Degradation via Association with the SCF Complex. 2018 Oct 15 Bmi1 is a polycomb group protein and regulator that stabilizes the ubiquitination complex PRC1 in the nucleus with no evidently direct link to the NF-κB pathway. In this study, we report a novel function of Bmi1: its regulation of IκBα ubiquitination in the cytoplasm. A deficiency of Bmi1 inhibited NF-κB-mediated gene expression in vitro and a NF-κB-mediated mouse model of arthritis in vivo. Mechanistic analysis showed that Bmi1 associated with the SCF ubiquitination complex via its N terminus and with phosphorylation by an IKKα/β-dependent pathway, leading to the ubiquitination of IκBα. These effects on NF-κB-related inflammation suggest Bmi1 in the SCF complex is a potential therapeutic target for various diseases and disorders, including autoimmune diseases.
30208508 Immunoglobulin A anti-phospholipid antibodies in Swedish cases of systemic lupus erythemat 2018 Oct Immunoglobulin (Ig) G- and IgM-class anti-cardiolipin antibodies (aCL) and lupus anti-coagulant (LA) are included in the 1997 update of the American College of Rheumatology (ACR-97) systemic lupus erythematosus (SLE) criteria. Despite limited evidence, IgA-aCL and IgA anti-β(2) -glycoprotein-I (anti-β(2) GPI) were included in the 2012 Systemic Lupus International Collaborating Clinics criteria. The present study aimed to evaluate IgG-/IgA-/IgM-aCL and anti-β(2) GPI occurrence in relation to disease phenotype, smoking habits, pharmacotherapy, anti-phospholipid syndrome (APS) and organ damage among 526 Swedish SLE patients meeting ACR-97. Patients with rheumatoid arthritis (n = 100), primary Sjögren's syndrome (n = 50) and blood donors (n = 507) served as controls. Anti-phospholipid antibodies (aPL) were analysed by fluoroenzyme-immunoassays detecting aCL/anti-β(2) GPI. Seventy-six (14%) SLE cases fulfilled the Sydney APS-criteria, and ≥ 1 aCL/anti-β(2) GPI isotype (IgG/IgA/IgM) occurred in 138 SLE patients (26%). Forty-five (9%) of the SLE cases had IgA-aCL, 20 of whom (4%) lacked IgG-/IgM-aCL. Seventy-four (14%) tested positive for IgA anti-β(2) GPI, 34 (6%) being seronegative regarding IgG/IgM anti-β(2) GPI. Six (1%) had APS manifestations but were seropositive regarding IgA-aCL and/or IgA anti-β(2) GPI in the absence of IgG/IgM-aPL and LA. Positive LA and IgG-aPL tests were associated with most APS-related events and organ damage. Exclusive IgA anti-β(2) GPI occurrence associated inversely with Caucasian ethnicity [odds ratio (OR) = 0·21, 95% confidence interval (CI) = 0·06-0·72) and photosensitivity (OR = 0·19, 95% CI = 0·05-0·72). Nephritis, smoking, LA-positivity and statin/corticosteroid-medication associated strongly with organ damage, whereas hydroxychloroquine-medication was protective. In conclusion, IgA-aPL is not rare in SLE (16%) and IgA-aPL analysis may have additional value among SLE cases with suspected APS testing negative for other isotypes of aPL and LA.
29518577 Reversibility of peripheral blood leukocyte phenotypic and functional changes after exposu 2018 Jun This study evaluated the short-term effects of tofacitinib treatment on peripheral blood leukocyte phenotype and function, and the reversibility of any such effects following treatment withdrawal in healthy volunteers. Cytomegalovirus (CMV)-seropositive subjects received oral tofacitinib 10 mg twice daily for 4 weeks and were followed for 4 weeks after drug withdrawal. There were slight increases in total lymphocyte and total T-cell counts during tofacitinib treatment, and B-cell counts increased by up to 26%. There were no significant changes in granulocyte or monocyte counts, or granulocyte function. Naïve and central memory T-cell counts increased during treatment, while all subsets of activated T cells were decreased by up to 69%. T-cell subsets other than effector memory cluster of differentiation (CD)4+, activated naïve CD4+ and effector CD8+ T-cell counts and B-cell counts, normalized 4 weeks after withdrawal. Following ex vivo activation, measures of CMV-specific T-cell responses, and antigen non-specific T-cell-mediated cytotoxicity and interferon (IFN)-γ production, decreased slightly. These T-cell functional changes were most pronounced at Day 15, partially normalized while still on tofacitinib and returned to baseline after drug withdrawal. Total natural killer (NK)-cell counts decreased by 33%, returning towards baseline after drug withdrawal. NK-cell function decreased during tofacitinib treatment, but without a consistent time course across measured parameters. However, markers of NK-cell-mediated cytotoxicity, antibody-dependent cellular cytotoxicity and IFN-γ production were decreased up to 42% 1 month after drug withdrawal. CMV DNA was not detectable in whole blood, and there were no cases of herpes zoster reactivation. No new safety concerns arose. In conclusion, the effect of short-term tofacitinib treatment on leukocyte composition and function in healthy CMV+ volunteers is modest and largely reversible 4 weeks after withdrawal.
28663326 Clinical associations of the positive anti Ro52 without Ro60 autoantibodies: undifferentia 2018 Jan AIMS: Autoantibodies targeting Ro52 and Ro60 antigens are historically reported as anti SSA/Ro. In general anti SSA/Ro results are either anti Ro52+Ro60+ or anti Ro52-Ro60+ antibodies. Anti Ro52 without anti Ro60 (Ro52+ Ro60-) antibodies are often not reported routinely. This study intends to review the potential significance of these autoantibodies in the management of connective tissue diseases. METHOD: A retrospective survey of Ro52+Ro60- was carried out as part of the service evaluation of extractable nuclear antigen antibodies (ENA) reporting from the immunology laboratory, the NHS Greater Glasgow and Clyde (GGC), UK. The clinical documents and laboratory results of 97 patients with Ro52+Ro60- and 100 patients with Ro52+Ro60+ were reviewed. RESULTS: Seventy-one patients (73%) with anti Ro52+Ro60- antibodies have been diagnosed with autoimmune conditions including undifferentiated connective tissue diseases (n=14, 14%), systemic lupus erythematosus (n=10, 10%), Sjögren's syndrome (n=10, 10%) and rheumatoid arthritis (n=13, 13%). Twenty-three patients (24%) with anti Ro52+Ro60- antibodies have no autoimmune features but were found to have significant clinical conditions including malignancies. In contrast, 87 patients (87%) with anti Ro52+Ro60+ antibodies have autoimmune conditions including Sjögren's syndrome (n=34, 34%), systemic lupus erythematosus (SLE; n=23, 23%), undifferentiated connective tissue diseases (n=12, 12%) and rheumatoid arthritis (n=6, 6%). CONCLUSION: Anti Ro52 without anti Ro60 (Ro52+Ro60-) antibodies should be reported. In the majority of patients these autoantibodies were associated with various autoimmune diseases. Anti Ro52+Ro60- antibodies were also found in patients with significant clinical conditions including malignancies even though there was no suggestion of autoimmunity at the time of testing.
30178172 Association between primary Sjogren's syndrome, arterial stiffness, and subclinical athero 2019 Feb In rheumatoid arthritis and systemic lupus erythematosus, cardiovascular disease is frequently one of the leading causes of mortality or morbidity. Studies have shown that acute systemic inflammation and chronic systemic vasculitis are associated with endothelial dysfunction and atherosclerotic plaque formation, subsequently leading to cardiovascular disease. This meta-analysis aimed to explore the association of subclinical atherosclerosis and arterial stiffness in primary Sjogren's syndrome. A comprehensive search of the MEDLINE and Embase databases was performed from date of inception through August 2017. The inclusion criterion was observational studies evaluating the association between primary Sjogren's syndrome, subclinical atherosclerosis, and arterial stiffness by measuring pulse wave velocity (PWV) and intima-media thickness (IMT). Definitions of PSS and methods to assess PWV and IMT were recorded for each study. Different locations of IMT were evaluated including common carotid, internal carotid, and femoral arteries. The pooled mean difference (MD) of PWV and IMT and 95% confidence interval (CI) were calculated using a random-effect meta-analysis. The between-study heterogeneity of effect size was quantified using the Q statistic and I(2). Data were extracted from eight observational studies involving 767 subjects. Pooled result demonstrated a significant increase in PWV in patients who have PSS compared with controls (MD = 1.30 m/s; 95% CI 0.48-2.12; p value = 0.002; I(2) = 85%). Patients with PSS also have higher IMT (MD = 0.08 mm; 95% CI 0.04-0.11; p value < 0.01; I(2) = 72%). Our study suggests that PSS is associated with arterial stiffness and subclinical atherosclerosis. Further studies need to be conducted to find the correlation of subclinical atherosclerosis in PSS with the cardiovascular event, the pathophysiological changes of arterial stiffness in PSS, and the benefit of statins, because controlling cardiovascular risk factors or disease activity could potentially help avoid progression of atherosclerosis to overt cardiovascular disease.
29174881 Reprint of "Anti-therapeutic antibodies and their clinical impact in patients treated with 2018 Jan Patients treated with the TNF antagonist adalimumab develop anti-therapeutic antibodies (ATA), the prevalence of which varies depending on the assay used. Most assays are compromised due to the presence of adalimumab in the clinical samples. Our objective was to develop an antibody assay, applicable for clinical testing, which overcomes the limitation of therapeutic interference and to further determine the relationship between ATA development, adalimumab levels and disease activity in patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA) or ankylosing spondylitis (AS). Use of an electrochemiluminescence platform permitted development of fit-for-purpose immunoassays. Serum samples from patients, taken prior to and at 12 and 24 weeks of treatment, were retrospectively analysed for levels of adalimumab and ATA. Overall, the antibody prevalence was 43.6% at 12 weeks and 41% at 24 weeks of treatment. Disruption of immune complexes by acid dissociation, a strategy often adopted for this purpose, only marginally increased the antibody prevalence to 48.7% and 46% at 12 and 24 weeks respectively. We found that antibody formation was associated with decreasing levels of circulating adalimumab, but no direct effect on disease activity was evident as assessed using DAS28 for RA patients and BASDAI for PsA and AS patients. However, a negative correlation of free adalimumab trough levels with disease activity scores was observed. Data showed that adalimumab levels can serve as an indicator of ATA development which can then be confirmed by ATA testing. Monitoring of both therapeutic and antibodies should be considered during adalimumab therapy to allow clinicians to personalise treatments for maximal therapeutic outcomes.
29541870 A Minimal Physiologically Based Pharmacokinetic Model with a Nested Endosome Compartment f 2018 Mar 14 We proposed here a minimal physiologically based pharmacokinetic (mPBPK) model for a group of novel engineered antibodies in mice and humans. These antibodies are designed with altered binding properties of their Fc domain with neonatal Fc receptor (FcRn) or the Fab domain with their cognate targets (recycling antibodies) in acidic endosomes. To enable simulations of such binding features in the change of antibody pharmacokinetics and its target suppression, we nested an endothelial endosome compartment in parallel with plasma compartment based on our previously established mPBPK model. The fluid-phase pinocytosis rate from plasma to endothelial endosomes was reflected by the clearance of antibodies in FcRn dysfunctional humans or FcRn-knockout mice. The endosomal recycling rate of FcRn-bound antibodies was calculated based on the reported endosomal transit time. The nonspecific catabolism in endosomes was fitted using pharmacokinetic data of a human wild-type IgG(1) adalimumab in humans and B21M in human FcRn (hFcRn) transgenic mice. The developed model adequately predicted the pharmacokinetics of infliximab, motavizumab, and an Fc variant of motavizumab in humans and the pharmacokinetics of bevacizumab, an Fc variant of bevacizumab, and a recycling antibody PH-IgG(1) and its non-pH dependent counterpart NPH-IgG(1) in hFcRn transgenic mice. Our proposed model provides a platform for evaluation of the pharmacokinetics and disposition behaviors of Fc-engineered antibodies and recycling antibodies.
30111894 PLD3 and PLD4 are single-stranded acid exonucleases that regulate endosomal nucleic-acid s 2018 Sep The sensing of microbial genetic material by leukocytes often elicits beneficial pro-inflammatory cytokines, but dysregulated responses can cause severe pathogenesis. Genome-wide association studies have linked the gene encoding phospholipase D3 (PLD3) to Alzheimer's disease and have linked PLD4 to rheumatoid arthritis and systemic sclerosis. PLD3 and PLD4 are endolysosomal proteins whose functions are obscure. Here, PLD4-deficient mice were found to have an inflammatory disease, marked by elevated levels of interferon-γ (IFN-γ) and splenomegaly. These phenotypes were traced to altered responsiveness of PLD4-deficient dendritic cells to ligands of the single-stranded DNA sensor TLR9. Macrophages from PLD3-deficient mice also had exaggerated TLR9 responses. Although PLD4 and PLD3 were presumed to be phospholipases, we found that they are 5' exonucleases, probably identical to spleen phosphodiesterase, that break down TLR9 ligands. Mice deficient in both PLD3 and PLD4 developed lethal liver inflammation in early life, which indicates that both enzymes are needed to regulate inflammatory cytokine responses via the degradation of nucleic acids.
30001173 Treponema denticola enolase contributes to the production of antibodies against ENO1 but n 2018 Autoantibodies against alpha-enolase (ENO1) are often detected in various infectious and autoimmune diseases. Anti-ENO1 antibody titers were reported to be associated with the severity of periodontitis in patients with rheumatoid arthritis. Because the enolase of the periodontal pathogen Treponema denticola (TdEno) has the highest homology with ENO1 among the enolases of human-associated bacteria, we hypothesized that anti-ENO1 autoantibodies produced during the immune response to TdEno may contribute to the progression of periodontitis and tested it in human and mouse systems. In human subjects with healthy periodontium or chronic periodontitis, a strong positive correlation between the levels of anti-TdEno and anti-ENO1 antibodies was observed. In addition, the purified anti-TdEno antibodies recognized ENO1 as well as TdEno in a dot blot, confirming the cross-reactivity between TdEno and ENO1. However, anti-ENO1 antibody titers were not associated with the severity of periodontitis. To further investigate the role of TdEno in the production of anti-ENO1 antibodies and the progression of periodontitis, mice received an oral gavage of P. gingivalis alone, subcutaneous immunization with TdEno alone, or both P. gingivalis oral gavage and TdEno immunization. Immunization with TdEno induced not only anti-TdEno but also anti-mouse Eno1 (mEno1) antibodies and increased the expression of TNFα in the gingival tissues. However, alveolar bone loss was not increased by TdEno immunization. In conclusion, autoreactive anti-ENO1/mEno1 antibodies that are produced as byproducts during the antibody response to TdEno play a minimal role in the progression of periodontitis in the absence of rheumatoid arthritis.
30102507 2018 Jul 11 This guideline covers diagnosing and managing rheumatoid arthritis. It aims to improve quality of life by ensuring that people with rheumatoid arthritis have the right treatment to slow the progression of their condition and control their symptoms. People should also have rapid access to specialist care if their condition suddenly worsens. NICE has also produced technology appraisal guidance on drug treatment for rheumatoid arthritis. WHO IS IT FOR? Healthcare professionals. Commissioners and providers. People with rheumatoid arthritis and their families and carers.
29697211 Molecular Profiling and Clonal Tracking of Secreted Rheumatoid Factors in Primary Sjögren 2018 Oct OBJECTIVE: Rheumatoid factors (RFs) are associated with systemic disease in primary Sjögren's syndrome (SS) and may be pathogenic as mixed cryoglobulins. Current detection methods cannot resolve RFs at a molecular level. This study was undertaken to perform the first proteomic and transcriptomic analysis of secreted and membrane-bound IgM-RF in primary SS and identify unique heavy-chain peptide signatures for RF clonotype tracking. METHODS: Purified heavy chains of serum RFs from 15 patients with primary SS were subjected to de novo mass spectrometric sequencing. The circulating B cell Ig repertoire was determined by massively parallel sequencing of IGH RNA from matched peripheral blood mononuclear cells (n = 7). RF-specific heavy-chain third complementarity-determining region (CDR3) peptides were identified by searching RF heavy-chain peptide sequences against the corresponding IGH RNA sequence libraries. Heavy-chain CDR3 peptides were used as biomarkers to track serum RF clonotypes using quantitative multiple reaction monitoring. RESULTS: Serum RFs were clonally restricted and composed of shared sets of IgM heavy-chain variable region (Ig V(H) ) 1-69, 3-15, 3-7, and 3-74 subfamilies. Cryoprecipitable RFs from patients with mixed cryoglobulinemia (MC) were distinguishable from nonprecipitating RFs by a higher frequency of amino acid substitutions and identification of stereotypic heavy-chain CDR3 transcripts. Potentially pathogenic RF clonotypes were detected in serum by multiple reaction monitoring years before patients presented with MC. Levels of Ig V(H) 4-34 IgM-RF decreased following immunosuppression and remission of MC. CONCLUSION: Cryoprecipitable RF clonotypes linked to vasculitis in primary SS have different molecular profiles than nonprecipitating RFs, suggesting different underlying mechanisms of production. The combined omics workflow presented herein provides molecular biomarkers for tracking and removal of pathogenic RF clones.
30899307 Lack of association of -863C/A (rs1800630) polymorphism of tumor necrosis factor-a gene wi 2019 Mar INTRODUCTION: Multifunctional pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) has been implicated in a variety of inflammatory diseases including rheumatoid arthritis (RA). TNF-α polymorphisms are mostly located in its promoter region and play a significant role in disease susceptibility and severity. We therefore sought to investigate TNFA -863C/A (rs1800630) polymorphism association with RA activity in our Pakistani study group. MATERIAL AND METHODS: A total of 268 human subjects were enrolled. Among them, 134 were RA patients and 134 were controls. In this study the physical parameters of RA patients were collected, and the disease activity was measured by DAS28. The genotypes were determined following the allele-specific PCR along with the pre-requisite internal amplification controls. Subsequently, data were analyzed statistically for any significant association including χ(2)/Fisher's exact test using GraphPad prism 6 software. RESULTS: We found that the TNF-α -863 C/A (rs1800630) variant was not differentially segregated between cases and controls in either genotype frequency, with χ(2) of 2.771 and a p-value of 0.2502, or allele frequency, with χ(2) of 2.741 and a p-value of 0.0978, with an odds ratio (95% CI) of 0.7490 (0.5317-1.055). CONCLUSIONS: The lack of positive association of TNF-α -863(rs1800630) polymorphism in our study group implies that TNF-α -863 polymorphism is not a susceptible marker to RA and cannot serve as a genetic factor for screening RA patients in Pakistan. There might be other factors that may influence disease susceptibility. However, further investigations on additional larger and multi-regional population samples are required to determine the consequences of genetic variations for disease prognosis.
35129926 2018 Jul Most people with rheumatoid arthritis (RA) have definite synovitis on clinical assessment, but there is sometimes uncertainty about the diagnosis when there is no definite synovitis. This can lead to a delay in starting treatment, which could affect prognosis. Use of ultrasound with clinical assessment may be more effective than clinical assessment alone at identifying synovitis and thereby diagnosing rheumatoid arthritis. Ultrasound may also allow healthcare professionals to be more confident about ruling out a diagnosis of rheumatoid arthritis.
30186495 Complement 3 glomerulonephritis in rheumatoid arthritis: A case report and follow-up. 2018 Sep Glomerulonephritis (GN) caused by rheumatoid arthritis may manifest as various pathological types; however, to the best of our knowledge, rheumatoid arthritis-associated complement 3 (C3)-GN has not been reported by any previous studies. C3GN is caused by dysregulation of the alternative pathway of complements, which is completely different from activation of the classic pathway of a typical autoimmune disease to cause renal damage. The present study describes a patient with a history of rheumatoid arthritis for 18 years, who presented with edema, proteinuria, hematuria, hypoproteinemia and a hypocomplementemic state. The pathological diagnosis was C3GN based on histological examination of a renal biopsy specimen. Hormone treatment on its own appeared to be effective and achieved complete clinical remission, while the follow-up of the condition remained stable.
30258513 Sonography of active rheumatoid arthritis during pregnancy: a case report and literature r 2018 Dec Disease activity in rheumatoid arthritis usually subsides in pregnancy, however a subset of patients have worsened symptoms with joint pain and swelling. Monitoring and mitigating disease activity in pregnancy is important for preventing deforming structural changes which can affect the ability of the patient to care for themselves and the newborn. Ultrasound is a safe and low-cost imaging modality for detecting active changes from an inflammatory arthritis, which can help guide management. We describe a case of an acute disease flare during pregnancy, readily detected with ultrasound, and present a review of sonographic evaluation of rheumatoid arthritis in pregnancy.
31213751 Evaluation of the electromyographic activity of masseter and temporalis muscles of women w 2018 Jan AIM: This study aimed to evaluate the electromyographic activity of the masseter and temporalis muscles of women with rheumatoid arthritis. METHODS: The sample comprised 28 women divided into two groups: 14 with rheumatoid arthritis [mean age: 52.2 ± standard deviation (SD): 3 years] and 14 without rheumatoid arthritis (mean age: 49.4 ± SD: 2.4 years). The women were paired by age and body mass index. The electromyographic activity of the masseter and temporalis muscles was analyzed in mandibular tasks: rest, right and left laterality, protrusion, maximal voluntary contraction with and without Parafilm M(®), habitual and non-habitual chewing. The MANOVA (multivariate analysis of variance) was used to compare the means of the two independent groups, considering as independent variable side and diagnosis of rheumatoid arthritis, and age as the covariate. The Bonferroni correction was used for the post hoc comparisons (p <0.05). RESULTS: Rheumatoid arthritis group presented an increase in the normalized electromyographic activity of the masticatory muscles and lower mean values for the habitual and non-habitual chewing. CONCLUSIONS: Women with rheumatoid arthritis showed functional alterations in the stomatognathic system, demonstrated through muscular hyperactivity and reduction of masticatory efficiency. HIPPOKRATIA 2018, 22(1): 3-9.
31061580 Rheumatoid subacromial-subdeltoid bursitis with rice bodies: A case report. 2019 May Subacromial-subdeltoid bursitis of a shoulder with rice bodies is relatively uncommon. The understanding of the pathogenesis of rice body formation is yet approximate only but some clinical conditions like rheumatoid arthritis, tuberculous arthritis, seronegative inflammatory arthritis, juvenile rheumatoid arthritis and osteoarthritis are related to it. We describe a case of a 44 years old female with subacromial-subdeltoid bursitis of her right shoulder with numerous rice bodies' formation as a presenting feature of rheumatoid arthritis. She underwent subacromial and subdeltoid bursectomy with the removal of rice bodies and had immediate improvement of symptoms.
30756056 Seronegative Bilateral Symmetrical Inflammatory Polyarthritis: Think Twice Before Starting 2018 The most common cause of bilateral symmetrical polyarthritis in the small joints is rheumatoid arthritis. However, if seronegative arthritis is involved, it could be the case that other underlying causes need to be diagnosed. This is particularly important for those coming from or living in developing countries where infectious causes should always be considered. The case of a young Nepali woman is presented in this article. She was referred as a case of seronegative rheumatoid arthritis for DMARDs therapy but this was not the case due to her origin from Nepal and seronegativity for RF, Anti-ccp, and ANA as well as faint macular skin lesions over her face and upper extremities, which the patients are not aware of. Consequently, skin biopsy was carried out which subsequently confirmed that the infectious cause of her polyarthritis was leprosy. LEARNING POINTS: Bilateral symmetrical seronegative inflammatory arthritis of rheumatoid type is very common.However, when both RF and anti-ccp are negative, other possible secondary causes including infection should be considered, especially in patients from areas where disease is endemic.In this case lepromatous leprosy was the cause of the patient's presumed rheumatoid arthritis and all her arthritis resolved after her leprosy had been treated.