Search for: rheumatoid arthritis    methotrexate    autoimmune disease    biomarker    gene expression    GWAS    HLA genes    non-HLA genes   

ID PMID Title PublicationDate abstract
27846765 Adult-onset Still's disease-like manifestation accompanied by the cancer recurrence after 2019 Jul A 72-year-old woman presented 9 months ago with skin rash on her bilateral forearms, which was followed by intermittent high fever, and stiffness and swelling of her bilateral fingers. She was diagnosed with seronegative rheumatoid arthritis (RA). She had a past history of breast cancer and had undergone breast preservation surgery 13 years previously. During admission in our hospital, she developed high fever and leukocytosis with a relapsing skin rash, sore throat, polyarthralgia and increased levels of serum ALT/AST and ferritin, all of which fulfilled Yamaguchi's criteria for adult-onset Still's disease (AOSD). While we tried to exclude other diseases that may show AOSD-like manifestations, pancytopenia rapidly developed and bone marrow biopsy strongly suggested the diagnosis of macrophage activating syndrome (MAS). Accordingly, steroid pulse therapy was begun, followed by oral glucocorticoid therapy. Thereafter, all of her symptoms improved, but systemic rash, inflammatory signs and pancytopenia gradually progressed. The results of bone marrow pathology, which returned 2 weeks after the beginning of treatment, revealed hemophagocytosis with CK7-positive/CK20-negative atypical cells that suggested recurrence of breast cancer in the bone marrow, thus all of her AOSD-like symptoms were considered to be paraneoplastic manifestations of late-onset metastatic breast cancer. She was treated successfully with chemotherapy. When we see the patients showing AOSD-like symptoms with a history of malignancy, we should consider the possibility of paraneoplastic syndrome due to cancer recurrence.
31130368 NF-κB-driven miR-34a impairs Treg/Th17 balance via targeting Foxp3. 2019 Aug The subset of regulatory T (Treg) cells, with its specific transcription Foxp3, is a unique cell type for the maintenance of immune homeostasis by controlling effector T (Teff) cell responses. Although it is common that a defect in Treg cells with Treg/Teff disorder causes autoimmune diseases; however, the precise mechanisms are not thoroughly revealed. Here, we report that miR-34a could attenuate human and murine Foxp3 gene expression via targeting their 3' untranslated regions (3' UTR). The human miR-34a, increased in peripheral blood mononuclear cells (PBMCs) and CD4(+) T cells from rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) patients, displayed a positive correlation with some serum markers of inflammation including rheumatoid factor (RF), anti-streptolysin antibody (ASO), erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) as well as Th17 signature gene RORγt, but inversely correlated with the mRNA expression levels of FOXP3. In addition, murine miR-34a levels were downregulated in TGF-β-induced Treg cells but upregulated in Th17 cells induced in vitro compared to activated CD4(+) T cells. It has also been demonstrated that elevated miR-34a disrupting Treg/Th17 balance in vivo contributed to the progress of pathogenesis of collagen induced arthritis (CIA) mice. Furthermore, IL-6 and TNF-α were responsible for the upregulation of miR-34a and downregulation of Foxp3, which was reverted by the addition of NF-κB/p65 inhibitor BAY11-7082, thus indicating that NF-κB/p65 inhibited Foxp3 expression in an miR-34a-dependent manner. Finally, IL-6 or TNF-α-activated p65 could bind to the miR-34a promotor and enhance its activity, resulting in upregulation of its transcription. Taken together, we show that NF-κB activated by inflammatory cytokines, such as IL-6 and TNF-α, ameliorates Foxp3 levels via regulating miR-34a expression, which provides a new mechanistic and therapeutic insight into the ongoing of autoimmune diseases.
31126347 Peripheral and central nervous system involvement in a patient with primary Sjögren's syn 2019 May 25 BACKGROUND: Primary Sjögren's syndrome is the second most common rheumatological disorder after rheumatoid arthritis. It typically presents as xerophthalmia and xerostomia in postmenopausal women. Involvement of the central nervous system has been recognized, although its pathogenesis and characteristics are poorly understood. Central nervous system complications are a diagnostic challenge and emphasize the need for systematic screening of patients with new peripheral and central neurological symptoms. CASE REPORT: We report a case of a 58-year-old Swiss woman presenting with rapidly progressive sensorimotor distal polyneuropathy together with new-onset generalized seizures. Initial magnetic resonance imaging (MRI) of the brain performed after the first seizure showed multiple, bihemispheric, confluent white matter hyperintensities with contrast enhancement. Follow-up imaging 3 days after the initial magnetic resonance imaging demonstrated a fulminant disease progression associated with the serious clinical deterioration of the patient. In light of the results of a minor salivary gland biopsy, autoantibody testing, nerve conduction studies, and cranial magnetic resonance imaging, primary Sjögren's syndrome with cryoglobulinemia type II was diagnosed. Response to plasmapheresis and subsequent administration of cyclophosphamide was favorable. CONCLUSION: Even though exocrinopathy is the hallmark of Sjögren's syndrome, systemic symptoms are observed in one-third of patients. There is an urgent need to better characterize the mechanisms underlying different disease phenotypes and to perform randomized controlled trials in order to provide tailored and evidence-based treatment for primary Sjögren's syndrome.
31823505 Serum levels of interleukin-34 and clinical correlation in patients with primary Sjögren' 2020 Mar OBJECTIVES: To measure the levels of serum interleukin (IL)-34 in patients with primary Sjögren's syndrome (pSS) and evaluate the cytokine's clinical association with the disease. METHODS: Serum samples were obtained from 66 pSS patients and 32 healthy controls (HCs) and measured by enzyme-linked immunosorbent assay for IL-34 levels. The clinical parameters, including autoantibodies, immunoglobulins (Igs), complements (Cs), inflammatory indicators, involvement of the blood system, lung and arthritis, were collected simultaneously. Two-sample t test was applied for comparison between 2 groups, and Pearson's correlation coefficient was used to assess the associations between IL-34 levels and laboratory parameters. RESULTS: Serum IL-34 levels were significantly elevated in pSS patients compared with HCs. Patients with anti-Ro/SSA antibody positivity showed higher serum IL-34 levels than those who were negative, as did the anti-La/SSB antibody-positive patients. Serum IL-34 levels were positively associated with the levels of rheumatoid factor, IgG and gamma-globulin, but not associated with IgA, IgM, C3, C4, erythrocyte sedimentation rate or C-reactive protein. For the pSS subgroups with and without leucopenia, thrombocytopenia, anemia or interstitial lung disease (ILD), there was no significant difference in serum IL-34 levels. Interestingly, the pSS patients with arthritis had higher levels of IL-34 compared with the no-arthritis patients. CONCLUSIONS: IL-34 may be involved in B cell activation and production of antibodies in pSS.
31241661 The evaluation of the Myxovirus Resistance 1 protein in serum and saliva to monitor diseas 2019 OBJECTIVE: Primary Sjögren's syndrome (pSjS) is a chronic autoimmune disease that causes dry eye and mouth. No laboratory parameters to monitor the activation of this disease have been identified. Therefore, any possible relationships between salivary and blood myxovirus resistance 1 (MX1) and pSjS must be prospectively studied. METHODS: Thirty female patients with pSjS, 30 women with rheumatoid arthritis (RA) without secondary Sjögren's syndrome (SjS) and 28 healthy control women were enrolled in this investigation. Analyses of MX1 by the enzyme-linked immunosorbent assay (ELISA) method, SS-A (Ro) and SS-B (La) tests by the strip immunoblot method, anti-nuclear antibody (ANA) tests by immunofluorescence and the measurement of serum rheumatoid factor (RF), C3, C4, immunoglobulin A (IgA), immunoglobulin M (IgM), and immunoglobulin G (IgG) were performed. RESULTS: The serum level of MX1 in patients without Raynaud phenomenon was higher than in those with Raynaud phenomenon (p:0.029, p<0.05, statistically significant). There was a statistically significant positive association between hemoglobin levels and MX1 serum levels. No statistically significant association was found among the other parameters. Low MX1 levels were shown to be associated with both a low disease activity score based on the European League Against Rheumatism (EULAR) Sjögren's Syndrome Disease Activity Index (ESSDAI) and hydroxychloroquine use in all patients. CONCLUSION: MX1 levels have a considerable impact on the assessment of the disease activity in SjS. We believe that more-comprehensive studies should be performed on patients with pSjS who do not use hydroxychloroquine to prove this relationship and that MX1 levels should be used as a routine marker for the assessment of pSjS disease activity. Further studies are needed to create awareness of the role that MX1 has in the diagnosis of pSjS, which may help to uncover novel pathways for new therapeutic modalities.
30990796 Transcription factor Fra-1 targets arginase-1 to enhance macrophage-mediated inflammation 2019 Apr 16 The polarization of macrophages is regulated by transcription factors such as nuclear factor kappa B (NF-κB) and activator protein 1 (AP-1). In this manuscript, we delineated the role of the transcription factor Fos-related antigen 1 (Fra-1) during macrophage activation and development of arthritis. Network level interaction analysis of microarray data derived from Fra-1- or Fra-2-deficient macrophages revealed a central role of Fra-1, but not of Fra-2 in orchestrating the expression of genes related to wound response, toll-like receptor activation and interleukin signaling. Chromatin-immunoprecipitation (ChIP)-sequencing and standard ChIP analyses of macrophages identified arginase 1 (Arg1) as a target of Fra-1. Luciferase reporter assays revealed that Fra-1 down-regulated Arg1 expression by direct binding to the promoter region. Using macrophage-specific Fra-1- or Fra-2- deficient mice, we observed an enhanced expression and activity of Arg1 and a reduction of arthritis in the absence of Fra-1, but not of Fra-2. This phenotype was reversed by treatment with the arginase inhibitor Nω-hydroxy-nor-L-arginine, while ʟ-arginine supplementation increased arginase activity and alleviated arthritis, supporting the notion that reduced arthritis in macrophage-specific Fra-1-deficient mice resulted from enhanced Arg1 expression and activity. Moreover, patients with active RA showed increased Fra-1 expression in the peripheral blood and elevated Fra-1 protein in synovial macrophages compared to RA patients in remission. In addition, the Fra-1/ARG1 ratio in synovial macrophages was related to RA disease activity. In conclusion, these data suggest that Fra-1 orchestrates the inflammatory state of macrophages by inhibition of Arg1 expression and thereby impedes the resolution of inflammation.
30936024 Incidence of Immune-Mediated Inflammatory Diseases Among Patients With Inflammatory Bowel 2019 Dec BACKGROUND & AIMS: It is not clear whether the co-occurrence of immune-mediated inflammatory diseases (IMIDs) affects the course of inflammatory bowel diseases (IBD). We investigated the occurrence of IMIDs in relation to onset of IBD and the effects of concurrent IMIDs on IBD outcomes in a nationwide study of the Danish population. METHODS: We used a nationwide cohort of all individuals diagnosed with IBD, including Crohn's disease (CD) or ulcerative colitis (UC), in Denmark from 2007 through 2016 (n = 14,377). Patients were match with individuals without IBD from the general population (controls, n = 71,885). All cohort members were followed from birth until 2016, their migration, or their death. The occurrence of IMIDs was assessed using the Danish national patient register and Registry of Medicinal Products Statistics. RESULTS: A total of 3,235 patients with a diagnosis of IBD (22.5%) has also received a diagnosis of an IMID; most IMIDs occurred before the onset of IBD (n = 2,600, 80.3%). The most common IMIDs observed were psoriasis, asthma, type 1 diabetes, and iridocyclitis. Patients with IBD treated with infliximab were at reduced risk of developing IMIDs (CD adjusted odds ratio [aOR], 0.52; 95% CI, 0.34-0.81 and UC aOR, 0.47; 95% CI, 0.29-0.76). Co-occurrence of IMIDs increased the risk of surgery in patients with CD that developed IMIDs after CD onset (aOR, 2.30; 95% CI, 1.46-4.20) but not in UC. CONCLUSIONS: In a nationwide study of the Danish population, 22.5% of patients with IBD also had at least 1 concurrent IMID. Co-occurrence of IMIDs increased the risk of surgery in patients with CD.
31132298 Tramadol for osteoarthritis. 2019 May 27 BACKGROUND: Tramadol is often prescribed to treat pain and is associated physical disability in osteoarthritis (OA). Due to the pharmacologic mechanism of tramadol, it may lead to fewer associated adverse effects (i.e. gastrointestinal bleeding or renal problems) compared to non-steroidal anti-inflammatory drugs (NSAIDs). This is an update of a Cochrane Review originally published in 2006. OBJECTIVES: To determine the benefits and harms of oral tramadol or tramadol combined with acetaminophen or NSAIDs in people with osteoarthritis. SEARCH METHODS: We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE and Embase databases, as well as the US National Institutes of Health and World Health Organization trial registries up to February 2018. We searched the LILACS database up to August 2015. SELECTION CRITERIA: We included randomized controlled trials (RCTs) that evaluated the effect of tramadol, or tramadol in combination with acetaminophen (paracetamol) or NSAIDs versus placebo or any comparator in people with osteoarthritis. DATA COLLECTION AND ANALYSIS: We used standard methodologic procedures expected by Cochrane. MAIN RESULTS: We included 22 RCTs (11 more than the previous review) of which 21 RCTs were included in meta-analyses for 3871 participants randomized to tramadol alone or tramadol in combination with another analgesic and 2625 participants randomized to placebo or active control. Seventeen studies evaluated tramadol alone and five evaluated tramadol plus acetaminophen. Thirteen studies used placebo controls and eleven studies used active controls (two trials had both placebo and active arms). The dose of tramadol ranged from 37.5 mg to 400 mg daily; all doses were pooled. Most trials were multicenter with a mean duration of two months. Participants were predominantly women with hip or knee osteoarthritis, with a mean age of 63 years and moderate to severe pain. There was a high risk of selection bias as only four trials reported both adequate sequence generation and allocation concealment. There was a low risk for performance bias as most studies blinded participants. There was a high risk of attrition bias as 10/22 trials showed incomplete outcome data. Most of the trials were funded by the pharmaceutical industry.Moderate quality evidence (downgraded due to risk of bias) indicated that tramadol alone and in combination with acetaminophen had no important benefit on pain reduction compared to placebo control (tramadol alone: 4% absolute improvement, 95% confidence interval (CI) 3% to 5%; 8 studies, 3972 participants; tramadol in combination with acetaminophen: 4% absolute improvement, 95% CI 2% to 6%; 2 studies, 614 participants).Fifteen out of 100 people in the tramadol group improved by 20% (which corresponded to a clinically important difference in pain) compared to 10/100 in the placebo group (5% absolute improvement). Twelve out of 100 people improved by 20% in the tramadol in combination with acetaminophen group compared to 7/100 in the placebo group (5% absolute improvement).Moderate quality evidence (downgraded due to risk of bias) indicated that tramadol alone and in combination with acetaminophen led to no important benefit in physical function compared to placebo (tramadol alone: 4% absolute improvement, 95% CI 2% to 6%; 5 studies, 2550 participants; tramadol in combination with acetaminophen: 4% absolute improvement, 95% CI 2% to 7%; 2 studies, 614 participants).Twenty-one out of 100 people in the tramadol group improved by 20% (which corresponded to a clinically important difference in physical function) compared to 16/100 in the placebo group (5% absolute improvement). Fifteen out of 100 people improved by 20% in the tramadol in combination with acetaminophen group compared to 10/100 in the placebo group (5% absolute improvement).Moderate quality evidence (downgraded due to risk of bias) indicated that, compared to placebo, there was a greater risk of developing adverse events with tramadol alone (risk ratio (RR) 1.34, 95% CI 1.24 to 1.46; 4 studies, 2039 participants) and tramadol in combination with acetaminophen compared to placebo (RR 1.91, 95% CI 1.32 to 2.76; 1 study, 308 participants). This corresponded to a 17% increase (95% CI 12% to 23%) with tramadol alone and 22% increase (95% CI 8% to 41%) with tramadol in combination with acetaminophen.The three most frequent adverse events were nausea, dizziness and tiredness. Moderate quality evidence (downgraded due to risk of bias) indicated that there was a greater risk of withdrawing from the study because of adverse events with tramadol alone compared to placebo (RR 2.64, 95% CI 2.17 to 3.20; 9 studies, 4533 participants), which corresponded to a 12% increase (95% CI 9% to 16%).Low quality evidence (downgraded due to risk of bias and inconsistency) indicated that there was a greater risk of withdrawing from the study because of adverse events with tramadol in combination with acetaminophen compared to placebo (RR 2.78, 95% CI 1.50 to 5.16; 2 studies, 614 participants), which corresponded to a 8% absolute improvement (95% CI 2% to 19%).Low quality evidence (downgraded due to risk of bias and imprecision) indicated that there was a greater risk of developing serious adverse events with tramadol alone compared to placebo (110/2459 participants with tramadol compared to 22/1153 participants with placebo; RR 1.78, 95% CI 1.11 to 2.84; 7 studies, 3612 participants), which corresponded to a 1% increase (95% CI 0% to 4%). There were no serious adverse events reported in one small study (15 participants) of tramadol with acetaminophen compared to placebo. AUTHORS' CONCLUSIONS: Moderate quality evidence indicates that compared to placebo, tramadol alone or in combination with acetaminophen probably has no important benefit on mean pain or function in people with osteoarthritis, although slightly more people in the tramadol group report an important improvement (defined as 20% or more). Moderate quality evidence shows that adverse events probably cause substantially more participants to stop taking tramadol. The increase in serious adverse events with tramadol is less certain, due to the small number of events.
31849513 Individualized Drug Repositioning For Rheumatoid Arthritis Using Weighted Kolmogorov-Smirn 2019 BACKGROUND: Existing drugs are far from enough for investigators and patients to administrate the therapy of rheumatoid arthritis. Drug repositioning has drawn broad attention by reusing marketed drugs and clinical candidates for new uses. PURPOSE: This study attempted to predict candidate drugs for rheumatoid arthritis treatment by mining the similarities of pathway aberrance induced by disease and various drugs, on a personalized or customized basis. METHODS: We firstly measured the individualized pathway aberrance induced by rheumatoid arthritis based on the microarray data and various drugs from CMap database, respectively. Then, the similarities of pathway aberrances between RA and various drugs were calculated using a Kolmogorov-Smirnov weighted enrichment score algorithm. RESULTS: Using this method, we identified 4 crucial pathways involved in rheumatoid arthritis development and predicted 9 underlying candidate drugs for rheumatoid arthritis treatment. Some candidates with current indications to treat other diseases might be repurposed to treat rheumatoid arthritis and complement the drug group for rheumatoid arthritis. CONCLUSION: This study predicts candidate drugs for rheumatoid arthritis treatment through mining the similarities of pathway aberrance induced by disease and various drugs, on a personalized or customized basis. Our framework will provide novel insights in personalized drug discovery for rheumatoid arthritis and contribute to the future application of custom therapeutic decisions.
30886993 Living life precariously with rheumatoid arthritis - a mega-ethnography of nine qualitativ 2019 BACKGROUND: Rheumatoid arthritis is an autoimmune disease that causes joint inflammation. It affects around 400,000 people in the UK and 1 million adults in the USA. Given the appropriate treatment, many can have relatively few symptoms. It is therefore important to understand what it is like to live with rheumatoid arthritis and gain insight into peoples' decisions about utilising healthcare. The aims of this study were: (1) to bring together qualitative evidence syntheses that explore patients' experience of living with rheumatoid arthritis and (2) develop a conceptual understanding of what it is like to live with rheumatoid arthritis. METHODS: We used the methods of mega-ethnography. The innovation of mega-ethnography is to use conceptual findings from qualitative evidence syntheses as primary data. We searched four bibliographic databases from inception until September 2018 to identify qualitative evidence syntheses that explored patients' experience of rheumatoid arthritis. RESULTS: We identified 373 qualitative evidence syntheses, removed 179 duplicates and screened 194 full text studies. We identified 42 qualitative evidence syntheses that explored the experience of pain or arthritis and 9 of these explored the experience of rheumatoid arthritis. We abstracted ideas into 10 conceptual categories: (1) rheumatoid arthritis is in control of my body (2) rheumatoid arthritis alters reciprocity; (3) rheumatoid arthritis is an emotional challenge; (4) rheumatoid arthritis disrupts my present and future self; (5) the challenge of balancing personal and work life; (6) I am trying to make sense of what is happening; (7) rheumatoid arthritis is variable and unpredictable; (8) rheumatoid arthritis is invisible; (9) I need a positive experience of healthcare, and (10) I need to reframe the situation. We developed a conceptual model underpinned by living life precariously with rheumatoid arthritis. CONCLUSIONS: This is the second mega-ethnography, or synthesis of qualitative evidence syntheses using the methods of meta-ethnography. Future research should consider the proliferation of qualitative evidence synthesis in order to avoid duplication of research effort. Our model for rheumatoid arthritis has some important clinical implications that might be transferable to other musculoskeletal conditions.
31814944 Hearing status in patients with rheumatoid arthritis. 2019 Fall BACKGROUND: Previous studies showed that one of the complications of rheumatoid arthritis disease was auditory disorder. The goal of the present study was to compare the auditory status in patients with rheumatoid arthritis and healthy individuals. METHODS: In the present case-control study, 30 normal persons and 60 persons with rheumatoid arthritis with mean age of 46.72 and standard deviation of 6.76 of both genders were appraised using pure tone audiometry, tympanometry and speech audiometry. The mean disease duration in patients with rheumatoid arthritis was 12.51±6.09 years. RESULTS: The frequency of hearing loss in rheumatoid arthritis group was significantly more than the control group (p=0.001). All patients had sensorineural hearing loss. Only in 5% of rheumatoid arthritis group, abnormal tympanometry (as type) was reported. Speech discrimination score analysis showed significant difference between the patients with rheumatoid arthritis and controls. In terms of hearing threshold level, the mean hearing threshold level (in 2000, 4000 and 8000 Hz frequencies) of the patients with rheumatoid arthritis was significantly higher than control group in both ears (p<0.05). A positive significant correlation was found among mean hearing threshold level in 4000 and 8000 Hz frequencies and rheumatoid arthritis duration in both ears. CONCLUSION: The frequency of hearing loss and the average hearing threshold in RA patients were higher than healthy individuals. The most common type hearing loss is sensorineural.
32226170 Rheumatoid neutrophilic dermatitis. 2019 Rheumatoid neutrophilic dermatitis is a rare extra-articular manifestation of rheumatoid arthritis, both seropositive and seronegative for rheumatoid factor. The condition most often presents as symmetric erythematous papules, nodules, plaques, and urticaria-like lesions in patients with severe, long-lasting rheumatoid arthritis. We report a case of a 65-year-old man with well-controlled rheumatoid arthritis, who developed rheumatoid neutrophilic dermatitis on the right lower leg. The biopsy of skin lesions revealed an intense, neutrophilic dermal infiltrate, microabscesses, and leukocytoclasis without vasculitis. The patient responded well to pulses of intravenous methylprednisolone. We present this patient due to the rarity of the disease and atypical unilateral manifestation involving the flexural surfaces of the lower leg.
31333917 Antibodies to Brewer's Yeast in Rheumatoid Arthritis. 2019 May 17 Antibodies to brewer's yeast or anti-Saccharomyces cerevisiae antibodies (ASCA) have been detected in 70% of patients with Crohn's disease and have become a part of the evaluation of a patient for Crohn's disease. Prior evaluation of these antibodies in rheumatoid arthritis have been inconsistent. In an initial small study, the levels of antibodies were elevated but not statistically significant. In a second large study from China, 40% of rheumatoid arthritis patients were positive for immunoglobulin A (IgA) ASCA and 20% positive for immunoglobulin G (IgG) ASCA. Our study was inspired by the observation that several seronegative patients with rheumatoid arthritis were positive for ASCA antibodies. Between January 1, 2016 and January 1, 2018, a total of 241 patients with clinical rheumatoid arthritis were evaluated for antibodies to IGA and IGG ASCA, rheumatoid factor, cyclic citrullinated peptide (CCP), and antinuclear antibody (ANA). Our results indicate that 158 (66%) of these patients were positive for ASCA; 70 (29%) of these patients were positive for ASCA but negative for other serologies; 62% of the patients were positive for rheumatoid factor. Our results also indicate that the percentage of rheumatoid factor (95%) and CCP positive (78%) patients in the ASCA negative group was higher than the percentage of rheumatoid factor positive (49%) and CCP positive (37%) patients in the ASCA positive group, suggesting serologic differences between the two groups. Only 4% of the rheumatoid patients were negative for all the evaluated serologies. The possible role of mannan, a mucopolysaccharide from the cell wall of Saccharomyces cerevisiae (S. cerevisiae) in producing rheumatoid arthritis is discussed.
31695961 Periodontitis and Rheumatoid Arthritis in sub-Saharan Africa, gaps and way forward: a syst 2019 Oct BACKGROUND: This review identified papers that described periodontitis and rheumatoid arthritis in sub-Saharan Africa. Only English language publications from January 2010 to December 2017 describing original research in sub-Saharan Africa on the association between periodontitis and rheumatoid arthritis were considered for this study. METHODS: Published databases: PubMed, Science direct and Google scholar, were searched using terms "periodontitis", "rheumatoid arthritis" and "Sub-Saharan Africa" to generate a set of putative studies. Articles with data on both rheumatoid arthritis and periodontitis compared to controls were selected. Studies on the association of periodontitis with cardiovascular disease, arthritis or rheumatoid arthritis alone were excluded. Data were extracted, critically appraised, and analyzed using a random-effect Mantel-Haenszel meta-analysis on plaque index, gingival index, pocket depth and clinical attachment loss. RESULTS: Three publications were selected for the systematic review and 2 for the meta-analysis. Two studies were from Sudan, and one was from Burina Faso. There was a significant increase in pocket depth (mean difference: 0.31; 95% CI: 0.21, 0.41; N= 274; (p ≤ 0.001) and clinical attachment loss (mean difference: 0.47; 95% CI: 0.22, 0.75; N= 274; (p ≤ 0.001) in participants with rheumatoid arthritis compared to normal controls. CONCLUSION: Findings from these combined studies show a significant relationship between periodontal disease and rheumatoid arthritis with increased periodontal pocket depth and clinical attachment loss. They also highlight the need for additional work especially in the area of associating rheumatoid arthritis with P. gingivalis, the oral microbiome and treating periodontal diseases to help in the management of rheumatoid arthritis.
31041286 Acute parvovirus B19 infection presenting as rheumatoid arthritis mimic. 2019 Mar Acute parvovirus B19 infection can cause acute symmetric polyarthritis indistinguishable from polyarticular rheumatoid arthritis. Most cases of acute arthritis due to parvovirus B19 are self-limiting and resolve with symptomatic treatment. We present a 65-year-old lady from Southern India who presented with history of fever and joint pain for 10 days. Clinical examination revealed symmetric inflammatory arthritis involving the appendicular skeleton with predominant involvement of bilateral metacarpophalageal joints. Laboratory investigations revealed elevated inflammatory markers with negative serology for rheumatoid arthritis. Parvovirus B19 IgM antibody tested positive. She was initiated on nonsteroidal anti-inflammatory drugs with which her symptoms resolved completely.
31092717 Sjögren Syndrome without Focal Lymphocytic Infiltration of the Salivary Glands. 2020 Mar OBJECTIVE: Primary Sjögren syndrome (SS) is characterized by a focal lymphocytic infiltrate in exocrine glands. We describe patients who lacked this key feature. METHODS: We evaluated patients with sicca in a comprehensive clinic at which medical, dental, and ophthalmological examinations were performed. All subjects underwent a minor salivary gland biopsy with focus score calculation. Extraglandular manifestations were also determined. We categorized subjects as high, intermediate, or low in terms of expression of interferon (IFN)-regulated genes. RESULTS: About 20% (51 of 229, 22%) of those classified as having primary SS had a focus score of zero. Compared to those with anti-Ro positivity and a focus score > 1.0, the patients with focus score of zero (who by classification criteria must be anti-Ro-positive) were statistically less likely to have anti-La (or SSB) and elevated immunoglobulin, as well as less severe corneal staining. The focus score zero patients were less likely to have elevated expression of IFN-regulated genes in peripheral blood mononuclear cells than anti-Ro-positive SS patients with a focal salivary infiltrate. CONCLUSION: There are only a few clinical differences between patients with primary SS with focus score zero and those with both anti-Ro and a focus score > 1.0. The small subset of focus score zero patients tested did not have elevated expression of IFN-regulated genes, but did have systemic disease. Thus, extraglandular manifestations are perhaps more related to the presence of anti-Ro than increased IFN. This may have relevance to pathogenesis of SS.
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.
31692611 Pneumocystis pneumonia in a treatment-naive rheumatoid arthritis patient. 2019 A HIV-negative, newly diagnosed patient with rheumatoid arthritis (RA) was found to have pneumocystis jiroveci pneumonia. The infection was treated with three weeks of atovaquone and corticosteroids. Clinicians should be aware of pneumocystis pneumonia as an infection in RA patients not receiving treatment.
31879467 Altering the natural history of rheumatoid arthritis: The role of immunotherapy and biolog 2020 Jan Rheumatoid Arthritis (RA) is an idiopathic disease characterized by systemic inflammation, persistent synovitis, and the presence of autoantibodies. Because of the musculoskeletal deformity caused by RA, multiple orthopaedic procedures are regularly performed as part of the treatment. The changing rates of surgery and the rise in new efficacious medical therapy have improved the prognosis for patients with RA. This review will discuss the natural history of rheumatoid arthritis, common medications used to treat it, how disease progression has changed as a function of new biologic immunotherapy, and the role of orthopaedic intervention in this new landscape of advanced rheumatoid care.
31579694 Periodontal Condition in Patients with Rheumatoid Arthritis: Effect of Anti-rheumatic Drug 2019 Sep STATEMENT OF THE PROBLEM: Rheumatoid arthritis and periodontitis are chronic inflammatory diseases with a possible bidirectional relationship. This link may be affected by many factors like drug consumption. PURPOSE: This study was designed to evaluate the periodontal condition in patients with rheumatoid arthritis, considering the effect of disease modifying anti-rheumatic drugs. MATERIALS AND METHOD: This case-control study included 25 newly diagnosed rheumatoid arthritis patients with negative history of taking anti-rheumatic drugs, 25 patients who received anti-rheumatic drugs for more than three years and 50 healthy individuals as a control group. Periodontal indices, including plaque index, gingival index, probing depth, clinical attachment loss, and rheumatologic indices were recorded and compared between these groups. RESULTS: Rheumatoid arthritis patients were significantly more affected by periodontitis compared with healthy subjects (p= 0.006). There was no significant difference in rheumatologic indices between patients with and without periodontitis. Clinical attachment loss in old rheumatoid arthritis patients and gingival index in newly diagnosed ones were significantly more compared to the control group (p= 0.003 and p< 0.001 respectively). We could not find a linear relationship between the severity of rheumatoid arthritis and chronic periodontitis (p= 0.1, r= -0.224). CONCLUSION: Periodontitis and clinical attachment loss were more in patients with rheumatoid arthritis than the healthy group, especially in drug consumers. Gingival index in patients without the history of consuming anti-rheumatic drugs was significantly higher than those who were drug consumers, indicating the effect of the medications on the signs of inflammation.