Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “inflammatory arthritis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2026

Genomic Structural Equation Modeling Identifies a Shared Inflammatory Genetic Dimension Across Inflammatory Arthritis Phenotypes and Biomarkers.

BACKGROUND: Inflammatory arthritis (IA), including rheumatoid arthritis (RA), psoriatic arthritis (PsA) and gout, shares systemic inflammatory features indexed by C-reactive protein (CRP) and interleukin-6 (IL-6), yet the extent of their common genetic basis remains unclear. AIMS: We aimed to delineate the shared genetic architecture across IA phenotypes and inflammatory biomarkers. MATERIALS AND METHODS: We applied genomic structural equation modelling (Genomic SEM) to GWAS summary statistics for RA, PsA, gout, CRP and IL-6, fitted a single common factor, and performed multivariate GWAS followed by fine-mapping, transcriptome-wide association, gene-based analysis, pathway enrichment, and cell-type and spatial mapping. RESULTS: A single common factor was fitted (CFI = 0.990, SRMR = 0.045). The multivariate GWAS identified 56 genome-wide significant SNPs across 10 independent lead loci, including one novel signal. Fine-mapping prioritized high-confidence variants near PTPN22, the CRP gene cluster and a urate-associated locus. Gene-level analyses converged on DCLRE1B, PTPN22, IL6R, NLRP3 and HNF1A, with pathway enrichment implicating inflammasome assembly and metabolic-inflammatory overlap. Cell-type enrichment highlighted myeloid populations, and spatial mapping localized signals to lung, kidney, mucosal epithelium and gastrointestinal tissues. DISCUSSION: These results delineate a shared inflammatory genetic dimension across IA phenotypes and biomarkers, anchored in immune, inflammasome, cytokine-receptor and metabolic pathways. CONCLUSION: Together, these findings provide a valuable framework for prioritizing candidate genes and cellular contexts for future investigation.

TWAS↗
PubMed2026

Definition and prevalence of residual disease in inflammatory arthritis: a systematic literature review and meta-analysis.

OBJECTIVE: To assess how residual disease (i.e., clinically relevant signs/symptoms despite achieving treatment targets) is defined in rheumatoid arthritis (RA), psoriatic arthritis (PsA) or axial spondyloarthritis (axSpA), and estimate the prevalence/severity of residual disease in these diseases. METHODS: Systematic review of original research in RA/PsA/axSpA. Two key residual disease components were extracted: (1) the patient's disease state (often remission/low disease activity) and (2) which residual signs/symptoms were measured, e.g. swollen joints or fatigue (indicators of residual disease). Frequencies of the disease states and indicators were described (Objective 1). Prevalence (%) and severity (absolute score on instrument, e.g. fatigue NRS) of residual disease was analysed by indicator, using random effects meta-analysis (&#x2265;4 studies) or descriptively (<4 studies) (Objective 2). RESULTS: Regarding residual disease definitions (59 studies), disease states were almost exclusively disease activity-based (>99%), but with much variation in specific instruments/thresholds. Across diseases, physician-reported (66%) and patient-reported (73%) indicators were used more often than laboratory indicators to define residual disease (46%). Especially peripheral joint counts, pain, physical function and CRP were frequently used (42-56% of studies). The prevalence of residual disease (84 studies) was notable. For example, 5-25% of RA and PsA patients in remission still had swollen joints, and up to one-third reported relevant pain or fatigue. For axSpA, evidence was limited. CONCLUSION: Residual disease definitions in RA/PsA/axSpA are based on various disease activity instruments/thresholds and indicators (signs/symptoms). Residual disease affects up to half of patients. Future research should aim for a consensus-based definition of residual disease.

Humans↗
PubMed1978

Role of Chlamydia trachomatis and HLA-B27 in sexually acquired reactive arthritis.

Inflammatory arthritis, tendinitis, and fasciitis after non-specific urethritis ("sexually acquired reactive arthritis" (SARA)) was studied prospectively in 531 men with non-specific urethritis, with particular reference to the frequency of isolation of Chlamydia trachomatis and the presence of HLA-B27. Satisfactory cultures were obtained from the urethral swabs from 384 patients; and HLA typing was performed on 482, of whom 30 (6%) were HLA-B27-positive. Arthritis developed in 16 patients, and five of the 14 (36%) with satisfactory cultures were positive for C trachomatis; 135 of the patients without arthritis were also positive for C trachomatis, an identical proportion. Seven of the 15 patients (40%) with arthritis who were HLA-typed were HLA-B27-positive. Six of the 30 patients with HLA-B27 developed peripheral arthritis in contrast to only nine of the 452 patients lacking the antigen, suggesting a tenfold increase susceptibility. C trachomatis, however, was no more prevalent in cultures from HLA-B27-positive men than from the others. Thus carriage of C trachomatis is unlikely to be influenced by HLA-B27. C trachomatis may be an important pathogen in some cases of SARA but does not appear to be an exclusive trigger factor for this condition.

Arthritis↗
PubMed1976

Circulating and intra-articular immune complexes in patients with rheumatoid arthritis. Correlation of 125I-Clq binding activity with clinical and biological features of the disease.

The correlation between the incidence and level of immune complexes in serum and synovial fluid and the various clinical and biological manifestations of rheumatoid arthritis has been studied. Immune complexes were quantitated using a sensitive radioimmunoassay, the 125I-Clq binding test, in unheated native sera and synovial fluids from 50 patients with seropositive (RA +) and 45 with seronegative (RA -) rheumatoid arthritis, 17 with other inflammatory arthritis, and 37 with degenerative and post-traumatic joint disease. The following observations were made: (a) when compared to the results from patients with degenerative and post-traumatic joint diseases, the 125I-Clq binding activity (Clq-BA) in synovial fluid was found to be increased (by more than 2 SD) in most of the patients with RA + (80%) and RA - (71%) and in 29% of patients with other inflammatory arthritis; the serum Clq-BA was also frequently increased in both RA + (76%) and RA - (49%) patients, but only exceptionally in patients with other inflammatory arthritis (6%); (b) a significant negative correlation existed between the Clq-BA and the immunochemical C4 level in synovial fluids from patients with RA + and RA -; (c) neither the serum nor the synovial fluid Clq-BA in rheumatoid arthritis significantly correlated with the erythrocyte sedimentation rate, the clinical stage of the disease, or the IgM rheumatoid factor titer; and (d) the serum Clq-BA in patients with rheumatoid arthritis and extra-articular disease manifestations (40 +/- 34% in those with RA +,32 +/- 29% in those with RA -) was significantly increased as compared to the serum Clq-BA in patients with joint disease alone (24 +/- 30% in those with RA +, 10 +/- 13% in those with RA -). Experimental studies were carried out in order to characterize the Clq binding material in rheumatoid arthritis. This material had properties similar to immune complexes: it sedimented in a high molecular weight range on sucrose density gradients (10-30S) and lost the ability to bind Clq after reduction and alkylation, or after acid dissociation at pH 3.8, or after passage through an anti-IgG immunoabsorbant. DNase did not affect the Clq BA. These results support the hypothesis that circulating as well as intra-articular immune complexes may play an important role in some pathogenetic aspects of rheumatoid arthritis. The 125I-Clq binding test may also be of some practical clinical value in detecting patients who have a higher risk of developing vasculitis.

Adult↗
PubMed1976

Noninfectious canine arthritis: the inflammatory, nonerosive arthritides.

Noninfectious, nonerosive arthritis was seen as an important manifestation of a number of chronic systemic diseases of the dog. Sixty-three dogs with this type of arthritis were seen at the Veterinary Medical Teaching Hospital during an 18-month period between 1973 and 1975. Of these dogs, 29 had systemic lupus erythematosus, 15 had arthritis in association with some chronic infectious disease process, and 19 had a similar type of arthritis, but without serologic evidence of systemic lupus erythematosus or any chronic infectious disease process.

Animals↗
PubMed1978

Prostaglandin production in arthritis.

Inflammatory cell populations from synovial effusions or synovial villi in rheumatoid arthritis have been cultured in vitro. Prostaglandin productive capacity, measured by radioimmunoassay, showed the polymorphonuclear leucocyte rich populations from synovial effusions to be poor sources of PGE production whereas the synovial fragments produced substantial amounts of PGE activity. It is suggested that the macrophage is the major source of local prostaglandin formation both in gout and rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1978

A systematic survey of the HLA B27 prevalence in inflammatory rheumatic diseases.

HLA B27 has been tested systematically in 246 patients attending a rheumatology clinic for chronic inflammatory arthritis or spondylitis. Patients were allocated to nine groups: typical ankylosing spondylitis, ankylosing spondylitis with moderate involvement without peripheral arthritis, ankylosing spondylitis with moderate involvement and with peripheral arthritis, juvenile chronic arthritis, Reiter's syndrome, Yersinia arthritis, arthropathies of inflammatory bowel disease, psoriatic arthritis, seronegative and seropositive rheumatoid arthritis. Except for seropositive rheumatoid arthritis, a significant association with HLA B27 antigen was found in all groups. In the seronegative rheumatoid arthritis group HLA B27 was present in 40% of the cases in contrast to 5.6% of the seropositive rheumatoid arthritis cases. These data confirm that a wide range of the so called "seronegative arthropathies" are associated with HLA B27 and suggest that sex and HLA B27 antigen are important factors in the manifestation of rheumatic disease. Women had less severe spondylitic changes but more peripheral arthritis of the small joints. Ankylosing spondylitis in its various forms had a comparable sex distribution despite relatively mild disease in females. The mean age of onset in the HLA B27 associated diseases was found to be significantly lower than in the seropositive rheumatoid arthritis group.

Arthritis, Juvenile↗
PubMed1979

Dermatological manifestations in psoriatic arthritis: a follow-up study.

Of 227 patients with psoriasis and rheumatic complaints, inflammatory arthritis was present in 168 patients, of whom 95 have been followed up for more than 5 years and 28 had been followed up for more than 10 years. In patients with psoriasis and inflammatory arthritis the majority were women, but in the Distal joint group, males predominated. The skin disease usually began on the arms and was restricted in extent, initially. It usually began before the arthritis. A few cases were apparently precipitated by trauma, but more by psychological factors. The course pursued by the skin lesions was generally favourable. The skin lesions were resistant to treatment in 20% of the patients. Puberty, pregnancy and the menopause had little effect on the skin lesions. Nail lesions were present in 80%, a greater frequency than that seen in uncomplicated psoriasis. These nail lesions began at a later age than the skin lesions, and commonly preceded the development of arthritis. There was a family history of psoriasis in 26% of first-degree relatives. A history of polyarthritis was obtained quite frequently, and of psoriatic arthritis in 3% of patients with Distal arthritis, and 2% of the Indistinguishable group. The arthritis was usually mild in degree. Ankylosing spondylitis occurred in 5% and sacro-iliitis in 19%. The sheep cell agglutination test for rheumatoid factor was negative in the majority of patients. It was positive in 16% and a fluctuating positive result was obtained in 10%.

Adolescent↗
PubMed1978

Rapid diagnosis of septic arthritis by quantitative analysis of joint fluid lactic acid with a monotest lactate kit.

The Monotest Lactate Kit (MLT) was compared with gas-liquid chromatography (GLC) for the rapid detection of septic arthritis. A total of 36 joint fluids were tested. Specimens were obtained from patients with septic arthritis (17 cases), inflammatory arthritis (18 cases), and degenerative arthritis (1 case). Specimens from 15 patients with bacterial arthritis had lactate levels above 65 mg/dl (mean, 318 mg/dl with the GLC method and 378 mg/dl with the MLT method). Three specimens from patients with gonococcal arthritis had levels that were not above 30 mg/dl (mean, 21 mg/dl with either the GLC or the MLT methods). Patients with inflammatory or degenerative disease yielded levels lower than 65 mg/dl (mean, 48 mg/dl with the GLC method and 46 mg/dl with the MLT method). Both methods proved to be equallly reliable in detecting septic arthritis, except for the gonococcal cases. Both methods are fast and easily adaptable to clinical laboratories; however, MLT was more definitive when quantitation was needed, required less fluid per speciment, and could be readily done at the bedside.

Adolescent↗
PubMed2025

Genome-Wide Aggregated Trans Effects Analysis Identifies Genes Encoding Immune Checkpoints as Core Genes for Rheumatoid Arthritis.

OBJECTIVE: The sparse effector "omnigenic" hypothesis postulates that the polygenic effects of common single nucleotide polymorphisms (SNPs) on a typical complex trait are mediated by trans effects that coalesce on expression of a relatively sparse set of core genes. The objective of this study was to identify core genes for rheumatoid arthritis by testing for association of rheumatoid arthritis with genome-wide aggregated trans effects (GATE) scores for expression of each gene as transcript in whole blood or as circulating protein levels. METHODS: GATE scores were calculated for 5,400 cases and 453,705 non-cases of primary rheumatoid arthritis in UK Biobank participants of European ancestry. RESULTS: Testing for association with GATE scores identified 16 putative core genes for rheumatoid arthritis outside the HLA region, of which six-TP53BP1, PDCD1, TNFRSF14, LAIR1, LILRA4, and IDO1-were supported by Mendelian randomization analysis based on the marginal likelihood of the causal effect parameter. Five of these 16 genes were validated by a reported association of rheumatoid arthritis with SNPs within 200 kb of the transcription site, eight by association of the measured protein level with rheumatoid arthritis in UK Biobank, 10 by experimental perturbation in mouse models of inflammatory arthritis, and two-CTLA4 and PDCD1-by evidence that drugs targeting the gene cause or ameliorate inflammatory arthritis in humans. Fourteen of these 16 genes are in pathways affecting immunity or inflammation, and six-CD5, CTLA4, TIGIT, LAIR1, TNFRSF14, and PDCD1-encode receptors that have been characterized as immune checkpoints exploited by cancer cells to escape the immune response. CONCLUSION: These results highlight the key role of immune checkpoints in rheumatoid arthritis and identify possible therapeutic targets.

Humans↗
PubMed1977

Comparison of the anti-inflammatory activity of Commiphora mukul (an indigenous drug) with those of phenylbutazone and ibuprofen in experimental arthritis induced by mycobacterial adjuvant.

In the present investigation a method of induction of experimental arthritis in animals was modified to provide a better model replica of human arthritis. Inflammatory syndrome, resembling rheumatoid arthritis in man, was induced in the right hock joint of albino rabbits by intra-articular injection of the killed mycobacterial adjuvant in liquid paraffin. Development of this arthritic syndrome was studied from a period of five months with and without drugs. Anti-inflammatory agents such as phenylbutazone, ibuprofen and fraction "A" of gum-guggual from Commiphora mukkul were administered orally at a daily dose of 100, 100 and 500 mg/kg, respectively, for a period of five months. All three drugs decreased the thickness of the joint swelling during the course of drug treatment. These results indicate the beneficial role of phenylbutazone, ibuprofen and fraction "A" of gum-guggul in experimental arthritis.

Animals↗
PubMed1977

Experimental E. coli arthritis in the rabbit. A model of infectious and post-infectious inflammatory synovitis.

Rabbit knee joints challenged with E. coli 06 underwent a self-limited infection lasting several weeks followed by a prolonged post-infectious inflammatory arthritis. The E. coli used did not possess collagenolytic activity nor did a variety of common aerobic clinical isolates. Articular cartilage destruction occurred by two basically different mechanisms: u) direct invasion of pannus at the juxtaarticular margins, and 2) fibrillation in cartilage to cartilage contact areas. Weekly measurement of intra-articular pH and temperature were correlated with bacteriologic findings and groww and microscopic pathologic events.

Animals↗
PubMed1976

Arthritis with an inflammatory dermatosis resembling Sweet's syndrome. Report of a unique case and review of the literature on arthritis associated with the inflammatory dermatoses.

A patient with a unique case of chronic episodic arthritis coincident with flares of acneform, pustular, nodular and ulcerating skin lesions was observed over a five-year period. This patient and a review of the literature on arthritis associated with the inflammatory dermatoses provide evidence which may interrelate several of these nosologically confusing skin conditions, e.g., the family of leukocytoclastic angiitides with the newly posited acute febrile neutrophilic dermatosis of Sweet. Systemic manifestations and a variety of acneform, pustular, nodular and ulcerating cutaneous lesions in the inflammatory dermatoses are best explained by small vessel involvement, with individual syndromes being determined by the type and degree of vascular change. Perivascular neutrophilic infiltration is the unifying histologic feature of these small vessel diseases. Neutrophil infiltration differentiates these entities, and our patient, from the histologically nonspecific inflammations of the skin, e.g., Behcet's disease and pyoderma gangrenosum, which, although capable of causing identically appearing skin lesions, consist predominantly of lymphocytic dermal infiltrates even in the earlier stages. It appears important to recognized these morphologically varied acute inflammatory dermatoses with perivascular neutrophilic infiltration in view of their systemic features and the dramatic efficacy of corticosteroid therapy.

Adult↗