244 The clinical phenotype of inflammatory arthritis correlates with synovial immune cell infiltration: results from the pathobiology of early arthritis cohort
Gloria Lliso RiberaFrances HumbyStephen KellyMyles LewisStefano BombardieriAlessandra NervianiRebecca HandsFabiola BeneChristopher D. BuckleyPeter C. TaylorIain B. McInnesCostantino Pitzalis
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Abstract:
treatment options for patients with rheumatoid arthritis (RA) who have failed a first TNFi.The risk of serious infection (SI) is similar between these two treatments during the first year.However, long-term data on risk of SI for RTX are scarce but required, in light of reports of reduction in IgG following repeated dosing.We compared the risk of SI over five years of treatment in patients with RA who had failed a first TNFi and then received either RTX or TNFi.Methods: This study used patients with RA registered with the BSRBR-RA, a large national prospective study in the UK established primarily to assess the long-term safety of exposure to biologic therapies in patients with RA.This analysis included patients treated with either a second TNFi or RTX after failing a first TNFi.Patients were followed until first SI, 90 days or nine months following last dose of TNFi or RTX respectively if treatment was discontinued, last recorded follow-up or the end of the fifth year after the switch, which ever came first.SI was defined as infection requiring intravenous antibiotics, hospitalisation or resulting in death.The risk of first SI was compared between TNFi and RTX using unadjusted, adjusted for sex and age, and propensity score adjusted Cox proportional hazard models.Results: This analysis included 3,419 TNFi-treated patients contributing 9,527 person-years (pyrs), median (IQR) exposure time per person 2.0 (0.8-3.3) years; and 1,396 RTX patients contributing 3,570 pyrs, median (IQR) exposure time 2.9 (1.7-3.9)years.A total of 362 and 135 first SI were reported in TNFi and RTX patients respectively, giving a crude incidence rate (95% CI) of 38 (34-42) SI/1,000 pyrs (TNFi) and 38 (32-45) SI/1,000 pyrs (RTX).The unadjusted, adjusted for sex and age, and propensity score adjusted hazard ratios (95%CI) for SI were 0.9 (0.8-1.1), 0.9 (0.7-1.0) and 0.9 (0.7-1.1) respectively.Conclusion: The risk of serious infections was comparable over five years of treatment between TNFi and RTX treatment in patients who had failed a single prior TNFi.Keywords:
Inflammatory arthritis
Infiltration (HVAC)
Clinical phenotype
Objective: Arthritis is one of the most common diseases in patients who have joint problems. Based on a patient’s WBC and polymorphonuclears count, it is divided into inflammatory and non-inflammatory types. IL-17 is an important cytokine causing inflammation in synovia. The objective of this research is to measure the level of IL-17 in joint fluid in order to differentiate inflammatory from non-inflammatory arthritis. Methods: In this case-control study, 40 cases were chosen: 20 patients who have inflammatory knee mono arthritis and 20 with non-inflammatory knee mono arthritis. Their demographic information including age, sex, and duration of disease was recorded by the questioners. After the patients’ consent was obtained, we sent their joint fluid samples to the lab to measure their levels of IL-17. Arthritis was considered inflammatory if there was more than 2000 WBC in one milliliter of joint fluid and non-inflammatory if there was less than 2000. We measured IL-17 using ELISA with KOMA BIOTECH kits. We analyzed the data using SPSS software. Results: In this study we had 18 males (45% of cases) and 22 females (55% of cases).The mean age and the duration of disease were 48+_15.96 Y and 8+_4.8 W respectively. Women had 40.9% inflammatory arthritis and 59.1% non-inflammatory arthritis. Men had 61.1% inflammatory and 38.9% non-inflammatory arthritis. No significant statistical difference was observed between the two groups (P-value=0.2). The means of age in patients who had inflammatory and non-inflammatory arthritis were 38.45+_13.44 and 57.55+_12.24 respectively which had a significant statistical difference (P-value<0.001). The means of disease duration in inflammatory and non-inflammatory arthritis were 5.84+_8.95 and 7.1+_3.24 W respectively (P-value=0.23). The means of the level of IL-17 in cases of inflammatory and non-inflammatory arthritis were 16.04+_5.74 and 8.83+_1.86pg/ml respectively which also had a significant statistical difference (P-value<0.001). To find a cut-off-point for IL-17 to differentiate the diagnosis of inflammatory from non-inflammatory arthritis we used an ROC diagram. The level of 10.5pg/ml of IL-17 is the cut-off-point to differentiate inflammatory from non-inflammatory knee mono arthritis. At this cut-off-point specificity, sensitivity, positive predictive value, and negative predictive value were 0.95, 0.90, 0.90, and 0.95 respectively. Conclusion: This study showed that by measuring the level of IL-17 in a patient, we can differentiate inflammatory from non-inflammatory arthritis.
Inflammatory arthritis
Knee arthritis
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Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disorder characterized by synovial inflammation and pannus formation leading to destruction of local articular structure, bone erosion and functional disabilities. Common research models of inflammatory arthritis in rodents e.g. collagen antibody-induced arthritis (CAIA) in mice are associated with pain, discomfort, and distress. Here we demonstrate in vivo assessment of CAIA mice using a transflection Raman setup. Mice with induced arthritis and controls were clinically and spectroscopically assessed for 14 days. Raman measurements of tibiotarsal joint bone density correlated well with volumetric bone mineral density (vBMD) in mice exhibiting clinical symptoms of arthritis.
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Background and aim The Montreal classification of disease behaviour in Crohn's disease describes progression of disease towards a stricturing and penetrating phenotype. In the present paper, we propose an alternative representation of the long-term course of Crohn's disease complications, the rolling phenotype. As is commonly observed in clinical practice, this definition allows progression to a more severe phenotype (stricturing, penetrating) but also, regression to a less severe behaviour (inflammatory, or remission) over time. Methods All patients diagnosed with Crohn's Disease between 01/01/1994 and 01/03/2008, managed at a single centre and observed for a minimum of 5 years, had development and resolution of all complications recorded. A rolling phenotype was defined at each time point based on all observed complications in the three years prior to the time point. Phenotype was defined as B1, B2, B3, or B23 (penetrating and stenotic). The progression over time of the rolling phenotype was compared to that of the cumulative Montreal phenotype. Results 305 patients were observed a median of 10.0 (Intraquartile range 7.3–13.7) years. Longitudinal progression of rolling phenotype demonstrated a consistent proportion of patients with B1 (70%), B2 (20%), B3 (5%) and B23 (5%) phenotypes. These proportions were observed regardless of initial phenotype. In contrast, the cumulative Montreal phenotype progressed towards a more severe phenotype with time (B1 (39%), B2 (26%), B3(35%) at 10 years). Conclusion A rolling phenotype provides an alternative view of the longitudinal burden of intra-abdominal complications in Crohn's disease. From this viewpoint, 70% of patients have durable freedom from complication over time (>3 years).
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Abstract We present PhenCards ( https://phencards.org ), a database and web server intended as a one-stop shop for previously disconnected biomedical knowledge related to human clinical phenotypes. Users can query human phenotype terms or clinical notes. PhenCards obtains relevant disease/phenotype prevalence and co-occurrence, drug, procedural, pathway, literature, grant, and collaborator data. PhenCards recommends the most probable genetic diseases and candidate genes based on phenotype terms from clinical notes. PhenCards facilitates exploration of phenotype, e.g., which drugs cause or are prescribed for patient symptoms, which genes likely cause specific symptoms, and which comorbidities co-occur with phenotypes.
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Animal models for inflammatory arthritides such as rheumatoid arthritis (RA) and psoriatic arthritis are widely accepted and frequently used to identify pathological mechanisms and validate novel therapeutic strategies. Unfortunately, many publications reporting on these animal studies lack detailed description and appropriate assessment of the distinct histopathological features of arthritis: joint inflammation, cartilage damage and bone erosion. Therefore, the European consortium BeTheCure, consisting of 38 academic and industrial partners from 15 countries, set as goal to standardise the histological evaluation of joint sections from animal models of inflammatory arthritis. The consensual approach of a task force including 16 academic and industrial scientists as well as laboratory technicians has resulted in the development of the Standardised Microscopic Arthritis Scoring of Histological sections ('SMASH') recommendations for a standardised processing and microscopic scoring of the characteristic histopathological features of arthritis, exemplified by four different rodent models for arthritis: murine collagen-induced arthritis, collagen-antibody-induced arthritis, human tumour necrosis factor transgenic Tg197 mice and rat pristane-induced arthritis, applicable to any other inflammatory arthritis model. Through standardisation, the SMASH recommendations are designed to improve and maximise the information derived from in vivo arthritis experiments and to promote reproducibility and transparent reporting on such studies. In this manuscript, we will discuss and provide recommendations for analysis of histological joint sections: identification of the regions of interest, sample preparation, staining procedures and quantitative scoring methods. In conclusion, awareness of the different features of the arthritis pathology in animal models of inflammatory arthritis is of utmost importance for reliable research outcome, and the standardised histological processing and scoring methods in these SMASH recommendations will help increase uniformity and reproducibility in preclinical research on inflammatory arthritis.
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Objective: To determine the lactic acid and lactate dehydrogenase levels in synovial fluid and differentiate between inflammatory and non-inflammatory arthritis.
Study Design: Cross-sectional study.
Place and Duration of Study: Department of Rheumatology, Liaquat National Hospital, Karachi, from Feb to May 2019.
Methodology: All patients of age >18 years, of either gender, who presented with knee joint effusion were enrolled in the study. Synovial fluid aspiration for the analysis of lactate and lactate dehydrogenase (LDH) was done for all patients.
Results: Seventy-seven patients were enrolled, of which 75 were included in the analysis. Two patients were excluded as one had lymphoma and the other had recent joint trauma. 31 (41.3 %) patients had non-inflammatory, or osteoarthritis, and 44 (58.7 %) had inflammatory arthritis. The mean value of synovial LDH in inflammatory and non-inflammatory arthritis was 737.38 ± 102.76 mmol/L and 265.5 ± 17.43 mmol/L, respectively, (p<0.001). The mean value of synovial lactate in inflammatory arthritis (32.16 ± 2.84 mmol/L) was higher than the mean value of synovial lactate in non-inflammatory arthritis (19.81 ± 1.08 mmol/L) (p<0.001). There mean plasma LDH in inflammatory arthritis and non-inflammatory arthritis was 495.77 ± 41.67 mg/dl and 437.90 ± 30.99 mg/dl, respectively (p>0.05). The plasma lactate in inflammatory arthritis and noninflammatory arthritis was 12.84 ± 0.59 mg/dl and 12.97 ± 0.78 mg/dl, respectively (p>0.05).
Conclusion: Synovial fluid lactic acid and synovial LDH can serve as rapid diagnostic and cost-effective tests to differentiate between non-inflammatory and inflammatory arthritis.
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The name of the first author was misspelled. The correct name should read: Shihua Zhang.
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