Molecular Pathophysiology of Gout

Objectives Periodontitis (PD) has been linked to arthritis in previous epidemiological observational studies; however, the results are inconclusive. It remains unclear whether the association between PD and arthritis is causal. The purpose of this study was to investigate the causal association of PD with arthritis, including rheumatoid arthritis (RA) and osteoarthritis (OA). Methods We performed a two-sample bidirectional Mendelian randomization (MR) analysis using publicly released genome-wide association studies (GWAS) statistics. The inverse-variance weighted (IVW) method was used as the primary analysis. We applied four complementary methods, including weighted median, weighted mode, MR-Egger regression and MR pleiotropy residual sum and outlier (MR-PRESSO) to detect and correct for the effect of horizontal pleiotropy. Results Genetically determined PD did not have a causal effect on OA (OR = 1.06, 95% CI: 0.99-1.15, P = 0.09) and RA (OR = 0.99, 95% CI: 0.87-1.13, P = 0.89). Furthermore, we did not find a significant causal effect of arthritis on PD in the reverse MR analysis. The results of MR-Egger regression, Weighted Median, and Weighted Mode methods were consistent with those of the IVW method. Horizontal pleiotropy was unlikely to distort the causal estimates according to the sensitivity analysis. Conclusions Our MR analysis reveals non-causal association of PD with arthritis, despite observational studies reporting an association between PD and arthritis.

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No Genetic Causal Association Between Periodontitis and Arthritis: A Bidirectional Two-Sample Mendelian Randomization Analysis

Whether the levels of procalcitonin (PCT) in the serum and synovial fluid are effective indicators for distinguishing septic arthritis (SA) from non-infectious arthritis remains controversial. The present study aimed to evaluate whether PCT levels in fresh serum or fresh joint fluid may be used in the differential diagnosis of SA from rheumatoid arthritis (RA), osteoarthritis (OA) and gouty arthritis (GA). From January 2012 to June 2013, 23 patients with knee SA, 21 patients with RA, 40 patients with OA and 11 patients with GA were enrolled in the current study. The levels of PCT were measured within 24 h after specimen collection at room temperature. An enzyme-linked fluorescence assay (ELFA) was used to detect the levels of PCT in the serum and synovial fluid. The correlations between the levels of PCT in the serum and synovial fluid and the arthritic patient groups were determined by the Nemenyi test. Areas under the receiver operating characteristic (ROC) curve were calculated to evaluate the accuracy of the correlations. The levels of PCT in the serum and joint fluid of the patients in the SA group were higher compared with those of the other groups (P<0.01) and there were no significant differences among the RA, OA and GA groups in these levels. A PCT level of <0.5 μg/l in the serum and synovial fluid had high specificity in the differential diagnosis of SA from RA, OA and GA. Synovial fluid PCT revealed significantly greater sensitivity than serum PCT. The accuracy of the differential diagnosis of SA by the serum levels of PCT was significantly lower than that by the synovial fluid levels of PCT. The levels of PCT in the serum and synovial fluid may be used as alternative laboratory indicators to distinguish between SA and the non-infectious types of arthritis; however, the PCT levels in fresh synovial fluid are more sensitive and accurate indicators than PCT levels in fresh serum.

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Procalcitonin levels in fresh serum and fresh synovial fluid for the differential diagnosis of knee septic arthritis from rheumatoid arthritis, osteoarthritis and gouty arthritis.

Differentiating septic arthritis from non-septic arthritis can be challenging as the clinical pictures are similar and an efficacious diagnostic test is not yet available. Our objectives in this study were to establish if procalcitonin (PCT) could be reproducibly measured from synovial fluid, if there is a difference in synovial procalcitonin values between patients with septic and non-septic arthritis, respectively, including those with implants and to determine cut-off levels that could be used as a practical tool in the management of these conditions. Using a standard serum assay, synovial fluid PCT levels were measured retrospectively in 26 septic and 50 non-septic predefined arthritis cases. The reproducibility of synovial PCT was also assessed at various concentrations. Synovial PCT can be measured and is reproducible. In this cohort, statistically significant higher synovial PCT levels were found in cases of septic arthritis than in non-septic arthritis. Sensitivities, specificities and positive and negative predictive values varied at different cut-off levels. The test could be added to other microbiological and biochemical tests and may be used to supplement other clinical, radiological and laboratory findings in the assessment of patients with acute painful joints. In our cohort, findings of very high synovial PCT levels supported an infection process, including in prosthesis-related infections. The high negative predictive value of low synovial PCT levels could exclude infection in both native and prosthetic joints. Larger prospective studies are needed to further validate these results and to examine the cost effectiveness of synovial PCT.

Measuring synovial fluid procalcitonin levels in distinguishing cases of septic arthritis, including prosthetic joints, from other causes of arthritis and aseptic loosening

Acute monoarthritis can be the initial manifestation of many joint disorders. The most common diagnoses in the primary care setting are osteoarthritis, gout, and trauma. It is important to understand the prevalence of specific etiologies and to use the appropriate diagnostic modalities. A delay in diagnosis and treatment, particularly in septic arthritis, can have catastrophic results including sepsis, bacteremia, joint destruction, or death. The history and physical examination can help guide the use of laboratory and imaging studies. The presence of focal bone pain or recent trauma requires radiography of the affected joint to rule out metabolic bone disease, tumor, or fracture. If there is a joint effusion in the absence of trauma or recent surgery, and signs of infection (e.g., fever, erythema, warmth) are present, subsequent arthrocentesis should be performed. Inflammatory synovial fluid containing monosodium urate crystals indicates a high probability of gout. Noninflammatory synovial fluid suggests osteoarthritis or internal derangement. Pitfalls in the diagnosis and early treatment of acute monoarthritis include failure to perform arthrocentesis, administering antibiotics before aspirating the joint when septic arthritis is suspected (or failing to start antibiotics after aspiration), and starting treatment based solely on laboratory data, such as an elevated uric acid level.

Acute Monoarthritis: Diagnosis in Adults.

Early in the evening, a 50-year-old man presents to the emergency department with a 24-hour history of pain and swelling in his right knee. He denies recent injury or trauma. He has no prior history of joint disease or joint surgery and has no family history of arthritis. His medical history

/pdf/acute-monoarthritis-what-is-the-cause-of-my-patient-s-5a9x38z8vz.pdf

Acute monoarthritis: What is the cause of my patient's painful swollen joint?

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Acute monoarthritis: What is the cause of my patient's painful swollen joint?