Abstract
The study aims were to verify the serum (S) and synovial fluid (SF) reference intervals (RIs) for human neutrophil defensins (HNP1-3); measure S and SF defensin concentrations in different types of SF, including non-inflammatory, inflammatory non-pyogenic, inflammatory pyogenic, and hemorrhagic; and to compare the HNP1-3 concentrations in SF and S with those of other inflammatory biomarkers. SF and S samples were collected from 92 patients. HNP1-3 concentrations were determined using enzyme-linked immunosorbent assays; glucose, lactate, interleukin-6, and procalcitonin using an automatic analyzer; and presepsin using a Pathfast system. There were 61 non-inflammatory, 11 inflammatory non-pyogenic, 11 inflammatory pyogenic, and 9 hemorrhagic SF. Non-inflammatory SF was divided into non-inflammatory normal and non-inflammatory osteoarthritis. The former was used to estimate the HNP1-3 RI in SF and S. The estimated HNP1-3 RIs of SF and S were 12.47-437.42 mg/L and 5.45-44.75 µg/L, respectively. HNP1-3 differed significantly between S and SF and individual groups of SF (P<0.001 and P=0.001, respectively). There were significant relationships between SF HNP1-3 and S HNP1-3 (P<0.001), S C-reactive protein (P<0.001), and S interleukin-6 (P=0.007), and between SF HNP1-3 and SF C-reactive protein (P=0.004) and SF interleukin-6 (P<0.001). The highest kappa coefficient was between SF HNP1-3 and SF interleukin-6 (κ=0.507). We validated the SF HNP1-3 diagnostic kit and demonstrated that SF and S HNP1-3 are promising biomarkers for distinguishing inflammatory from non-inflammatory joint diseases.
Highlights
Joint effusion can have different etiologies, associated appearances, and biochemical and microscopic characteristics
These authors studied this marker in the synovial fluid of 157 patients diagnosed with different joint infections, such as periprosthetic joint infection (PJI) and infectious arthritis, as well as arthrosis, reactive arthritis, and rheumatoid arthritis
They set the cut-off concentration of synovial fluid (SF) HNP1–3 at 62.5 mg/L when comparing the results of patients with infectious arthritis versus aseptic patients with osteoarthritis
Summary
Joint effusion can have different etiologies, associated appearances, and biochemical and microscopic characteristics. Dungl et al.[1] divides joint effusions into noninflammatory, inflammatory, and pyogenic. It is debatable whether any effusion (increase in intra-articular fluid) can be fully non‐inflammatory. It is crucial to understand the nature of the process. It can be inflammation provoked by mechanical factors leading to cartilage abrasion and the production of microscopic cartilage particles (initially only as a manifestation of delamination of the surface layer of the cartilage). Many systemic diseases lead to arthritis with overproduction of joint fluid. The crucial fact is that the aforementioned types of inflammation are free of microorganisms
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