23 research outputs found

    CD64 as a potential biomarker in septic arthritis

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    Background Traditional inflammatory markers are generally unhelpful in discerning septic arthritis from inflammatory joint disease due to their lack of specificity. We wished to explore the discriminatory power of the novel inflammatory marker, Fc-gamma-receptor type 1, CD64, in patients presenting with acute arthritis. Methods Patients were recruited prospectively in the time period June 2009 to December 2011. Thirty-six patients presenting with an acute flare of chronic rheumatic arthritis, 31 with crystal-induced arthritis and 23 with septic arthritis were included. Traditional inflammatory markers, CD64 and procalcitonin (PCT) were measured and their diagnostic abilities were compared. Results CD64 and PCT both demonstrated a specificity of 98%, but poor sensitivities of 59% and 52%, respectively. White blood cell count (WBC), and erythrocyte sedimentation rate (ESR) did not have significant discriminatory power, while C-reactive protein (CRP) proved to have the best diagnostic accuracy as measured by area under the ROC curve (AUC 0.92, 95% confidence-interval 0.87-0.98). Subgroup analysis excluding patients with septic arthritis without concurrent bacteremia, and likewise exclusion of the patients with septic arthritis caused by coagulase negative staphylococci, both improved the diagnostic accuracy of CD64 and PCT, but not of WBC and CRP.</p< Conclusions CD64 and PCT are highly specific for infectious disease, but they predominantly measure bacteremia. Their use in hospital practice has yet to be defined, and especially so in localized infections

    Independence, institutionalization, death and treatment costs 18 months after rehabilitation of older people in two different primary health care settings

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    <p>Abstract</p> <p>Background</p> <p>The optimal setting and content of primary health care rehabilitation of older people is not known. Our aim was to study independence, institutionalization, death and treatment costs 18 months after primary care rehabilitation of older people in two different settings.</p> <p>Methods</p> <p>Eighteen months follow-up of an open, prospective study comparing the outcome of multi-disciplinary rehabilitation of older people, in a structured and intensive Primary care dedicated inpatient rehabilitation (PCDIR, n=202) versus a less structured and less intensive Primary care nursing home rehabilitation (PCNHR, n=100). Participants: 302 patients, disabled from stroke, hip-fracture, osteoarthritis and other chronic diseases, aged ≥65years, assessed to have a rehabilitation potential and being referred from general hospital or own residence. Outcome measures: Primary: Independence, assessed by Sunnaas ADL Index(SI). Secondary: Hospital and short-term nursing home length of stay (LOS); institutionalization, measured by institutional residence rate; death; and costs of rehabilitation and care. Statistical tests: T-tests, Correlation tests, Pearson’s χ<sup>2</sup>, ANCOVA, Regression and Kaplan-Meier analyses.</p> <p>Results</p> <p>Overall SI scores were 26.1 (SD 7.2) compared to 27.0 (SD 5.7) at the end of rehabilitation, a statistically, but not clinically significant reduction (p=0.003 95%CI(0.3-1.5)). The PCDIR patients scored 2.2points higher in SI than the PCNHR patients, adjusted for age, gender, baseline MMSE and SI scores (p=0.003, 95%CI(0.8-3.7)). Out of 49 patients staying >28 days in short-term nursing homes, PCNHR-patients stayed significantly longer than PCDIR-patients (mean difference 104.9 days, 95%CI(0.28-209.6), p=0.05). The institutionalization increased in PCNHR (from 12%-28%, p=0.001), but not in PCDIR (from 16.9%-19.3%, p= 0.45). The overall one year mortality rate was 9.6%. Average costs were substantially higher for PCNHR versus PCDIR. The difference per patient was 3528€ for rehabilitation (p<0.001, 95%CI(2455–4756)), and 10134€ for the at-home care (p=0.002, 95%CI(4066–16202)). The total costs of rehabilitation and care were 18702€ (=1.6 times) higher for PCNHR than for PCDIR.</p> <p>Conclusions</p> <p>At 18 months follow-up the PCDIR-patients maintained higher levels of independence, spent fewer days in short-term nursing homes, and did not increase the institutionalization compared to PCNHR. The costs of rehabilitation and care were substantially lower for PCDIR. More communities should consider adopting the PCDIR model.</p> <p>Trial registration</p> <p>Clinicaltrials.gov ID NCT01457300</p

    Cellular inflammatory response to persistent localized Staphylococcus aureus infection: phenotypical and functional characterization of polymorphonuclear neutrophils (PMN)

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    Persistent, localized Staphylococcus aureus infections, refractory to antibiotic treatment, can result in massive tissue destruction and surgical intervention is often the only therapeutic option. In that context, we investigated patients with S. aureus-induced infection at various sites, apparent as either olecranon bursitis, empyema of the knee joint or soft tissue abscess formation. As expected, a prominent leucocyte infiltrate was found, consisting predominantly of polymorphonuclear neutrophils (PMN) (up to 75%) and to a lesser extent of T lymphocytes and natural killer (NK) cells. In line with their bactericidal capacity, PMN expressed the high-affinity receptor for IgG, CD64 and the lipopolysaccharide (LPS) receptor CD14; moreover, the oxygen radical production in response to the bacterial peptide f-MLP was enhanced, while chemotactic activity was greatly reduced. The more intriguing finding, however, was that a portion of PMN had acquired major histocompatibility complex (MHC) class II antigens and CD83, indicative of a transdifferentiation of PMN to cells with dendritic-like characteristics. Of note is that a similar transdifferentiation can be induced in PMN in vitro, e.g. by gamma interferon or by tumour necrosis factor alpha. Co-cultivation of transdifferentiated PMN with autologous T lymphocytes resulted in prominent T cell proliferation, provided that S. aureus enterotoxin A was added. Taken together, persistent S. aureus infection induces PMN to acquire characteristics of dendritic cells, which in turn might promote the local immune response

    C-reactive protein-mediated phagocytosis and phospholipase D signalling through the high-affinity receptor for immunoglobulin G (FcγRI)

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    C-reactive protein (CRP) is the prototypic acute-phase protein in man which performs innate immune functions. CRP-mediated phagocytosis may be indirect, through activation of complement and complement receptors, or direct, through receptors for the Fc portion of immunoglobulin G (IgG; FcγRs) or even a putative CRP-specific receptor. No strong evidence has been shown to indicate which receptors may be responsible for phagocytosis or signalling responses. Using BIAcore technology, we confirm that CRP binds directly to the extracellular portion of FcγRI with a threefold higher affinity than IgG (K(D) = 0·81 × 10(−9) m). Binding is Ca(2+) dependent and is inhibited by IgG1 but not by phosphorylcholine (PC). CRP opsonization (using CRP concentrations within the normal human serum range) of PC-conjugated sheep erythrocytes increased phagocytosis of these particles by COS-7 cells transfected with FcγRI-II chimaera or FcγRI/γ-chain. Interferon-γ-treated U937 cells, which signal through FcγRI to activate phospholipase D (PLD) in response to cross-linked IgG, were also activated by CRP without any requirement for further cross-linking. These studies indicate that CRP is capable of binding to and cross-linking FcγRI thereby resulting in PLD activation and increased phagocytosis. Uptake by FcγRI has been reported to promote various acquired immune responses suggesting that CRP could act in a similar way
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