Objective. To quantify potential risk factors for septic arthritis, in order to identify a basis for prevention.
Methods. The occurrence of potential risk factors for septic arthritis in patients ...with joint diseases attending a rheumatic disease clinic was prospectively monitored at 3‐m onth intervals over a period of 3 years. Potential risk factors investigated were type of joint disease, comorbidity, medication, joint prosthesis, infections, and invasive procedures. The frequencies of risk factors in patients with and those without septic arthritis were compared using multiple logistic regression analysis.
Results. There were 37 patients with and 4,870 without septic arthritis. Risk factors for developing septic arthritis were age ≥80 years (odds ratio OR = 3.5, 95% confidence interval 95% CI 1.4–8.6), diabetes mellitus (OR = 3.3, 95% CI 1.1–10.1), rheumatoid arthritis (OR = 4.0, 95% CI 1.9–8.3), hip and/or knee prosthesis (OR = 15, 95% CI 4.1–54.3), joint surgery (OR = 5.1, 95% CI 2.2–11.9), and skin infection (OR = 27.2, 95% CI 7.6–97.1)
Conclusion. These findings indicate that preventive measures against septic arthritis in patients with joint diseases should mainly be directed at those with joint prostheses and/or skin infection.
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Objective. To assess the outcome and adverse prognostic factors of bacterial arthritis (BA).
Methods. In a prospective community survey of BA, data were collected at the time of diagnosis and at a ...mean of 2 years later. A poor patient outcome was defined as death due to BA or severe overall functional deterioration. A poor joint outcome was defined as amputation, arthrodesis, prosthetic surgery, or severe functional deterioration. Possible prognostic factors were analyzed by univariate analysis.
Results. BA was diagnosed in 154 patients, 121 adults and 33 children. One‐half of the adults had a preexisting joint disease and 29% of the infected joints contained synthetic material. The patient outcome was poor in 21% of all patients, and the joint outcome was poor in 33% of the surviving patients. Adverse prognostic factors were an older age, preexisting joint disease, and an infected joint containing synthetic material. These factors were interrelated. There was no association between a poor outcome and young age, comorbidity, immunosuppressive medication, functional class, multiple infected joints, type of microorganism, or treatment delay.
Conclusion. BA had a poor outcome in almost one‐half of the patients. Patients who were older, had a preexisting joint disease, and/or had an infected joint containing synthetic material had the poorest prognosis.
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Objective
In a sibpair study of osteoarthritis (OA) patients, we investigated whether, upon stimulation with lipopolysaccharide (LPS), variations in the innate ex vivo production of interleukin‐1β ...(IL‐1β), IL‐1 receptor antagonist (IL‐1Ra), IL‐10, and tumor necrosis factor α (TNFα) in whole‐blood assays contribute to the risk of OA.
Methods
Data from 305 patients with OA at multiple sites (hand, knee, hip, and spine), whose median age was 60 years (range 43–79 years), were compared with those from 137 controls. OA was defined in accordance with the American College of Rheumatology criteria. Whole‐blood samples were stimulated with LPS (10 ng/ml). In the supernatants, cytokines were measured by enzyme‐linked immunosorbent assay. Odds ratios (ORs) were used as measures of the relative risk of OA in relation to quartiles of IL‐1β, IL‐1Ra, TNFα, and IL‐10 production. The ORs were adjusted for sex and age, and 95% confidence intervals (95% CIs) were computed using robust standard errors to take into account the intrafamily effect.
Results
Subjects in the highest quartile of IL‐1β and IL‐1Ra had an increased risk of OA (OR 3.3, 95% CI 1.4–7.9 and OR 8.0, 95% CI 3.7–17.4, respectively), while subjects in the lowest quartile of IL‐10 had a 3‐fold increased risk of OA (OR 3.1, 95% CI 1.5–6.5). High innate ex vivo production of TNFα was not associated with an increased risk of OA.
Conclusion
Subjects with a high innate ex vivo production of IL‐1β and IL‐1Ra and low innate ex vivo production of IL‐10 have an increased risk of OA. These results suggest that a proportion of the genetic susceptibility to OA may be encoded for by variations in innate cytokine activity.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
In a sibpair study of osteoarthritis (OA) patients, we investigated whether, upon stimulation with lipopolysaccharide (LPS), variations in the innate ex vivo production of interleukin-1beta ...(IL-1beta), IL-1 receptor antagonist (IL-1Ra), IL-10, and tumor necrosis factor alpha (TNFalpha) in whole-blood assays contribute to the risk of OA.
Data from 305 patients with OA at multiple sites (hand, knee, hip, and spine), whose median age was 60 years (range 43-79 years), were compared with those from 137 controls. OA was defined in accordance with the American College of Rheumatology criteria. Whole-blood samples were stimulated with LPS (10 ng/ml). In the supernatants, cytokines were measured by enzyme-linked immunosorbent assay. Odds ratios (ORs) were used as measures of the relative risk of OA in relation to quartiles of IL-1beta, IL-1Ra, TNFalpha, and IL-10 production. The ORs were adjusted for sex and age, and 95% confidence intervals (95% CIs) were computed using robust standard errors to take into account the intrafamily effect.
Subjects in the highest quartile of IL-1beta and IL-1Ra had an increased risk of OA (OR 3.3, 95% CI 1.4-7.9 and OR 8.0, 95% CI 3.7-17.4, respectively), while subjects in the lowest quartile of IL-10 had a 3-fold increased risk of OA (OR 3.1, 95% CI 1.5-6.5). High innate ex vivo production of TNFalpha was not associated with an increased risk of OA.
Subjects with a high innate ex vivo production of IL-1beta and IL-1Ra and low innate ex vivo production of IL-10 have an increased risk of OA. These results suggest that a proportion of the genetic susceptibility to OA may be encoded for by variations in innate cytokine activity.
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BFBNIB, FZAB, GIS, IJS, KILJ, OILJ, SBCE, SBMB, UL, UPUK
Objective. Prednisone is frequently used in the treatment of elderly‐onset rheumatoid arthritis (RA), but the balance between efficacy and toxicity, including the effect on bone mass, has not been ...investigated in long‐term studies. This prospective, randomized study was undertaken to compare disease activity and bone mass during long‐term treatment with prednisone versus chloroquine in this patient population.
Methods. Patients with active RA diagnosed at age ≥ 60 were randomized to receive prednisone (15 mg/day for 1 month, with the dosage tapered as low as possible thereafter) (n = 28) or chloroquine (n = 28). Patients who did not show a response received other second‐line drugs as an adjunct to prednisone or as a replacement for chloroquine. Bone mass was measured by dual‐energy x‐ray absorptiometry. The study duration was 2 years.
Results. During the 2 years, treatment with other second‐line drugs was needed for 12 patients in the prednisone group (43%) and 8 in the chloroquine group (29%). Functional capacity and disease activity improved significantly in both groups and did not differ significantly between the groups, except for a greater improvement in the prednisone group at 1 month. Radiographic scores for joint destruction progressed similarly in both groups. There was a nonsignificant excess bone loss of 1.8% in the spine and 1.5% in the hip in the prednisone group, compared with the chloroquine group.
Conclusion. Neither treatment was entirely satisfactory since a significant number of patients needed an additional second‐line drug over the 2‐year period.
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