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Sökning: L773:2326 5205 OR L773:2326 5191 > (2015-2019)

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  • Ahmad Kiadaliri, Aliasghar, et al. (författare)
  • Rheumatoid arthritis as underlying cause of death in 31 countries, 1987-2011: Trend analysis of WHO mortality database
  • 2017
  • Ingår i: Arthritis & Rheumatology. - : Wiley. - 2326-5205 .- 2326-5191. ; 69:8, s. 1560-1565
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective To examine trends in rheumatoid arthritis (RA) as an underlying cause of death (UCD) in 31 countries across the globe during 1987-2011. Methods Data on mortality and population were collected from the World Health Organization mortality database and the United Nations. Age-standardized mortality rates (ASMR) were calculated by means of direct standardization. We applied joinpoint regression analysis for trend analysis. Between-country disparities were examined using between-country variance, and Gini coefficient. Due to low numbers of deaths, we smoothed our ASMR using a three-year moving average. The changes in number of RA deaths between 1987 and 2011 were decomposed using two counterfactual scenarios. Results The absolute number of deaths with RA registered as UCD declined from 9281 (0.12% of all-cause deaths) in 1987 to 8428 in 2011 (0.09% of all-cause deaths). The mean ASMR declined from 7.1/million person-years in 1987-89 to 3.7 in 2009-11 (48.2% reduction). Reduction of 25% or more in ASMR occurred in 21 countries while a corresponding increase was observed in 3 countries. There was a persistent reduction in RA mortality and, on average, the ASMR declined by 3.0% per year. The absolute and relative between-country disparities declined over the study period.CONCLUSION: Mortality rates attributable to RA have declined globally. However, there were substantial between-country disparities in RA mortality, though the disparities decreased over time. Population aging combined with fall in RA mortality may lead to an increase in the economic burden of disease that should be taken into consideration in policy-making. This article is protected by copyright. All rights reserved.
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  • Ali, Abukar, 1988, et al. (författare)
  • Antibiotic-killed Staphylococcus aureus induces destructive arthritis in mice.
  • 2015
  • Ingår i: Arthritis & rheumatology (Hoboken, N.J.). - : Wiley. - 2326-5205 .- 2326-5191. ; 67:1, s. 107-116
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Permanent reduction in joint function is a severe post-infectious complication in patients with Staphylococcus aureus septic arthritis. This reduction in joint function might be caused by persistent joint inflammation after the adequate eradication of bacteria by antibiotics. Methods: We studied whether antibiotic-killed S. aureus induced joint inflammation in mice and elucidated the molecular and cellular mechanism of this type of arthritis. Results: The intraarticular injection of antibiotic-killed S. aureus induced mild to moderate synovitis and bone erosions that lasted for a minimum of 14 days. The frequency and severity of synovitis were significantly reduced in tumor necrosis factor receptor 1 (TNFR1), receptor for Advanced Glycation End Products (RAGE), and toll like receptor 2 (TLR2) knockout mice compared with wild-type animals. The combined depletion of monocytes and neutrophils resulted in a significantly lower frequency of synovitis. Among bacterial factors, insoluble cell debris played a more important role than bacterial DNA or soluble components in inducing joint inflammation. Importantly, anti-TNF therapy abrogated the joint inflammation induced by antibiotic-killed S. aureus. Conclusion: Antibiotic-killed S. aureus induced and maintained the joint inflammation that is mediated through TLR2, TNFR1, and RAGE receptor. The cross-talk between neutrophils and monocytes is responsible for this type of arthritis. Anti-TNF therapy might be used as a novel therapeutic strategy, in combination with antibiotics, to treat staphylococcal septic arthritis. © 2014 American College of Rheumatology.
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  • Arnaud, Laurent, et al. (författare)
  • Effect of Corticosteroids and Cyclophosphamide on Sex Hormone Profiles in Male Patients With Systemic Lupus Erythematosus or Systemic Sclerosis
  • 2017
  • Ingår i: Arthritis & Rheumatology. - : WILEY. - 2326-5191 .- 2326-5205. ; 69:6, s. 1272-1279
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) are autoimmune diseases that predominantly affect female patients, and therefore fewer investigations have been conducted in men. The aim of this study was to analyze sex hormone levels in male patients with SLE and those with SSc, compared to matched controls, in relation to the use of corticosteroids and cyclophosphamide (CYC).Methods: Sex hormone levels were measured in fasting blood samples from male patients with SLE (n=71) and those with SSc (n=29) and compared to population-based, age-matched male controls. Relevant hormone profiles were identified using cluster analysis.Results: Male SLE patients had higher levels of luteinizing hormone (LH) (P<0.0001) and more frequent bioactive testosterone deficiency (P=0.02) than their matched controls. The current dosage of prednisolone correlated inversely with the levels of bioactive testosterone (r=-0.36, P=0.03). Cluster analysis identified a subset of SLE patients with increased levels of follicle-stimulating hormone, LH, and prolactin as well as lower levels of bioactive testosterone (P<0.0001) in relation to higher daily doses of prednisolone. In male SSc patients, levels of testosterone (P=0.03) and bioactive testosterone (P=0.02) were significantly lower than those in matched controls. Use of CYC during the previous year was associated with lower bioactive testosterone levels in both SLE patients (P=0.02) and SSc patients (P=0.01), after adjustment for age.Conclusion: The results of this study highlight the negative impact of corticosteroids on gonadal function in men with SLE. Furthermore, use of CYC during the year prior to study inclusion impaired bioactive testosterone levels in male patients with either SLE or SSc. Physicians should be more aware of the possibility of hypogonadism in male patients with autoimmune diseases. The need for hormonal supplementation remains to be formally evaluated in these patients.
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  • Askling, Johan, et al. (författare)
  • Is Rheumatoid Arthritis a Mortal Disease?
  • 2017
  • Ingår i: Arthritis & Rheumatology. - : Wiley-Blackwell. - 2326-5191 .- 2326-5205. ; 69:8, s. 1509-1511
  • Tidskriftsartikel (refereegranskat)
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