Suchergebnisse

IntroductionRheumatoid arthritis (RA) imposes a considerable burden on society in terms of morbidity, long-term disability, and costs. RA prevalence is poorly described in Australia, and linked health datasets can provide a more meaningful picture for RA epidemiology in the Australian population.
Objectives and ApproachWe extracted data on all patients identified in the WA Hospital Morbidity Data Collection between 1995 and 2014, with the International Classification of Diseases (ICD) codes for RA (ICD 10 M05.00–M06.99, and the corresponding ICD 9 codes). We estimated RA point- and period prevalence rates per 1000 hospital separations and annual average percentage changes, with the total number of hospital separations each year obtained from the Australian Institute of Health and Welfare, which served as the denominator.
ResultsA total of 17,125 patients were admitted to WA hospitals with a diagnostic code for RA over the study period (1995-2014). The total number of hospital separations for RA patients was 50,353, indicating an average of three hospital separations per patient over twenty years. The RA prevalence was 3.4 per 1000 separations over the study period, with a -2.89% annual average decrease since 1995.The RA point prevalence remained constant in the early part of the study period, at 7.9 per 1000 separations, then decreased in the later years, from 3 per 1000 separations in 2009 to 1.9 per 1000 separations in 2014.
Conclusion / ImplicationsThese data demonstrate that hospitalisation for RA has decreased considerably in WA over the last two decades. As this decrease roughly coincides with the introduction of biological drug treatment for RA, the reduced need for hospital admission is likely due to improvements in RA management.

Background/ObjectivePatients with IgA vasculitis (IgAV aka Henoch Schonlein) may require aggressive initial treatment, are prone to disease relapses and may have sustained abnormal IgA responsiveness. We investigated whether the relatively rare diagnosis of childhood IgAV is associated with subsequent comorbidity, hospitalisation and interventions.
MethodsUsing linked administrative health data from the Western Australian Rheumatic Disease Registry we performed an observational cohort study comparing hospitalisation and ED visit rates(per 1000 person years), comorbidity accrual (Charlson comorbidity index; CCI) and procedures between 494 IgAV patients < 20 years and 1385 matched controls over a twenty-year period.
ResultsHospitalisation was proportionally (73.5 vs 51.5%) and by rate (21.7 vs 18.9; rate ratio 1.15, p<0.01) increased in IgAV patients. IgAV patients more often underwent diagnostic and medical procedures than controls, who had higher rates of surgical interventions. ED visit frequency (25 vs 16%) and rate (10.8 vs 8.43, rate ratio 1.29, (p<0.01) was also increased in IgAV patients, who more often accrued peptic ulcer and renal disease than controls and had an increased accrual of CCI ≥3.
Conclusions/ImplicationsA diagnosis of IgAV in childhood significantly increases the risk and rate of subsequent hospital admission, ED visits and accrual of severe comorbidity. Although often considered a self-limiting disease, the occurrence of childhood IgAV signifies the presence of a sustained predisposition to illness, likely related to abnormal IgA functioning.

Ankylosing spondylitis (AS) is a common, highly heritable, inflammatory arthritis for which HLA-B*27 is the major genetic risk factor, although its role in the aetiology of AS remains elusive. To better understand the genetic basis of the MHC susceptibility loci, we genotyped 7,264 MHC SNPs in 22,647 AS cases and controls of European descent. We impute SNPs, classical HLA alleles and amino-acid residues within HLA proteins, and tested these for association to AS status. Here we show that in addition to effects due to HLA-B*27 alleles, several other HLA-B alleles also affect susceptibility. After controlling for the associated haplotypes in HLA-B, we observe independent associations with variants in the HLA-A, HLA-DPB1 and HLA-DRB1 loci. We also demonstrate that the ERAP1 SNP rs30187 association is not restricted only to carriers of HLA-B*27 but also found in HLA-B*40:01 carriers independently of HLA-B*27 genotype. ; We thank all participating subjects with AS and healthy individuals who provided the DNA and clinical information necessary for this study. This work was in part funded by grants from Arthritis Research UK (19536 and 18797), the NIHR Oxford comprehensive Biomedical Research Centre (immunity and inflammation theme A93081) and NIHR Thames Valley collaborative research network and National Ankylosing Spondylitis Society (UK). SPARCC was established through the support of the Arthritis Society of Canada. Support was received from National Institutes of Health/National Institute of Allergy and Infectious Diseases grant 1U01AI09090-01. This work was supported in part by grant PI12/02587 (Inst. Carlos III, Spain) and by European Union 'Fondos FEDER'. Support was received from Agence Nationale de la Recherche (grant ANR 2010 GEMISA and Investissements d'Avenir programme ANR-11-IDEX-0005-02), the Société Française de Rhumatologie (SFR) and the Arthritis Foundation. M.W. is funded by the Intramural Research Program, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health. M.A.B. is funded by a National Health and Medical Research Council (Australia) Senior Principal Research Fellowship. D.M.E. is funded by an Australian Research Council Future Fellowship (FT130101709). P.I.W.d.B. is funded in part by the Netherlands Organization for Scientific Research (VIDI Vernieuwingsimpuls project 016.126.354) and by the National Institutes of Health (1R01AR062886-1). ; Peer reviewed