A multilevel analysis on the relationship between neighbourhood poverty and public hospital utilization: is the high Indigenous morbidity avoidable?

<p>Abstract</p> <p>Background</p> <p>The estimated life expectancy at birth for Indigenous Australians is 10-11 years less than the general Australian population. The mean family income for Indigenous people is also significantly lower than for non-Indigenous people. In this paper we examine poverty or socioeconomic disadvantage as an explanation for the Indigenous health gap in hospital morbidity in Australia.</p> <p>Methods</p> <p>We utilised a cross-sectional and ecological design using the Northern Territory public hospitalisation data from 1 July 2004 to 30 June 2008 and socio-economic indexes for areas (SEIFA) from the 2006 census. Multilevel logistic regression models were used to estimate odds ratios and confidence intervals. Both total and potentially avoidable hospitalisations were investigated.</p> <p>Results</p> <p>This study indicated that lifting SEIFA scores for family income and education/occupation by two quintile categories for low socio-economic Indigenous groups was sufficient to overcome the excess hospital utilisation among the Indigenous population compared with the non-Indigenous population. The results support a reframing of the Indigenous health gap as being a consequence of poverty and not simplistically of ethnicity.</p> <p>Conclusions</p> <p>Socio-economic disadvantage is a likely explanation for a substantial proportion of the hospital morbidity gap between Indigenous and non-Indigenous populations. Efforts to improve Indigenous health outcomes should recognise poverty as an underlying determinant of the health gap.</p

Genetic association analyses implicate aberrant regulation of innate and adaptive immunity genes in the pathogenesis of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a genetically complex autoimmune disease characterized by loss of immune tolerance to nuclear and cell surface antigens. Previous genome-wide association studies (GWAS) had modest sample sizes, reducing their scope and reliability. Our study comprised 7,219 cases and 15,991 controls of European ancestry, constituting a new GWAS, a meta-analysis with a published GWAS and a replication study. We have mapped 43 susceptibility loci, including ten new associations. Assisted by dense genome coverage, imputation provided evidence for missense variants underpinning associations in eight genes. Other likely causal genes were established by examining associated alleles for cis-acting eQTL effects in a range of ex vivo immune cells. We found an over-representation (n = 16) of transcription factors among SLE susceptibility genes. This finding supports the view that aberrantly regulated gene expression networks in multiple cell types in both the innate and adaptive immune response contribute to the risk of developing SLE

The end of the Australia antigen? An ecological study of the impact of universal newborn hepatitis B vaccination two decades on

Background: A universal newborn hepatitis B (HBV) vaccination program was introduced in the Northern Territory of Australia in 1990, followed by a school-based catch-up program. We evaluated the prevalence of hepatitis B infection in birthing women up to 20 years after vaccination and compared this to women born before the programs commenced. Methods: A cohort of birthing mothers was defined from Northern Territory public hospital birth records between 2005 and 2010 and linked to laboratory confirmed notifications of chronic HBV, based principally on a record of hepatitis B surface antigen detection. Prevalence of HBV was compared between women born before or after implementation of the newborn and catch-up vaccination programs. Findings: Among 10797 birthing mothers, 138 (1.3%) linked to a chronic HBV record. HBV prevalence was substantially higher in Aboriginal women compared to non-Indigenous women (2.4% versus 0.04%; p<0.001). Among 5678 Aboriginal women, those eligible for catch-up and newborn HBV vaccination programs had a significantly lower HBV prevalence than older women born prior to the programs: HBV prevalence respectively 2.2% versus 3.5%, (OR 0.61, 95%CI 0.43-0.88) and 0.8% versus 3.5% (OR 0.21, 95%CI 0.11-0.43). This represents a risk reduction of respectively 40% and 80% compared to unvaccinated women. Interpretation: The progressively greater reduction in the prevalence of chronic HBV in adult Aboriginal women co-inciding with eligibility for catch-up and newborn vaccination programs is consistent with a significant impact from both programs. The use of data derived from antenatal screening to track ongoing vaccine impact is applicable to a range of settings globally. © 2012 Elsevier Ltd

PTPN22 Association in Systemic Lupus Erythematosus (SLE) with Respect to Individual Ancestry and Clinical Sub-Phenotypes

Protein tyrosine phosphatase non-receptor type 22 (PTPN22) is a negative regulator of T-cell activation associated with several autoimmune diseases, including systemic lupus erythematosus (SLE). Missense rs2476601 is associated with SLE in individuals wit

Association of a functional IRF7 variant with systemic lupus erythematosus

Basic and Translational Research: 1.1 Genomics, genetic basis of disease, HLA/T cell recognitionOBJECTIVE: Previous genome wide association study conducted in a population of European ancestry identified rs4963128, a KIAA1542 SNP 23kb telomeric to IRF7, in strong association with SLE. This study was undertaken to investigate whether genetic polymorphism within IRF7 is a risk factor for the development of SLE. METHODS: A total of 5024 individuals from multiple ethnic groups …link_to_OA_fulltextThe 14th Congress of Asia Pacific League of Associations for Rheumatology, Hong Kong, China, 11-15 July 2010. In International Journal of Rheumatic Diseases, 2010, v. 13 suppl. 1, p. 9, abstract no. 069