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1.  A study of racial/ethnic differences in treatment preferences among lupus patients 
Rheumatology (Oxford, England)  2012;51(9):1697-1706.
Objectives. To determine whether there are racial/ethnic differences in the willingness of SLE patients to receive CYC or participate in clinical trials, and whether demographic, psychosocial and clinical characteristics contribute to these differences.
Methods. Data from 120 African-American and 62 white lupus patients were evaluated. Structured telephone interviews were conducted to determine treatment preferences, as well as to study characteristics and beliefs that may affect these preferences. Data were analysed using serial hierarchical multivariate logistic regression and deviances were calculated from a saturated model.
Results. Compared with their white counterparts, African-American SLE patients expressed less willingness to receive CYC (67.0% vs 84.9%, P = 0.02) if their lupus worsened. This racial/ethnic difference remained significant after adjusting for socioeconomic and psychosocial variables. Logistic regression analysis showed that African-American race [odds ratio (OR) 0.29, 95% CI 0.10, 0.80], physician trust (OR 1.05, 95% CI 1.00, 1.12) and perception of treatment effectiveness (OR 1.40, 95% CI 1.22, 1.61) were the most significant determinants of willingness to receive CYC. A trend in difference by race/ethnicity was also observed in willingness to participate in a clinical trial, but this difference was not significant.
Conclusion. This study demonstrated reduced likelihood of accepting CYC in African-American lupus patients compared with white lupus patients. This racial/ethnic variation was associated with belief in medication effectiveness and trust in the medical provider, suggesting that education about therapy and improved trust can influence decision-making among SLE patients.
doi:10.1093/rheumatology/kes128
PMCID: PMC3418647  PMID: 22653381
systemic lupus erythematosus; racial inequities; patient decision-making; patient preferences; cyclophosphamide
2.  Network Analysis of Associations between Serum Interferon Alpha Activity, Autoantibodies, and Clinical Features in Systemic Lupus Erythematosus 
Arthritis and rheumatism  2011;63(4):1044-1053.
Background
Interferon-alpha (IFN-α) is a primary pathogenic factor in systemic lupus erythematosus (SLE), and high IFN-α levels may be associated with particular clinical manifestations. The prevalence of individual clinical and serologic features differs significantly by ancestry. We used multivariate and network analyses to detect associations between clinical and serologic disease manifestations and serum IFN-α activity in a large diverse SLE cohort.
Methods
1089 SLE patients were studied (387 African-American, 186 Hispanic-American, and 516 European-American). Presence or absence of ACR clinical criteria for SLE, autoantibodies, and serum IFN-α activity data were analyzed in univariate and multivariate models. Iterative multivariate logistic regression was performed in each background separately to establish the network of associations between variables that were independently significant following Bonferroni correction.
Results
In all ancestral backgrounds, high IFN-α activity was associated with anti-Ro and anti-dsDNA antibodies (p-values 4.6×10−18 and 2.9 × 10−16 respectively). Younger age, non-European ancestry, and anti-RNP were also independently associated with increased serum IFN-α activity (p≤6.7×10−4). We found 14 unique associations between variables in network analysis, and only 7 of these associations were shared by more than one ancestral background. Associations between clinical criteria were different in different ancestral backgrounds, while autoantibody-IFN-α relationships were similar across backgrounds. IFN-α activity and autoantibodies were not associated with ACR clinical features in multivariate models.
Conclusions
Serum IFN-α activity was strongly and consistently associated with autoantibodies, and not independently associated with clinical features in SLE. IFN-α may be more relevant to humoral tolerance and initial pathogenesis than later clinical disease manifestations.
doi:10.1002/art.30187
PMCID: PMC3068224  PMID: 21162028
systemic lupus erythematosus; interferon alpha; autoantibodies; ancestry
3.  Osteopontin Alleles Are Associated with Clinical Characteristics in Systemic Lupus Erythematosus 
Variants of the osteopontin (OPN) gene have been associated with systemic lupus erythematosus (SLE) susceptibility and cytokine profiles in SLE patients. It is not known whether these alleles are associated with specific clinical phenotypes in SLE. We studied 252 well-characterized SLE patients from a multiethnic cohort, genotyping the rs11730582, rs28357094, rs6532040, and rs9138 SNPs in the OPN gene. Ancestry informative markers were used to control for genetic ancestry. The SLE-risk allele rs9138C in the 3′ UTR region was associated with photosensitivity in lupus patients across all ancestral backgrounds (meta-analysis OR = 3.2, 95% CI = 1.6–6.5, P = 1.0 × 10−3). Additionally, the promoter variant rs11730582C demonstrated suggestive evidence for association with two hematologic traits: thrombocytopenia (OR = 2.1, P = 0.023) and hemolytic anemia (OR = 2.6, P = 0.036). These clinical associations with SNPs in the promoter and 3′ UTR regions align with previously reported SLE-susceptibility SNPs in OPN and suggest potential roles for these variants in antibody-mediated cytopenias and skin inflammation in SLE.
doi:10.1155/2011/802581
PMCID: PMC3205903  PMID: 22131818
4.  DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice 
The Journal of Clinical Investigation  2008;118(7):2516-2525.
Chronic inflammation increases cancer risk. While it is clear that cell signaling elicited by inflammatory cytokines promotes tumor development, the impact of DNA damage production resulting from inflammation-associated reactive oxygen and nitrogen species (RONS) on tumor development has not been directly tested. RONS induce DNA damage that can be recognized by alkyladenine DNA glycosylase (Aag) to initiate base excision repair. Using a mouse model of episodic inflammatory bowel disease by repeated administration of dextran sulfate sodium in the drinking water, we show that Aag-mediated DNA repair prevents colonic epithelial damage and reduces the severity of dextran sulfate sodium–induced colon tumorigenesis. Importantly, DNA base lesions expected to be induced by RONS and recognized by Aag accumulated to higher levels in Aag-deficient animals following stimulation of colonic inflammation. Finally, as a test of the generality of this effect we show that Aag-deficient animals display more severe gastric lesions that are precursors of gastric cancer after chronic infection with Helicobacter pylori. These data demonstrate that the repair of DNA lesions formed by RONS during chronic inflammation is important for protection against colon carcinogenesis.
doi:10.1172/JCI35073
PMCID: PMC2423313  PMID: 18521188

Results 1-4 (4)