Why do patients want to have their blood tested? A qualitative study of patient expectations in general practice

BACKGROUND: General practitioners often take their impression of patients' expectations into account in their decision to have blood tests done. It is commonly recommended to involve patients in decision-making during consultations. The study aimed to obtain detailed information on patients' expectations about blood tests. METHODS: Qualitative study among patients in waiting rooms of general practices. Each patient was presented with a short questionnaire about their preferences in terms of diagnostics. Patients who would like blood tests to be done were interviewed. RESULTS: Fifty-seven (26%) of the 224 respondents wanted blood tests. Twenty-two were interviewed. Patients overestimated the qualities of blood tests. Favourable test results were regarded as proof of good health. Patients regarded blood tests as a useful instrument to screen for serious disorders, and were confirmed in this belief by people in their social environment and by the media. Many patients expected their GP to take an active test ordering approach, though some indicated that they might be convinced if their GP proposed a wait-and-see policy. CONCLUSIONS: GPs' perceptions about patient expectations seem justified: patients appear to have high hopes for testing as a diagnostic tool. They expect diagnostic certainty without mistakes and a proof of good health. The question is whether it would be desirable to remove patients' misconceptions, allowing them to participate in policy decisions on the basis of sound information, or whether it would be better to leave the misconceptions uncontested, in order to retain the 'magic' of additional tests and reassure patients. We expect that clarifying the precise nature of patients' expectations by the GP may be helpful in creating a diagnostic strategy that satisfies both patients and GPs. GPs will have to balance the benefits of reassuring their patients by means of blood tests which may be unnecessary against the benefits of avoiding unnecessary tests. Further research is needed into the effects of different types of patient information and the effects of testing on satisfaction and anxiety

Association of IFIH1 and pro-inflammatory mediators: Potential new clues in SLE-associated pathogenesis

This study was supported by the National Institute of Allergy, Immunology and Infectious Diseases, Office of Research on Women’s Health, National Institute of General Medical Sciences, and the National Institute of Arthritis, Musculoskeletal and Skin Diseases under award numbers U01AI101934, R01AI024717, U19AI082714, U54GM104938, P30GM103510, P30GM110766, P30AR053483, RC1AR058554, U34AR067392, and HHSN266200500026C. This publication is the sole responsibility of the authors and does not represent the views of the National Institutes of Health.Antiviral defenses are inappropriately activated in systemic lupus erythematosus (SLE) and association between SLE and the antiviral helicase gene, IFIH1, is well established. We sought to extend the previously reported association of pathogenic soluble mediators and autoantibodies with mouse Mda5 to its human ortholog, IFIH1. To better understand the role this gene plays in human lupus, we assessed association of IFIH1 variants with soluble mediators and autoantibodies in 357 European-American SLE patients, first-degree relatives, and unrelated, unaffected healthy controls. Association between each of 135 genotyped SNPs in IFIH1 and four lupus-associated plasma mediators, IL-6, TNF-α, IFN-β, and IP-10, were investigated via linear regression. No significant associations were found to SNPs orthologous to those identified in exon 13 of the mouse. However, outside of this region there were significant associations between IL-6 and rs76162067 (p = 0.008), as well as IP-10 and rs79711023 (p = 0.003), located in a region of IFIH1 previously shown to directly influence MDA-5 mediated IP-10 and IL-6 secretion. SLE patients and FDRs carrying the minor allele for rs79711023 demonstrated lower levels of IP-10, while only FDRs carrying the minor allele for rs76162067 demonstrated an increased level of IL-6. This would suggest that the change in IP-10 is genotypically driven, while the change in IL-6 may be reflective of SLE transition status. These data suggest that IFIH1 may contribute to SLE pathogenesis via altered inflammatory mechanisms.Yeshttp://www.plosone.org/static/editorial#pee

CD27-IgD- memory B cells are modulated by in vivo interleukin-6 receptor (IL-6R) blockade in rheumatoid arthritis

Introduction Enhanced B cell activity, particularly memory B cells have gained interest in evaluating response during therapies with biologics. CD27-IgD- double-negative (DN) B cells lacking the conventional memory marker CD27 are reported to be part of the memory compartment, however, only scarce data is available for rheumatoid arthritis (RA). We therefore focused on DN B cells in RA, studied their isotypes and modulation during interleukin-6 receptor (IL-6R) inhibition by tocilizumab (TCZ). Methods DN B cells were phenotypically analyzed from 40 RA patients during TCZ at baseline week 12, week 24 and 1 year. A single B cell polymerase chain reaction (PCR) approach was used to study Ig receptors, VH gene rearrangements and specific isotypes. Results Phenotypic analysis showed a significantly expanded population of DN B cells in RA which contain a heterogeneous mixture of IgG-, IgA- and IgM-expressing cells with a clear dominance of IgG+ cells. DN B cells carry rearranged heavy chain gene sequences with a diversified mutational pattern consistent with memory B cells. In contrast to tumor necrosis factor alpha (TNF-α) inhibition, a significant reduction in mutational frequency of BCR gene rearrangements at week 12, 24 and 1 year (P <0.0001) was observed by in vivo IL-6R inhibition. These changes were observed for all BCR isotypes IgG, IgA and IgM at week 12, 24 and 1 year (P <0.0001). IgA-RF, IgA serum level and IgA+ DN B cells decreased significantly (P <0.05) at week 12 and week 24 during TCZ. Patients with a good European League Against Rheumatism (EULAR) response to TCZ had less DN B cells at baseline as compared to moderate responders (P = 0.006). Univariate logistic regression analysis revealed that the frequency of DN B cells at baseline is inversely correlated to a subsequent good EULAR response (P = 0.024) with an odds ratio of 1.48 (95% confidence interval as 1.05 to 2.06). Conclusions In RA, the heterogeneous DN B cell compartment is expanded and dominated by IgG isotype. TCZ can modulate the mutational status of DN Ig isotype receptors over 1 year. Interestingly, the frequency of DN B cells in RA may serve as a baseline predictor of subsequent EULAR response to TCZ