An intervention designed to improve sensory impairments in the elderly and indoor lighting in their homes: an exploratory randomized controlled trial

Background: Vision and hearing impairments in the elderly (aged over 80 years) and poor indoor lighting conditions in a home-care setting are risk factors for functional decline, reduced social participation, withdrawal, and accidents. Objective: We aimed to evaluate the changes in vision, hearing, and lighting conditions in the homes of participants aged over 80 years after implementation of a clinical intervention. Methods: We undertook an exploratory randomized, controlled experimental study of sensory impairments and lighting conditions in the homes of elderly aged over 80 years who received home care. The intervention group (IG) received advice and encouragement to improve their vision, hearing, and indoor lighting conditions in the home, with a 10-week follow-up period. The control group (CG) received their usual care and underwent the same vision and hearing tests but were provided no intervention. Results: Vision and hearing (self-assessed) and tested by Wilcoxon rank-sum test were significantly better (P=0.025 and P=0.008, respectively) in the IG after the intervention and follow-up. The test between the groups showed a significance of P=0.026 for visual acuity and P=0.098 for pure-tone average. The maximum and minimum lighting levels were significantly improved in the IG after the intervention (P=0.002 and P=0.039, respectively) but were unchanged in the CG. Conclusion: Several of the IG participants did not follow all of the advice; however, among those who did, vision, hearing, and lighting conditions were all significantly improved. It appears that modest interventions have great potential for improving vision and hearing. Older patients in the home-care setting cannot be expected to take the necessary action to improve their sensory impairments by themselves. They require close monitoring, help from a specialist, and help to improve the indoor lighting conditions in their homes

Increased levels of BAFF in patients with Systemic Lupus Erythematosus are associated with acute phase reactants, independent of BAFF genetics: a case control study

This article is part of Gro Østli Eilertsen's doctoral thesis. Available in Munin at http://hdl.handle.net/10037/3594Objectives. To determine whether increased levels of B-cell activating factor (BAFF) in patients with SLE are due to disease activity or genetic variations in the promoter region of the BAFF gene and BAFF gene expression. Methods. The case-control study included 101 SLE patients and 111 healthy controls. Five single nucleotide polymorphisms (SNPs) in the BAFF promoter region were investigated by melting point analysis: c.-2841 (T > C), c.-2704 (T > C), c.-2701 (A > T), c.-871 (C > T) and c.-514 (A > G). BAFF mRNA levels were determined by real-time PCR (BAFF-RQ) and serum BAFF (s-BAFF) levels were measured by ELISA. Independent predictors that might be correlated with increased s-BAFF in SLE patients were analysed by multivariate regression methods. Results. Although s-BAFF levels were increased in SLE patients (1.73 vs 0.98 ng/μl, P < 0.001), no specific BAFF genotype was found to associate with SLE. The different genotypes defined by the investigated SNPs were identified both in SLE patients and healthy controls with similar frequencies. No association was found between BAFF genotype and BAFF-RQ. s-BAFF was independent of other factors, correlated with CRP (β = 0.40, P < 0.001) and physician's visual analogue score (R = 0.21, P = 0.046) and inversely with haemoglobin (β = -0.32, P < 0.001) and IgA (β = -0.33, P = 0.001). Conclusions. Increased s-BAFF levels in SLE patients are associated with the acute-phase responses, CRP and haemoglobin, but probably not dependent on BAFF genotype or expression. This indicates that s-BAFF production occurs at sites of inflammation

Smoking associates with increased BAFF and decreased interferon-γlevels in patients with systemic lupus erythematosus

Objective - In SLE, smoking increases the burden of cutaneous disease and organ damage, and leads to premature mortality. However, the effect of smoking on disease manifestations and cytokine levels of patients with SLE is unclear. This study compared characteristics of patients with SLE across smoking status, and determined the association of smoking with serum cytokine levels. Method - A cross-sectional study of patients with SLE (n=99) during a research visit in which smoking status was ascertained. Smoking status was compared across classification criteria (American College of Rheumatology Classification Criteria for SLE (ACR97)), disease activity (SLE Disease Activity Index), autoantibody levels, accrued damage (Systemic Lupus International Collaborating Clinics/ACR Damage Index), and circulating concentrations of serum interferon-gamma (IFN-γ), interleukin (IL)-1β, IL-4, IL-6, IL-10, IL-12, IL-17, B cell-activating factor (BAFF), tumour necrosis factor-alpha, transforming growth factor beta 1 (TGF-β1), macrophage inflammatory protein 1 alpha (MIP-1α), MIP-1β and monocyte chemoattractant protein 1. Linear regression models determined the association between smoking and cytokine levels, adjusting for age and sex, clinical characteristics (model 1), and anti-inflammatory (IL-4, IL-10 and TGF- β1) and regulatory (IL-1β) cytokines (model 2). Results - Among patients with SLE (97.9% ANA+; mean 48.48 years old; 86.9% female; mean 10 years of disease duration), 35.4% (n=35 of 99) were smoking (an average of 7 cigarettes/day for 24 years). Smokers had increased odds of prevalent ACR97 malar rash (OR 3.40, 95% CI 1.23 to 9.34) and mucosal ulcers (OR 3.31, 95% CI 1.36 to 8.05). Smokers had more arthritis (OR 3.19, 95% CI 1.19 to 8.60), migraine (OR 2.82, 95% CI 1.07 to 7.44), Raynaud’s phenomenon (OR 5.15, 95% CI 1.95 to 13.56) and increased non-steroidal anti-inflammatory drug use (OR 6.88, 95% CI 1.99 to 23.72). Smoking associated with 27% increased BAFF levels (95% CI 6% to 48%) and 42% decreased IFN-γ levels (95% CI −79% to −5%) in model 2. Conclusion - In patients with SLE, smoking independently associated with increased BAFF and decreased IFN-γ levels, and an increased frequency of arthritis, migraine and Raynaud’s phenomenon. Smoking cessation is advisable to reduce systemic inflammation, reduce disease activity and improve host defence

Clinical epidemiology of Systemic Lupus Erythematosus with emphasis on nephritis and autoantibody production

Systemisk Lupus Erythematosus (SLE) er en kronisk sykdom der immunforsvaret produserer antistoffer som kan angripe kroppens egne organer. I 1997 ble klassifikasjonskriteriene for å stille diagnosen endret slik at flere typer autoantistoffer ble inkludert. For å undersøke mulige endringer etter innføring av de nye 1997 klassifikasjonskriteriene for SLE, delte vi inn pasientene i to grupper. En ny gruppe som fikk diagnosen basert på de nye klassifikasjonskriteriene, og en ”eldre” gruppe som tidligere var diagnostisert basert på kriterier fra 1982. Ved å sammenligne disse to gruppene, fant vi ut at den nye gruppen ble diagnostisert tidligere i sykdomsforløpet og en større andel hadde fått tidlig behandling i form av immundempende –, blodtrykks – og blodfortynnende medikamenter. Den nye gruppen hadde også en mildere sykdom, økt overlevelse og færre hadde nyresykdom. Dette betyr at ved å diagnostisere SLE tidlig vha. de nye klassifikasjonskriteriene fra 1997 og behandle mer aggressivt, forebygges nyresykdom og overlevelse øker. Slike funn er ikke påvist tidligere. Vi sammenlignet blodprøver av SLE-pasienter med en kontrollgruppe, men fant ingen genetiske forskjeller på BAFF-molekylet. Hos SLE-pasienter så vi derimot en klar korrelasjon mellom BAFF og akuttfase reaktanter. Dette betyr at BAFF har en større rolle ved vevsbetennelse enn ved produksjon av autoantistoffer

Soluble erythropoietin receptor levels associate with inflammatory mediators but not with disease activity or cumulative organ damage in patients with systemic lupus erythematosus

The erythropoietin receptor (EpoR) stimulates erythrocyte proliferation after erythropoietin binding. EpoR belongs to the cytokine receptor superfamily and can be found on macrophages and endothelial cells. As there are no data on the role of EpoR systemic autoimmune diseases, we investigated the role of soluble EpoR (sEpoR) in patients with systemic lupus erythematosus (SLE). In a cross-sectional study we recorded clinical characteristics, disease activity (SLEDAI-2K) and organ damage (SDI). sEpoR, autoantibodies and cytokines were measured by enzyme-linked immunosorbent assay (ELISA) in SLE patients (n = 100) and compared with a rheumatoid arthritis (RA) cohort (n = 57) and a cohort with non-inflammatory back pain (NIBP; n = 89). Data were analysed with non-parametric techniques. We found no significant difference in sEpoR levels across the SLE, RA and NIBP groups and sEpoR levels were similar in patients with (6% of SLE and 31% of RA) or without anaemia. sEpoR levels were unrelated to haemoglobin levels, SLEDAI-2K or SDI scores, but in both cohorts correlated with levels for C-reactive protein (CRP), interleukin-6 (IL-6), tumour necrosis factor (TNF) and IL-1 (all P  < 0.001). sEpoR levels are not involved in anaemia or erythropoietin resistance in SLE and RA patients, but closely mirror the underlying inflammatory process. This suggests that increased shedding of sEpoR during inflammation occurs at other sites than bone marrow

Hypocomplementemia as a Risk Factor for Organ Damage Accrual in Patients with Systemic Lupus Erythematosus

While it is a common practice to monitor complement levels in patients with systemic lupus erythematosus to aid in flare prediction and detection, it is unclear if this strategy is helpful in preventing subsequent organ damage. We studied longitudinal complement levels in 102 SLE patients during a median follow-up of 13.8 years (IQR 7.0, 23.1). Low complement was defined as C3 p p p = 0.9), frequency (SDI > 0, n = 60), and type of organ damage accrual were similar for patients with and without HC (OR 1.08, p > 0.20). Intermittent or sustained HC has no predictive value for damage accrual in SLE or the underlying disease activity over time. This together with significant discrepancies in the concurrence of low C3, C4, and anti-dsDNA Ab indicates frequent activation of the complement pathway by other factors than immune complexes in SLE

Increased levels of BAFF in patients with Systemic Lupus Erythematosus are associated with acute phase reactants, independent of BAFF genetics: a case control study

Objectives. To determine whether increased levels of B-cell activating factor (BAFF) in patients with SLE are due to disease activity or genetic variations in the promoter region of the BAFF gene and BAFF gene expression. Methods. The case-control study included 101 SLE patients and 111 healthy controls. Five single nucleotide polymorphisms (SNPs) in the BAFF promoter region were investigated by melting point analysis: c.-2841 (T > C), c.-2704 (T > C), c.-2701 (A > T), c.-871 (C > T) and c.-514 (A > G). BAFF mRNA levels were determined by real-time PCR (BAFF-RQ) and serum BAFF (s-BAFF) levels were measured by ELISA. Independent predictors that might be correlated with increased s-BAFF in SLE patients were analysed by multivariate regression methods. Results. Although s-BAFF levels were increased in SLE patients (1.73 vs 0.98 ng/μl, P < 0.001), no specific BAFF genotype was found to associate with SLE. The different genotypes defined by the investigated SNPs were identified both in SLE patients and healthy controls with similar frequencies. No association was found between BAFF genotype and BAFF-RQ. s-BAFF was independent of other factors, correlated with CRP (β = 0.40, P < 0.001) and physician's visual analogue score (R = 0.21, P = 0.046) and inversely with haemoglobin (β = -0.32, P < 0.001) and IgA (β = -0.33, P = 0.001). Conclusions. Increased s-BAFF levels in SLE patients are associated with the acute-phase responses, CRP and haemoglobin, but probably not dependent on BAFF genotype or expression. This indicates that s-BAFF production occurs at sites of inflammation

BAFF expression is increased in Lupus Nephritis and associated with activation of C1 inhibitor, α-1-acid-glycoprotein and endothelial markers.

B cell activating factor (BAFF) inhibitor therapy has recently been approved for non-renal Systemic Lupus Erythematosus (SLE). While BAFF plays a role in experimental lupus nephritis (LN), its role human LN is not well studied. Case control study in 102 SLE patients, 30 with LN (+LN) and 72 without LN (-LN) and 31 healthy controls. We analysed BAFF mRNA expression in PBMCs (BAFF-RQ) and serum BAFF (s-BAFF) levels and investigated their relation with clinical, histological- and additional acute phase proteins. Results: s-BAFF and BAFF-RQ were increased in +LN patients compared to controls, but their expression did not correlate with ISN/RPS class, Activity- or Chronicity index on biopsy. s-BAFF correlated with levels of anti-nucleosome antibodies, C1 inhibitor and α-1-acid-glycoprotein (AGP), while BAFF-RQ correlated inversely with Factor VIII. s-BAFF and BAFF mRNA levels are increased in LN patients, but do not reflect histological disease severity. The association of increased BAFF expression with both pro- and anti-inflammatory markers and reduced endothelial activation suggest that BAFF inhibition in LN may have diverse effects

The Influence of the 1997 Updated Classification Criteria for Systemic Lupus Erythematosus : Epidemiology, Disease Presentation, and Patient Management

The influence of the 1997 updated classification criteria for systemic lupus erythematosus: epidemiology, disease presentation, and patient management. Eilertsen GØ, Becker-Merok A, Nossent JC. Department of Rheumatology, Medical School, University of Tromsø, 9037 Tromsø, Norway. [email protected] OBJECTIVE: The 1997 update of the American College of Rheumatology classification criteria (ACR97) for systemic lupus erythematosus (SLE) has not been validated. We determined to what extent their introduction influenced the epidemiology and clinical characteristics of the disease in northern Norway. METHODS: Annual incidence and point-prevalence rates, clinical manifestations, and outcome were determined in an inception cohort of patients with SLE in northern Norway, included between 1996 and 2006, using ACR97 criteria (97acr). These findings were compared with a cohort from the same area enrolled 1978-1995 using the 1982 revised criteria ACR82 (82acr). RESULTS: The mean annual incidence of SLE was 3.00 for cohort 97acr (n = 58) versus 2.63 for cohort 82acr (n = 81) (p = 0.5). All patients in the 97acr cohort also fulfilled the 1982 criteria; however, significantly fewer patients presented with discoid rash [odds ratio (OR) 0.31)], arthritis (OR 0.24), renal (OR 0.28) or hematological disorder (OR 0.27), and significantly more with anti-dsDNA (OR 2.57) and antiphospholipid antibodies (OR 27.9). Initial treatment with intravenous pulse methylprednisolone (OR 9.23), azathioprine (OR 6.32), and low-dose aspirin (OR 20.9) was increased in cohort 97acr. Five- (95.2%) and 10-year survival (91.9%) rates were also improved for cohort 97acr. CONCLUSION: The ACR97 criteria set has construct validity compared to the ACR82 criteria set. SLE incidence remains unchanged in northern Norway, but a significant reduction of renal disease and further improvements in survival rates occurred simultaneously with increased serological surveillance with ELISA-based assays and early immunosuppressive and anticoagulant therapy