The ASAS Health Index and Environmental Factors Item Set: validity and reliability of the Swedish translations in Swedish patients with ankylosing spondylitis.

OBJECTIVES: To translate the Assessment of SpondyloArthritis international Society (ASAS) Health Index (HI) Environmental Factors Item Set (EFIS) into Swedish and culturally adapt it for a Swedish context, and to assess the construct validity of the Swedish version of the ASAS HI and test-retest reliability in ASAS HI and EFIS in Swedish patients with ankylosing spondylitis (AS). METHOD: Translation and cross-cultural adaptation of the EFIS were carried out according to a forward-backward procedure consisting of five steps. The construct validity of the ASAS HI was tested using Spearman correlation with standard health outcomes for axial spondyloarthritis (axSpA). Reliability was analysed by internal consistency with the Cronbach's alpha coefficient for ASAS HI, and test-retest reliability with intraclass correlation coefficients (ICCs) for ASAS HI and kappa agreement for the individual items of EFIS. RESULTS: The translation of EFIS showed acceptable face and content validity. ASAS HI showed an acceptable internal consistency (Cronbach's alpha 0.79), and excellent test-retest reliability (ICC 0.87). Test-retest reliability for EFIS showed varied results, with kappa agreement for the individual items ranging from poor (-0.027) to good (0.80). CONCLUSIONS: The Swedish version of ASAS HI proved to be valid and reliable and is recommended for assessing the impact of AS on global functioning and health. A Swedish version of EFIS has been produced and uploaded on the ASAS website. The EFIS proved to have acceptable face and content validity, and may contribute to the contextual interpretation of the ASAS HI.

Distinctive gut microbiomes of ankylosing spondylitis and inflammatory bowel disease patients suggest differing roles in pathogenesis and correlate with disease activity.

BACKGROUND: Multiple studies have confirmed dysbiosis in ankylosing spondylitis (AS) and inflammatory bowel disease (IBD); however, due to methodological differences across studies, it has not been possible to determine if these diseases have similar or different gut microbiomes. RESULTS: In this study, faecal and intestinal biopsies were obtained from 33 Australian AS patients (including 5 with concomitant IBD, 'AS-IBD'), 59 IBD patients and 105 healthy controls. Stool samples were also obtained from 16 Italian AS patients and 136 Swedish AS patients. Focusing on the Australian cohort, AS, AS-IBD and IBD patients differed from one another and from healthy controls in both alpha and beta diversity. AS patients with and without clinical IBD could be distinguished from one another with moderate accuracy using stool microbiome (AUC=0.754). Stool microbiome also accurately distinguished IBD patients from healthy controls (AUC=0.757). Microbiome composition was correlated with disease activity measured by BASDAI and faecal calprotectin (FCP) levels. Enrichment of potentially pathogenic Streptococcus was noted in AS, AS-IBD and IBD patients. Furthermore, enrichment of another potentially pathogenic genus, Haemophilus, was observed in AS, AS-IBD, IBD, AS patients with increased BASDAI, and IBD patients with faecal calprotectin >100 µg/mg. Apart from these genera, no other taxa were shared between AS and IBD patients. CONCLUSIONS: In conclusion, the distinct gut microbiome of AS and AS-IBD patients compared to IBD patients and healthy controls is consistent with immunological and genetic evidence suggesting that the gut plays a different role in driving AS compared with IBD. However, enrichment of two potentially pathogenic genera in both diseases suggests that the presence of a shared/common microbial trigger of disease cannot be discounted.

Factors associated with changes in volumetric bone mineral density and cortical area in men with ankylosing spondylitis: a 5-year prospective study using HRpQCT.

Patients with ankylosing spondylitis (AS) have impaired volumetric bone mineral density (vBMD) assessed with high-resolution peripheral computed tomography (HRpQCT). This first longitudinal HRpQCT study in AS shows that cortical and trabecular vBMD decreased at tibia and that signs of inflammation were associated with cortical bone loss at tibia and radius. INTRODUCTION: Patients with ankylosing spondylitis (AS) have reduced volumetric bone mineral density (vBMD) in the peripheral skeleton assessed with high-resolution peripheral quantitative computed tomography (HRpQCT). The aims were to investigate longitudinal changes in vBMD, cortical area, and microarchitecture and to assess factors associated with changes in vBMD and cortical area in men with AS. METHODS: HRpQCT of radius and tibia was performed in 54 men with AS at baseline and after 5 years. Univariate and multivariable linear regression analyses were used. RESULTS: At tibia, there were significant decreases exceeding least significant changes (LSC) in cortical and trabecular vBMD, mean (SD) percent change -1.0 (1.9) and -2.7 (5.0) respectively (p<0.001). In multivariable regression analyses, increase in disease activity measured by ASDAS_CRP from baseline to follow-up was associated with decreases in cortical vBMD (ß -0.86, 95% CI -1.31 to -0.41) and cortical area (ß -1.66, 95% CI -3.21 to -0.10) at tibia. At radius, no changes exceeded LSC. Nonetheless, increase in ASDAS_CRP was associated with decreases in cortical vBMD, and high time-averaged ESR was associated with decreases in cortical area. Treatment with TNF inhibitor ≥ 4 years during follow-up was associated with increases in cortical vBMD and cortical area at tibia, whereas exposure to bisphosphonates was associated with increases in cortical measurements at radius. No disease-related variables or treatments were associated with changes in trabecular vBMD. CONCLUSION: The findings in this first longitudinal HRpQCT study in patients with AS strengthen the importance of controlling disease activity to maintain bone density in the peripheral skeleton.

Concomitant Ro/SSA and La/SSB antibodies are biomarkers for the risk of venous thromboembolism and cerebral infarction in primary Sjögren's syndrome.

BACKGROUND: To assess the risk of incident cardiovascular disease in patients with primary Sjögren's syndrome, overall and stratified by Ro/SSA and La/SSB autoantibody status. METHODS: A cohort of patients with primary Sjögren's syndrome in Sweden (n = 960) and matched controls from the general population (n = 9035) were included, and data extracted from the National Patient Register to identify events of myocardial infarction, cerebral infarction and venous thromboembolism. Hazard ratios were estimated using cox proportional hazard regressions. RESULTS: During a median follow-up of 9.5 years, the overall hazard ratio (HR) was 1.6 (95% CI 1.2-2.1) for myocardial infarction, 1.2 (95% CI 0.9-1.7) for cerebral infarction and 2.1 (95% CI 1.6-2.9) for venous thromboembolism. Patients positive for both Ro/SSA and La/SSB autoantibodies had a substantially higher risk of cerebral infarction (HR 1.7, 95% CI 1.0-2.9) and venous thromboembolism (HR 3.1, 95% CI 1.9-4.8) than the general population. These risks were not significantly increased in Ro/SSA- and La/SSB-negative patients. Among autoantibody-positive patients, the highest HR of cerebral infarction was seen after ≥10 years disease duration (HR 2.8, 95% CI 1.4-5.4), while the HR for venous thromboembolism was highest 0-5 years after disease diagnosis (HR 4.7, 95% CI 2.3-9.3) and remained high throughout disease duration. CONCLUSIONS: Primary Sjögren's syndrome is associated with a markedly increased risk of cardiovascular disease and the presence of Ro/SSA and La/SSB autoantibodies identify the subgroup of patients carrying the highest risk. These findings suggest that monitoring and prevention of cardiovascular disease in this patient group should be considered.

Infections increase the risk of developing Sjögren's syndrome.

OBJECTIVE: Environmental factors have been suggested in the pathogenesis of rheumatic diseases. We here investigated whether infections increase the risk of developing primary Sjögren's syndrome (pSS). METHODS: Patients with pSS in Sweden (n = 945) and matched controls from the general population (n = 9048) were included, and data extracted from the National Patient Register to identify infections occurring before pSS diagnosis during a mean observational time of 16.0 years. Data were analysed using conditional logistic regression models. Sensitivity analyses were performed by varying exposure definition and adjusting for previous health care consumption. RESULTS: A history of infection associated with an increased risk of pSS (OR 1.9, 95% CI 1.6-2.3). Infections were more prominently associated with the development of SSA/SSB autoantibody-positive pSS (OR 2.7, 95% CI 2.0-3.5). When stratifying the analysis by organ system infected, respiratory infections increased the risk of developing pSS, both in patients with (OR 2.9, 95% CI 1.8-4.7) and without autoantibodies (OR 2.1, 95% CI 1.1-3.8), whilst skin and urogenital infections only significantly associated with the development of autoantibody-positive pSS (OR 3.2, 95% CI 1.8-5.5 and OR 2.7, 95% CI 1.7-4.2). Furthermore, a dose-response relationship was observed for infections and a risk to develop pSS with Ro/SSA and La/SSB antibodies. Gastrointestinal infections were not significantly associated with a risk of pSS. CONCLUSIONS: Infections increase the risk of developing pSS, most prominently SSA/SSB autoantibody-positive disease, suggesting that microbial triggers of immunity may partake in the pathogenetic process of pSS.

Comparison of agreement between internet-based registration of patient-reported outcomes and clinic-based paper forms within the Swedish Rheumatology Quality Register.

Objective: The Swedish Rheumatology Quality Register has implemented an internet-based method (PER) for registering patient-recorded outcome measures. The aim of this study was to compare the agreement between visual analogue scales (VASs) reported via PER and clinic-based reporting using paper forms. Methods: In a cross-sectional study (70 patients), the results of 79 registrations of VASs for global health, pain, and fatigue from PER were compared with corresponding clinic-based paper registrations. For patients with polyarthritis, 28-joint count Disease Activity Scores (DAS28) were computed. Patients with axial disease also completed Bath Ankylosing Spondylitis Disease Activity Index and Functional Index (BASDAI and BASFI) questionnaires. Mean differences and intraclass correlation coefficients (ICCs) were calculated. Agreement was visualized using Bland-Altman plots. Results: No statistically significant differences in VASs were found comparing PER and paper forms for VAS Global, VAS Pain, and VAS Fatigue (p = 0.295, 0.463, and 0.288, respectively). ICCs for VAS Global, Pain, and Fatigue ranged from 0.889 to 0.952, indicating excellent agreement. Bland-Altman plots for VAS did not show any proportional bias. The mean difference for DAS28 calculated by VASs from paper vs PER was -0.02 (n = 65, p = 0.660), and the mean difference for BASDAI was 0.04 (n = 11, p = 0.742). ICCs for DAS28 and BASDAI were 0.962 and 0.985, respectively. Of the participating patients, 60% preferred PER. Conclusion: Internet-based reporting for patient-reported outcomes in a clinical setting resulted in similar data for VASs and corresponding disease activity scores to clinic-based reporting on paper forms.

Hepatocyte growth factor is a potential biomarker for osteoproliferation and osteoporosis in ankylosing spondylitis.

We explored relations between serum hepatocyte growth factor (HGF), disease activity, osteoproliferation, and bone mineral density (BMD) in ankylosing spondylitis (AS), in comparison with healthy controls. HGF was increased especially in male AS patients and smokers and associated with both lower BMD and more chronic radiographic changes in the spine. INTRODUCTION: Ankylosing spondylitis (AS) is characterized by both osteoproliferation and increased bone loss. Biomarkers are requested to predict the processes. The aims of this study were to compare serum levels of hepatocyte growth factor (HGF), matrix metalloproteinase-3 (MMP-3), and vascular endothelial growth factor (VEGF) in AS patients with healthy controls (HC) and to explore the associations with disease activity, osteoproliferation, and bone mineral density (BMD). METHODS: Serum from AS patients (modified NY-criteria) and HC was analyzed for HGF, MMP-3, and VEGF with ELISA. Disease activity parameters were collected. Osteoproliferation was assessed with modified Stoke Ankylosing Spondylitis Spine Score (mSASSS) and BMD was measured in femoral neck. RESULTS: Totally, 204 AS patients and 80 sex and age matched HC were included. Serum HGF was higher in the AS patients compared with the HC, whereas serum MMP-3 and VEGF were not. Serum HGF was also higher in smokers and in the male AS patients positively correlated with age, BASMI, and mSASSS, and negatively correlated with BMD. The biomarkers were all positively associated with ESR, CRP, and WBC. In multiple linear regression analysis serum HGF remained associated with higher mSASSS and lower BMD, after adjusting for age, sex, CRP, smoking, and body mass index. CONCLUSIONS: Serum HGF was increased in male AS patients and associated with higher mSASSS and lower BMD. In addition, serum HGF was positively associated with risk factors for osteoproliferation such as age, CRP and smoking. HGF could be a potential biomarker of importance for the bone metabolism in AS. TRIAL REGISTRATION: NCT00858819.

The vitamin D status in ankylosing spondylitis in relation to intestinal inflammation, disease activity, and bone health: a cross-sectional study.

UNLABELLED: We assessed the vitamin D status in ankylosing spondylitis (AS) patients and healthy controls in the late winter when no vitamin D is produced by the sunlight. The vitamin D status was often poor, but not lower in AS and not associated with disease activity or signs of gut inflammation. INTRODUCTION: The aims of the study were to investigate the vitamin D levels attained mainly by dietary intake in ankylosing spondylitis (AS) in comparison with healthy controls and in relation to gut inflammation, measured indirectly by fecal calprotectin, disease activity, osteoproliferation, bone mineral density (BMD), and vertebral fractures. METHODS: Serum 25-hydroxy vitamin D (25(OH)D) was measured in 203 AS patients and 120 healthy controls at the end of "the vitamin D winter," when the out-door UVB irradiation is too low to allow synthesis of vitamin D3 in the skin at the latitude of Gothenburg, Sweden. Fecal calprotectin was measured in stool samples. Disease activity was assessed with CRP, ESR, ASDASCRP, BASDAI, BAS-G, BASFI, and BASMI. Lateral spine radiographs were scored for osteoproliferation and vertebral fractures using the mSASSS and Genant scores. BMD was measured in the lumbar spine and femoral neck. RESULTS: Vitamin D insufficiency (a serum 25(OH)D <50 nmol/L) was found in approximately 50 % of the AS patients, but serum 25(OH)D was not different from healthy controls and not significantly correlated with fecal calprotectin, gastrointestinal symptoms, disease activity parameters, mSASSS, BMD, or vertebral fractures. CONCLUSIONS: The vitamin D status was often poor in the late winter in AS but not different from the healthy controls. No evidence for a connection between subclinical gut inflammation, malabsorption, and hypovitaminosis D was found. Serum 25(OH)D was not associated with disease activity, osteoproliferation, BMD, or vertebral fractures. We suggest that the lower vitamin D levels in AS, previously found by others, may be caused by reduced out-door UVB exposure.

Validity of ankylosing spondylitis and undifferentiated spondyloarthritis diagnoses in the Swedish National Patient Register.

OBJECTIVES: Epidemiological studies of spondyloarthritis (SpA), using ICD codes from the Swedish National Patient Register (NPR), offer unique possibilities but hinge upon an understanding of the validity of the codes. The aim of this study was to validate the ICD codes for ankylosing spondylitis (AS) and undifferentiated SpA (uSpA) in the NPR against the established classification criteria [modified New York (mNY), Assessment of SpondyloArthritis international Society (ASAS), Amor, and European Spondyloarthropathy Study Group (ESSG) criteria]. METHOD: All patients with an ICD-8/9/10 code of AS or uSpA in the NPR 1966-2009 at a visit to a specialist in rheumatology or internal medicine or corresponding hospitalization, alive and living in Sweden 2009, were identified (n=20,089). Following a structured procedure to achieve geographical representativeness, 500 random patients with a diagnosis of AS or uSpA in 2007-2009 were selected. Based on a structured review of clinical records, positive predictive values (PPVs) for fulfilling the criteria sets were calculated. RESULTS: For those having received an ICD code for AS, the PPVs for fulfilling the mNY criteria or any set of SpA criteria were 70% and 89%, respectively. For those with an uSpA diagnosis (and never an AS diagnosis), the corresponding PPVs were 20% and 79%. The subset with both AS and uSpA diagnoses (overlap=12%) were as likely to fulfil the mNY criteria as the group that had been coded as AS only. CONCLUSIONS: The diagnosis codes for AS or uSpA had high PPVs, suggesting that our case identification in the Swedish NPR can be used for nationwide, population-based, epidemiological studies of these diseases.

Prevalence of diastolic dysfunction in patients with ankylosing spondylitis: a cross-sectional study.

OBJECTIVES: To determine the prevalence of diastolic dysfunction (DD) in patients with ankylosing spondylitis (AS) by following recommended criteria from the American Society of Echocardiography (ASE) and using single variables reflecting DD. METHOD: A total of 187 patients with AS (105 men; mean age 51 ± 13 years; mean duration of disease 15 ± 11 years) fulfilled the inclusion criteria and underwent pulsed-wave and tissue Doppler imaging. RESULTS: By following ASE recommended criteria, we observed that 12% of patients with AS had mild DD. We also compared single standard Doppler values with normal age-stratified reference values and showed a wide variation in the number of patients with AS outside the 95% confidence interval (CI) of normal values depending on the variable chosen (ranging from 1.1% to 30.5%). CONCLUSIONS: By following recommended criteria, our cross-sectional study shows that DD was infrequent and mild in patients with AS.

Genetic variants in CARD8 but not in NLRP3 are associated with ankylosing spondylitis.

OBJECTIVES: The NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome is important for interleukin-1beta (IL-1ß) processing as part of an innate immune response. Caspase recruitment domain family, member 8 (CARD8) is an inhibitor of nuclear factor kappa B (NF-κB) and possibly also a part of the NLRP3 inflammasome. The objective of this study was to evaluate one single nucleotide polymorphism (SNP) in CARD8 and three SNPs in NLRP3 in ankylosing spondylitis (AS) susceptibility and disease phenotype. METHOD: We recruited 492 AS patients from Southern Sweden fulfilling the modified New York criteria for AS, and assessed phenotypic characteristics from medical records and questionnaires. Patients with psoriasis or clinically overt inflammatory bowel disease (IBD) were excluded, as were patients without human leucocyte antigen B27 (HLA-B27). Three NLRP3 SNPs (rs35829419, rs4353135, and rs10733113) and one SNP in CARD8 (rs2043211) were genotyped by commercially available TaqMan assays, and the results compared at genotype and allele levels to those of 793 population-based controls. In a subgroup of the patients (n = 169), faecal calprotectin was assessed as a marker of subclinical intestinal inflammation. RESULTS: The minor allele (A) of CARD8-C10X (rs2043211) was associated with a decreased risk of AS in a dominant model [odds ratio (OR) 0.74, 95% confidence interval (CI) 0.54-0.94, p = 0.012] and at the allelic level (OR 0.81, 95% CI 0.68-0.97, p = 0.02), but was not associated with levels of faecal calprotectin. There was no association regarding NLRP3 SNPs and AS susceptibility, and none of the investigated SNPs were associated with iritis, anti-tumour necrosis factor (anti-TNF) therapy, or peripheral joint involvement. CONCLUSION: In a Swedish population, the minor allele of CARD8-C10X is associated with a decreased risk of AS, but not with levels of faecal calprotectin or disease phenotype.

A 5-year prospective population-based study of juvenile chronic arthritis: onset, disease process, and outcome.

OBJECTIVES: To investigate, in a population-based cohort of patients with juvenile chronic arthritis (JCA), onset characteristics, progression, outcome, and prognostic factors longitudinally for 5 years. METHODS: This cohort consisted of 132 incidence cases identified between 1984 and 1986 in southwestern Sweden followed for 5 years with annual reports of subgroup, joint assessment, disease activity, eye examinations, laboratory measurements, and medication. At the 5-year follow-up, the Childhood Health Assessment Questionnaire (Child-HAQ) was evaluated. European League Against Rheumatism (EULAR) criteria for diagnosis and disease activity were used. RESULTS: During the 5 years only four patients were lost to follow-up, 34% changed subgroup and 8% developed uveitis. At the 5-year follow-up the disease was active in 12% of the patients, stable in 28%, inactive in 25%, and in remission in 34%. Among those examined, 24% had radiological changes, of whom half had advanced changes. The Child-HAQ median score at the 5-year follow-up was 0.13 (range 0.0-1.9). The number of involved joints at inclusion correlated positively with active disease at the 5-year follow-up. Age at disease onset, the number of involved joints, and the number of joints with arthritis correlated positively with continuous disease and Child-HAQ score. CONCLUSION. Our study shows a diverse disease course during the first 5 years of JCA where one-third changed subgroup and two-thirds did not reach remission. Age of disease onset, the number of involved joints, and the number of joints with arthritis at inclusion were associated with poor outcome at the 5-year follow-up.

Decreased serum levels of TGF-ß1 are associated with renal damage in female patients with systemic lupus erythematosus.

INTRODUCTION: Transforming growth factor ß1 (TGF-ß1) has a large role in the control of autoimmunity. TGF-ß1 production by lymphocytes is reduced in systemic lupus erythematosus (SLE). Decreased levels of TGF-ß1 might associate to disease susceptibility, activity and organ damage in SLE. However, the correlation between TGF-ß1 levels and severity of renal damage in SLE has not been examined. METHODS: The present study was undertaken to assess the serum levels of total and active TGF-ß1 in 150 female patients with SLE and 31 healthy women. Simple and multiple regression analyses between TGF-ß1 levels and the diseases-related variables were performed in patients with SLE. RESULTS: Serum levels of both total and active TGF-ß1 were significantly reduced in patients with SLE compared with levels in healthy controls (p < 0.01). Total TGF-ß1 levels correlated positively with white blood cell, platelet counts, calculated glomerular filtration rate (GFR), and active TGF-ß1 level, and inversely with erythrocyte sedimentation rate (ESR). In multiple regression analysis, ESR and platelet counts remained determinants of total TGF-ß1. Total TGF-ß1 levels were lower in patients with high disease activity (SLEDAI > 10) and severe organ damage (SLICC > 3). Significantly lower levels of total TGF-ß1 were found in patients with severe renal damage, i.e. lower TGF-ß1 in patients with 24-h urine protein over 3.5 g than in those with below 3.5 g (p < 0.05); lower TGF-ß1 in patients with GFR less than 50 ml/min than in those with over 50 ml/min (p < 0.05). In contrast, active TGF-ß1 only correlated with platelet counts. There was no association between renal damage and the levels of active TGF-ß1. CONCLUSION: This study demonstrates significantly reduced serum levels of both total and active TGF-ß1 in women with SLE compared with healthy women. Total TGF-ß1 levels are correlated negatively with ESR and positively with blood platelets. Total TGF-ß1 levels were lower in SLE patients with high disease activity and severe organ damage. Importantly, the severity of the renal damage was associated with decreased serum levels of total TGF-ß1, suggesting that TGF-ß1 might be involved in pathogenesis of renal damage caused by lupus nephritis.

Health-related quality of life in systemic lupus erythematosus and its association with disease and work disability.

OBJECTIVES: To determine the health-related quality of life (HRQOL) and its relationship to disease variables, vertebral fractures, and employment status in female patients with systemic lupus erythematosus (SLE). METHODS: HRQOL was assessed with the Swedish version of the Medical Outcomes Study (MOS) 36-Item Short Form Survey (SF-36) in female patients (n=163) and in age- and sex-matched controls (n=1045). Associations between the SF-36 score and demographics, disease variables, prevalent vertebral fractures, and employment status were analysed. RESULTS: The SLE patients, aged 20 to 82 years, scored significantly lower than the controls on all SF-36 subscales. Patients with vertebral fractures were older, had greater disease damage, and lower physical functioning (PF) than patients without fractures. Of the SLE patients of working age (n=142), 54% worked full or part time. These patients scored their HRQOL significantly higher (better) than patients not working. Being able to work was significantly associated with low age and high scores in PF and role physical (RP): the area under the receiver operating characteristic (ROC) curve for these variables was 0.82, confidence interval 0.75-0.89. CONCLUSIONS: HRQOL is substantially lower in SLE than in the general population but working ability indicates better health. We encourage further research regarding the effects on HRQOL by preventive actions taken against work disability in SLE.

The use of complementary and alternative medicine in outpatients with inflammatory rheumatic diseases in Sweden.

OBJECTIVES: To study the use of complementary and alternative medicine (CAM) drugs and methods in patients with inflammatory rheumatic diseases, at rheumatology clinics in western Sweden, and to investigate possible associations between CAM-using habits and other characteristics of the patients. METHODS: Randomly selected rheumatology outpatients were asked to complete questionnaires about CAM usage, diagnoses, medication, quality of life (using the 36-item Short Form Health Survey, SF-36), fatigue (using the 20-item Multiple Fatigue Inventory, MFI-20), the Health Assessment Questionnaire (HAQ), and visual analogue scales (VAS) for global health, pain, and fatigue. RESULT: A total of 200 patients were included, 137 women and 63 men, mean age 55+/-16 and 54+/-15 years, respectively. Ongoing CAM use was reported by 58 patients (29%): 45 (22.5%) were taking CAM drugs, 20 (10%) were using CAM methods. Altogether 130 patients (65%) had used CAM at some time of their lives; 103 patients (51%) had used CAM drugs ever and 90 patients (45%) had used CAM methods ever. Women used more CAM drugs compared with men. Younger patients used more CAM. CAM use was associated with parameters indicating poorer health, mental component score (MCS) and physical component score (PCS) of SF-36, and VAS for global health and fatigue. Ongoing CAM method was associated with less use of immunomodulatory drugs. CONCLUSION: CAM use is widespread among rheumatology patients in Sweden. A total of 65% of the patients had experience of CAM treatment. Female sex, younger age, and poor health were associated with CAM utilization.

Resistin in serum is associated with higher levels of IL-1Ra in post-menopausal women with rheumatoid arthritis.

OBJECTIVES: The aim of this study was to investigate associations between serum levels of resistin, an adipokine and markers of inflammation, bone metabolism, plasma lipids and kidney function in post-menopausal RA patients and to evaluate if HRT during 2 yrs affected resistin levels. METHODS: Eighty-eight women were randomly allocated to receive HRT, vitamin D(3) and calcium or vitamin D(3) and calcium alone. Serum levels of resistin, IL-1beta, IL-1 receptor antagonist (IL-1Ra), IL-6, IL-6 soluble receptor, TNF-alpha were measured by ELISA, markers of bone metabolism, carboxyterminal cross-linked telopeptide of type I collagen (ICTP) and carboxyterminal propeptide of type I procollagen by RIA, ESR, CRP, Hb, creatinine and lipids by standard laboratory techniques, BMD and total lean mass (TLM) by DXA and joint destruction by Larsen score. Resistin was also measured in 42 healthy control women. RESULTS: There was no difference in resistin concentration between patients and healthy controls. Resistin was significantly correlated with IL-1Ra, CRP, TNF-alpha, ICTP, glucocorticosteroids and Larsen score and inversely with BMD, hip and with TLM. In multiple regression analysis, IL-1Ra, TLM and use of corticosteroids remained determinants of resistin. Patients treated with HRT displayed significant increase in resistin compared with controls in the first but not the second year. CONCLUSIONS: Resistin was associated with increased inflammation, particularly by the acute-phase reactant IL-1Ra antagonizing IL-1beta, joint destruction, glucocorticosteroids and with reduced BMD and TLM. These findings suggest resistin being a significant mediator in the inflammatory process in RA. Further studies examining the mechanisms behind the relation between resistin and IL-1Ra are encouraged. HRT does not seem to have important long-term effect on resistin.

Prevalence and risk factors of osteoporosis in female SLE patients-extended report.

OBJECTIVES: To determine the frequency of osteoporosis and possible risk factors of low bone mineral density (BMD) in women with systemic lupus erythematous (SLE) in western Sweden. In addition, to evaluate if adequate anti-osteoporotic treatment was provided. METHODS: BMD was measured at radius, lumbar spine and hip by dual X-ray absorptiometry (DXA). An 'expected' control BMD was calculated for each patient. Simple and multiple linear regression analyses were performed to determine associations between BMD and demographic and disease-related variables. RESULTS: One hundred and sixty-three women were included. Median age was 47 (20-82) yrs, 89 (55%) were post-menopausal and 85 (52%) were taking glucocorticosteroids. BMD was significantly reduced in all measured sites compared with expected BMD. Thirty-seven (23%), 18 (11%) and 6 (4%) of the patients were osteoporotic in at least one, two and three or more measured locations. Bisphosphonates were used by 23 (27%) of patients taking glucocorticosteroids and 13 (35%) with osteoporosis. High age and low weight or BMI were associated with low BMD in all measured sites. In total hip, high SLICC/American Collage of Rheumatology (ACR), ESR and 'combinations of DMARD' were additional markers of low BMD. High S-creatinine was associated with low BMD in lumbal spine whereas high S-creatinine and CRP were markers in radius. CONCLUSION: Women with SLE are at greater risk of osteoporosis compared with controls and few are treated adequately. Factors associated with low BMD in SLE are high age and low weight but also markers of inflammation, impaired kidney function and disease damage, however glucocorticosteroids were not associated.

Radiographic joint destruction in postmenopausal rheumatoid arthritis is strongly associated with generalised osteoporosis.

OBJECTIVES: To investigate determinants of joint destruction and reduced bone mineral density (BMD) in postmenopausal women with active rheumatoid arthritis (RA) not treated with bisphosphonates or hormone replacement therapy and to evaluate if there are common markers of erosive disease and bone loss. METHODS: BMD was measured using dual x ray absorptiometry and joint damage was examined by x ray examination according to the Larsen method in 88 patients with RA. Associations between BMD and Larsen score, and between demographic and disease related variables, including proinflammatory cytokines, HLA-DR4 epitopes, and markers of bone and cartilage turnover, were examined bivariately by simple and multiple linear regression analyses. RESULTS: 49/88 (56%) patients had osteoporosis in at least one site. Reduced BMD and increased joint destruction were associated with: at the forearm and femoral neck, high Larsen score, low weight, and old age (R(2)=0.381, p<0.001; R(2)=0.372, p<0.001, respectively); at the total hip, low weight, high Larsen score, and dose of injected glucocorticosteroids (R(2)=0.435, p<0.001); at the lumbar spine, low weight, reduced cartilage oligomeric matrix protein, and increased carboxyterminal propeptide of type I procollagen (R(2)=0.248, p<0.001). Larsen score was associated with long disease duration and increased C reactive protein (CRP) (R(2)=0.545, p<0.001). CONCLUSIONS: Osteoporosis is common in postmenopausal patients with RA. Low weight and high Larsen score were strongly associated with BMD reduction. Increased CRP and long disease duration were determinants of erosive disease in postmenopausal women with RA. These findings indicate common mechanisms of local and generalised bone loss in RA.