Methods. Rabbits, injected with methylprednisolone (MPSL; 20 mg/kg), were divided into four groups: (i) MPSL alone; MPSL injection only, (ii) MPSL+needling; 2 days after MPSL injection, a hole (1.2 mm diameter) was drilled from the outer cortex 2.5 cm distal to the proximal end of the greater trochanter, (iii) MPSL+saline; 2 days after MPSL injection, 2 ml saline was injected directly into the bone marrow cavity, and (iv) MPSL+BMT; 2 days after MPSL injection, 1 x 10⁷/2 ml bone marrow cells (BMCs) were injected directly into the bone marrow cavity. Platelets, fibrinogen, prothrombin time and total cholesterol in peripheral blood were measured before and after treatment. Tissues were stained with haematoxylin and eosion and terminal deoxynucleotidyl-mediated deoxyuridine triphosphate nick-end labelling stain and immunostained for VEGF, while cell proliferation and viability of whole BMCs in the femur were analysed by cell cycle analysis and [³H]-thymidine uptake.

Results. The ON incidence in rabbits treated with MPSL alone, MPSL+needling and MPSL+saline was 72.7, 70.0 and 66.7%, respectively, while in the MPSL+BMT group, the incidence was 0%. Serological findings in the MPSL+BMT group were almost normalized. VEGF and TUNEL staining were reduced in the MPSL+BMT group compared with all other groups. There were significantly fewer BMCs in G1 phase from the MPSL+BMT group than the other groups, while uptake of [³H]-thymidine was significantly increased.

Conclusion. Direct injection of autologous BMCs into femurs prevents corticosteroid-induced ON following treatment with high-dose, short-term steroids.

Methods. Cytosolic protein extracts obtained from RA (n = 14) and SpA patients (n = 14) were analysed by gel electrophoresis and western blotting. Citrullinated vimentin isoforms were visualized by a combination of anti-modified citrulline (AMC) staining and anti-vimentin detections (V9, H-84). This was subsequently confirmed by immunoprecipitation. Autoantibody detection was verified using sera obtained form RA (n = 6) and SpA (n = 6) patients.

Results. A specific cluster of spots displayed on the 2D gel images of cytosolic synovial tissue extracts, was identified by mass spectrometry as vimentin. Interestingly, our results suggested that these isoforms could be the result of caspase cleavage. In addition, these cleaved forms of vimentin were found to be citrullinated in synovial cytosolic protein extracts of inflammatory arthritides, mainly in RA patients. Caspase-3 is able to cleave vimentin at amino acid 85. Western blot analysis with a specific antibody against amino acids 1–84 of vimentin (H-84) confirmed that the citrullinated isoforms of vimentin were lacking this part of the protein. These results were also confirmed by immunoprecipitation of vimentin derived from cytosolic protein extracts of RA and SpA patients. Furthermore, the presence of autoantibodies against these citrullinated processed forms of vimentin was found to be predominantly associated with RA patients.

Conclusions. These findings show the presence of processed citrullinated vimentin in inflammatory arthritides, mainly in RA and suggest a possible origin of the ACPA immune response in RA.

Methods. Male DBA/1 mice from different litters were caged together at the age of 8 weeks. Treatment with zoledronic acid (ZA) (100 ng/g) or placebo was started at the age of 10 weeks and administered every 2 weeks. Clinical incidence and severity of arthritis were evaluated twice a week until the age of 26 weeks. At this point, bone density measurements were performed, mice were sacrificed and severity of arthritis was evaluated by histology.

Results. Treatment with ZA did not affect incidence or clinical severity of arthritis in male DBA/1 mice. ZA treatment significantly increased bone mineral density and content as demonstrated by dual X-ray densitometry and peripheral quantitative CT. However, the treatment did not affect histomorphological appearance of arthritis or ankylosis.

Conclusions. These data suggest that bone erosion at the enthesis does not necessarily precede entheseal ankylosis. Therefore, these observations further support the concept that inflammation and new tissue formation in SpA are at least partially uncoupled events and may be different therapeutic targets.

Methods. Receptor expression and IFN synthesis were measured in T cells of patients with active disease by cytofluorometry and compared with expression in patients in remission and in healthy donors.

Results. During active disease, a small but conspicuous population of CD8+CD28+CD11b+ was found which produced IFN. In healthy donors and in patients in remission or undergoing immunosuppressive therapy, CD11b was exclusively associated with CD8+CD28– cells, the latter being more frequent in patients with long-lasting or severe disease. In vitro experiments confirmed that CD11b is up-regulated when T cells are activated. After multiple rounds of restimulation, the CD11b expression persists whereas CD28 expression is lost, compatible with the notion that CD8+CD28+CD11b+ represents a transient phenotype in the course of T-cell activation. The IFN-producing T cells activated polymorphonuclear neutrophils (PMN) to express MHC class II, thus generating the same PMN phenotype as in patients with active ANCA-associated vasculitis. A similar PMN phenotype could be generated by cultivation with supernatants of activated T cells or by IFN alone, but not by antibodies to proteinase 3.

Conclusions. In active primary vasculitis, a small population of CD8+ T cells, identified by the expression of CD11b, expands, producing IFN. These T cells could activate PMN, thus generating a long-living and potentially destructive PMN phenotype.

Methods. The polymorphisms 869T/C and –509C/T were determined in 73 gout patients and 114 healthy controls among male Taiwanese using the PCR–restriction fragment length polymorphism method. Each patient was matched with 1–2 controls by age within 1–2 yrs. The tophus number was measured from all the patients’ arms and legs.

Results. Neither 869T/C nor –509C/T showed a significant association between patients and controls in the proportions of genotypes, allele frequency or dominant and recessive models. The mean number of tophi for all patients was 1.53 ± 3.44, showing a significant difference in distribution among the genotypes at polymorphism 869T/C (P = 0.006), but not those in polymorphism –509C/T (P > 0.05). Those carrying genotype CC at polymorphism 869T/C have a mean number of tophi 0.35 (± 1.11), which is significantly lower than those carrying genotype TT (3.73 ± 4.67; P < 0.05). Those with genotype TT at polymorphism 869T/C also had 11.06 times the likelihood of having at least one tophus compared with the genotype CC after adjustment of hyperuricaemia (95% CI = 1.84, 66.36; P = 0.009). However, except for the tophus number, these two polymorphisms did not show any significant association with the clinical characteristics or biochemical markers.

Conclusions. The polymorphism 869T/C in TGF-β1 gene has a significant association with the occurrence of tophus in gout patients.

Methods. To investigate the anti-proteasome response in more detail and to disclose reactivities against former neglected subunits, two-dimensional electrophoresis followed by immunoblotting was used. As a novel antigen source, the immunosubunits LMP2 (β1i) and LMP7 (β5i) were expressed as recombinant proteins and employed in ELISA.

Results. The subunits Iota (1) and Zeta (5) of the outer rings as well as the catalytic subunit Delta (β1) and all three immunosubunits [MECL-1 (β2i), LMP2 (β1i) and LMP7 (β5i)] of the inner rings of the proteasome were identified as autoantigens for the first time. Using a panel of anti-proteasome antibody-positive sera of patients with SLE, autoimmune myositis (PM/DM) and primary Sjögren's syndrome (pSS), an autoimmune response was documented against LMP2 (β1i) and LMP7 (β5i) in all three patient groups in ELISA.

Conclusions. The frequent autoimmune response against LMP2 (β1i) and LMP7 (β5i) might indicate a role of inflammatory processes in the primary induction of the anti-proteasomal immune reaction, while the diversity of the humoral response against the proteasome system supports the assumption of a specific antigen-driven process leading to these extended autoimmune reactivities.

Methods. The effects of diacerein, celecoxib, diclofenac, meloxicam and indomethacin on prostaglandin (PG) E2 production, cyclo-oxygenase-2 (COX-2) protein expression, nitrite levels, presence of MMP-1 and -13, and activation of nuclear factor-B (NF-B) were studied on stimulated OA synoviocytes and chondrocytes.

Results. Diacerein and NSAIDs inhibited IL-1β-stimulated NF-B activation in synoviocytes and chondrocytes except indomethacin in synoviocytes. Diacerein further increased COX-2 protein expression and PGE2 synthesis in synoviocytes stimulated with IL-1β, while no effect was observed on stimulated chondrocytes. NSAIDs diminished until almost basal levels PGE2 release in both cells and, surprisingly, these drugs also diminished COX-2 protein expression both in synoviocytes and chondrocytes. With regard to structural mediators, diacerein decreased MMP-13 levels in synoviocytes but did not modify MMP-1 presence. NSAIDs induced a significant increase in MMP-1 levels in both cell types and in MMP-13 levels in chondrocytes.

Conclusions. Diacerein does not seem to reduce but rather increase inflammatory mediators in synoviocytes, while it does not overall affect chondrocyte inflammatory profile.

Methods. Totally, 181 patients with TA and 177 healthy controls are genotyped by PCR-RFLP method for the SNP rs2476601 (A/G) of PTPN22 gene. Polymorphic region was amplified by PCR and digested with Xcm I enzyme.

Results. Detected frequencies of heterozygous genotype (AG) were 5.1% (9/177) in control group and 3.8% (7/181) in TA group (P = 0.61, odds ratio: 0.75, 95% CI: 0.3, 2.0). No association with angiographic type, vascular involvement or prognosis of TA was observed either.

Conclusion. The distribution of PTPN22 polymorphism did not reveal any association with TA in Turkey.

Methods. To evaluate the effects of dexamethasone (Dex) on Anx-A1 expression, human peripheral blood T cells were incubated with Dex and then analysed by real-time PCR and western blotting. Similar experiments were carried out in vivo by measuring Anx-A1 levels in T cells from patients with RA before and after administration of steroids.

Results. Incubation of T cells with Dex decreased Anx-A1 levels in a time-dependent fashion and almost abolished its expression after 12 h. Stimulation of T cells pre-incubated with Dex for 12 h with anti-CD3/CD28 led to significant reduction of IL-2 production. Addition of human recombinant Anx-A1 to Dex-treated cells reversed the inhibitory effects of the steroids on anti-CD3/CD28-induced IL-2 production. Treatment of RA patients with steroid decreased Anx-A1 expression in T cells.

Conclusions. GCs suppress Anx-A1 expression in T cells in vitro and in vivo. These results provide evidence for a novel pathway by which steroids regulate the adaptive immune response and suggest that Anx-A1 may represent a target for the treatment of autoimmune diseases.

Methods. A systematic review of the literature was performed to identify all RCTs involving exclusively JIA patients. Two investigators independently assessed the identified articles for six quality indicators: generation of allocation sequence, allocation concealment, masking, intention-to-treat (ITT) analysis, dropout rates and clearly stated primary outcome.

Results. Fifty-two RCTs involving JIA patients were assessed. Generation of allocation sequence was unclear in 79% of the studies. Reporting of allocation concealment was adequate in only one-third of the studies. Masking was adequate in 73%, inadequate in 19% and unclear in 8% of the reports. ITT analysis was employed in 37% of the reports. Per-protocol analysis was used in 40% and in 23% the method was unclear. Most of the reports (67%) had dropout rates ≤20%. About half of the reports (n = 25) failed to show a significant effect of the experimental treatment. No significant associations were found between the study results and quality indicators. With the exception of adequate masking and dropout rate, all quality indicators showed a trend of improvement over the decades.

Conclusions. The quality of RCTs in JIA based on the selected indicators was poor. Although there were some positive changes over time, the reporting and methodological quality of trials should be improved. New, more powerful and acceptable RCT designs should be developed in this patient population.

Methods. Twelve SLE-RSA pregnant patients were treated with high-dose IVIg and compared with 12 SLE-RSA pregnant patients treated with prednisolone and NSAIDs. They were evaluated for the clinical response [lupus activity index-pregnancy (LAI-P) scale] and for ANA, anti-dsDNA, anti Ro/SS-A or La/SS-B, aCL, LAC, C4, C3 before and during pregnancy, and before and after each treatment course. Pregnancy outcome in the two groups was also evaluated.

Results. The groups characteristics were homogeneous at the beginning of pregnancy. A beneficial clinical response following IVIg treatment was noted in all patients and mean LAI-P decreased from 0.72 ± 0.43 at the beginning of pregnancy to 0.13 ± 0.19 at the end of pregnancy (P < 0.0001). Antibodies and complement levels tended to normalize in most of the patients. These clinical and laboratory improvements were significant with respect to the control group. Pregnancy was successfully carried out in 12/12 (100%) SLE-RSA patients with a mean Apgar score of 8.92. Three patients in the control group got aborted (25%).

Conclusions. IVIg has a high response rate among SLE-RSA pregnant patients and may be considered safe and effective.

Methods. Twelve senior students were trained in PAL and the gait, arms, legs, spine (GALS) screening technique for musculoskeletal system (MSS) examination. The students recruited and trained 45 year-2 students in the use of GALS. Nineteen students were recruited by a physiotherapist for GALS training tutorials. Trainee responses were compared by analysis of pre/post training confidence (using 100 mm visual analogue scale), course experience questionnaires (using a 5-point Likert scale) including free text comments, and in end of year examinations.

Results. Trainee confidence increased after PAL training from 3.7 to 89.9 (P < 0.0001). There were no significant differences in confidence levels from student trainees after PAL when compared with expert-led teaching. Results from course experience questionnaires demonstrated benefits in all parameters investigated with all students recommending PAL training. No differences between PAL and expert-led training were observed. Free-text comments showed that PAL-trained students perceived that this learning technique has potential to be applied to other areas of training, an observation not raised by expert-trained students. Examination results revealed that PAL-trained and expert-tutored students were respectively, 1.4 and 1.3 times more likely to pass the MSS examination, when compared with students undertaking standard training (P < 0.002 and P = 0.0001, respectively).

Conclusion. PAL is a useful adjunct to musculoskeletal clinical skills training. Students using PAL techniques offered a comparable level of training with that provided by an expert.

Methods. A cohort of 146 patients from the Kuopio 2000 Arthritis Survey having RA, AS, PsA, ReA, uSpA or undifferentiated arthritis were studied. Autoantibodies binding citrullinated types I and II carboxytelopeptides were measured in two different inhibition ELISA assays. Sera from 135 adult persons were used as controls.

Results. In RA, the sensitivities were 0.83 with long type I telopeptide and 0.78 with long type II telopeptide and the respective specificities were 0.94 and 0.93, while the corresponding values in other inflammatory joint diseases were much lower. The likelihood ratio in RA increased with longer peptides from 4.20 to 14.06 for type I telopeptide and from 2.74 to 11.67 for type II telopeptide.

Conclusion. The antibody assay using long telopeptide from type I collagen was the most specific and sensitive method in every diagnostic category, although in the arthritides other than RA, binding was much less abundant and possibly citrulline-independent.

Methods. Sixty children aged 7–18 yrs with juvenile idiopathic arthritis and >4 joints involved were recruited. Children underwent a physical examination. The Childhood HAQ was completed by both the children and their parents. Children also completed questionnaires for depression (Birleson Depression Inventory; BDI), anxiety (Revised Children's Manifest Anxiety Scale; RCMAS) and peer, emotional and behavioural problems (Strengths and Difficulties Questionnaire; SDQ). Clinical information was extracted from the hospital records.

Results. Self-reported psychological functioning (depression, anxiety, and behaviour) was not different from the normal population. Parent-reported emotional difficulties on the SDQ were somewhat elevated. There were no significant correlations between psychological functioning and physician-rated disease activity score or the number of active joints at the time of assessment. Furthermore, no differences in psychological functioning were found between children with or without significantly raised inflammatory markers. All aspects of psychological function (depression, anxiety and behaviour) correlated moderately with physical function (r_s = 0.49, 0.41, 0.46, respectively; all P < 0.01).

Conclusions. Children and adolescents with polyarthritis are not at significantly elevated risk of psychological difficulties. Poor psychological outcome was associated with more severe physical disability but not with the level of disease activity.

Methods. Dual-centre, double-blind placebo-controlled randomized study of 9 months’ duration. Ninety-seven patients with RA were randomized to take either 10 g of cod liver oil containing 2.2 g of n-3 EFAs or air-filled identical placebo capsules. Documentation of NSAID daily requirement, clinical and laboratory parameters of RA disease activity and safety checks were done at 0, 4, 12, 24 and 36 weeks. At 12 weeks, patients were instructed to gradually reduce, and if possible, stop their NSAID intake. Relative reduction of daily NSAID requirement by >30% after 9 months was the primary outcome measure.

Results. Fifty-eight patients (60%) completed the study. Out of 49 patients 19 (39%) in the cod liver oil group and out of 48 patients 5 (10%) in the placebo group were able to reduce their daily NSAID requirement by >30% (P = 0.002, chi-squared test). No differences between the groups were observed in the clinical parameters of RA disease activity or in the side-effects observed.

Conclusions. This study suggests that cod liver oil supplements containing n-3 fatty acids can be used as NSAID-sparing agents in RA patients.

Methods. In this article, the authors performed a systematic review of all currently available randomized controlled trials (RCTs) fulfilling the inclusion criteria, by using a recently developed rating system aimed to assess the strength of evidence with regard to the methodological quality of the trials.

Results. Compared with other non-disciplinary treatments, moderate evidence of higher effectiveness for multidisciplinary interventions was shown. In contrast to no treatment or standard medical treatment, strong evidence was detected in favour of multidisciplinary treatments. The evidence that comprehensive inpatient programmes were more beneficial that outpatient programmes was moderate. Fibromyalgia and chronic back pain patients tended to profit more substantially than patients with diverse origins or chronic pain diagnoses. No evidence was found that treatment variables, such as duration or programme components, were influential for the success of the intervention.

Conclusion. A standard of multidisciplinary programmes should be internationally established to guarantee generally good outcomes in the treatment of chronic pain. Our results highlight the lack of quality of design, execution or reporting of many of the RCTs included in this article. Future studies should more specifically focus on differential effects of treatment components and patient variables, allowing the identification of subgroups, which most probably would profit from multidisciplinary pain programmes.

Methods. Consecutive outpatients with an episode of shoulder pain were prospectively included in the study. They were examined by a rheumatologist and, within 3 days, an MRI was done. Sensitivity, specificity, positive and negative predictive values, and accuracy of PE manoeuvres were calculated using a 2 x 2 table.

Results. Fourteen males and 16 females were included. All the tests exhibited acceptable sensitivity. As a result Yocum manoeuvre was considered the most sensitive and most accurate for SIS. With regard to SSB, the Gerber test was the most sensitive. The majority of the PE manoeuvres showed low specificity.

Conclusions. Most PE manoeuvres identify reasonably well subacromial impingement of the shoulder, although, in general, they have low specificity. The Yocum test has the best sensitivity and precision. Our data suggest that imaging techniques should be recommended to better define shoulder lesions.

Methods. We evaluated 155 patients with SLE by using objective tests for diagnosing ASO, IHD and CVD and laboratory tests including ELISA for aCL/β2-glycoprotein I antibodies (aCL/β2-GPI) and anti-phosphatidylserine/prothrombin antibodies (anti-PS/PT).

Results. Twenty-five (16.1%) of the 155 SLE patients were diagnosed with ASO. Both aCL/β2-GPI and anti-PS/PT levels were significantly higher in SLE patients with ASO (mean ± s.e., 104.3 ± 38.8 U/ml for aCL/β2-GPI, P < 0.01; 72.6 ± 48.9 U/ml for anti-PS/PT, P < 0.05) than in SLE patients without ASO (22.8 ± 9.9 U/ml for aCL/β2-GPI; 18.3 ± 4.4 U/ml for anti-PS/PT). Multivariate logistic analysis including aCL/β2-GPI, anti-PS/PT and traditional risk factors (hypercholesterolaemia, hypertension and diabetes mellitus) confirmed that the presence of aCL/β2-GPI was the most significant risk factor for ASO in SLE patients [odds ratio (OR) 3.45; 95% CI 1.40, 8.56; P < 0.01]. Furthermore, the prevalence of ASO was associated strongly with IHD (OR 11.8; 95% CI 3.45, 40.1; P < 0.0001) but not CVD (OR 1.84; 95% CI 0.65, 5.21; P = 0.25).

Conclusions. The presence of aCL/β2-GPI contributes to the risk of development of ASO, which may represent an important mechanism for the pathogenesis of IHD in patients with SLE.

Methods. One hundred patients of South Asian origin (50 RA; 50 SLE) and 100 patients of White British/Irish origin (50 RA; 50 SLE) were recruited. Demographic and disease-related details and responses to the Beliefs about Medicines Questionnaire (BMQ), the SF-36 and the HAQ were collected.

Results. Patients of South Asian origin had significantly higher General Overuse (GO), General Harm (GH) and Specific Concern (SC) scores compared with patients of White British/Irish origin. Forward stepwise multivariable regression analysis showed that ethnic origin was an independent predictor of the GO, GH and SC scores with patients of South Asian origin having higher scores in these three scales of the BMQ.

Conclusion. RA and SLE patients of South Asian origin have very high levels of concern about DMARDs and are generally worried about prescribed medicines. This may have an impact on adherence in this group of patients and further work is needed to understand the reasons underlying these beliefs.

Methods. An RA research database was constructed by identifying hospitalized RA patients from the Hospital Discharge Register and cancer patients from the Cancer Registry. Earlier studies from Sweden have shown that some 75% of RA patients have been hospitalized at some time point. Follow-up of 42 262 RA patients was carried out from year 1980 to 2004 including separate follow-ups for shorter intervals. Standardized incidence ratios (SIRs) were calculated for cancer in RA patients by comparing with subjects without RA.

Results. Many cancers were in excess in RA patients, especially Hodgkin disease, non-Hodgkin lymphoma and squamous cell skin cancer; a novel association was found for non-thyroid endocrine tumours. Colon, rectal and endometrial cancers were decreased in RA patients. When RA patients were first hospitalized after 1999, the SIRs for melanoma, squamous cell skin and upper aerodigestive tract cancers and for leukaemia were increased compared with previous periods.

Conclusions. This study, the largest so far published, quantified the increased and decreased site-specific risks of cancer in RA patients. The recent increases in the risks of squamous cell skin and upper aerodigestive tract cancers, melanoma and leukaemia call for continuous vigilance and recording of changes in treatment.

Methods. A total of 92 patients with LN who underwent renal biopsy in our hospital were re-classified according to the ISN/RPS 2003 criteria.

Results. The mean patient age was 36.8 yrs and the median observation period was 65 months. The relative frequency for each class was as follows: Class I (minimal mesangial LN) 0%, Class II (mesangial proliferative LN) 13%, Class III (focal LN) 17%, Class IV (diffuse LN) 60% and Class V (membranous LN) 10%. Within Class IV, diffuse segmental (Class IV-S) was 25% and diffuse global (Class IV-G) 75%. During the observation period, renal function was more likely to deteriorate in Class IV-G cases than in Class IV-S cases. Importantly, when Class IV-G was subdivided into cases involving active lesion alone [IV-G (A)] or chronic lesion [IV-G (A/C)], the majority of cases in IV-G (A) was nephrotic, but responded well to therapy. In contrast, renal function declined only in IV-G (A/C) cases. Patients with Class IV-G (A/C) had persistent proteinuria in spite of intensified therapies. Moreover, the higher proportion of chronic lesions was related with the deterioration of renal function.

Conclusions. This study showed that in Class IV-G cases, renal outcome differed in the presence of chronicity. Chronicity could be a critical factor in predicting outcome. Thus, the revised classification of LN is clinically valuable in identifying different renal outcomes among patients with diffuse LN.

Methods. Five hundred and fifty Chinese patients with primary systemic vasculitis diagnosed in our referral diagnostic centre during the past 10 years were retrospectively studied. Four hundred and ninety-three out of 550 were ANCA positive. We compared the new consensus algorithm and the 1994 Chapel Hill Consensus Conference (CHCC) definitions supplemented with surrogate parameters, in the same cohort of patients with primary systemic vasculitis.

Results. Applying the CHCC definitions with surrogate parameters, the diagnoses were Churg–Strauss syndrome (CSS) (n = 0), WG (n = 127), microscopic polyangiitis (MPA) (n = 363), PAN (n = 4) and unclassified (n = 56). Using the new consensus algorithm, the diagnoses were CSS (n = 2), WG (n = 199), MPA (n = 329), PAN (n = 0) and unclassified (n = 20).

Conclusions. Watts’ algorithm was a useful method to classify patients into a single category, with less unclassified patients and without overlapping diagnosis, which allows their use in epidemiological studies.

Methods. Using data from 14 664 participants aged 20 yrs and older in The US Third National Health and Nutrition Examination Survey (1988–1994), we examined the relation between the levels of HbA1c, other biomarkers and serum uric acid levels using multivariate linear regressions stratified by gender.

Results. The serum uric acid levels increased with increasing serum HbA1c levels up to the category of 6–6.9%, and thereafter decreased with further increasing HbA1c levels (a bell-shaped relation). Compared with a HbA1c level of <5%, the multivariate differences among women were 26.8 µmol/l for HbA1c of 6–6.9% and –25.6 µmol/l (95% CI –42.8, –8.3) for HbA1c ≥9%. The corresponding multivariate differences among men were 8.3 µmol/l (95% CI –3.0, 19.6) and –64.8 µmol/l (95% CI –46.0, –84.5), which were both significantly different from those among women (P-values for interaction by sex <0.001). Fasting glucose levels also showed a bell-shaped relation with serum uric acid levels. Individuals with diabetes showed lower serum uric acid levels and the association was larger among men (P-value for interaction, 0.007). Serum uric acid levels increased linearly with increasing fasting serum C-peptide levels, serum insulin levels or insulin resistance (multivariate P-values for trend, <0.001).

Conclusions. Individuals with moderately elevated HbA1c levels (i.e. pre-diabetes) may be at a higher risk of hyperuricaemia and gout, particularly in women, whereas individuals with diabetes or highly elevated HbA1c levels may be at a lower risk of these conditions, particularly in men.

Methods. We compared risk factors for CVD between 102 consecutive PsA patients and 82 controls, adjusting for BMI. We also assessed the role of inflammation on the CVD risk factor by using a BMI and high-sensitivity CRP (hsCRP)-adjusted model.

Results. The BMI of PsA patients were significantly higher than healthy controls. After adjusting for the BMI, PsA patients still have a higher prevalence of diabetes mellitus (DM) [odds ratio (OR) 9.27, 95% CI 2.09, 41.09) and hypertension (OR 3.37, 95% CI 1.68, 6.72), but a lower prevalence of low high density lipoprotein (HDL) cholesterol (OR 0.16, 95% CI 0.07, 0.41). PsA patients have significantly increased systolic and diastolic blood pressures, insulin resistance and inflammatory markers (hsCRP and white cell count) compared to controls. PsA patients have higher HDL cholesterol and apolipoprotein (Apo) A1 levels; and lower total cholesterol (TC) and low density lipoprotein cholesterol levels; and a lower TC/HDL ratio. However, the Apo B level (P < 0.05), and the Apo B/Apo A1 ratio (P = 0.07) were higher in PsA patients. Further adjustment for hsCRP level rendered the differences in the prevalence of hypertension and DM; the TC, and sugar levels; and white cell count non-significant between the two groups; while the differences in other parameters remained significant.

Conclusion. These data support the hypothesis that PsA may be associated with obesity, hypertension, dyslipidaemia and insulin resistance because of the shared inflammatory pathway.

Methods. A prospective cohort study with 6 months follow-up was carried out in The Netherlands, including 587 patients with a new episode of shoulder pain. Patients were categorized as having acute (symptoms <6 weeks), subacute (6–12 weeks) or chronic (>3 months) shoulder pain. The course of shoulder pain, functional disability and quality of life was analysed over 6 months. Patient and disease characteristics, including physical and psychosocial factors, were investigated as possible predictors of outcome using multivariable regression analyses.

Results. Acute shoulder symptoms showed the most favourable course over 6 months follow-up, with larger pain reduction and improvement of functional disability. Patients with chronic shoulder symptoms showed the poorest results. The multivariable regression analysis showed that predictors of a better outcome at 6 months for acute shoulder pain were lower baseline disability scores and higher baseline pain intensity (explained variance 46%). Predictors of a better outcome for chronic shoulder pain were lower scores on pain catastrophizing and higher baseline pain intensity (explained variance 21%).

Conclusions. The results indicate that, besides a different course of symptoms in patients presenting with acute or chronic shoulder pain, predictors of outcome may also differ with psychosocial factors being more important in chronic shoulder pain.