Methods. Peripheral blood monocytes were isolated from RA patients and differentiated into macrophages by M-CSF (15 ng/ml). Under CypA stimulation (200 ng/ml), the protein release and activation of MMPs were detected by gelatin zymography and invasion assay. Human monocyte cell line THP-1 cells were selected for the advanced searching for potential interaction between CypA and CD147 in production of MMPs and cell adhesion to extracellular matrix (ECM).

Results. CypA significantly increased production and activation of MMP-9, not MMP-2, in the monocytes/macrophages derived from RA SF. CSA and HAb18G/CD147 antagonistic peptide AP-9 against CD147, respectively, dramatically decreased MMP-2 and MMP-9 expression, both in the absence or presence of CypA. Similar effects of CypA on MMP-9 production and cell invasion were observed in THP-1 cells. CypA-induced nuclear factor B (NF-B) activity for MMP-9 transcription were strongly blocked by extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK) inhibitors (U0126 and SP600125, respectively), but not by p38 mitogen-activated protein kinase (MAPK) inhibitors (SB203580). CypA also induced calcium mobilization and increased the adhesion of THP-1 cells to ECM.

Conclusions. These findings suggest that in RA, the abundant CypA, by its direct binding to CD147, up-regulates MMP-9 expression and adhesion of monocytes/macrophages to ECM, and the cyclophilin-CD147 interactions might contribute to the destruction of cartilage and bone.

Methods. Case–control study in an established pSS cohort with PCR–RFLP genotyping for four SNPs (-2841 T->C, -2704 T->C, -2701 T->A, -871 C->T), which tag a haplotype block in the 5' regulatory region of the BAFF gene and s-BAFF determination by ELISA.

Results. s-BAFF levels were elevated in Ro/La-positive pSS patients (n = 85, 1770 pg/ml) compared with both Ro/La-negative pSS patients (n = 27, 1193 pg/ml) and controls (n = 59, 1171 pg/ml), P < 0.001. s-BAFF increased with diversification of the anti-Ro/La antibody response, but was not correlated with age, RF or immunoglobulin G levels. There were four common BAFF haplotypes. While the CTAT haplotype was associated with Ro/La-positive pSS [odds ratio (OR) 2.6; 95% CI 1.7, 4.1; P = 0.00004], the TTTT haplotype was associated with elevated s-BAFF in autoantibody-positive pSS (n = 85; 88% females; P = 0.008). The shared -871 T allele had no independent contribution to disease susceptibility or s-BAFF.

Conclusions. Disease susceptibility for Ro/La-positive pSS is increased with the CTAT haplotype, but not associated with high s-BAFF levels. Elevated s-BAFF levels in pSS are associated with the TTTT haplotype and may be a secondary phenomenon in Ro/La-positive pSS. While both haplotypes carry the -871 T allele, this allele is not independently associated with disease susceptibility.

Methods. Human synovial tissue was obtained from RA and OA patients and aryl hydrocarbon receptor (AhR) expression in these tissues was evaluated using immunohistochemistry and real-time PCR. Expression of various cytokines was measured by real-time PCR following stimulation of RA synoviocytes with different concentrations of TCDD. To study the role of AhR, we treated RA synoviocytes with -naphthoflavone, a known AhR antagonist. To evaluate which signal transduction pathways were stimulated by the TCDD–AhR interaction, we used inhibitors of nuclear factor-B (NF-B) and extra-cellular stimulus-activated kinase (ERK).

Results. Higher AhR mRNA and protein levels were observed in RA synovial tissue than in OA tissue. TCDD up-regulated the expression of IL-1β, IL-6 and IL-8 through binding to AhR, and this effect was transmitted via the NF-B and ERK signalling cascades. AhR expression in synovial cells was up-regulated by TNF-.

Conclusion. TNF- activates AhR expression in RA synovial tissue, and that cigarette smoking and exposure to TCDD enhances RA inflammatory processes. TCDD induces inflammatory cytokines via its association with AhR, resulting in stimulation of the NF-B and ERK signalling cascades. Thus TCDD exposure, such as smoking exacerbates RA pathophysiology.

Methods. Primary cultures of chondrocytes from OA patients were stimulated with IL-1β. The production of reactive oxygen species, nitrite, PGE₂, TNF- and IL-1 receptor antagonist (IL-1Ra) were measured in the presence or absence of CORM-2. The expression of nitric oxide synthase-2 (NOS-2), cyclo-oxygenase-2 (COX-2) and microsomal PG E synthase-1 (mPGES-1) was followed by western blot and real-time PCR. Activation of nuclear factor-B (NF-B) and hypoxia inducible factor-1 (HIF-1), and phosphorylation of NF-B inhibitory protein (IB) were determined by ELISA.

Results. CORM-2 decreased the production of oxidative stress, nitrite and PGE₂. In addition, CORM-2 inhibited IL-1β-induced TNF- but enhanced IL-1Ra production. Treatment of chondrocytes with CORM-2 strongly down-regulated NOS-2 and mPGES-1 protein expression, whereas COX-2 was reduced to a lesser extent. These changes were accompanied by a significant decrease in mRNA expression for NOS-2 and mPGES-1. CORM-2 showed a concentration-dependent inhibition of DNA-binding activity for p65 NF-B and HIF-1. IB phosphorylation was also reduced by CORM-2 treatment.

Conclusions. These data have opened new mechanisms of action for CORM-2, raising the prospect that CO-releasing molecules are an interesting strategy for the development of new treatments in articular conditions.

Methods. Expression of an extensive panel of chemokine receptors and adhesion molecules on matched CD4⁺ and CD8⁺ T cells from peripheral blood (PB) and synovial fluid (SF) was analysed by multicolour flow cytometry. Migration assays and flow-based adhesion assays were used to assess the functional consequences of any differences in the expression of chemokine and adhesion receptors.

Results. CD4⁺ and CD8⁺ T cells from PB and SF expressed unique yet consistent patterns of chemokine and adhesion receptors. SF CD8⁺ T cells were much less promiscuous in their expression of chemokine receptors than SF CD4⁺ T cells. The ₆β₁ integrin was highly expressed on PB CD4⁺ T cells, but not on PB CD8⁺ T cells. Laminin, the ligand for ₆β₁, retained CD4⁺ T cells, but less so CD8⁺ T cells, within inflamed synovial tissue.

Conclusion. Infiltrating PB CD4⁺ T cells, but not CD8⁺ T cells, express functional levels of the ₆β₁ integrin. We propose that this leads to their retention within the rheumatoid synovium in perivascular cuffs, which are defined and delineated by the expression of laminin.

Methods. Peripheral blood mononuclear cells (PBMC) were isolated from 19 paediatric patients with SLE and from 17 healthy age-matched controls. PBMC from both cohorts were cultured in the absence of exogenously added stimuli, and leucocyte PD-L1 expression was measured by flow cytometry.

Results. Immature mDC and monocytes (Mo) from healthy children expressed little PD-L1 at initial isolation, but spontaneously up-regulated PD-L1 by 24 h. In contrast, both mDC and Mo from patients with active SLE failed to up-regulate PD-L1 over a 5 day time course, expressing this protein only during disease remissions.

Conclusions. These data are the first to link active lupus with reversibly decreased PD-L1 expression on professional APC, suggesting a novel mechanism for loss of peripheral tolerance in SLE.

Methods. To clarify this situation we have performed a systematic literature search to find randomized controlled trials comparing the efficacy of eradication in patients receiving NSAIDs to prevent ulcer development.

Results. Seven randomized controlled trials and one meta-analysis were identified. There were three papers on NSAID-naive patients. According to this data, NSAID-naive users benefit from testing for H. pylori infection and subsequent H. pylori eradication therapy prior to the initiation of NSAID. In contrast, H. pylori eradication alone does not protect chronic NSAID users with recent ulcer complications from further gastrointestinal (GI) events. To prevent recurrent ulcer bleeding long-term acid suppressive therapy is needed.

Conclusions. In conclusion, ulcer risk reduction after H. pylori eradication therapy is clearly more marked in patients beginning NSAID therapy than in patients who were already receiving and tolerating NSAID therapy. Thus, the management of H. pylori infection and the prevention of GI complications in NSAID users need to be individualized on the basis of recently published data.

Methods. Serum 25OHD requests were matched to electronic medical records from rheumatology and metabolic bone clinics (April 2006–March 2007). Data were analysed separately for two groups, ‘Documented osteoporosis/osteopaenia’ (Group 1) and ‘General rheumatology outpatients’ (Group 2, sub-divided by diagnosis). Hypovitaminosis D was defined by 25OHD levels <50 nmol/l. Values were compared with healthy adults to calculate geometric z-scores.

Results. A total of 263 patients were included (Group 1, n = 122; Group 2, n = 141) with an overall median 25OHD of 44 nmol/l.The 25OHD level among general rheumatology patients (median 39 nmol/l, mean z score –1.2, was statistically significantly lower than among osteoporotic/osteopaenic patients (median 49 nmol/l, mean z score of –0.9, p < 0.05 for the difference). 25OHD was lower in inflammatory arthritis and chronic pain/fibromyalgia than in other groups. Prescribing was recorded in 100 in Group 1 (of whom 95% were prescribed calcium/800 IU cholecalciferol) and 83 in Group 2 (91% calcium/800 IU). Only 31% of the patients with 25OHD <50 nmol/l would have been identified using general guidelines for screening patients at ‘high risk’ of hypovitaminosis D.

Conclusions. Improved guidelines for managing hypovitaminosis D in rheumatology patients are needed. We found a high prevalence of hypovitaminosis D among secondary care patients in rheumatology and widespread supplementation with 800 IU cholecalciferol. Substantially reduced levels of serum 25OHD were identified among patients with inflammatory arthritis and chronic pain.

Methods. Analysis of the medical records of 1442 SLE patients who were regularly followed up in a tertiary teaching medical centre from 2000 to 2005.

Results. Among 1442 SLE patients, 240 patients (17%) developed at least one episode of bacteraemia, corresponding to an incidence of 92.7 cases/1000 hospital admissions. Since SLE diagnosis, the overall survival of our patients was 92% at 5 yrs, 86% at 10 yrs and 79% at 15 yrs. However, after one episode of bacteraemia, the survival decreased to 76% at 30 days and 67% at 360 days. Of the 336 episodes of bacteraemia, 167 were community-acquired (49.7%) and 169 were nosocomial (50.3%). Staphylococcus aureus was the leading cause of Gram-positive bacteraemia. Among Gram-negative bacteria, non-typhoidal Salmonella and Escherichia coli were the most common species. Community-acquired Salmonella and Streptococcus bacteraemia were more common than nosocomial infections. Klebsiella and Acinetobacter spp. were significantly more responsible for nosocomial than community-acquired bacteraemia. Patients infected with Acinetobacter, Klebsiella or Pseudomonas had lower probabilities of 14-day survival (71.4, 55.6, 42.9%, respectively).

Conclusions. Among SLE patients, an episode of bacteraemia was associated with an unfavourable long-term outcome. The bacterial species significantly influenced short-term survival. Therefore, when empiric antibiotic therapy is initiated in SLE patients who are suspected of bacteraemia, we suggest use of antibiotics that are effective against Pseudomonas, Klebsiella, Acinetobacter, S. aureus, and E. coli.

Method. Thirty-eight subjects with active AS were randomized to receive MTX (MTX group) or placebo (placebo group) for 22 weeks. Both groups received infliximab for three infusions of 5 mg/kg at week 16, 18 and 22 and were followed up until week 30. MRI changes in the spine were assessed before and after infusion.

Results. The Assessments in Ankylosing Spondylitis (ASAS) 20 response at week 16 was 5.4% in the MTX group vs 15.8% in the placebo group (P = 0.17). In the MTX group, 5.4, 31.6, 52.6 and 63.2% of patients vs 15.8, 21.1, 57.9 and 68.4% patients in the placebo group achieved ASAS20 at week 16, 18, 22, 30, respectively. There were no significant differences between the two groups at any time points. Likewise, the secondary outcome showed no significant differences between the two groups. MRI changes in 31 subjects showed an overall improvement of 36.4% but the changes were not significant between the two groups.

Conclusions. Combination MTX with infliximab is as safe and as effective as infliximab monotherapy in the treatment of AS with a significant improvement in ASAS20 and in the different core sets in assessment. MRI improvements were also seen. However, there was no additional clinical or MRI improvement with the addition of MTX to infliximab in AS.

Methods. A postal questionnaire was sent to all GPs in Norfolk. It was designed to test GPs ability to identify symptoms suggestive of IBP in patients with back pain. It also enquired whether GPs considered other features of SpA. Their perceptions of usefulness of various investigations when considering a diagnosis of AS, management and their unmet needs were recorded.

Results. A total of 62% of completed questionnaires were returned. Only 5% of GPs could identify all eight features known to be indicative of IBP, 78% between four and eight and 17% identified less than four features. GPs had a range of views regarding the utility of a positive family history, HLA-B27, use of X-ray and physiotherapy in patients with suspected IBP. GPs awareness of the associated features of SpA was low. There were inconsistencies in the use of diagnostic tests and management of AS. Improving musculoskeletal education in primary care was identified as one of the unmet needs by the majority of GPs.

Conclusions. In a survey of GPs, we identified inconsistencies in their perceptions and approach to the diagnosis and management of AS. Education in primary care and the wider use of diagnostic algorithms may improve early detection and hence outcome of AS.

Methods. RCTs in non-renal SLE were identified using PubMed (1975–2007). Inclusion/exclusion criteria, trial quality (5-point scale) and results of each study were recorded. The inclusion/exclusion criteria were compared with an SLE database to determine the proportion of patients from the database who would theoretically be eligible for these trials. For each negative study, we calculated the post hoc study power. We also looked for temporal improvements of trials in the literature and examined if pharmaceutical involvement influenced trial quality.

Results. Sixty-four articles were included; the mean power of 30 negative studies was 24.6 ± s.e.m. 3.9% (range 2.5–81.1%). Only one study had a power > 80%. Overall, potential eligibility of SLE patients in the database was 45.1 ± s.e.m. 3.6%. Only 14 studies (21.9%) were of good quality. Fortunately, RCT quality is improving over time (trials <1995, compared with 1996–2002 and >2003; P < 0.001). Trials with pharmaceutical involvement had a significantly higher number of enrollees and better study quality.

Conclusions. Negative RCTs in SLE were mostly underpowered but the generalizability of these trials was high. Determination of study power and the impact of eligibility criteria on generalizability of study results are crucial in the design of clinical trials to ensure applicability to clinical practice.

Methods. A detailed questionnaire survey on CMV infection was carried out against rheumatic disease patients hospitalized in member hospitals, and the obtained clinical and/or laboratory data were analysed.

Results. Out of 7377 patients, 151 were diagnosed as having CMV infection. The underlying diseases ranged broadly, but SLE, microscopic polyangiitis, and dermatomyositis were the most common. Four were diagnosed histopathologically, and the others via positive CMV antigenaemia. In addition to oral corticosteroid for all but one patient, 81 were treated with pulsed methylprednisolone (MPSL), 64 with cyclophosphamide (CYC) and 36 with other immunosuppressants. Forty-four had a fatal outcome, for which presence of clinical symptoms, other infectious complications, lymphopenia, an older age (>59.3 yrs) and the use of pulsed MPSL were significant risk factors (P < 0.05) by univariate analysis. Multivariate analysis retained the first three (P < 0.05). The CMV antigenaemia count was significantly higher for the symptomatic than asymptomatic [10.1 (0.0–2998.0) vs 4.0 (1.3–1144.4)/10⁵ PMNs, respectively, P < 0.05; threshold count: 5.6/10⁵ PMNs]. No treatment benefit by anti-viral agent was observed as for survival.

Conclusion. CMV infection was mostly diagnosed by antigenaemia, and occurred among patients under strong immunosuppressive therapy using pulsed MPSL and/or immunosuppressants. Lymphopenia, presence of symptoms and other infections are significant risk factors for a poor outcome and pulsed MPSL and an older age may predict it. Patients were prone to be symptomatic with anti-genaemia count over 5.6/10⁵ PMNs.

Method. We conducted a retrospective study of 485 patients with SLE attending a UK tertiary referral centre, followed up over 27 yrs. Demographics, clinical features, serological features, treatment and outcome data were assessed.

Results. Seven out of 485 patients (1.4%) had evidence of gangrene or CPI with onset at any stage of SLE disease from presenting feature to 27 yrs after SLE onset, aPL and LAC were over-represented in the CPI patients. All had active SLE at the time of CPI. All seven were treated with intravenous (IV) epoprostenol infusion and aPL-positive patients were anti-coagulated. One patient failed to respond to this treatment and to IV calcitonin gene-related peptide but responded to B-cell depletion therapy using rituximab. Five out of the seven patients suffered digit loss with auto-amputation.

Conclusion. CPI is a rare but potentially devastating complication of SLE associated with aPL, LAC and active SLE. B-cell depletion therapy with rituximab may be an option in severe ischaemia not improving with IV epoprostenol.

Methods. A 48-week comparative, prospective study of patients with active RA [mean 28-joint disease activity score (DAS28): 6.81], despite MTX (n = 48), or LEF (n = 42), or CSA (n = 38) treatment, in whom ANK (100 mg/daily SC) was given with corticosteroid cream topical application.

Results. At 24 and 48 weeks the patient percentages meeting the ACR20 response criteria were 57 and 73%, respectively, 33 and 41% met ACR50, while 15 and 23% met ACR70. Significant improvements in number of swollen and tender joints, HAQ, pain, global disease assessment, CRP and haemoglobin from baseline to 24 and 48 weeks were evident. DAS28 decreased at 24 weeks (– 1.68; 95% CI – 1.46, – 1.90; P < 0.0001), as well as at study end (– 2.24; 95% CI – 2.01, – 2.47; P < 0.0001). Subgroup analysis revealed a significantly weaker response in terms of pain and DAS28 in patients treated with concomitant CSA. The most common ANK-related adverse event was injection-site reaction (29%), being less frequent in male patients, as well as in patients treated with CSA. There were 17 withdrawals, 6 of them due to inefficacy. No opportunistic infections or new safety signals were observed.

Conclusion. Considering the limitations of an open-label study, addition of ANK appears to be an effective and well-tolerated treatment option for many RA patients with inadequate responses to non-biologic DMARDs in clinical practice.

Methods. The patients were divided into responders (DAS28 dropped by >1.2) and non-responders. These groups were compared for demographics, DAS28 at the two pre-assessments 1 month apart and at baseline. Exposure to intramuscular, oral and IA steroids in the 3 months period before the baseline DAS28 was recorded.

Results. At 6-month assessment in 256 patients, 82.8% were responders with no demographic differences between them and non-responders. Although the first pre-assessment score was not significantly different (6.8 vs 6.6), the second pre-assessment score (7.1 vs 6.7) and the baseline DAS (7.2 vs 6.3) were lower in the non-responders (P < 0.04 and P < 0.001, respectively). Comparing the differences in DAS28 from the first pre-assessment to baseline, the responders had increased by 0.4, and the non-responders had decreased by 0.4, (P < 0.001). If the first pre-assessment score had been taken as the baseline DAS28, then 9.4% of responders would be re-classified as non-responders, and 31.8% of non-responders would be re-classified as responders. The proportion of patients who had steroid treatment within the 3 months period before the baseline DAS28 did not differ significantly between the responders and non-responders (34% vs 41%, P = 0.38).

Conclusion. Baseline DAS28 is critical in classifying responders at the 6-month assessment.

Methods. Two hundred and seventy-one healthy community-dwelling adults with no history of knee injury, knee pain or clinical knee OA had an MRI performed on their dominant knee at baseline and 2 yrs later to assess the relationship between the presence of BMLs at baseline and change in tibiofemoral cartilage defects and tibial cartilage volume over 2 yrs.

Results. BMLs were present in 37 (14%) subjects. Cartilage defects were more likely to progress rather than remain stable or regress in subjects with BMLs compared with those without BMLs (P = 0.04). The odds of cartilage defects progressing in the tibiofemoral compartment of the knee where BMLs were present compared with where BMLs were absent was 2.6 (95% CI 1.2, 5.3; P = 0.01). Where ‘very large’ BMLs were present, there was a trend for increased annual tibial cartilage volume loss (46.4 mm³/yr; P = 0.07).

Conclusions. These data suggest that BMLs are associated with change in knee cartilage over 2 yrs in asymptomatic subjects. Increased progression of cartilage defects is seen with increasing size of BMLs. It will be important to determine in future studies whether BMLs directly cause change in cartilage over 2 yrs, or act as a marker of another factor that facilitates these changes.

Methods. We retrospectively reviewed clinical, biological and radiological data of children with CRMO at five French paediatric centres. Outcome data were obtained through review of hospital charts and questionnaires sent to all patients to assess disease activity and educational and vocational achievement.

Results. Forty patients were assessed (34 females and 6 males) with a median age at diagnosis of 11.5 yrs (range 2–17). Median number of initial bony lesions was 2 at onset, and 3.5 over disease course. Median time since diagnosis was 3.5 yrs (range 0.5–15) and median duration of active disease 2.7 yrs (range 0.5–13.5). Nine (22.5%) patients had psychological or physical sequelae. Twenty-nine children (72.5%) responded to the questionnaire. Twenty-six had no physical disability as judged by the HAQ 0–1, two had moderate disability (HAQ: 1–2) and one had severe disability (HAQ: 2–3). Seventeen patients (58.6%) had active disease at follow-up (after 6 months to 15 yrs since diagnosis) and continued to have pain (median value of visual analogue scale: 10/100). CRMO had interfered with patient's education in two cases.

Conclusions. Clinical outcome of children with CRMO is generally good, but a sizeable proportion of patients have active disease at follow-up, and a minority of patients can have a severe and prolonged disease course despite intensive treatments. Further studies are required to determine predictive factors for severe disease.

Methods. We describe five patients with SLE and antibody deficiency, and review the literature exploring the relationship between the two.

Results. Various types of antibody deficiency syndromes, including common variable immunodeficiency (CVID), IgA deficiency, IgM deficiency, drug-induced hypogammaglobulinaemia and hypogammaglobulinaemia secondary to nephrotic syndrome can occur in SLE. Antibody deficiency states can be treated with antibiotics and replacement immunoglobulin therapy (particularly CVID) but sometimes close monitoring is all that is required.

Conclusion. Measurement of immunoglobulin levels is useful in SLE to identify coexisting antibody deficiency and the later development of hypogammaglobulinaemia. This allows monitoring and appropriate treatment to be instituted.

Methods. Charts of 53 LV-GCA patients and 53 GCA controls were reviewed following a predetermined protocol. Telephone interviews of patients or their primary care physicians were conducted. Forty LV-GCA patients underwent follow-up duplex ultrasound examinations of proximal arm arteries.

Results. The mean observation time was 50 (s.d. ± 31) months. None of the LV-GCA patients developed ischaemic arm complications. In 30%, proximal arm artery wall swelling disappeared completely. It decreased in 53%. In 8% it remained unchanged, in 5% it increased and in 5% arteries occluded with collateral flow. After the start of treatment, anterior ischaemic optic neuropathy developed neither in LV-GCA patients nor in GCA controls, amaurosis fugax occurred in 4 and 6%, arterial hypertension in 53 and 66%, strokes in 9 and 9%, myocardial infarction in 2 and 2%, diabetes mellitus in 30 and 25%, osteoporosis in 38 and 23%, and osteoporotic fractures in 15 and 4%, respectively. Mean corticosteroid dose was 3.7 mg/day. Mean duration of therapy was 42 months. All differences were insignificant. Four LV-GCA patients developed vasculitic popliteal artery stenoses.

Conclusions. The prognosis of LV-GCA is benign with regard to ischaemic complications. Proximal artery wall swelling decreases in most cases. Its course is similar to GCA without proximal arm arteritis.

Methods. Large-window videodensitometry with sodium fluorescein was performed in 38 SSc patients and 20 healthy controls. Capillary permeability was expressed as the average relative light intensity over the first 7 min [I_av(7)] after appearance of fluorescein in skin capillaries.

Results. Capillary permeability, expressed as I_av(7) was significantly decreased in patients with SSc (47.3 ± 15.0% vs 57.6 ± 9.4% in controls, P = 0.007), as was capillary density (12 ± 6/mm² vs 26 ± 11/mm², P < 0.001). Adjustment for capillary density in multivariate regression analysis demonstrated that differences in I_av(7) between SSc patients and controls were related to differences in capillary density, BMI and high density lipoprotein cholesterol.

Conclusion. At the level of the ankle decreased capillary permeability was found in SSc patients, related to decreased capillary density. Microvascular involvement in SSc is widespread, but no evidence was established for increased capillary permeability at the level of individual capillaries as a generalized phenomenon.

Methods. We designed a web-based register with the intention to make it easy to use for participating physicians and at the same time accurate and up-to-date. Security demands were taken into account to secure the safety of the patient data.

Results. The web-based register was tested with data from 161 juvenile idiopathic arthritis patients from nine different centres. Internal validity was obtained and user-friendliness guaranteed. To secure the completeness of the data automatically generated e-mail alerts were implemented into the web-based register. More transparency of data was achieved by including the option to automatically generate interim reports of data in the web-based register. The safety was tested and approved.

Conclusions. By digitalizing the CRF we achieved our aim to provide easy, rapid and safe access to the database and contributed to a new way of data collection. Although the web-based register was designed for the current multi-centre observational study, this type of instrument can also be applied to other types of studies. We expect that especially collaborative study groups will find it an efficient tool to collect data.

Methods. Three groups were investigated. A healthy volunteer group (1) was injected with capsaicin into the volar aspect of one forearm. A group of patients with RA (2) was also injected with capsaicin. A control group of healthy volunteers (3) was not injected with capsaicin. All groups were tested for hyperalgesia and allodynia every 10 min for 1 h following the injection using quantitative sensory testing.

Results. A total of 9/14 healthy volunteers (Group 1) and 10/14 patients with RA (Group 2) demonstrated contralateral sensitization that subsided within 1 h following intradermal capsaicin injection. A total of 2/23 control subjects (Group 3) demonstrated positive responses with the monofilaments. The frequency of the contralateral responses in the experimental groups compared with the control group is significant (P < 0.05). The peak hyperalgesia was relatively delayed contralaterally compared with the ipsilateral side (35 min vs 15 min). The area of sensitization, where present, was reduced compared with the ipsilateral side (5–50%).

Conclusions. This is the first demonstration of a contralateral response following a unilateral stimulus in man. Bilateral neural pathways mediating contralateral responses may have a role in the pathophysiology of chronically painful or inflammatory diseases and a confounding influence on using the contralateral limb as a control experimentally. We did not find that a systemic inflammatory disease sensitized for this phenomenon.

Methods. A retrospective, non-randomized, cross-sectional study was performed in a cohort of 145 patients with AS in Hong Kong. Participants completed questionnaires on sociodemographics, work status and out-of-pocket expenses. Health resources consumption was recorded by chart review. Functional impairment and disease activity were measured using the Bath Ankylosing Spondylitis Functional Index (BASFI) and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), respectively. Patients’ QoL was assessed using the Short Form-36 (SF-36).

Results. The mean age of the patients was 40 yrs with mean disease duration of 10 yrs. The mean BASDAI score was 4.7 and BASFI score was 3.3. Annual total costs averaged USD 9120. Direct costs accounted for 38% of the total costs while indirect costs accounted for 62%. Costs of technical examinations represented the largest proportion of total cost. Patients with AS reported significantly impaired QoL. Functional impairment became the major cost driver of direct costs and total costs.

Conclusion. There is a substantial societal cost related to the treatment of AS in Hong Kong. Functional impairment is the most important cost driver. Treatments that reduce functional impairment may be effective to decrease the costs of AS and improve the patient's QoL, and ease the pressure on the healthcare system.

Methods. One hundred and forty-eight women with no clinical knee OA were recruited from a previous population-based cross-sectional study of healthy women aged 40–67 yrs. MRI was performed at baseline and at 2 yrs, to assess patella cartilage and bone volume. Self-reported exercise was assessed by questionnaire.

Results. Annual loss of patella cartilage volume was 1.6% (95% CI 1.2, 1.9). Age was positively associated with patella cartilage volume loss after adjustment for confounders (P = 0.05). For every 1 mm³ increase in patella bone volume at baseline, annual cartilage loss was reduced by 8.05 mm³ (95% CI 12.91, 3.19; P < 0.001). Fortnightly participation in exercise promoting an increased heart and respiratory rate for at least 20 min also tended to be associated with a reduced rate of patella cartilage volume loss (P = 0.09).

Conclusion. Among middle-aged women with no clinical knee OA, advancing age expedites the rate of patella cartilage volume loss, while increased patella bone volume and exercise participation tends to be associated with a reduction in the rate of patella cartilage volume loss. Interventions targeting modifiable factors, such as physical activity, warrant further investigation as they may help to prevent patellofemoral OA.