Osimertinib is the first line treatment for metastatic epidermal growth factor receptor (EGFR) mutation positive non-small cell lung cancer (NSCLC), and second line treatment for patients with acquired resistant T790M mutation. Interstitial lung disease (ILD) is a rare but potentially life-threatening complication from osimertinib thus drug discontinuation is recommended for grade 2 or above ILD. The risk of ILD associated with EGFR tyrosine kinase inhibitor (TKI) rechallenge with osimertinib versus first or second generation EGFR TKI remains unclear.

Background Blockade of JAK, preferably JAK1, by upadacitinib is a feasible approach to achieve erosion repair as it 1) is approved for the treatment of rheumatoid arthritis (RA), 2) effectively controls the inflammation and 3) targets pathogenic pathways that influence local bone homeostasis in the joint. Objectives To evaluate whether inhibition of JAK1 could lead to erosion repair on high-resolution peripheral quantitative computer tomography (HR-pQCT) in patients with active RA. Methods This was a 24-week, single-centered, prospective, non-randomized pilot study. We enrolled 20 adult patients with active RA (Disease activity score 28-C-reactive protein [DAS28-CRP] > 3.2) and ≥1 bone erosion on HR-pQCT. They were given upadacitinib 15mg once daily for 6 months. HR-pQCT of the 2-4 metacarpophalangeal (MCP) head was done at baseline and 6 months. The serum inflammatory cytokine profile and bone-cartilage interface biomarkers were also checked before and after treatment. The primary outcome was the change of erosion volume on HR-pQCT. Secondary outcomes included change in RA disease activity and serum biomarkers, as well as predictors of response to treatment. Erosion regression was defined as decrease in volume exceeding the smallest detectable change. Results The baseline clinical characteristics of the recruited patients were shown in Table 1. Of the 20 patients, 11 (55%) patients failed to respond to 3 or more csDMARDs. At 24-week, there was significant improvement in mean DAS28 (-1.75, p<0.001). Erosion regression was seen in 8 (40%) patients on HR-pQCT. Although no significant change in overall median erosion volume before and after upadacintinib (0.07 [-0.90-0.76mm3] mm3, p=0.904) was noted, the deterioration was less obvious compared to a historic cohort of 20 patients with similar age and disease activity on csDMARDs (median erosion volume change in 6 months: 0.67 mm3). There was significant reduction in the serum level of bone resorption marker C1M before and after treatment, which was not seen in the historic cohort. Significant reduction in various inflammatory cytokines (e.g. TNF-α, IL-6) was also noted after treatment. When patients were stratified according to whether or not they had failed multiple csDMARDs, significantly high proportion of patients in the non-multiple-DMARDs failure group had volume regression in at least one erosion compared to those in the failure group (75% vs 25%, p=0.04). There was improvement in mean total erosion volume in the non-failure group (-0.33±1.33 mm3), whereas mean erosion volume in the failure group worsened (2.09±7.62 mm3). One patient developed chest infection requiring hospitalization and withdrew from the study. No other serious adverse event was noted. Conclusion The results of the study suggested upadacitinib was clinically efficacious in refractory RA disease and could retard erosion progression. Regression of erosion was possible, particularly in those with limited csDMARDs exposure. Whether earlier JAK1 inhibition could lead to better structural outcome warrants further investigations. REFERENCES: NIL. Acknowledgements: NIL. Disclosure of Interests Ho SO Speakers bureau: Abbvie, Boehringer Ingelheim, Fosun Industrial, GSK, Janssen, Pfizer, Consultant of: Abbvie, GSK, Grant/research support from: Fosun Industrial, Isaac T. Cheng: None declared, Martin Li: None declared, Chun Kwok Wong: None declared, Lai-Shan Tam Consultant of: AbbVie, AstraZenaca, Boehringer Ingelheim, Eli Lilly, Janssen, Pfizer, and Sanofi, Grant/research support from: Amgen, Boehringer Ingelheim, GSK, Janssen, Novartis and Pfizer.

Background Psoriatic Arthritis (PsA) is a complex, heterogeneous disease with chronic inflammation. Disease manifestations include the peripheral joint inflammation, dactylitis, enthesitis and skin psoriasis. Chronic inflammation is associated with structural damage, which jeopardize long-term functional ability. Sensitive biomarkers reflecting disease activity in various disease domains are lacking. Objectives To define the molecular basis of inflammation in different disease domains through comparative profiling of serum proteins. Methods This is a cross-sectional study in patients with PsA. Clinical assessment of inflammation in the peripheral joint (clinical Disease Activity in Psoriatic Arthritis [cDAPSA] and swollen joint count), dactylitis digit count, skin (Psoriasis Activity and Severity Index [PASI]) and enthesis (Leeds enthesitis index) were performed. Blood samples were collected for biomarker assay including 48 cytokines, chemokines, growth and angiogenic factors using the Bio-Rad Bioplex assay1 (Table 1). Levels of selected serum proteins were compared between different disease activity scores across various domains using adjusted linear regression with least absolute shrinkage and selection operator (LASSO) modeling. Results 100 PsA patients were recruited (age: 51±11 years, male: 52 (52%), disease duration: 9.0±3 years). The cohort had moderate disease activity (DAPSA: 24.4±14.6; PASI: 6.0±7.2). 53 (53%) and 11 (11%) patients were using conventional synthetic disease modifying anti-rheumatic drugs (csDMARDs) and biologic DMARDs (bDMARDs) respectively. Using LASSO regression analysis, biomarkers correlating with peripheral joint inflammation were IFN-γ, IL6, SCF and MCP1, while MIP-1α and β-NGF were related to dactylitis. Biomarkers correlating with skin severity were IP10, M-CSF and eotaxin, while IL8, M-CSF and CTACK were related to enthesitis. Details of biomarkers independent predicting various disease severity are listed in table 2-3. Conclusion Comparative serum protein biomarker profiling represents a viable method for distinguishing active inflammation in the various disease domains which may be a step forward towards personalized medicine.cDAPSA - clinical Disease Activity in Psoriatic Arthritis; IFN-γ - Interferon-γ; IL – interleukin; SCF - Stem Cell Factor; MCP1 - Monocyte chemoattractant protein 1; MIP-1- Macrophage inflammatory protein 1α; β-NGF - Nerve growth factor; IP10 - Interferon gamma-induced protein 10; M-CSF - Macrophage colony-stimulating factor; CTACK - Cutaneous T cell- attracting chemokine.cDAPSA - clinical Disease Activity in Psoriatic Arthritis; IFN-γ - Interferon-γ; IL – interleukin; SCF - Stem Cell Factor; MCP1 - Monocyte chemoattractant protein 1; MIP-1 - Macrophage inflammatory protein 1α; β-NGF - Nerve growth factor; IP10 - Interferon gamma-induced protein 10; M-CSF - Macrophage colony-stimulating factor; CTACK - Cutaneous T cell- attracting chemokine. REFERENCES: NIL. Acknowledgements: NIL. Disclosure of Interests None Declared.Table 2LASSO regression on various disease activity scores across various disease domainsTable 3Biomarker independently correlating with various disease severity scores across various disease domains

Background: While carotid ultrasound (US) has been advocated for cardiovascular (CV) risk screening in patients with rheumatoid arthritis as various traditional scores underestimate CV risk, whether subclinical carotid atherosclerosis (SCA) is associated with coronary atherosclerosis on coronary computed tomography angiography (CCTA) in patients with psoriatic arthritis (PsA) remains uncertain. Objectives: This study aimed to identify carotid US parameters which can discriminate PsA patients with coronary artery disease (CAD) and obstructive CAD (O-CAD), and determine the utility in combination with Framingham Risk Score (FRS). Methods: Ninety-one PsA patients (56 males; age: 50±11years, disease duration: 9.4±9.2years) without overt CV diseases were recruited. Carotid intima-media thickness (cIMT), presence of plaque and total plaque area (TPA) were determined by high-resolution US. CAD was defined as the presence of any coronary plaque on CCTA. O-CAD was defined as >50% stenosis of the lumen. FRS <10% indicates low CV risk, 10-19% indicates intermediate risk while ≥20% indicates high risk (1). Results: Thirty-five (38%) patient had carotid plaque. Fifty-five (60%) patients had CAD and 9 (10%) patients had O-CAD. 53 (58%), 25 (17%) and 13 (14%) were classified as low, moderate and high CV risk according to the FRS respectively. FRS underestimated the CV risk as only 11/55 (20%) of subjects with CAD were correctly identified as having high CV risk by FRS (Figure 1). Fifteen patients out of 53 (28%) with low CV risk based on FRS were reclassified as high CV risk by the presence of carotid plaque. Nine out of these 15 (60%) had CAD and 1/15 (6.7%) had O-CAD. Concerning the carotid ultrasound parameters, cIMT (mean and maximum) and TPA were increased in both the CAD+ and O-CAD+ group compared to those without CAD or O-CAD (Table 1). Multivariate logistic regression analysis revealed that mean cIMT (OR=1.06, 95% CI:1.01-1.11, p =0.013) was an independent explanatory variables associated with CAD. Meanwhile, mean cIMT (OR=1.06, 95%CI: 1.01-1.11, p =0.013) maximum cIMT (OR=1.06, 95%CI: 1.00-1.13, p =0.043), and TPA (OR=1.55, 95%CI: 1.01-2.36, p =0.043) were independent explanatory variables associated with O-CAD after adjusting for covariates. Based on Receiver Operating Curve (ROC) analysis, an optimal cut off for FRS at 5% and mean cIMT at 0.62mm yield 63% sensitivity and 73% specificity for the presence of CAD (AUC: 0.71, p =0.001). Table 1. Relationship between carotid ultrasound parameters and the presence and extent of coronary artery disease on coronary computed tomography angiography. Coronary artery disease No (n=37) Yes (n=54) p Mean carotid IMT, mm 0.63 ± 0.12 0.69 ± 0.1 0.017 Maximum carotid IMT, mm 0.77 ± 0.17 0.84 ± 0.14 0.040 Carotid Plaque, n, % Absence 26 46.4% 30 53.6% 0.156 Presence 11 31.4% 24 68.6% Total plaque area, mm 2 0.0 [0,6] 0.0 [0, 10.8] 0.059 Obstructive coronary artery disease No (n=82) Yes (n=9) p Mean carotid IMT, mm 0.65 ± 0.12 0.76 ± 0.07 0.011 Maximum carotid IMT, mm 0.80 ± 0.16 0.93 ± 0.14 0.020 Carotid Plaque, n, % Absence 53 93.0% 4 7.0% 0.235 Presence 29 85.3% 5 14.7% Total plaque area, mm 2 0.0 [0, 7.0] 6.0 [0, 15.3] 0.103 IMT-intima media thickness; coronary computed tomography angiography. Conclusion: Increased cIMT and TPA were associated with CAD and O-CAD in PsA patients while the presence of carotid plaque alone was insufficient to discriminate patient with or without CAD. A combination of US parameters should be considered for CV risk stratification in patients with PsA. References: [1]Ford ES et al., J Am Coll Cardiol . 2004;43(10):1791-6. Disclosure of Interests: Isaac T. Cheng: None declared, Ka Tat Wong: None declared, Edmund Li: None declared, Priscilla C Wong: None declared, Billy Tin Lok Lai: None declared, Cheuk Wan Yim: None declared, Shirley King Yee Ying: None declared, Kitty Yan Kwok: None declared, Martin Li: None declared, Tena K. Li: None declared, Jack Jock Wai Lee: None declared, Alex Pui Wai Lee: None declared, Lai-Shan Tam Grant/research support from: Janssen, Pfizer, Novartis, Speakers bureau: Abbvie, Lilly, Sanofi

Objectives Many in vitro studies have investigated the mechanism by which mechanical signals are transduced into biological signals that regulate bone homeostasis via periodontal ligament fibroblasts during orthodontic treatment, but the results have not been systematically reviewed. This review aims to do this, considering the parameters of various in vitro mechanical loading approaches and their effects on osteogenic and osteoclastogenic properties of periodontal ligament fibroblasts. Methods Specific keywords were used to search electronic databases (EMBASE, PubMed, and Web of Science) for English-language literature published between 1995 and 2017. Results A total of 26 studies from the 555 articles obtained via the database search were ultimately included, and four main types of biomechanical approach were identified. Compressive force is characterized by static and continuous application, whereas tensile force is mainly cyclic. Only nine studies investigated the mechanisms by which periodontal ligament fibroblasts transduce mechanical stimulus. The studies provided evidence from in vitro mechanical loading regimens that periodontal ligament fibroblasts play a unique and dominant role in the regulation of bone remodelling during orthodontic tooth movement. Conclusion Evidence from the reviewed studies described the characteristics of periodontal ligament fibroblasts exposed to mechanical force. This is expected to benefit subsequent research into periodontal ligament fibroblasts and to provide indirectly evidence-based insights regarding orthodontic treatment. Further studies should be performed to explore the effects of static tension on cytomechanical properties, better techniques for static compressive force loading, and deeper analysis of underlying regulatory systems.

Background Patients with rheumatoid arthritis(RA) had increased risk of cardiovascular disease(CVD). IL-33, a member of the IL-1 family, plays an important role in the pathogenesis of RA and development of CVD. Yet, plasma IL-33 level was not detectable in most subjects which limits it’s utility as a biomarker for CVD. Meanwhile, microRNAs(miRNAs) targeting IL-33 gene expression might play a role. Objectives To ascertain if dysregulated miRNAs targeting IL-33 gene expression in earlyRA patients were associated with subclinical atherosclerosis progression Methods 73 ERA patients were recruited for this 1 year cohort study. Potential miRNAs binding to IL-33 gene were predicted by miRanda. 10 miRNAs with the highest possibility of targeting functional sites of IL-33 gene were quantified in cell free plasma samples. cel-miR-39 was used as spike-in control. Carotid plaque(CP) was identified using high-resolution ultrasound annually. Plaque progression(PP) was defined as an increased region harbouring plaque. Results CPs were identified in 25 (34%) and 31 (43%) subjects at baseline and month 12 respectively. 16 (22%) subject had plaque progression(PP +group). At baseline, subjects in PP +group were older, with lower pain and patient global scores, a higher proportion on conventional synthetic DMARDs, and higher cardiovascular risk compared to patients without plaque progression (PP-) (table 1). Plasma level of miR-382–5 p in the PP +group was significantly higher than that in the PP- group after adjusting for baseline difference (table 1). Using multivariate logistic regression, miRNA-382–5 p was an independent predictor for plaque progression(OR:2.534, 95%CI=1.079–5.952, p=0.033) after adjustment of baseline characteristics. [AUC:0.66,95% CI:0.51–0.81,p=0.048]. Other independent predictor included higher baseline Framingham risk score, diastolic BP and lower pain score. Conclusions miR-382–5 p was an independent predictor for progression of subclinical atherosclerosis and may serve as a novel biomarker for cardiovascular risk assessment in ERA patients. Acknowledgements Acknowledgement to Hong Kong Society of Rheumatology Project Fund for supporting this project. Disclosure of Interest None declared

Background Carotid Atherosclerosis is associated with compromised volumetric bone mineral density and microstructures in patients with inflammatory arthritis Objectives The aim of this study was to explore the relationship between volumetric bone mineral density (vBMD)/microstructural features and presence of carotid plaque (CP) in patients with inflammatory arthritis. Methods 175 inflammatory arthritis patients (81 [46%] PsA, 94 [54%] RA; 70 [40%] males; age: 53±12 years) were recruited into an ongoing prospective study assessing the relationship between inflammation, osteoporosis and carotid atherosclerosis. Carotid plaque and intima-media thickness (IMT) were measured by carotid ultrasound. Areal BMD (aBMD) was measured by dual energy X-ray absorptiometry (DXA). Microstructure features and vBMD of distal radius were measured using high-resolution peripheral quantitative computed tomography (HR-pQCT). Results No patients had established cardiovascular disease (CVD). Data from 172 patients at baseline were analyzed for this cross-sectional study. Patients were sub grouped according to the presence or absence of carotid plaque (CP+ group, n=68 [40%]) and CP- group, n=132 [60%]). CP+ group were older (59±10 vs 49±11, p<0.001), more likely to be male (54% vs 31%, p=0.002), had higher systolic blood pressure (130±19 vs 124±17 mmHg, p=0.034) and CVD risk (15.7±14.2 vs 7.9±8.6, p<0.001) according to the Framingham Risk Score (FRS) then the CP- group. aBMD, vBMD and microstructure were significantly compromised in the CP+ group. Distal radius aBMD, distal radius total vBMD, trabecular (Tb) vBMD, Tb thickness, cortical (Ct.) vBMD, Ct. thickness and bone volume fraction were 5% (p=0.004), 12% (p<0.001), 8% (p=0.007), 8% (p=0.004), 4% (p=0.007), 10% (p=0.001) and 8% (p=0.007) lower in the CP+ group. The differences remained significant after adjustment for gender, disease type and FRS (Table 1). Conclusions Inflammatory arthritis patients with carotid plaque had lower aBMD, vBMD and compromised bone microstructure in the distal radius even after adjustment for gender, disease type and FRS, suggesting that inflammation may be the common link for both conditions. Disclosure of Interest None declared

Background Expression of several miRNAs occurs in the plasma and synovial fluid of patients with established rheumatoid arthritis (RA). We found that microRNA-143–3 p (miR-143–3 p), miR-145–5 p, and miR-99b-5p expression was associated with greater erosion volume in early RA (ERA)EULAR 2018-abstract no 1980). Whether these miRNAs are associated with bone erosion and joint inflammation on magnetic resonance imaging (MRI) is unknown. Objectives To determine whether plasma cell-free circulating miRNAs are associated with (a) bone erosion and (b) inflammation severity on MRI in patients with ERA. Methods 66 ERA patients were recruited at presentation for this cross-sectional study. 60 of these 66 patients (90.9%) were treatment naïve. MRI of the most severely affected wrist was performed in all patients. The degree of bone damage (i.e. erosions), bone inflammation (osteitis) and soft tissue inflammation (synovitis/tenosynovitis) was scored on MRI (a) semi-quantitatively using the Rheumatoid Arthritis MRI score (RAMRIS) for scoring the severity of erosions, bone marrow oedema, synovitis and tenosynovitis; and (b) quantitatively by measuring synovial and tenosynovial volume (mm3). The three most dysregulated miRNAs (miR-143–3 p, miR-145–5 p, and miR-99b-5p) identified in our previous ERA study were validated by TaqMan® qRT-PCR in all patients. Results Expression of miR-99b-5p was higher in ERA patients with erosions (1.28±0.61) on MRI than those without erosions (0.23±0.43, p<0.05). Subdivided according to mean RAMRIS synovitis score (5.69), miR-99b-5p expression was higher in ERA patients with relatively more synovitis (0.75±1.24) on MRI than those with relatively less synovitis (0.34±1.14, p<0.05). Bone marrow oedema or tenosynovitis on MRI were not found to be associated with specific miRNA expression. Expression of miR-99b-5p did, however, correlate with synovial (r=0.443, p=0.018) and tenosynovial volume (r=0.423, p=0.025) on MRI. Linear regression analysis revealed miR-99b-5p expression to be independently associated with both increased synovial volume (B=15.65, 95% CI 3.42~27.89, p=0.014) and increased tenosynovial volume (B=7.39, 95% CI 0.41~14.38, p=0.039) (Table). Table 1 Univariate and multivariate analysis for factors associated with synovial volume and tenosynovitis volume at baseline in all ERA patients Conclusions Increased cell-free circulating miR-99b-5p is associated with increased synovial and tenosynovial volume as well as more severe bone erosion in ERA patients at presentation. Whether it may serve as a biomarker for monitoring the progression of synovitis and damage would need to be addressed in prospective studies. Acknowledgements This study was partly supported by the Health and Medical Research Fund (project no 10110071). Disclosure of Interest None declared

Background Bone erosions are a key feature of rheumatoid arthritis (RA) reflecting both disease severity and disease progression. Recent studies using HR-pQCT demonstrated impairment in the bone microstructure of the metacarpophalangeal (MCP) joints of ACPAs-positive healthy individuals despite no signs of arthritis. In patients with established RA, ACPAs and rheumatoid factor (RF) showed an additive effect on erosion number and erosion size. Furthermore, RF influences erosion size only in ACPAs-positive but not in ACPAs-negative patients. Objectives To determine the effect of high titre of anticitrullinated protein antibodies (ACPAs) and rheumatoid factor (RF) on the number and size of bone erosions in patients with early rheumatoid arthritis (ERA) by high-resolution peripheral quantitative computed tomography (HR-pQCT) at baseline and whether these antibodies are associated with the progression of erosion after one year of follow-up. Methods In the cross-sectional study, HR-pQCT of the second metacarpophalangeal joint (MCP2) was performed in 124 patients with ERA at baseline, images were analysable in 117 patients. Erosions were visualized in 72 patients and parameters of bone erosions were assessed. In the prospective study, 63 ERA patients who had completed one year of follow-up with repeat HR-pQCT scan were also analysed. The number and volume of the erosions as well as bone mineral density (BMD) surrounding erosion were quantified. Data on demographic and disease-specific parameters including ESR, CRP, DAS 28, ACPAs and RF levels and treatment were recorded. Results At baseline, 90/117 patients were both ACPAs and RF positive (ACPAs+/RF+ group), 7/117 were only RF (RF+), 13/117 were only ACPAs (ACPAs+) and 7/117 were antibody negative (non-ACPAs+/RF+ group, n=27). Erosion depth and volume were increased in the ACPAs+/RF+ group compared with the non-ACPAs+/RF+ group (both P<0.05) (Table 1). Independent explanatory variables associated with a larger erosion volume included RF>16U (P=0.012), older age (P=0.003) and a higher damage joint count (P=0.028). Images from 63 patients who completed 12 months follow-up were analysed. Erosion volume were significantly lower in patients who achieved simplified disease activity score (SDAI) remission at 12 months compared to those who did not (P=0.045). Linear regression analysis indicated that independent predictors for an increase in erosion volume included RF>16U (P=0.032) and a higher damage joint count (P=0.009) at baseline and failure to achieve SDAI remission at 1 year (P=0. 043). Conclusions ACPAs and RF show an additive effect on erosion volume in ERA patients. Higher RF titre was associated with larger erosion volume at baseline and predicted progression of erosion volume after adjusting for baseline parameters and treatment response. Disclosure of Interest None declared

BACKGROUND:Non-ionizing radiation imaging assessment has been advocated for the patients with adolescent idiopathic scoliosis (AIS). As one of the radiation-free methods, ultrasound imaging has gained growing attention in scoliosis assessment over the past decade. The center of laminae (COL) method has been proposed to measure the spinal curvature in the coronal plane of ultrasound image. However, the reliability and validity of this ultrasound method have not been validated in the clinical setting. OBJECTIVES:To evaluate the reliability and validity of clinical ultrasound imaging on lateral curvature measurements of AIS with their corresponding magnetic resonance imaging (MRI) measurements. METHODS:Thirty curves (ranged 10.2°-68.2°) from sixteen patients with AIS were eligible for this study. The ultrasound scan was performed using a 3-D ultrasound unit within the same morning of MRI examination. Two researchers were involved in data collection of these two examinations. The COL method was used to measure the coronal curvature in ultrasound image, compared with the Cobb method in MRI. The intra- and inter-rater reliability of the COL method was evaluated by intra-class correlation coefficient (ICC). The validity of this method was analyzed by paired Student's t-test, Bland-Altman statistics and Pearson correlation coefficient. The level of significance was set as 0.05. RESULTS:The COL method showed high intra- and inter-rater reliabilities (both with ICC (2, K) >0.9, p<0.05) to measure the coronal curvature. Compared with Cobb method, COL method showed no significant difference (p<0.05) when measuring coronal curvature. Furthermore, Bland-Altman method demonstrated an agreement between these two methods, and Pearson's correlation coefficient (r) was high (r>0.9, p<0.05). CONCLUSION:The ultrasound imaging could provide a reliable and valid measurement of spinal curvature in the coronal plane using the COL method. Further research is needed to validate the proposed ultrasound measurement in larger clinical trial and to optimize the ultrasound scanning and measuring procedure.

Background Data from observational studies showed that the effects of long-term anti-TNF-α therapy on arterial stiffness and intima-media thickness (IMT) progression in patients with ankylosing spondylitis (AS) were inconsistent. Objectives To ascertain the efficacy of with golimumab compared to placebo in the prevention of atherosclerosis and arterial stiffness in patients with AS. Methods A randomized, double-blind, placebo-controlled study in which AS patients with active disease were treated with golimumab 50mg daily (n=20) and placebo (n=21) for 12 months. Patients were assessed every 3 monthly. Patients from the placebo group who failed to achieve ASAS20 response at 6 months were permitted to escape to receive open-label golimumab. IMT, pulse wave velocity (PWV) and augmentation index (AIx) were measured at baseline, 6 and 12 months. We hereby report the results of the first 6 months. Results At 6 months, 11/20 (55%) and 3/21 (14%) patients from the golimumab and placebo groups respectively achieved an ASAS 20 response (p = 0.006). There was no significant difference in the change of the vascular parameters between the two groups. Nonetheless, within group comparison showed that in the placebo group, significantly greater progression of the mean IMT (from 0.51 ± 0.07 mm at baseline to 0.53 ± 0.08 mm at 6 months, p = 0.044) and PWV (from 12.2± 1.6 m/s at baseline to 12.6 ± 1.3m/s, p = 0.028) were observed in the placebo group, while the maximum IMT (from 0.54 ± 0.08 mm at baseline to 0.56 ± 0.10 mm at 6 months, p = 0.085) and AIx (12.4 ± 10.3% at baseline to 11.6 ± 10.9%, p=0.7) remained unchanged. The vascular parameters of the golimumab group remained unchanged (mean IMT from 0.52 ± 0.07 mm at baseline to 0.54 ± 0.09 mm at 6 months, p = 0.099; maximum IMT from 0.56 ± 0.09 mm at baseline to 0.56 ± 0.10 mm at 6 months, p = 0.852; AIx from 11.4 ± 11.8 % at baseline to 13.1 ± 10.9 %, p=0.454; and PWV from 12.4 ± 1.5m/s at baseline to 12.4 ± 1.6 m/s, p = 0.855). Compared with the placebo group, there was a significantly greater reduction in the laboratory parameters of inflammation (ESR and CRP), accompanied by significantly greater reduction in the physician’s global assessment, pain and BASDAI in the golimumab group. Significantly greater increase in the total cholesterol (TC) and high density lipoprotein (HDL) cholesterol levels were observed in the golimumab group, nonetheless, no significant differences in the changes of the TC/HDL or other cardiovascular risk factors were observed between the two groups Conclusions Uncontrolled inflammation may result in a significant progression in IMT and PWV in patients with AS, which may be prevented by golimumab over a period of 6-month, suggesting that effective suppression of inflammation may prevent progression of subclinical atherosclerosis and improving vascular function. Acknowledgements This study is supported by an educational grant from Janssen Pharmaceutical (Hong Kong). The study drugs were provided by Janssen Pharmaceutical (Hong Kong). Disclosure of Interest None Declared

This study aimed to improve the effectiveness of orthotic treatment for the patients with AIS using the three-dimensional clinical ultrasound (3D CUS) method in which the optimal location of pressure pad of spinal orthosis was determined with the assistance of ultrasound image analysis.

Patient with moderate AIS is usually prescribed with spinal orthosis aiming to mechanically support and prevent the spine from further deterioration. In the conventional fitting method, pre-brace X-ray is the main reference, thus, the pressure pad of spinal orthosis may not be accurately located to the strategic areas because the spinal deformities could change 3-dimensionally once pressure pad is applied. A high correlation (r > 0.98) between Cobb's angle and spinous process angle (SPA) was found in the recent studies. With the advancements of 3D clinical ultrasound (3D CUS), tracing SPA along a scoliotic spine becomes possible and this can be used to estimate Cobb's angle. This study aimed to evaluate the effect of pressure pad location of spinal orthosis in the treatment of AIS and 3D CUS was used to trace SPA for estimation of Cobb's angle. The in-brace X-rays were assessed for confirmation of treatment effectiveness. The subjects were divided into ultrasound-guided fitting group A (n=21) and conventional fitting group B (n=22). In the group A, pressure pads were tested at 5 locations - the prescribed location as in the conventional fitting (referred to the pre-brace X-ray), and 1 cm and 2 cm above and below the prescribed location, and 3D CUS was applied to trace the SPA in these 5 pad locations, and the pad location with the lowest estimated Cobb's angle was selected in the final fitting. The assessments of in-brace X-rays showed that the mean Cobb's angle of group A decreased from 28.9° (pre-brace) to 18.6° (immediate in-brace) while the mean Cobb's angle of group B decreased from 27.1° (pre-brace) to 22.5° (immediate in-brace). There was a significant difference (p < 0.05) in the correction of Cobb's angle between the two groups. The results showed that accurate pressure pad location does play an important role in the reduction of Cobb's angle and 3D CUS can be considered as a non-invasive and effective assessment tool to improve orthotic treatment of AIS.

Objective: To ascertain the effect of rosuvastatin on carotid atherosclerosis and arterial stiffness in patients with rheumatoid arthritis (RA).Methods: Fifty RA patients were randomized in a double-blind placebo-controlled trial to receive 10 mg rosuvastatin (n = 24) or placebo (n = 26). Patients were followed prospectively every 3 months for 12 months. Intima-media thickness (IMT), augmentation index (AIx), and subendocardial viability ratio (SEVR) were measured at baseline, 6 and 12 months.Results: Rosuvastatin resulted in statistically significant reductions of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), and urate levels vs. placebo. However, rosuvastatin had no significant effect on changes in inflammatory markers, including C-reactive protein (CRP) levels [from 2.9 (1.4-11.0) to 3.1 (0.9-13.3) mg/L in the rosuvastatin group compared with from 5.8 (2.6-14.2) to 4.4 (1.2-12.3) mg/L in the placebo group]. Nonetheless, a significant improvement in the Disease Activity Score (DAS) and a reduction in fibrinogen level was observed at 6 and 12 months compared with baseline in the rosuvastatin group. The treatment group exhibited a significant increase in SEVR (from 157 +/- 28% to 163 +/- 33% in the rosuvastatin group compared with from 143 +/- 18% to 143 +/- 26% in the placebo group, p = 0.023), but no significant effect was observed in the changes in IMT and AIx.Conclusion: Our data suggest that rosuvastatin has a modest anti-inflammatory effect in RA patients with low disease activity in terms of reduction in DAS and fibrinogen level. Rosuvastastin may also improve subendocardial perfusion and lower the urate level.

Spinal orthosis is generally applied to the patients with adolescent idiopathic scoliosis (AIS) during puberty to mechanically support the spine and prevent further deterioration. However, the optimum location of pressure is not easy to be determined and the X-ray taken is not a real time presentation of the spinal curvature. With the advancement of clinical ultrasound, tracing spinal processes along a scoliotic spine becomes possible, which means spinous process angle (SPA) can be obtained from ultrasound images. Moreover, SPA is found to be highly correlated with Cobb's angle. Since the outcome of orthotic intervention for AIS is considered to be associated with accurate orthosis fitting, this study seeks to apply three-dimensional (3-D) ultrasound in the fitting procedure of spinal orthosis for patients with AIS. The accuracy of pressure pad location in brace can help to improve the effectiveness of spinal orthosis treatment. By means of the ultrasound assessments, spinous process angle is examined and used as the parameter to evaluate the optimal location for pressure pad. The intra-rater reliability [ICC (1, 3)] for using ultrasound to measure SPA is >0.9 (p<0.05). Furthermore, the correlation between Cobb's angle estimated from the measurement of SPA in 3-D ultrasound images and Cobb's angle measured from X-ray is highly significant (R=0.98, p<0.01). According to these findings, ultrasound can be further developed as a non-invasive real-time assessment tool for spinal curvature especially in fitting stage to improve the treatment effect of the spinal orthosis.

OBJECTIVE:To examine the distribution of traditional and novel risk factors of cardiovascular disease (CVD) in patients with PsA compared with healthy controls.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.

The adverse effect of disease and chronic corticosteroid therapy on bone mineral density (BMD) in patients with systemic lupus erythematosus (SLE) has been reported in several studies of Caucasian populations. As the factors controlling bone homeostasis may be different in Asian populations, we measured BMD in 52 pre-menopausal Chinese women (mean age 34.1 +/- 8.0 yr) with SLE (mean disease duration 6.4 +/- 4.5 yr) treated with prednisone (mean daily dose 11.4 +/- 10.8 mg/day). Lumbar spine, hip (total and subregions) and total body BMDs were measured in the SLE patients using dual-energy X-ray absorptiometry (DEXA), and compared with those from healthy controls matched for age, sex and body mass index. Compared to controls, SLE patients were found to have lower BMD (g/cm2) at several sites: the lumbar spine (0.98 vs 0.90, P = 0.001), Ward's triangle (0.72 vs 0.67, P = 0.03), total body (1.04 vs 1.01, P = 0.04) and total hip (0.87 vs 0.82, P = 0.05). There was no correlation between BMD at any region and duration of disease, activity of disease or prednisone therapy (mean daily dose, cumulative dose or treatment duration). When BMDs were compared between controls and SLE patients, subgrouped according to those not on calcium and those arbitrarily receiving calcium supplements (1 g/day), significantly lower BMDs were found in those not on calcium compared to both controls and SLE patients on calcium. BMDs in SLE patients on calcium were not different from those in controls. The low prevalence of osteoporosis in our SLE patients (4-6%) suggests significant loss of BMD in Chinese SLE patients on corticosteroid therapy is less than that reported in Caucasians (12-18%).