Aim:  This is a rheumatoid arthritis (RA) descriptive study, the first of its kind carried out in Malaysia. Methods:  This descriptive study involved 1084 RA patients’ epidemiological and clinical data taken from Selayang, Putrajaya, Taiping and Seremban hospitals from June 2004 to December 2005. Results:  One thousand and eighty‐four RA patients'data were analysed; 960 (88.6%) patients were female and 124 (11.4%) were male, approximately 8 : 1 M : F ratio. The majority of the patients were Indian (591; 54.5%), followed by the Malays (340; 31.4%), Chinese (126; 11.6%), indigenous (13; 1.2%) and others (14; 1.3%). Mean age was 49.6 ± 11.8 years with the youngest being 15 years and the oldest 88 years of age. Mean age for males was 52.0 ± 12.0 and females 49.3 ± 11.7 years (P = 0.017). Most of these patients were housewives (565; 52.1%), followed by paid workers (266; 24.5%), retired patients (80; 7.4%), unemployed (76; 7.0%) and others (97; 8.9%). Mean duration of illness was 8.4 ± 6.7 years; 805 (74.3%) patients were relatively new patients (≤ 2 years illness duration) and 279 (25.7%) patients had illness duration > 2 years. Eight hundred and six (74.4%) were seropositive RA patients and 385 (35.5%) had presence of deformity. The majority of patients were treated with methotrexate (178; 16.4%), followed by combination of methotrexate, sulfasalazine and hydroxychloroquine (143; 13.2%), leflunomide (140; 12.9%), sulfasalazine (133; 12.3%) and combination of methotrexate and sulfasalazine (108; 10%). Conclusion:  In the above study, the majority of patients were female (960; 88.6%), Indian (591; 54.5%), had a mean age of 49.6 ± 11.8 years, most were housewives with a mean duration of illness of 8.4 ± 6.7 years and were treated with methotrexate (178; 16.4%). The results of the study may help Malaysian rheumaologists to understand their patients better and treat RA holistically.

Background:The mechanisms affecting anti-RA33 antibody’s involvement in RA pathogenesis is still unclear. Refining our understanding of anti-RA33’s role in RA in relation to known RA-associated genes and serological elements is needed.Objectives:We investigated the relationship between RA-associated HLA-DRB1 epitope (SE) allele and presence of anti-RA33 antibodies in different serological subsets of rheumatoid arthritis in a Malaysian population.Methods:Serum samples from 550 RA cases comprising seronegative (negative for anti-CCP2, IgG and IgM, n=250), seropositive (triple-autoantibody positive, n=150), singular anti-CCP2 positive (n=100), and double RF positive RA (n=50) were chosen from the Malaysian Epidemiological Investigations of RA (MyEIRA) case-control study. Three hundred MyEIRA population controls were used for comparison. All serum samples were assayed using a commercial anti-RA33 ELISA kit. All genetic samples were genotyped for four-digit HLA-DRB1 alleles using the PCR-SSO method on Luminex platform.Results:The proportions of anti-RA33 positive was 20.9% in all RA cases (i.e. 34% in RF only positive RA; 25% in seropositive RA; 18% in seronegative RA and 18% in anti-CCP2 only positive RA). The HLA-DRB1 shared epitope alleles were significantly associated with anti-RA33 positive in the seropositive RA subgroup (OR=6.9, 95% CI 1.4-34.8; p=0.02). We observed significant association between anti-RA33 negative and HLA-DRB1 SE alleles among the seropositive RA patients (OR=4.5, 95% CI 2.8-7.2; p<0.001) and among CCP only positive RA (OR=4.4; 95% CI 2.6-7.4; p<0.01). No association was observed between anti-RA33 status and HLA-DRB1 SE alleles in seronegative RA and RF only positive RA.Conclusion:The HLA-DRB1 SE alleles increased the risk of seropositive and CCP only positive RA independent of anti-RA33 positivity.References:[1]Boeters, Debbie M et al. “The 2010 ACR/EULAR criteria are not sufficiently accurate in the early identification of autoantibody-negative rheumatoid arthritis: Results from the Leiden-EAC and ESPOIR cohorts.” Seminars in arthritis and rheumatism vol. 47,2 (2017): 170-174.[2]de Brito Rocha, Sara et al. “Clinical and pathophysiologic relevance of autoantibodies in rheumatoid arthritis.” Advances in rheumatology (London, England) vol. 59,1 2. 17 Jan. 2019.Acknowledgements:The authors would like to thank the Director General of Health, Ministry of Health Malaysia for supporting this study. The authors are also indebted to participants for their kind participation. This study was financially supported by the Ministry of Health, Malaysia (JPP-IMR 08-012).Disclosure of Interests:None declared

Background:Osteoporosis (OS) is common in rheumatic diseasas (RMD). OS fracture leads to morbidity and premature mortality. The treatment for OS is well established with good long term safety profile. Oral bisphosphonate (BIS) is recommended as initial treatment option for both postmenopausal and glucocorticoid induced OS. Denosumab (DSB), is the noninferior alternative option. Despite its efficacy, DSB was linked with elevated infection risk in non RMD. Yet, data in RMD is lacking.Objectives:To determine the infection risk and associated factors in RMD patients receiving DSB.Methods:This is retrospective cohort study. Data was extracted from medical database (between Jan 2010 & Dec 2018) at Selayang Hospital, Malaysia. Descriptive statistical analysis, logistic regression (LR) and cox (proportional hazard) regression [CPHR] were the analysis methods.Results:50 cases were analysed. 96% were female. The median age was 72.5 ± 12.7 years. The primary rheumatological disorders were rheumatoid arthritis (48%), OS (24%) and systemic lupus erythematosus (10%). 92% had ≥ 1 comorbidity including metabolic/cardiovascular diseases (74%), chronic lung diseases (CLD) (40%) and diabetes mellitus (DM) (22%). 54% had disease modifying anti rheumatic drug (DMARD) therapy; majority (59.2%) received single conventional synthetic DMARD. Only 7.4% received combination biologic DMARD therapy. 28% had received prednisolone therapy, with dose < 7.5mg OD in 78.6%.The median age at DSB initiation was 71 ± 12.4 years. 38% had fracture history and 88% had received previous OS treatment.In total, 13 infection episodes were recorded. The infection risk was 26% & incidence rate was 134 cases per 1000 person-years. 84.6% required hospitalisation and 38.5% were severe cases. The mortality rate was 23.1%. The mean DSB treatment duration to first infection was 15.46 ± 11.9 months.Univariate LR showed infection risk and hospitalisation were higher with longer DSB treatment duration, OR 1.062 (95% CI: 1.010 - 1.117), p = 0.018) & OR 1.057 (95% CI: 1.003 - 1.114, p = 0.037), respectively. These risks were lower in absence of steroid use, OR 0.2 (95% CI: 0.051 - 0.784, p = 0.021) and OR 0.215 (95% CI: 0.052 - 0.889, p = 0.034), respectively. Additionally, infection risk was lower in absence of CLD, OR 0.188 (95% CI: 0.048 - 0.742, p = 0.017) and hospitalisation was lower without concomitant DM, OR 0.050 (95% CI: 0.050 — 0.950, p = 0.043). Yet, multivariate LR did not infer the above predictions, after adjustment made for age, gender, rheumatological diseases, comorbidity, DMARD therapy and steroid dosing. For severe infection and case fatality, no predictive factors were identified.CPHR showed patients without steroid use had lower fatality risk, HR 0.077 (95% CI: 0.007 - 0.864, p = 0.038). With confounding factors (age, gender, previous infection and comorbidity), the observed difference was insignificant.Conclusion:Risk of infection and hospitalisation could be higher in rheumatic patients receiving longer DSB treatment duration. Concomitant comorbidities (CLD and DM) might increase the risk of infection and/or hospitalisation.References:[1]Cummings SR, San Martin J, McClung MR, Siris ES, Eastell R, Reid IR, et al. Denosumab for prevention of fractures in postmenopausal women with osteoporosis. N Engl J Med 2009;361:756–65.[2]Watts NB, Roux C, Modlin JF, Brown JP, Daniels A, Jackson S, Smith S, Zack DJ, Zhou L, Grauer A, Ferrari S. Infections in postmenopausal women with osteoporosis treated with denosumab or placebo: coincidence or causal association? Osteoporos Int. 2012;23(1):327–337.[3]Prabhakaran S, Pritchard C. Comparison of infection rates in patients receiving denosumab, denosumab and biologics and biologics alone in a suburban rheumatology clinic [abstract]. Arthritis Rheumatol 2014;66 Suppl 10:S409.[4]Bray V, Bagley A, West S, Etzel C, Kremer J, Kolfenbach J. Infection risk among patients receiving concurrent denosumab and biologic or non-biologic DMARD therapy: An analysis of the ConsortiumAcknowledgements:We would like to thank the Director General of Health Malaysia for his permission for this poster presentation.Disclosure of Interests:None declared.

BackgroundFamily history of rheumatoid arthritis (RA) is a surrogate for an individual's genetic and partly environmental risk of developing RA. It is assessed daily in clinical practice and its magnitude and pattern of distribution may provide information on the RA etiology.ObjectivesWe investigated the association between family history of RA and the risk of anti-citrullinated peptide antibody (ACPA)-positive and ACPA-negative RA in the Malaysian population.MethodsData from the Malaysian Epidemiological Investigation of Rheumatoid Arthritis (MyEIRA) population-based case-control study involving 1,055 early RA cases and 1,055 age, sex and residential area-matched controls were analyzed. Information from interview-reported family history of RA or rheumatic stiff back among first degree relatives was used to estimate the risk of developing ACPA-positive and ACPA negative RA. The odds ratio (OR) with 95% confidence interval (CI) was calculated.ResultsIn this study, 64% of the RA patients were ACPA-positive and 40% of the overall RA carried HLA-DRB1 shared epitope (SE) alleles. Family history of RA was significantly associated with an increased risk of developing RA in the Malaysian population (RA versus controls, 17.0% vs. 7.7%, OR 2.4, 95% CI 1.8–3.2, p<0.0001). The association between positive family history and risk of RA was uniformly observed for the ACPA-positive RA (OR 2.5, 95% CI 1.8–3.3, p<0.0001) and ACPA-negative RA (OR 2.3, 95% CI 1.6–3.2, p<0.0001) subsets, respectively. A dramatically increased risk for ACPA-positive RA was seen in individuals who both were having positive family history of RA and carried HLA-DRB1 SE alleles (OR 14.7, 95% CI 7.7–27.8). We also observed a lesser risk magnitude in the ACPA-negative RA patients (OR 5.7, 95% CI 2.7–11.9).ConclusionsOur data demonstrate that family history of RA remains an important clinical risk factor for RA. In addition, positive family history of RA was associated with an increased risk of developing both the ACPA-positive and ACPA-negative RA in the Malaysian population, suggesting that the two RA subsets are similar in genetic risk factors that overlap with these diseases.References Frisell T, Saevarsdottir S, Askling J. Family history of rheumatoid arthritis: an old concept with new developments. Nat Rev Rheumatol. 2016 Jun;12(6):335–43.Frisell T, Hellgren K, Alfredsson L, Raychaudhuri S, Klareskog L, Askling J. Familial aggregation of arthritis-related diseases in seropositive and seronegative rheumatoid arthritis: a register-based case-control study in Sweden. Ann Rheum Dis. 2016 Jan;75(1):183–9. Disclosure of InterestNone declared