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ID PMID Title PublicationDate abstract
29479472 Moderate use of alcohol is associated with lower levels of C reactive protein but not with 2018 OBJECTIVES: Moderate alcohol consumption is protective against rheumatoid arthritis (RA) development and associated with lower levels of systemic inflammation in RA and in the general population. We therefore hypothesised that moderate alcohol consumption is associated with less severe local inflammation in joints in RA, detected by MRI. Since asymptomatic persons can have low-grade MRI-detected inflammation, we also hypothesised that alcohol consumption is associated with the extent of MRI inflammation in asymptomatic volunteers. METHODS: 188 newly presenting patients with RA and 192 asymptomatic volunteers underwent a unilateral contrast-enhanced 1.5T MRI of metacarpophalangeal, wrist and metatarsophalangeal joints. The MRIs were scored on synovitis, bone marrow oedema and tenosynovitis; the sum of these yielded the MRI inflammation score. MRI data were evaluated in relation to current alcohol consumption, categorised as non-drinkers, consuming 1-7 drinks/week, 8-14 drinks/week and >14 drinks/week. Association between C reactive protein (CRP) level and alcohol was studied in 1070 newly presenting patients with RA. RESULTS: Alcohol consumption was not associated with the severity of MRI-detected inflammation in hand and foot joints of patients with RA (P=0.55) and asymptomatic volunteers (P=0.33). A J-shaped curve was observed in the association between alcohol consumption and CRP level, with the lowest levels in patients consuming 1-7 drinks/week (P=0.037). CONCLUSION: Despite the fact that moderate alcohol consumption has been shown protective against RA, and our data confirm a J-shaped association of alcohol consumption with CRP levels in RA, alcohol was not associated with the severity of joint inflammation. The present data suggest that the pathophysiological mechanism underlying the effect of alcohol consists of a systemic effect that might not involve the joints.
29100671 "NETtling" the host: Breaking of tolerance in chronic inflammation and chronic infection. 2018 Mar How and why we break tolerance to self-proteins still remains a largely unanswered question. Neutrophils have been identified as a rich source of autoantigens in a wide array of autoimmune diseases that arise as a consequence of different environmental and genetic factors, e.g. rheumatoid arthritis (RA), lupus, vasculitis, cystic fibrosis (CF) etc. Specifically, neutrophil extracellular trap (NET) formation has been identified as a link between innate and adaptive immune responses in autoimmunity. Autoantigens including neutrophil granular proteins (targeted by anti-neutrophil cytoplasmic antibodies, ANCA) as well as post-translationally modified proteins, i.e. citrullinated and carbamylated proteins targeted by anti-citrullinated protein antibodies (ACPA) and anti-carbamylated protein antibodies (ACarPA), respectively, localize to the NETs. Moreover, NETs provide stimuli to dendritic cells that potentiate adaptive autoimmune responses. However, while NETs promote inflammation and appear to induce humoral autoreactivity across autoimmune diseases, the antigen specificity of autoantibodies found in these disorders is striking. These unique autoantigen signatures suggest that not all NETs are created equal and that the environment in which NETs arise shapes their disease-specific character. In this review article, we discuss the effects of different stimuli on the mechanism of NET formation as well as how they contribute to antigen specificity in the breaking of immune tolerance. Specifically, we compare and contrast the autoreactive nature of NETs in two settings of chronic airway inflammation: one triggered by smoking, a recognized environmental NET stimulus in RA patients, and one mediated by Pseudomonas aeruginosa, the most prevalent lung pathogen in CF patients. Finally, we draw attention to novel findings that, together with the specific environmental/chemical stimuli, should be taken into account when investigating how and why antigen specificity arises in the context of NET formation.
28646319 Presence of enthesopathy in patients with primary Sjogren's syndrome: ultrasonographic stu 2018 Jan BACKGROUND: Musculoskeletal findings in Sjögren's syndrome are arthralgia, arthritis, myalgia, myositis, fibromyalgia, and chronic fatigue. Enthesis zones are important in the formation of pain in the musculoskeletal system. Musculoskeletal ultrasound (US) may show subclinical enthesitis in the synovial joints and in the axial skeleton before joint swelling in inflammatory diseases characterized by arthritis. OBJECTIVE: In this study, we aimed to determine the presence of enthesopathy using the Madrid sonographic enthesitis index (MASEI) in patients with primary Sjögren's syndrome (PSS). PATIENTS AND METHODS: Consecutive patients with PSS and age-matched healthy controls were included in this study. All the patients met the 2002 American College of Rheumatology/European League against Rheumatism classification criteria for PSS. The demographic characteristics of the patients were recorded. Six enthesis sites were evaluated using gray-scale and Doppler US with a linear transducer, and they were scored using the MASEI. They were assessed by the EULAR Sjögren's syndrome disease activity index (ESSDAI). RESULTS: We evaluated 40 patients with PSS (average age 48.67 ± 11.23 years) and 30 healthy controls (average age 45.40 ± 8.24 years). Patients with PSS had significantly higher MASEI scores than the healthy controls. Plantar fascia, Achilles tendon, and distal patellar tendons were significantly thicker in the PSS group than in the healthy controls. The MASEI total score had a positive correlation with age. There was no correlation between MASEI total score and BMI and ESSDAI. CONCLUSION: In this study, it was shown that the MASEI scores assessed by US were significantly higher in patients with PSS than in healthy controls. Plantar fascia, Achilles tendon, and distal patellar tendon were significantly thicker in the PSS group than in the healthy controls. This result suggests that PSS may be one of the causes of musculoskeletal pain that can be seen in patients with PSS. Our study was the first study to use an enthesis index ultrasonographically in patients with PSS. In addition, it is the first study to investigate the relationship between the presence of enthesopathy and disease activity by means of US.
29968328 Significance of combined anti-CCP antibodies and rheumatoid factor in a New Zealand cohort 2018 Jul BACKGROUND: Systemic sclerosis (SSc) can present as an overlap syndrome with rheumatoid arthritis (SSc-RA overlap). OBJECTIVE: To evaluate the frequency of rheumatoid factor (RF) and anticyclic citrullinated peptide antibodies (anti-CCP) in our SSc cohort and their association with clinical features. METHODS: Data were gathered prospectively from the Waikato Hospital Systemic Sclerosis Clinics. Patients with SSc and SOS (systemic sclerosis overlap syndrome) underwent baseline auto-antibody profiling including RF and anti-CCP along with annual clinical review. RESULTS: Our cohort comprised of 132 patients (two had incomplete data); 115 (87.1%) were female. Out of 89 limited cutaneous SSc (lcSSc) patients, arthralgia, synovitis, contractures, tendon crepitus and erosions on imaging were found in three, 10, 31, five and nine patients, respectively. Within the 33 diffuse cutaneous SSc (dcSSc) patients, arthralgia, synovitis, contractures, tendon crepitus and erosion were found in 15, five, 27, five and one patient, respectively. In the 10 SOS patients, arthralgia, synovitis and contractures were found in six, three and two patients; none had tendon crepitus or erosions. RF positivity was found in 15.7%, 9% and 20% of patients with lcSSc, dcSSc and SOS, and anti-CCP positivity was found in 13.5%, 6.1% and 0% in lcSSc, dcSSc and SOS patients. A statistically significant relationship of double antibody positivity with arthralgia (P = 0.03) and erosions (P < 0.001) was found. Anti-CCP positivity association with erosions was significant at P = 0.007. CONCLUSION: Our study confirms that articular manifestations are common in SSc. Statistically significant associations of double antibody positivity with arthralgia and erosions were demonstrated. Significant association between anti-CCP antibody and erosions was also confirmed.
30578887 Venlafaxine and carvedilol ameliorate testicular impairment and disrupted spermatogenesis 2019 Feb 1 Testicular impairment has been commonly described in long-standing rheumatoid arthritis (RA) patients. Since depression and cardiovascular disorders are the most disturbing co-morbidities of RA, investigating the efficacy of the anti-depressant venlafaxine or the beta-blocker carvedilol in RA-associated testicular dysfunction may add to their clinical utility for RA patients. Previously, both agents have demonstrated significant in vivo anti-oxidant and anti-inflammatory actions. In the current study, venlafaxine (50 mg/kg/day) and carvedilol (10 mg/kg/day) were orally administered to adjuvant arthritic rats for 20 days. Interestingly, venlafaxine and carvedilol effectively suppressed paw edema and mitigated the testicular histopathological aberrations and the disrupted spermatogenesis. Both drugs enhanced testicular steroidogenesis through upregulation of 3β-HSD, 17β-HSD and StAR gene expression with concomitant augmentation of serum testosterone. They also blunted the inflammatory burden via attenuation of myeloperoxidase, TNF-α and the protein expression of NF-κBp65 along with elevation of IL-10. They attenuated testicular oxidative perturbations via lowering lipid peroxides and nitric oxide and boosting glutathione levels. With regard to apoptosis, the two agents lowered the protein expression of caspase-3, cleaved caspase-3, cleaved PARP, Bax and p53, promoting germ cell survival. They also modulated the AMPK/ERK signaling via lowering of p-AMPK and upregulation of p-ERK1/2 along with PI3K/AKT/mTOR transduction by enhancing the PI3Kp110α, p-AKT and p-mTOR protein expression. Together, the present work demonstrates the beneficial effects of venlafaxine and carvedilol in RA testicular dysfunction and impaired spermatogenesis via modulation of AMPK/ERK and PI3K/AKT/mTOR signaling and intervention with the testicular oxidative stress, inflammation and apoptosis.
28838228 Red blood cell distribution width is useful in discriminating adult onset Still's disease 2018 Nov BACKGROUND/AIMS: Red blood cell distribution width (RDW) is a value representing the heterogeneity in the size of red blood cell, and it is usually used in distinguishing types of anaemia. Recently, it was reported that it could reflect the burden of inflammation in diverse diseases and their prognosis. Hence, in this study, we investigated whether RDW may contribute to discriminating adult onset Still's disease (AOSD) from sepsis in serious febrile patients within 24 hours after hospitalization. METHODS: We reviewed the medical records and enrolled 21 AOSD patients, 27 sepsis patients and 30 matched healthy controls. We collected at least two laboratory results of variables including RDW within 24 hours after hospitalization, and we calculated their mean values. RESULTS: Sepsis patients showed the significantly increased median white blood cell count, compared to AOSD patients (14,390.0/mm3 vs. 12,390.0/mm3 , p = 0.010). The median RDW in sepsis patients was higher than that in AOSD patients (15.0% vs. 13.3%, p = 0.001), and furthermore, the median RDW in both patient-groups was significantly higher than that in healthy controls. In contrast, the median ferritin level in sepsis patients was lower than that in AOSD patients (544.0 mg/dL vs. 3,756.6 mg/dL, p = 0.001). In multivariate analysis, RDW ≥ 14.8% (odds ratio, 17.549) and ferritin < 2,251.0 mg/dL (odds ratio, 32.414) independently suggested sepsis more than AOSD in patients initially presenting with fever requiring hospitalization. CONCLUSION: RDW might be a rapid and helpful marker for a differential diagnosis between AOSD from sepsis at an early phase.
28972439 Suppressor of TCR signaling-2 (STS-2) suppresses arthritis development in mice. 2018 Jul OBJECTIVES: Suppressor of TCR signaling-2 (STS-2) is one of the RA susceptibility genes identified in genome-wide association studies (GWAS). We tried to verify the involvement of STS-2 on the development of autoimmune arthritis in a mouse model. METHODS: STS-2 knock-out (KO) and wild type (WT) mice were immunized with chicken type II collagen (CII). For CD4(+) helper T cell (Th) subset analysis, intracellular cytokines in splenocytes and lymph node cells were stained and analyzed by flow cytometry. Regulatory T cell (Treg) function was analyzed by co-culturing effector CD4(+)T cells and Tregs collected from non-immunized mice. RESULTS: CII-immunized STS-2 KO mice developed arthritis more frequently than WT mice. Although the T cell activation profile and Th subset in spleen and LNs were similar between STS-2 KO and WT mice, STS-2 KO mice showed increased IL-2-producing CD4(+)T cells in spleen when compared with WT mice. Accordingly, STS-2 KO CD4(+)T cells promoted IL-2 production by TCR stimulation. However, STS-2 KO Tregs normally suppressed T cell proliferation. CONCLUSION: We proved that STS-2 is involved in the arthritis development by collagen-induced arthritis. Higher IL-2 production from STS-2 KO T cells is suggested to have a main pathogenic role in arthritis development.
30079897 Diagnostic dilemma between sarcoidosis and primary Sjögren syndrome: mimicry, concomitanc 2018 Both sarcoidosis and primary Sjögren syndrome (pSS) are multisystem disorders of unknown etiology, which share certain clinical features, making the differential diagnosis a real challenge in clinical practice. Several published case reports and case series have posed the question as to whether there is a real association - mimicry between the two diseases or it is just coincidence. We attempt, after systematic and comprehensive research of the relevant published literature, to present all those data, clinical or paraclinical, which could be useful in the diagnostic approach and the distinguishment of the two diseases. It is certain that, besides the classic diagnostic methods, emerging is the role of immunology and genetics on this direction, although not established yet.
29566725 Interleukin-37 is increased in adult-onset Still's disease and associated with disease act 2018 Mar 22 BACKGROUND: Interleukin (IL)-37 has been known to play an immunosuppressive role in various inflammatory disorders, but whether it participates in the regulation of pathogenesis of adult-onset Still's disease (AOSD) has not been investigated. In this study, we examined serum IL-37 levels and their clinical association with AOSD, and we explored the anti-inflammatory effects of IL-37 on peripheral blood mononuclear cells (PBMCs) from patients with AOSD. METHODS: Blood samples were collected from 62 patients with AOSD and 50 healthy control subjects (HC). The serum IL-37 levels were determined using an enzyme-linked immunosorbent assay (ELISA). The correlations of serum IL-37 levels with disease activity, laboratory values, and inflammatory cytokines in AOSD were analyzed by Spearman's correlation test. The correlations between serum IL-37 levels and clinical manifestations were analyzed by Mann-Whitney U test. PBMCs from ten patients with AOSD were stimulated with recombinant human IL-37 protein, and expression levels of tumor necrosis factor (TNF)-α, IL-6, IL-10, IL-1β, and IL-18 were determined by qRT-PCR and ELISA. RESULTS: A significantly higher IL-37 protein level was observed in patients with AOSD than in HC. Serum IL-37 levels correlated with systemic score, laboratory values, IL-1β, IL-18, and IL-10 in patients with AOSD. The expression levels of IL-37 were closely related to the patients with AOSD who also had fever, skin rash, lymphadenopathy, splenomegaly, myalgia, and arthralgia. Moreover, the production of proinflammatory cytokines such as IL-6, IL-1β, TNF-α, and IL-18 in PBMCs from patients with AOSD was obviously attenuated after recombinant human IL-37 stimulation. CONCLUSIONS: Increased expression of IL-37 and its positive correlation with disease activity suggest its involvement in AOSD pathogenesis. More importantly, IL-37 inhibits the expression of proinflammatory cytokines in PBMCs from patients with AOSD, indicating the potential anti-inflammatory role of IL-37 in AOSD. Thus, IL-37 may be a novel disease activity biomarker and research target in AOSD.
29149922 Gastrointestinal and Hepatic Disease in Sjogren Syndrome. 2018 Feb Sjogren syndrome (SS) is a lymphocyte-mediated, infiltrative autoimmune disorder characterized by destruction of exocrine glands leading to secretory dysfunction. The typical manifestations include xerostomia and xerophthalmia; however, extensive gastrointestinal involvement is increasingly being recognized, emphasizing the variable and systemic nature of SS.
31037163 Pathological changes of renal biopsy in Sjögren Syndrome. 2018 We are presenting the case of a 53-year-old woman with a history of Sjögren syndrome and a secondary antiphospholipid syndrome admitted at the Nephrology department for the evaluation of renal failure. The patient was initially diagnosed with tubulointerstitial nephritis and subsequently a membranoproliferative type I glomerulonephritis, secondary to cryoglobulins during the course of the disease. Repeated renal biopsies were required to confirm the diagnosis.
30459471 Diagnostic accuracy of salivary gland ultrasonography with different scoring systems in Sj 2018 Nov 20 Noninvasive objective salivary gland ultrasonography (SGU) had been widely used to evaluate major salivary gland involvement in primary Sjögren's syndrome (pSS) and treatment responses. However, the evaluation score, diagnostic sensitivity, and diagnostic specificity significantly varied among clinical studies. We conducted this meta-analysis to assess the diagnostic accuracy of different SGU scoring systems using the American-European Consensus Group criteria. Of the 1301 articles retrieved from six databases, 24 met the criteria for quality assessment and 14 for meta-analyses. The pooled sensitivities were 75% (0-4) with I(2) = 92.0%, 84% (0-16) with I(2) = 63.6%, and 75% (0-48) with I(2) = 90.9%; the pooled specificities were 93% (0-4) with I(2) = 71.5%, 88% (0-16) with I(2) = 65.4%, and 95% (0-48) with I(2) = 83.9%; the pooled diagnostic odds ratios were 71.26 (0-4) with I(2) = 0%, 46.3 (0-16) with I(2) = 73.8%, and 66.07 (0-48) I(2) = 0%; the areas under the SROC curves were 0.95 (0-4), 0.93 (0-16), and 0.94 (0-48). These results indicated that the 0-4 scoring system has a higher specificity and a less heterogeneity than other systems, and could be used as a universal SGU diagnostic standard.
30031495 Systemic Lupus Erythematosus, Sjögren Syndrome, and Mixed Connective Tissue Disease in Ch 2018 Aug Juvenile systemic lupus erythematosus (jSLE), mixed connective tissue disease (jMCTD), and Sjögren syndrome (jSS) are systemic autoimmune and inflammatory disorders with distinct patterns of organ involvement. All are characterized by autoantibody formation, with antinuclear (ANA) and anti-double-stranded DNA common in jSLE, ANA with high-titer ribonucleoprotein antibody in jMCTD, and Sjögren syndrome A and Sjögren syndrome B antibodies + ANA in jSS. Recognition, monitoring, and management for primary care providers are discussed, focusing on the role of primary physicians in recognizing and helping maintain optimal health in children with these potentially life-threatening diseases.
29305014 NF-κB and the Transcriptional Control of Inflammation. 2018 The NF-κB transcription factor was discovered 30 years ago and has since emerged as the master regulator of inflammation and immune homeostasis. It achieves this status by means of the large number of important pro- and antiinflammatory factors under its transcriptional control. NF-κB has a central role in inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, and autoimmunity, as well as diseases comprising a significant inflammatory component such as cancer and atherosclerosis. Here, we provide an overview of the studies that form the basis of our understanding of the role of NF-κB subunits and their regulators in controlling inflammation. We also describe the emerging importance of posttranslational modifications of NF-κB in the regulation of inflammation, and highlight the future challenges faced by researchers who aim to target NF-κB transcriptional activity for therapeutic benefit in treating chronic inflammatory diseases.
30034820 Ankle arthroplasty: A review and summary of results from joint registries and recent studi 2018 Jun Total ankle arthroplasty offers a reasonable alternative to ankle arthrodesis in carefully selected patients.It is debatable whether rheumatoid arthritis patients have better outcomes compared with those who have ankle arthroplasty for either primary osteoarthritis or post-traumatic arthritis.Aseptic loosening and infection are the most common complications requiring revision.It is worth noting that some of the best survival rates are seen in the surgeon-designer case series.The uncemented mobile or fixed bearing prostheses have better outcomes compared with their older counterparts.There is no convincing evidence to suggest superiority of one design over another among the currently available prostheses.Ankle arthroplasty surgery has a steep learning curve; the prosthesis choice should be driven by the surgeon's training and experience. Cite this article: EFORT Open Rev 2018;3:391-397. DOI: 10.1302/2058-5241.3.170029.
30155621 Fibroblasts and Osteoblasts in Inflammation and Bone Damage. 2018 This review discusses the important role fibroblasts play in the process of inflammation and the evidence that these cells may drive the persistence of inflammation. Fibroblasts are key components of the stroma normally involved in maintenance of extracellular matrix and tissue function; however, the term 'fibroblast' is used to describe a heterogeneous population of cells that vary in phenotype both between and within anatomical sites. Fibroblasts possess Toll-like receptors allowing them to respond to pathogen and damage-related signals by producing proinflammatory mediators such as IL-6, PGE(2), and GM-CSF and can produce a range of chemokines such as CXCL12, CXCL13, and CXCL8 which attract B and T lymphocytes, monocytes, and neutrophils to sites of inflammation. Interactions between leukocytes and fibroblasts can facilitate increased survival of the leukocytes and modulate phenotypes leading to differential gene expression in the presence of mediators involved in inflammation. Fibroblasts also contribute to collateral tissue damage during inflammation through the production of members of the metalloproteinase family and cathepsins and also through induction of osteoclastogenesis leading to increased bone resorption rates. In persistent diseases, fibroblasts obtain an imprinted, aggressive phenotype leading to the production of higher basal levels of proinflammatory cytokines and the ability to damage tissue in the absence of continual stimuli. This aggressive phenotype offers an attractive new target for therapeutics that could help alleviate the burden of persistent inflammation.
29995301 Total Joint Arthroplasty in Patients with Inflammatory Rheumatic Diseases. 2018 Aug Since its introduction, total joint arthroplasty (TJA) has improved the quality of life of patients with degenerative joint disorders. In the last decades, a number of conventional and biological disease-modifying antirheumatic drugs have become available for the treatment of patients with inflammatory rheumatic diseases (IRD), leading to a reduction in the need to undergo TJA. However, TJA is still frequently performed in IRD patients. Both rheumatologists and orthopedics should be aware that patients with IRD have a peculiar perioperative risk profile due to disease-related, patient-related, and surgery-related risk factors. On the basis of current evidence, TJA is a safe procedure for IRD patients as long as an accurate risk stratification and a multidisciplinary approach are applied. We here describe the current strategies for an appropriate surgical management of osteoarthritis in IRD patients and the fascinating opening perspectives that surgeons and clinicians may expect in the future.
30701839 Comorbidities in inflammatory joint and spine diseases in XXI century. 2018 Dec 30 AIM: The evaluation the occurrence of comorbidities in patients with inflammatory diseases of the spine and joints and the assessment of the general changes in comorbidities at the beginning of the XXI century compared to previous period. MATERIALS AND METHODS: Comorbidity was analyzed in 245 patients with spondyloarthritis who participated in the scientific program PROGRESS. Validated comorbidity assessment indices were used in the study. The analysis of 96 sources of literary bases RISC and PubMed were used in literature analysis. The results of their own observation and literary search were compared. RESULTS: According to the patients' cards, an analysis of the structure of comorbidities was conducted in 221 patients: 207 (93.66%) patients with spondyloarthritis had two or more comorbidities. The most common diseases were diseases of gastrointestinal tract (60.6%) and cardiovascular pathology (58.3%), secondary osteoarthritis (60.2%). According to literature sources, most of the comorbidities and spondyloarthritis are interrelated pathogenetically and undergo a change in the profile of rheumatic and/or related diseases undergo simultaneous changes. The emergence of new diseases in the structure of comorbidity and new drugs requires the development of recommendations that take into account the presence of comorbidity in patients with a rheumatic diseases. CONCLUSION: Most patients with spondyloarthritis has comorbidity. The change in rheumatic and non-rheumatic diseases that occurs in the 21st century has a mutual influence, changing the profile of patients and determining the change in the tactics of their management.
29971163 Burden of Depression among Working-Age Adults with Rheumatoid Arthritis. 2018 OBJECTIVE: This study estimated the excess clinical, humanistic, and economic burden associated with depression among working-age adults with Rheumatoid Arthritis (RA). METHODS: A retrospective cross-sectional study was conducted among working-age (18 to 64 years) RA patients with depression (N = 647) and without depression (N = 2,015) using data from the nationally representative Medical Expenditure Panel Survey for the years 2009, 2011, 2013, and 2015. RESULTS: Overall, 25.8% had depression. In adjusted analyses, adults with RA and depression compared to those without depression were significantly more likely to have pain interference with normal work (severe pain: AOR = 2.22; 95% CI = 1.55, 3.18), functional limitations (AOR = 2.17; 95% CI = 1.61, 2.94), and lower mental health HRQoL scores. Adults with RA and depression had significantly higher annual healthcare expenditures ($14,752 versus 10,541, p < .001) and out-of-pocket spending burden. Adults with RA and depression were more likely to be unemployed and among employed adults, those with depression had a significantly higher number of missed work days annually and higher lost annual wages due to missed work days. CONCLUSIONS: This study highlights the importance of effectively managing depression in routine clinical practice of RA patients to reduce pain and functional limitations, improve quality of life, and lower direct and indirect healthcare costs.
30323555 A descriptive analysis of real-world treatment patterns of innovator (Remicade(®)) and bi 2018 PURPOSE: Biosimilar IFX (CT-P13) received marketing approval in Turkey for treatment of rheumatologic diseases, including ankylosing spondylitis, psoriatic arthritis, rheumatoid arthritis (RA), inflammatory bowel disease (IBD), and psoriasis. Population data on real-world treatment patterns of CT-P13 following marketing approval in European countries are largely unreported. This study examined the prescribing and medication utilization patterns of innovator infliximab (IFX) and CT-P13 in Turkey for patients with RA or IBD naïve to either IFX. MATERIALS AND METHODS: Adult patients with ≥1 diagnosis claim for RA or IBD and ≥1 claim for IFX or CT-P13 were identified in the Turkish Ministry of Health database during the following identification periods: 1 Oct 2014-30 May 2015 (RA) and 1 Oct 2014-31 Dec 2015 (IBD). Continuous medical and pharmacy coverage for ≥12 months before and after the date of the first dose (index) IFX or CT-P13 was also required. Separate analyses were done for each population. RESULTS: Seven hundred and seventy nine adult RA and 581 IBD patients met the selection criteria. The majority of RA (74%; n=575) and IBD patients (87%; n=504) were initiated on IFX. The average study observation period was 16 months for the RA and 12 months for the IBD population. Over the observation periods, discontinuation among RA patients occurred in 42% of IFX and 63% of CT-P13 while discontinuation in the IBD cohort occurred in 38% of IFX; and 62% of CT-P13. CONCLUSION: In this population-based study, more IFX-naïve RA and IBD patients were initially treated with IFX than CT-P13. Discontinuation and switching were observed more often and earlier among patients treated with CT-P13 regardless of disease state. Further studies are needed to understand the reasons for these observed differences.