Based on our findings, we suggest that the leptin present in the articular joint fluid protects articular chondrocytes against cumulative mechanical load and detrimental stresses throughout a lifetime, delaying the onset of degenerative changes in chondrocytes. We can further hypothesize that leptin protects articular chondrocytes against destructive stimuli even in the joints of osteoarthritis (OA) patients.

Background Neurological manifestations in systemic lupus erythematosus (SLE) are diverse. Because of its varied manifestations and low prevalence, the ACR has developed nomenclature and case definitions for neuropsychiatric SLE (NPSLE) to facilitate clinical research. Brain MRI has been used for the evaluation of neurologic symptoms. Objectives The purpose of this study was to identify characteristic brain MRI findings in NPSLE and to investigate the association between brain MRI findings and NPSLE manifestations. Methods In total, 145 brain MRIs in 126 patients with NPSLE from 2002 to 2013 from three tertiary university hospitals were retrospectively reviewed. The images were evaluated for the presence of white matter hyperintensity (WMH), gray matter hyperintensity (GMH), parenchymal defects, atrophy, enhancement, and the abnormalities in diffusion-weighted image (DWI). The number, size and location of WMH,GMH and parenchymal defects were evaluated. The NPSLE manifestations of each patient were classified according to the 1999 ACR case definitions for NPSLE syndromes. The associations between MRI findings and manifestations of NPSLE were examined. Results In total, 103 MRIs (71.0%) exhibited abnormalities among the 145 MRIs reviewed. There were 172 NP events that encompassed 16 of 19 NP syndromes. The most common MRI abnormalities were WMHs. One or more WMHs were found in 84 MRIs (57.9%) among the total 145 MRIs. GMHs were observed in 42 MRIs (29.0%). GMHs tended to involve much larger areas than WMHs. Patients with cerebrovascular disease or seizures were more likely to have GMHs than patients with other NP manifestations. 33 MRIs among 42 MRIs which had GMHs also exhibited WMHs. Parenchymal defects were found in 35 MRIs (24.1%). Atrophy was detected in 26 MRIs (17.9%). Brain MRIs were enhanced in 21 of the 126 cases that had undergone enhancement. Patients who had seizures were more likely to demonstrate MRI enhancement than patients with other NP manifestations. DWIs were obtained in 102 MRIs and abnormal DWIs were obtained in 18 MRIs cases. Patients with cerebrovascular disease were more likely to have GMH, parenchymal defects and abnormal DWI than patients with other NP manifestations Number of MRIs (%) Abnormalities of MRI WMH GMH Parenchymal defect Atrophy Enhancement Acute confusion 13 (9.0%) 10 7 3 3 5 3 Anxiety disorder 1 (0.7%) 0 0 0 0 0 0 Aseptic meningitis 6 (4.1%) 4 3 0 1 0 2 Cerebrovascular disease 33 (22.7%) 33 27 15 15 5 4 Cognitive dysfunction 4 (2.7%) 3 3 0 1 3 0 Demyelinating disease 2 (1.4%) 2 2 1 1 0 1 Headache 33 (22.7% ) 17 12 6 2 4 2 Mood disorder 1 (0.7%) 0 0 0 0 0 0 Movement disorder 5 (3.4%) 4 4 0 1 1 0 Psychosis 4 (2.7%) 3 2 0 1 1 1 Seizure 23 (15.9%) 17 14 12 5 5 7 Autonomic disorder 3 (2.1%) 0 0 0 0 0 0 Cranial neuropathy 12 (8.3%) 7 7 2 2 0 0 Mononeuropathy 3 (2.1%) 1 1 1 1 0 0 Myasthenia gravis 0 (0%) 0 0 0 0 0 0 Polyneuropathy 2 (1.4%) 2 2 2 2 2 1 Total 145 (100%) 103 84 42 35 26 21 Conclusions Diverse brain MRI abnormalities w...

Background Pulmonary arterial hypertension (PAH) is a major cause of mortality in connective tissue disease (CTD). Objectives The survival rates and mortality-predictive factors of a nationwide registry of Korean patients with CTD-PAH were determined. Methods Patients with CTD-PAH were enrolled between April 2008 and December 2012. Hemodynamic parameters and clinical data (WHO-functional class [FC], organ involvement, laboratory tests, and treatment agents) were recorded. Survival rates were calculated by using the Kaplan–Meier method. Mortality-associated factors were examined by Cox proportional hazards regression analysis. Results In total, 174 incident PAH cases (61 with systemic lupus erythematosus, 50 with systemic sclerosis, 10 with mixed CTD, 22 with rheumatoid arthritis [RA], and 31 with other CTDs) were diagnosed by right heart catheterisation or Doppler echocardiography. Of these, 25 (14%) died during the 3.8±2.7 year follow-up period after PAH diagnosis. The 1 and 3 year survival rates were 90.7% and 87.3%, respectively. Compared to the other CTD-PAHs, RA-PAH had the lowest survival rates (56% 3 year survival; p=0.022). Multiple regression analysis revealed that low DLCO, pleural effusion, and diabetes mellitus were poor prognostic factors (p=0.008, 0.04, and 0.009, respectively). Anti-UI-RNP antibody positivity was protective (p=0.022). In patients with WHO-FC III/IV, patients who received vasodilators had lower mortality than those who did not (p=0.038). Conclusions In Korean patients with CTD-PAH, the 3 year survival rate was 87%. Low DLCO, pleural effusion, and DM were independent poor prognostic factors. Anti-UI-RNP antibody was protective. Prompt PAH-specific vasodilator therapy may improve the survival of patients with severe CTD-PAH. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.1271

BackgroundThe NLRP3 inflammasome, a member of the NLR family, is a key player in the production of uric acid-mediated IL-1β and is an important cytoplasmic protein complex involved in gouty inflammation. Recent single-nucleotide polymorphism (SNP) studies suggested that genetic alternations of several target molecules such as CARD8 and P2X7R contribute to the process of NLRP3 inflammasome activation.ObjectivesThe aim of this study was to determine the association between P2X7R rs3751142 and CARD8 rs2043211 polymorphisms and gout susceptibility in male Korean subjects.MethodsThis study enrolled a total 242 male patients with gout and 280 healthy controls. The polymorphisms of two individual genes including rs3751142 (C>A) in the P2X7R gene and rs2043211 (A>T) in the CARD8 gene were assessed using Taq-Man analysis. Statistical analyses were performed using the Chi-square test, Kruskal-Wallis test, and logistic regression analyses.ResultsA difference in genotypic frequency of the P2X7R rs3751142 and CARD8 rs2043211 genes was not detected between gout and control patients. Clinical parameters including age, onset age, disease duration, body mass index, and serum uric acid levels were not different among the three genotypes for either P2X7R or CARD8 (p>0.05 for all). A pair-wise comparison of P2X7R rs3751142 and CARD8 rs2043211 genotype combinations revealed a protective effect of P2X7R/CARD8 AA/AA against gout susceptibility (OR=0.023, 95% CI 0.874–0.999).ConclusionsThis study revealed that genetic variability of the P2X7R rs3751142 and CARD8 rs2043211 genes might, in part, be associated with susceptibility for gout.ReferencesMartinon F, Pétrilli V, Mayor A, et al. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature 2006;440:237–41.Choe JY, Jung HY, Park KY, et al. Enhanced p62 expression through impaired proteasomal degradation is involved in caspase-1 activation in monosodium urate crystal-induced interleukin-1b expression. Rheumatology (Oxford) 2014;53:1043–53.Yang SK, Kim H, Hong M, et al. Association of CARD8 with inflammatory bowel disease in Koreans. J Hum Genet 2011;56:217–23.Chen Y, Ren X, Li C, et al. CARD8 rs2043211 polymorphism is associated with gout in a Chinese male population. Cell Physiol Biochem 2015;35:1394–400.Gu BJ, Zhang W, Worthington RA, et al. A Glu-496 to Ala polymorphism leads to loss of function of the human P2X7 receptor. J Biol Chem 2001;276:11135–42.Disclosure of InterestNone declared