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Autoimmune diseases (AIDs) are complex diseases characterized by persistent or recurrent inflammation, alteration of immune response, and production of specific autoantibodies. It is known that different AIDs share several susceptibility genetic loci. Tumor necrosis factor alpha inducible protein 3 (TNFAIP3) encodes the ubiquitin-modifying enzyme A20, which downregulates inflammation by restricting NF-κB, a transcription factor that regulates expression of various proinflammatory genes. Variants in TNFAIP3 gene have been described as associated with susceptibility to several AIDs. Here, we analyzed two TNFAIP3 polymorphisms in Italian patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and primary Sjogren’s syndrome (pSS), to verify if the genetic variability of TNFAIP3 gene is involved in genetic predisposition to AIDs also in the Italian population. We recruited 313 SLE patients, 256 RA patients, 195 pSS patients, and 236 healthy controls. Genotyping of rs2230926 and rs6920220 in TNFAIP3 gene was performed by an allelic discrimination assay. We carried out a case/control association study and a genotype/phenotype correlation analysis. A higher risk to develop SLE was observed for rs2230926 (P=0.02, OR=1.92). No association was observed between this SNP and the susceptibility to pSS or RA. However, the rs2230926 variant allele seems to confer a higher risk to develop lymphoma in pSS patients, while in RA patients, the presence of RF resulted significantly associated with the variant allele. Regarding the rs6920220 SNP, we observed a significant association of the variant allele with SLE (P=0.03, OR=1.53), pSS (P=0.016, OR=1.69), and RA (P=0.0001, OR=2.35) susceptibility. Furthermore, SLE patients carrying the variant allele showed a higher risk to develop pericarditis, pleurisy, and kidney complications. Our results support the importance of the TNFAIP3 gene variant role in the development of different autoimmune diseases in the Italian population and furtherly confirm a sharing of genetic predisposing factors among these three pathologies.

Despite the high prevalence of diabetic neuropathy, its early start, and its impact on quality of life and mortality, unresolved clinical issues persist in the field regarding its screening implementation, the understanding of its mechanisms, and the search for valid biomarkers, as well as disease-modifying treatment. Genetics may address these needs by providing genetic biomarkers of susceptibility, giving insights into pathogenesis, and shedding light on how to select possible responders to treatment. After a brief summary of recent studies on the genetics of diabetic neuropathy, the current review focused mainly on microRNAs (miRNAs), including the authors’ results in this field. It summarized the findings of animal and human studies that associate miRNAs with diabetic neuropathy and explored the possible pathogenetic meanings of these associations, in particular regarding miR-128a, miR-155a, and miR-499a, as well as their application for diabetic neuropathy screening. Moreover, from a genetic perspective, it examined new findings of polymorphisms of miRNA genes in diabetic neuropathy. It considered in more depth the pathogenetic implications for diabetic neuropathy of the polymorphism of MIR499A and the related changes in the downstream action of miR-499a, showing how epigenetic and genetic studies may provide insight into pathogenetic mechanisms like mitochondrial dysfunction. Finally, the concept and the data of genotype-phenotype association for polymorphism of miRNA genes were described. In conclusion, although at a very preliminary stage, the findings linking the genetics and epigenetics of miRNAs might contribute to the identification of exploratory risk biomarkers, a comprehensive definition of susceptibility to specific pathogenetic mechanisms, and the development of mechanism-based treatment of diabetic neuropathy, thus addressing the goals of genetic studies.

Background The clinical manifestations of recent syphilis can be variable, with typical and atypical patterns. Several conditions may cause atypical clinical aspects, including human immunodeficiency virus (HIV) co-infection. Besides the clinical features, co-infections may completely alter syphilis serological tests, causing interpretative difficulties and diagnostic delays. Aim of the work is to describe the difficulties encountered during the diagnostic evaluation of atypical skin manifestations and of the serology for syphilis of an HIV-infected patient who had contracted it several times. Case presentation In 2020, a 52-year old HIV-positive bisexual male patient was admitted to our department with a 4-month history of moderately itchy cutaneous lesions localized at his neck, trunk and arms. In 2013, the patient presented with a classic syphilitic roseola of the trunk and a secondary syphilis was diagnosed, with increased levels of rapid plasma reagin (RPR), Treponema pallidum hemagglutination assay (TPHA), anti-Treponema pallidum IgM and IgG Index. A second episode occurred in 2018, as a primary syphilis with multiple ulcerative lesions of the penis, and increased levels of RPR, IgG and IgM. In 2019, a further episode of secondary syphilis was treated with Doxycycline. In 2020, erythematous and papular lesions with vesicular components and urticarial erythema multiforme (EM)-like lesions were present at the neck, trunk and arms. Serological tests and Nucleic Acid Amplification Test (NAAT) for Treponema Pallidum were performed, as well as a cutaneous biopsy with histological and immunohistochemical evaluation of one lesion. NAAT was negative for T. pallidum . Serological test results were discordant with a new syphilis infection, showing only increased levels of RPR and anti-Treponema IgG. The cutaneous biopsy revealed a non specific histological pattern, while the immunohistochemical evaluation with anti-spirochetal antibodies was mandatory for the diagnosis of recent syphilis, showing clusters of rod-shaped elements, some of which with spiral form, focally present at the epidermis and adnexal structures. Conclusions Nowadays, syphilis may present with atypical clinical and serological features. Physicians should be aware of these possible alterations and consider syphilis even in case of uncommon clinical aspect and unclear serological tests. Cutaneous biopsy and immunohistochemical exam may be mandatory for the diagnosis.

Background:Psoriatic arthritis (PsA) is a chronic inflammatory disease, characterized by heterogeneous articular and periarticular manifestations. The achievement of remission or low disease activity is the goal of therapy. However, some patients experience primary failure and lack or loss of response to cs-, b- and ts-DMARDs. The treatment response could be affected by multiple factors, including epigenetic factors. Recently, some studies have suggested the possible involvement of lncRNAs in modulating treatment response [1]. In this context, the identification of genetic and epigenetic factors associated to treatment response could help to define new biomarkers for a more effective and personalized therapy.Objectives:The main aim of this study was to prospectively investigate lncRNAs potentially related to treatment response in a cohort of PsA patients treated with TNFi and IL17i, to identify potential predictors of drug treatment effectiveness. In addition, we analysed retrospectively a cohort of PsA patients treated with TNFi to look for possible association between lncRNAs genetic variants and the response after 6 and 12 months of TNFi.Methods:For the expression study, a cohort of 48 PsA patients starting a TNFi (n=28) or IL17i (n=20) drugs was recruited, monitoring their treatment response for 12 months in order to identify subgroup of patients Reponder e Non-Responder. For the genotyping study, we retrospectively analysed 163 PsA patients treated with TNFi. For each patient was estimated the Disease Activity in Psoriatic Arthritis (DAPsA) score at 6 and 12 months after the beginning of therapy. The expression level of lncRNA was analysed in a panel of 84 lncRNAs, after the extraction of total RNA from PBMCs. Then we validated the differentially expressed lncRNAs, resulted from the array experiments, by qRT-PCR using specific primer assay. Web-based data analysis tool (NPInter v4.0 and DIANALncBase v3) were used to confirm miRNA target genes of the validated lncRNAs. For the genotyping study, we extracted genomic DNA from PBMCs and we performed allelic discrimination assay by TaqMan assays. We evaluated a possible association between the selected SNPs and the response to therapy at 6 and 12 months from the beginning of the TNFi treatment, using the clinical parameter of DAPsA value.Results:We observed a significant difference in the expression level between Responder and non-Responder patients, of 4 lncRNAs in the group of PsA patients treated with TNFi and of 3 lncRNAs in the group of patients treated with IL17i. Then, we confirmed a significant decrease of MEG3 expression in non-Responder patients compared to Responder patients, both considering the whole cohort (P= 0.01) and stratifying patients by drugs (P= 0.05 and P= 0.03, respectively for TNFi and IL17i) (Figure 1). In addition, we observed an association between the variant allele of rs7158663 and a lower expression of MEG3 compared to the wild-type allele, although without statistical significance. We also observed that the variant allele of rs941576 (MEG3) was associated with a better response at T6 and T12, with a linear decrease of mean DAPsA value among wildtype, heterozygous and homozygous variant patients. Interestingly, we noticed that the variant allele of rs941576 SNV resulted associated with a better response regarding joints involvement. Indeed, the number of TJ and SJ decreases more in patients carrying the variant allele, both at T6 and T12 (P= 0.0006 and P= 0.032, respectively) (Table 1).Conclusion:Our study suggests a possible role, both in terms of genetic variability and expression, of the lncRNA MEG3 in the treatment response to TNFi and IL17i in PsA patients.REFERENCES:[1] De Benedittis G, Latini A, Ciccacci C, et al. Impact of TRAF3IP2, IL10 and HCP5 Genetic Polymorphisms in the Response to TNF-i Treatment in Patients with Psoriatic Arthritis. J Pers Med. 2022;12(7):1094.Acknowledgements:NIL.Disclosure of Interests:None declared.

Background:Telomeres are specific regions of repetitive nucleotide sequences that protect chromosome ends and preserve genetic information. In each cell division, telomeres shorten, leading finally to apoptosis and cell cycle arrest when reaching a critical point. The telomere-associated protein (telomeric repeat-binding factor 1 [TERF1]) is essential for the maintenance of telomeres, acting as an inhibitor of telomerase, and its levels correlate with telomere length (TL).Shortened telomeres have been demonstrated in Rheumatoid Arthritis (RA). Furthermore, they are a recognized risk factor for idiopathic pulmonary fibrosis. Few data are present in the literature regarding TL in RA-associated interstitial lung disease (RA-ILD), while no data are present regarding TERF1 in RA and RA-ILD.Objectives:We aimed to evaluate the TL and TERF1 expression levels in RA-ILD.Methods:TL and TERF1 expression levels were evaluated in patients with RA-ILD compared to age-matched RA patients without lung involvement (RA-non-ILD) and healthy controls. Genomic DNA and total RNA were isolated from peripheral blood mononuclear cells. Relative TL was measured using real-time quantitative polymerase chain reaction (qPCR) assay, which quantifies a ratio of telomeric repeat copy signal and a reference single-copy gene (human beta globin) signal. Expression analysis of TERF1 was performed by qPCR assay. T-test was used to compare mean TL and TERF1 expression data among the different phenotypic groups. RA patients were divided according to whether their TL fell within or above the first quartile of the cohort. A multivariate logistic regression analysis was used to correct the p-value for sex, age and disease duration.Results:Eighty-nine RA patients were included (mean age 63.6 ± 13.8 years, median disease duration 9 [IQR 8.4-11.6] years): 42 RA-ILD and 47 RA-non-ILD. 21 age- and sex-matched controls were collected. RA-ILD patients were older and with minor disease duration than RA-non-ILD patients. They exhibited higher disease activity, CRP levels, positivity for RF and ACPA, and were more treated with bDMARDs than RA-non-ILD patients (Table 1). TL in all patients was significantly shorter compared to controls (p = 0.0016). RA-ILD patients presented significantly shorter TL compared to controls (p = 0.00001) and compared to RA-non-ILD (p = 0.0006) (Figure 1A). In the multivariate regression analysis, TL was reduced in RA-ILD compared with RA-non-ILD when adjusted for sex, age and disease duration (p<0.001). After patients stratification according to their TL, it is observed that the prevalence of ILD was significantly higher in patients with short vs normal-length telomeres (82.6% vs 34.8% p=0.00008). In RA-ILD, TL correlated negatively with disease duration (p= 0.007 r= -0.408). TERF1 expression levels were reduced in RA compared with controls (p= 2.17E-17). Both RA-ILD patients and RA-non-ILD patients exhibited reduced TERF1 expression levels than controls (p= 3.37E-10 and p= 2.78E-10, respectively. Figure 1B). TERF1 levels correlated positively with TL (p= 0.004 r= 0.328).Conclusion:Telomere shortening is a feature of immunosenescence and it has been linked to more severe articular disease. Shorter TL and reduced TERF1 expression levels characterize RA. In particular, RA-ILD patients displayed higher disease activity, negative prognostic factors, received more biologic treatments, and exhibited shorten TL than RA-non-ILD patients suggesting that TL might represent a hallmark of a more aggressive disease with lung involvement.Table 1.Figure 1.Acknowledgements:NIL.Disclosure of Interests:None declared.

Psoriatic arthritis (PsA) is a chronic inflammatory joint disease typically associated with psoriasis and classified in the group of spondyloarthritis (1). The pathogenesis is based on an interplay of different genes interacting with several environmental factors including stress, trauma, infections, triggering an inflammatory response related to the activation of innate and acquired immunity in different tissues and organs (2). However, the risk for the development of PsA is not clearly understood. The aim of this study was to evaluate, in a cohort of Italian PsA out-patients of the Rheumatology Unit of the University of Rome Tor Vergata, the association of genetic variants in candidate genes for PSA susceptibility and their possible contribute in the modulation of clinical and laboratory features. The genes were selected according to previous studies describing these genes as involved in susceptibility to rheumatoid arthritis (RA) (3), since a common genetic background can be shared between these diseases. Nine SNPs (single nucleotide polymorphism) in eight candidate genes were analysed: STAT4 (rs7574865), TRAF3IP2 (rs33980500), TNFAIP3 (rs6920220 and rs2230926), MIR146A (rs2910164), PSORS1C1 (rs2233945), IL-10 (rs1800872), HCP5 (rs3099844) and ERAP1 (rs27524). Polymorphisms were analysed in 163 consecutive PsA out-patients and 198 healthy controls (HC). Genotyping was performed by allelic discrimination by TaqMan assay. Alleles frequencies differences between cases and controls or between phenotypic groups were compared using Pearson's χ 2 test. We have observed an association between PSA susceptibility and the variant alleles of STAT4 [OR= 1.60 (1.15-2.21), P= 0.005], TRAF3IP2 [OR= 1.65 (1.01-2.65), P= 0.04], ERAP1 [OR= 1.40 (1.05-1.85), P= 0.02] and TNFAIP3 (rs6920220) [OR= 1.75 (1.19-2.57), P= 0.004]. On the contrary, the variant allele of IL-10 polymorphism seems to play a protective role [OR= 0.74 (1.05-1.85), P= 0.05]. Moreover, in order to define a genetic risk profile, we have counted the total number of risk alleles in each subject, considering as risk alleles the allelic variant of rs7574865 (STAT4), rs33980500 (TRAF3IP2), rs6920220 (TNFAIP3) and rs27524 (ERAP1) SNPs. Then, we have compared the risk allele number distribution between patients and HC (Fig.1). Classes with 3 or more risk alleles are significantly more represented in patients than in HC (OR= 2.03, P=0.004). The risk to develop the disease increases significantly in subjects with at least four risk alleles (OR= 2.96, P=0.002). We confirm the associations between five SNPs, already studied in RA, and PSA susceptibility, suggesting a common inflammatory pathway in chronic inflammatory rheumatological diseases. Moreover, we show how the genotyping of only few associated SNPs could help to define a genetic risk profile for PSA development. [1]Calabresi E, et al. One year in review 2019: psoriatic arthritis. Clin Exp Rheumatol. 2020;38:1046-55. [2]Chimenti MS, Triggianese P, De Martino E, Conigliaro P, Fonti GL, Sunzini F, Caso F, Perricone C, Costa L, Perricone R. An update on pathogenesis of psoriatic arthritis and potential therapeutic targets. Expert Rev Clin Immunol. 2019 Aug;15(8):823-836. [3]Ciccacci C, et al. Polymorphisms in STAT-4, IL-10, PSORS1C1, PTPN2 and MIR146A genes are associated differently with prognostic factors in Italian patients affected by rheumatoid arthritis. Clin Exp Immunol. 2016;186:157-63. None declared [Display omitted]

The resistivity and thermal coefficient of resistivity (TCR), of metallic matrix composites, MMCs, aluminum–carbon nanotube, Al-CNT, were studied under high vacuum in the temperature interval from RT to 800 K. The samples shaped as small cylinders and containing single-walled CNTs or multi-walled CNTs were sintered at 625 °C. The resistivity of sintered samples of pure Al was found three orders of magnitude higher with respect to bulk, having the former a density value equal to 98.8 % of bulk Al. The explored range of the CNT concentration was within 5 wt%. At the highest CNT concentrations, the trend of resistivity against temperature was found negative being more pronounced for composites with MWCNTs. For Al-SWCNT composites, at around 3.3 wt% (4.2 vol%), TCR is practically independent from temperature; for Al-MWCNT, the TCR zero-crossing occurs at different compositions depending on temperature. Higher is the temperature, lower is the TCR zero-crossing composition. Resistivity data were discussed in the framework of the Matthiessen’s rule and sound evidences were shown that no Al₄C₃ formation was detected at working temperatures.

Background:Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) presents with a high prevalence of pulmonary fibrosis. Pulmonary fibrosis confers a worse prognosis to RA-ILD. There are no well stablished serum biomarkers for the identification of fibrotic versus non-fibrotic RA-ILD. This study reports the baseline plasma biomarkers analysed in RA-ILD individuals, both with and without pulmonary fibrosis, who are being closely monitored for two years as part of the BERTHA study (NCT04136223).Objectives:Investigate whether exploratory plasma biomarkers differ between RA-ILD with and without pulmonary fibrosis.Methods:All consecutive adult RA-ILD participants seen in five Brazilian rheumatologic centers between March 2021 – July 2022 were included in the study (ethical approval n.3.799.253). Patients with mMRC dyspnea score 5, use of long-term oxygen supplementation, significant pulmonary hypertension, and comorbidities with an impact in the respiratory system were excluded. At baseline, participants underwent high resolution computed tomography (HRCT) of the chest and blood draw. HRCTs were visually assessed by two independent radiologists and quantitatively analyzed by lung densitometry (Chest Imaging Platform software). Pulmonary fibrosis was defined on visual assessment of HRCT by the unequivocal presence of traction bronchiectasis and/or honeycombing. Plasma was analyzed for known biomarkers associated with pulmonary fibrosis, namely anti-CCP, MMP-7, SP-D, CCL-8, CA125, and CA19.9. The novel biological markers, tetrahydrobiopterin (BH4) and neopterin, associated with inflammation and oxidative stress, were also assessed. All laboratory analyses were performed in a central laboratory (LABOX, Federal University of Santa Catarina). Mean differences between participants with and without pulmonary fibrosis were evaluated using a two-sample T-test or Mann-Whitney U test.Results:95 RA-ILD participants were included (Table 1). Articular disease activity did not differ between groups. Pulmonary fibrosis was present in 84 % of participants [kappa radiologists: 0.65 (95CI 0.45-0.84)]. Patients with pulmonary fibrosis were older with worse pulmonary function (FVC % predicted 75±16 vs. 83±16, p=0.038, and DLCO %predicted 68±21 vs. 93±5, p=0.014), worse 6-minute walking distance (361±61m vs. 419±116m, p=0.023), and with more extensive disease in the HRCT (% HAA 12.3±6.8 vs. 6.6±3.8, p=0.004). No difference was observed in baseline plasma biomarkers between participants with or without pulmonary fibrosis (Table 1).Conclusion:At baseline, participants with RA-ILD and pulmonary fibrosis did not differ from RA-ILD participants without pulmonary fibrosis in terms of MMP-7, SP-D, CCL-8, CA125, and CA19.9. New plasma biomarkers, BH4 and neopterin, also did not differ between groups. As per BERTHA protocol, participants will be followed for more two years and the prognostic value of these plasma biomarkers will be assessed.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of Interests:Leticia Kawano-Dourado For Boehringer Ingelheim and Roche, From Boehringer Ingelheim and Bristol-Myers-Squibb, Karina Bonfiglioli For Roche, Lilly, BMS, Ana Cristina Medeiros-Ribeiro To Roche, Lilly and BMS, Licia Mota Boehringer Ingelheim, Lilly, BMS, Alisson Pugliesi Roche, Lilly, BMS, Luciana Muniz Boehringer Ingelheim, Roche, Lilly, Daniel Strabelli: None declared, Marcio Sawamura: None declared, Andrea Shimabuco: None declared, Sandra Pasoto: None declared, Luciana Teófilo Lourenconi: None declared, Fernanda L F B Riscado: None declared, Cleandro Albuquerque: None declared, Tassiane R C M Morais: None declared, Clemilda C da Silva: None declared, Ana Carolina Londe: None declared, Luciana C Palhares: None declared, Romuel Barros: None declared, Luis F Marqueze: None declared, Juliana D R Lindenau: None declared, Yara C N Muniz: None declared, Rachel H V Machado: None declared, Thabata S Veiga: None declared, Viviane B Bezerra: None declared, Leila O Silva: None declared, Jackeline O Gomes: None declared, Debora H K Miyada: None declared, Samira M Tokunaga: None declared, Tiago Mendonça: None declared, Bruno G Baldi Boehringer and Roche, Alexandra Latini: None declared.

The Absorb biovascular scaffold (BVS) is a bioresorbable, everolimus-eluting scaffold whose data on real-world patients with complex lesions are limited. Short-term follow-up from recent studies point to a higher rate of 30-day thrombosis than observed with drug-eluting stents. We aimed to understand the short-term safety and efficacy of BVS. Registro Absorb Italiano (RAI, ClinicalTrials.gov:NCT02298413) is an Italian, prospective, multicenter registry not funded, whose aim is to investigate BVS performance through a 5-year follow-up of all consecutive patients who have undergone successful implantation of ≥1 BVS in different clinical/lesion subsets. Co-primary end points were target lesion revascularization and definite/probable thrombosis. Secondary end point was the occurrence of device-oriented cardiac events. The registry involved 23 centers, with patient enrollment from October 2012 to December 2015. We here report the 30-day outcomes of the whole population of the registry. We enrolled 1,505 consecutive patients, of which 82% were men and 22.4% diabetic. At presentation, 59.6% of the patients had an acute coronary syndrome, including 21% ST-elevation myocardial infarction. All lesions were pre-dilated and in 96.8% of the cases BVS was post-dilated. At 30 days, the co-primary study end point target lesion revascularization occurred in 0.6% of patients and definite/probable BVS thrombosis in 0.8%. There were 2 cases of cardiac and overall death (0.13%). Device-oriented cardiac events occurred in 1% of the patients. In conclusion, our data of consecutive patients suggest that current use of BVS in a wide spectrum of coronary narrowings and clinical settings is associated with good outcome at 30 days.

BackgroundSystemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex pathogenesis in which genes and environmental factors interact leading to a protean clinical picture. Treat-to-target recommendations have identified ‘remission’ as a target in SLE, since achievement of remission improves the outcome and is associated with decreased damage progression. Nonetheless, predicting factors for the achievement of remission are lacking. It is likely that genes associated with SLE pathogenesis may influence the disease course.ObjectivesThus, our aim was to analyse previously identified loci associated with SLE in a cohort of SLE patients to evaluate their influence on remission achievement.MethodsWe recruited 117 Italian SLE patients. A panel of 34 SNPs in 19 genes involved in immune response, autophagy and inflammation, was selected. SNPs genotyping was performed by allelic discrimination assay by TaqMan assays (Applied Biosystems, Foster City, CA, USA) and ABI PRISM 7000. The main clinical/laboratory features (including injury index and disease activity) were collected on an electronic platform. Remission was defined according to Zen et al.1 and evaluated over 5 years. A genotype/phenotype correlation analysis was performed.ResultsThe variant alleles of rs7574965 (STAT4) (p<0.001) and rs2910164 (MIR146a) (p=0.031) were significantly associated with lack of achievement of 5 years remission in SLE. Specifically, patients carrying the C allele of MIR146a were less likely to achieve 5 years remission (p=0.01, OR 0.235, 95% CI 0.074–0.752) as well as to achieve remission after 1, 2 and 3 years of evaluation (p=0.002, p=0.001, p=0.002, respectively). Among the clinical and laboratory features, 5 years remission was less likely to be achieved by patients who had arthritis in their clinical history (p=0.007), and who tested positive for anti-dsDNA (p=0.005). In a multinomial logistic regression analysis, arthritis (p=0.022, Exp(B)=0.255, 95% CI 0.079–0.820), anti-dsDNA (p=0.003, Exp(B)=0.166, 95% CI 0.051–0.537) and MIR146a rs2910164 gene variant (p=0.046, Exp(B)=0.250, 95% CI 0.064–0.974) were confirmed to be independent risk factors for unreached 5 years remission (table 1).Abstract FRI0260 – Table 1REMISSIONExp(B)Exp (B) 95% CI LowerUpperArthritis025500790,82anti-dsDNA016600510537STAT403540,111139mir146A0,2500640974ConclusionsWe describe for the first time the contribution of STAT4 and MIR146a SNPs as predicting factors for the achievement of 5 years remission in SLE. No genetic study has been performed so far in SLE, while a genetic profile of patients may be useful to predict the disease outcome.Reference[1] Zen, et al. Ann Rheum Dis. 2017Mar;76(3):562–565.Disclosure of InterestNone declared