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We included 600 patients between December 2018 and March 2020. Among these 600 patients, 95 were excluded due to missing data (absence of recorded triage score) or lost to follow-up. Flow chart of patient screening and inclusion is provided in Fig. 1.
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Entre 2018 et 2020, les patients qui se sont présentés aux urgences de l'Institut de cardiologie de Montréal pour une TA élevée ont été recrutés dans le cadre d'une étude observationnelle prospective comprenant une entrevue téléphonique structurée post-hoc et un examen des dossiers médicaux. Cinq sources de référence possibles ont été prédéterminées. Nous avons fourni des proportions et des intervalles de confiance à 95 %.
Results: In may 2018 baseline and clinical information were available of near 4000 patients in the Eurofever registry. Of the 36 patients classified as PAPA syndrome, 2 were excluded from the study. 34 PAPA patients, from 11 different centers, were analysed: the genotype was confirmatory in 29 patients, while in 5 was not available. 10 patients were of the same family, in 4 cases one parent was affected (2 included in the registry), while in other 8 patients the family history was negative. At the time of enrolment, 15 patients were in the paediatric age, while 19 were adults. The mutations detected in the PSTPIP1 gene were E250Q (13 pts), E250K (5 pts), A230T (3 pts), G258A (3 pts), E277D (2 pts), E257G (1 pt), G940A (1pts) and R365W (1 pts).
Results: ARPC1B-deficient zebrafish were significantly smaller, and monocytes migrated slower compared to WT fish in response to injury. In the patient LCLs, loss of ARPC1B protein, compensatory upregulation of isoform ARPC1A, and loss of total F-actin were confirmed. Patient 1 LCLs were unusually adherent in the absence of stimulation, suggesting constitutive activation. To measure activation, LCLs were stimulated with anti-IgG to measure calcium flux; Patient 1 had a statistically significant higher calcium flux peak compared to control. To address whether Arp2/3 function was compromised, LCL lysates were stimulated with (activating domain) VCA and actin assembly was measured. Although both ARPC1B and ARPC1A isoforms were found to interact with VCA and full-length WASP in immunoprecipitation experiments, VCA-induced actin polymerization in cell lysates was completely abolished in Patients 1-3. Patient 1 was treated with an allogeneic HSCT in January 2018.
Methods: We performed the genetic analysis of the ADA2 gene and measured ADA2 activity of the patients from 2016 to 2018 in Japan. Multi-omics analysis had been done in 4 out of 8 DADA2 patients and 4 healthy donors using their peripheral blood mononuclear cells (PBMCs). The samples were taken before and after introduction of anti-TNFα agents (meaning acute and remission phase) in the patients.
Methods: DNAs from 577 patients clinically suspected for SAIDs (age 3 months to 79 years) were sequenced by NGS between September 2014 and December 2018. The libraries were prepared using Nextera (Illumina) or SureSelect (Agilent) Target Enrichment Capture custom kits. Sequencing reactions were performed on MiSeq or NextSeq500 equipment (Illumina). The mutations were classified according to a 5-class scale provided by the Infevers database or according to the American College of Medical Genetics and Genomics (ACMG) guidelines. Epidemiological data, clinical symptoms and biological markers were collected on a form provided with all genetic diagnosis requests.
Methods: We reviewed all ADA2 Sanger sequencing results of individuals tested between 2014 and 2018, including confirmatory testing in referral patients, and determined the diagnostic yield of this method in patients we suspected to have DADA2 based on clinical phenotype. We then analyzed if subsequent ADA2 enzyme assay and/or MLPA further increased our diagnostic yield.
Methods: We retrospectively reviewed patients with clinical and/ or genetically proven monogenic AIDs other than FMF seen between 1990 and 2018 at 10 rheumatology clinics from seven Arab countries. Data were collected at the last follow-up visit comprising history of consanguinity, age at onset and diagnosis, follow-up duration, clinical and laboratory findings, as well as the damage accrual and death related to monogenic AIDs.
Methods: We carried out a descriptive retrospective analysis of pediatric patients with auto-inflammatory diseases who were seen and managed at a single tertiary center, in Riyadh, Saudi Arabia, between 2004 and 2018. Multiple measures were investigated including time of disease onset, clinical features, investigations, treatment, and outcome.
Methods: 40 adults patients referring to the Rheumatology Unit of Padova University Hospital affected by FMF, TRAPS and HIDS and 40 healthy subjects were recruited between March and June 2018. Fasting blood samples were collected in order to determinate calcium (Ca), phosphorus (P), magnesium (Mg), 24-h urine calcium, 24-h urine phosphorus, albumin, parathyroid hormone (PTH), Vitamin D, creatinine, serum amyloid A (SAA), c-terminal telopeptide of type I collagen (CTX), bone alkaline phosphatase (b-ALP). Moreover, serum OPG and RANK-L were determined by a commercially available ELISA kit (Pantec, Turin, Italy). Femur and lumbar dual-energy X-ray absorptiometry (DXA) was performed with the QDR Bone Densitometer Discovery (Hologic Inc.,Waltham, MA). Trabecular Bone Score (TBS) was calculated on DXA lumbar images, using iNsight Software (version 1.8.0.0; Medimaps, Merignac, France). The statistical analysis was performed using Mann-Whitney U Test.
M. Finetti: None Declared, I. Gueli: None Declared, J. Frenkel: None Declared, S. Ozen: None Declared, H. Lachmann: None Declared, F. De Benedetti: None Declared, I. Koné-Paut: None Declared, C. Wouters: None Declared, P. Brogan: None Declared, H. Girschick: None Declared, B. Neven: None Declared, A. Martini Grant / Research Support from: The Gaslini Hospital, which is the public Hospital where AM worked till 31/dec/2018as a full time public employee, has received contributions from the following industries:Abbvie, Ablynx, Aim Group, Amgen, Astrazeneca, Biogen, BMS, Boehringer, Celgene, Emd Serono, GSK, Janssen, Novartis, Pfizer, R-Pharm. This money has been reinvested for the research activities of the hospital in a fully independent manner without any commitment with third parties., N. Ruperto Grant / Research Support from: The Gaslini Hospital, where NR works as full-time public employee, has received contributions (> 10.000 USD each) from the following industries in the last 3 years: BMS, Eli-Lilly, GlaxoSmithKline, F Hoffmann-La Roche, Janssen, Novartis, Pfizer, Sobi. This funding has been reinvested for the research activities of the hospital in a fully independent manner, without any commitment with third parties.,Speaker Bureau of: NR has received honoraria for consultancies or speaker bureaus (
Methods: We analyzed mutations of 22 genes related to autoinflammatory diseases as follows: TNFRSF1A, MEFV, NLRP3, MVK, NOD2, IL1RN, NLRP12, PSTPIP1, PSMB8, PSMB9, PSMA3, PSMB4, POMP, NLRC4, PLCG2, HMOX1, CECR1, COPA, TNFAIP3, FAM105B, RNF31, RBCK1,in 84 patients with fever of unknown origin who introduced to our hospital from May 2017 to June 2018. Genetic analysis was performed by the next generation sequencer. Furthermore, we investigated precise clinical features in 53 cases.
Methods: The data were extracted from the Eurofever registry, which is hosted in the PRINTO website ( printo.it). From February 2015 we started the longitudinal collection of follow-up data with particular focus on treatment, modification of the clinical picture, onset of complication/adverse events. We have enrolled patients included in the registry up to 28 September 2018.
I. Gueli: None Declared, M. Finetti: None Declared, F. De Benedetti: None Declared, J. Anton Lopez: None Declared, M. Alessio: None Declared, J. Frenkel: None Declared, L. Cantarini: None Declared, R. Gallizzi: None Declared, J. Sanchez Manubens: None Declared, M. Cattalini: None Declared, E. Papadopoulou-Alataki: None Declared, R. Cimaz: None Declared, D. Rigante: None Declared, A. N. Olivieri: None Declared, P. Dolezalova: None Declared, A. Martini Grant / Research Support from: The Gaslini Hospital, which is the public Hospital where AM worked till 31/dec/2018as a full time public employee, has received contributions from the following industries:Abbvie, Ablynx, Aim Group, Amgen, Astrazeneca, Biogen, BMS, Boehringer, Celgene, Emd Serono, GSK, Janssen, Novartis, Pfizer, R-Pharm. This money has been reinvested for the research activities of the hospital in a fully independent manner without any commitment with third parties., N. Ruperto Grant / Research Support from: The Gaslini Hospital, where NR works as full-time public employee, has received contributions (> 10.000 USD each) from the following industries in the last 3 years: BMS, Eli-Lilly, GlaxoSmithKline, F Hoffmann-La Roche, Janssen, Novartis, Pfizer, Sobi. This funding has been reinvested for the research activities of the hospital in a fully independent manner, without any commitment with third parties.,Speaker Bureau of: NR has received honoraria for consultancies or speaker bureaus ( 041b061a72