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234 results on '"Berkun, Y."'

2. AB1166 MYOCARDITIS FOLLOWING mRNA COVID VACCINE COMPARED TO PAEDIATRIC MULTISYSTEM INFLAMMATORY SYNDROME MULTICENTER RETROSPECTIVE STUDY

Author

Butbul, Y., primary, Kaidar, K., additional, Hashkes, P. J., additional, Dizitzer, Y., additional, Kanteman, I., additional, Berkun, Y., additional, Eisenstein, E. M., additional, Hamad Saied, M., additional, Goldzweig, O., additional, Heshin-Bekenstein, M., additional, Ling, E., additional, Feldon, M., additional, Tal, R., additional, Amarilyo, G., additional, and Harel, L., additional

Published
2022
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3. Development of a New International Antiphospholipid Syndrome Classification Criteria Phase I/II Report: Generation and Reduction of Candidate Criteria

Author

Barbhaiya, M., Zuily, S., Ahmadzadeh, Y., Amigo, M. -C., Avcin, T., Bertolaccini, M., Branch, D. W., de Jesus, G., Devreese, K. M. J., Frances, C., Garcia, D., Guillemin, F., Levine, S. R., Levy, R. A., Lockshin, M. D., Ortel, T., Seshan, S. V., Tektonidou, M., Wahl, D., Willis, R., Naden, R., Costenbader, K., Erkan, D., Agmon-Levin, N., Aguilar, C., Alba, P., Alpan, O., Ambrozic, A., Amoura, Z., Andrade, D., Andrade, L., Appenzeller, S., Esen, B. A., Atsumi, T., Berkun, Y., Cabral, A., Canaud, G., Cervera, R., Chen, P., Chighizola, C., Cimaz, R., Cohen, H., Costedoat-Chalumeau, N., Crowther, M., Cuadrado, M. J., de Groot, P. G., de Moerloose, P., Derksen, R., Diz-Kucukkaya, R., Dorner, T., Fortin, P., Giannakopoulos, B., Gomez-Puerta, J. A., Gonzalez, E. B., Inanc, M., Kenet, G., Khamashta, M., Kriegel, M., Krilis, S., Laskin, C., Massicotte, P., Mccarty, G., Meroni, P. L., Mikdashi, J., Myones, B., Pengo, V., Petri, M., Roubey, R., Sammaritano, L., Sanna, G., Sciascia, S., Signorelli, F., Soybilgic, A., Tincani, A., Woller, S., and Yelnik, C.

Subjects
Antiphospholipid Syndrome, Consensus, Delphi Technique, Humans, Predictive Value of Tests, Rheumatology, Severity of Illness Index, CONSENSUS STATEMENT, Potential candidate, AMERICAN-COLLEGE, Article, DISEASE, Reduction (complexity), 03 medical and health sciences, 0302 clinical medicine, Antiphospholipid syndrome, RHEUMATOLOGY/EUROPEAN LEAGUE, Nominal group technique, Medicine and Health Sciences, Hierarchical organization, Medicine, CLINICAL-SIGNIFICANCE, computer.programming_language, 030203 arthritis & rheumatology, RISK, VENOUS THROMBOEMBOLISM, Information retrieval, business.industry, SYSTEMIC-SCLEROSIS, medicine.disease, Phase i ii, MYOCARDIAL-INFARCTION, ANTIBODIES, Report generation, business, computer, Delphi
Abstract

Objective : An international multidisciplinary initiative, jointly supported by the American College of Rheumatology and European Alliance of Associations for Rheumatology, is underway to develop new rigorous classification criteria to identify patients with high likelihood of antiphospholipid syndrome (APS) for research purposes. The present study was undertaken to apply an evidence- and consensus-based approach to identify candidate criteria and develop a hierarchical organization of criteria within domains. Methods : During phase I, the APS classification criteria steering committee used systematic literature reviews and surveys of international APS physician scientists to generate a comprehensive list of items related to APS. In phase II, we reviewed the literature, administered surveys, formed domain subcommittees, and used Delphi exercises and nominal group technique to reduce potential APS candidate criteria. Candidate criteria were hierarchically organized into clinical and laboratory domains. Results : Phase I generated 152 candidate criteria, expanded to 261 items with the addition of subgroups and candidate criteria with potential negative weights. Using iterative item reduction techniques in phase II, we initially reduced these items to 64 potential candidate criteria organized into 10 clinical and laboratory domains. Subsequent item reduction methods resulted in 27 candidate criteria, hierarchically organized into 6 additive domains (laboratory, macrovascular, microvascular, obstetric, cardiac, and hematologic) for APS classification. Conclusion : Using data- and consensus-driven methodology, we identified 27 APS candidate criteria in 6 clinical or laboratory domains. In the next phase, the proposed candidate criteria will be used for real-world case collection and further refined, organized, and weighted to determine an aggregate score and threshold for APS classification.

Published
2021

4. POS1183 OUTCOMES OF COVID-19 INFECTION AMONG CHILDREN AND YOUNG PEOPLE WITH PRE-EXISTING RHEUMATIC AND MUSCULOSKELETAL DISEASES

Author

Kearsley-Fleet, L., primary, Lawson-Tovey, S., additional, Costello, R. E., additional, Belot, A., additional, Aeschlimann, F., additional, Melki, I., additional, Koné-Paut, I., additional, Clemente, D., additional, Pinedo Gago, M. C., additional, Svestkova, N., additional, Vinšová, N., additional, Hamad Saied, M., additional, Berkun, Y., additional, Wulffraat, N., additional, Eulert, S., additional, Scirè, C. A., additional, Strangfeld, A., additional, Mateus, E., additional, Machado, P., additional, Uziel, Y., additional, and Hyrich, K., additional

Published
2021
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6. Efficacy and safety of canakinumab, a long acting fully human anti-Interleukin-1β antibody, in systemic juvenile idiopathic arthritis with active systemic features: results from a phase III study

Author

McCann L, Ozdogan H, Rutkowska-Sak L, Ferrandiz MA, Wulffraat NM, Brik R, Kallinich T, Erguven M, Berkun Y, Constantin T, Quartier P, Horneff G, Brunner H, Ruperto N, Lheritier K, Preiss R, Tseng L, Martini A, and Lovell DJ

Subjects
Pediatrics, RJ1-570, Diseases of the musculoskeletal system, RC925-935
Published
2011
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17. Early changes in gene expression and inflammatory proteins in systemic juvenile idiopathic arthritis patients on canakinumab therapy

Author

Brachat A. H., Grom A. A., Wulffraat N., Brunner H. I., Quartier P., Brik R., McCann L., Ozdogan H., Rutkowska-Sak L., Schneider R., Gerloni V., Harel L., Terreri M., Houghton K., Joos R., Kingsbury D., Lopez-Benitez J. M., Bek S., Schumacher M., Valentin M. -A., Gram H., Abrams K., Martini A., Lovell D. J., Nirmala N. R., Ruperto N., Cuttica R., Emminger W., Lauwerys B., Wouters C., Goffin L., Sztajnbok F., Radominski S., Oliveira S., Haddad E., Kone-Paut I., Desjonqueres M., Fischbach M., Thon A., Foell D., Weibarth-Riedel E., Horneff G., Trauzeddel R., Berner R., Kallinich T., Trachana M., Constantin T., Barash J., Berkun Y., Uziel Y., Corona F., Alessio M., Cimaz R., Viola S., Flato B., Ferrandiz M., Calvo I., Anton J., Robledillos J. C., Gamir M. L., Magnusson B., Hofer M., Unsal E., Erguven M., Ozen S., Wilkinson N., Chieng A., Ramanan A., Foster H., Nistala K., Higgins G., Marzan K., Schikler K., Morris P., Brachat, A. H., Grom, A. A., Wulffraat, N., Brunner, H. I., Quartier, P., Brik, R., Mccann, L., Ozdogan, H., Rutkowska-Sak, L., Schneider, R., Gerloni, V., Harel, L., Terreri, M., Houghton, K., Joos, R., Kingsbury, D., Lopez-Benitez, J. M., Bek, S., Schumacher, M., Valentin, M. -A., Gram, H., Abrams, K., Martini, A., Lovell, D. J., Nirmala, N. R., Ruperto, N., Cuttica, R., Emminger, W., Lauwerys, B., Wouters, C., Goffin, L., Sztajnbok, F., Radominski, S., Oliveira, S., Haddad, E., Kone-Paut, I., Desjonqueres, M., Fischbach, M., Thon, A., Foell, D., Weibarth-Riedel, E., Horneff, G., Trauzeddel, R., Berner, R., Kallinich, T., Trachana, M., Constantin, T., Barash, J., Berkun, Y., Uziel, Y., Corona, F., Alessio, M., Cimaz, R., Viola, S., Flato, B., Ferrandiz, M., Calvo, I., Anton, J., Robledillos, J. C., Gamir, M. L., Magnusson, B., Hofer, M., Unsal, E., Erguven, M., Ozen, S., Wilkinson, N., Chieng, A., Ramanan, A., Foster, H., Nistala, K., Higgins, G., Marzan, K., Schikler, K., and Morris, P.

Subjects
Male, 0301 basic medicine, SJIA, Juvenile, Arthritis, 0302 clinical medicine, Monoclonal, Gene expression, Child, Oligonucleotide Array Sequence Analysis, Immunoassay, biology, Interleukin-18, Antibodies, Monoclonal, Interleukin-1β, Child, Preschool, Female, Interleukin 18, Biomarkers, Canakinumab, Juvenile idiopathic arthritis, Adolescent, Arthritis, Juvenile, Down-Regulation, Gene Expression Profiling, Humans, Interleukin-6, Transcriptome, Young Adult, Research Article, Human, medicine.drug, medicine.medical_specialty, Antibodies, Monoclonal, Humanized, Antibodies, 03 medical and health sciences, Juvenile idiopathic arthriti, Internal medicine, medicine, Journal Article, Preschool, Interleukin 6, 030203 arthritis & rheumatology, Oligonucleotide Array Sequence Analysi, business.industry, Microarray analysis techniques, Interleukin-1 beta, Biomarker, medicine.disease, Rheumatology, Gene expression profiling, 030104 developmental biology, Immunology, biology.protein, business
Abstract

Novartis Pharma Background: Canakinumab is a human anti-interleukin-1 beta (IL-1 beta) monoclonal antibody neutralizing IL-1 beta-mediated pathways. We sought to characterize the molecular response to canakinumab and evaluate potential markers of response using samples from two pivotal trials in systemic juvenile idiopathic arthritis (SJIA). Methods: Gene expression was measured in patients with febrile SJIA and in matched healthy controls by Affymetrix DNA microarrays. Transcriptional response was assessed by gene expression changes from baseline to day 3 using adapted JIA American College of Rheumatology (aACR) response criteria (50 aACR JIA). Changes in pro-inflammatory cytokines IL-6 and IL-18 were assessed up to day 197. Results: Microarray analysis identified 984 probe sets differentially expressed (>= 2-fold difference P < 0.05) in patients versus controls. Over 50% of patients with >= 50 aACR JIA were recognizable by baseline expression values. Analysis of gene expression profiles from patients achieving = 50 aACR JIA response at day 15 identified 102 probe sets differentially expressed upon treatment (>= 2-fold difference P < 0.05) on day 3 versus baseline, including IL-1 beta, IL-1 receptors (IL1-R1 and IL1-R2), IL-1 receptor accessory protein (IL1-RAP), and IL-6. The strongest clinical response was observed in patients with higher baseline expression of dysregulated genes and a strong transcriptional response on day 3. IL-6 declined by day 3 (>= 8-fold decline P < 0.0001) and remained suppressed. IL-18 declined on day 57 (>= 1.5-fold decline, P

Published
2017

21. THU0571 Preliminary Response To Janus Kinase Inhibition with Baricitinib in Chronic Atypical Neutrophilic Dermatosis with Lipodystrophy and Elevated Temperatures (CANDLE)

Author

Montealegre, G.A., primary, Reinhardt, A., additional, Brogan, P., additional, Berkun, Y., additional, Zlotogorski, A., additional, Brown, D., additional, Gao, L., additional, Dare, J.A., additional, Schalm, S., additional, Klausmeier, T.L., additional, Murias, S., additional, Chapelle, D., additional, Kim, H., additional, Judd, S., additional, O'Brien, M., additional, de Jesus, A.A., additional, Kost, B., additional, Paul, S.M., additional, Colbert, R.A., additional, Brofferio, A., additional, Lee, C., additional, Hadigan, C., additional, Heller, T., additional, Waldman, M., additional, Rother, K.I., additional, and Goldbach-Mansky, R., additional

Published
2016
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24. Preliminary response to Janus kinase inhibition with baricitinib in chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperatures (CANDLE)

Author

Montealegre, G, primary, Reinhardt, A, additional, Brogan, P, additional, Berkun, Y, additional, Zlotogorski, A, additional, Brown, D, additional, Chira, P, additional, Gao, L, additional, Dare, J, additional, Schalm, S, additional, Merino, R, additional, Chapelle, D, additional, Kim, H, additional, Judd, S, additional, O'Brien, M, additional, De Jesus, A Almeida, additional, Kim, Y, additional, Kost, B, additional, Huang, Y, additional, Paul, S, additional, Brofferio, A, additional, Lee, C-C, additional, Hadigan, C, additional, Heller, T, additional, Minniti, C, additional, Rother, K, additional, and Goldbach-Mansky, R, additional

Published
2015
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25. The EULAR/PRINTO/PRES criteria for Henoch-Schönlein purpura, childhood polyarteritis nodosa, childhood Wegener granulomatosis, and childhood Takayasu arteritis: ankara 2008. part ii: final classification criteria

Author

Ozen, S, Pistorio, A, Iusan, Sm, Bakkaloglu, A, Herlin, T, Brik, R, Buoncompagni, A, Lazar, C, Bilge, I, Uziel, Y, Rigante, D, Cantarini, L, Hilario, Mo, Silva, Ca, Alegria, M, Norambuena, X, Belot, A, Berkun, Y, Amparo Ibanez, E, Olivieri, An, Alpigiani, Mg, Rumba, I, Sztajnbok, F, Tambic Bukovac, L, Breda, L, Al Mayouf, S, Mihaylova, D, Chasnyk, V, Sengler, C, Klein Gitelman, M, Djeddi, D, Nuno, L, Pruunsild, C, Brunner, J, Kondi, A, Pagava, K, Pederzoli, S, Martini, Alberto, and Ruperto, N.

Published
2010

27. The mosaic of autoimmunity: hormonal and environmental factors involved in autoimmune diseases--2008

Author

Shoenfeld, Y., Zandman Goddard, G., Stojanovich, L., Cutolo, M., Amital, H., Levy, Y., Abu Shakra, M., Barzilai, O., Berkun, Y., Blank, M., De Carvalho Jf, Andrea Doria, Gilburd, B., Katz, U., Krause, I., Langevitz, P., Orbach, H., Pordeus, V., Ram, M., Toubi, E., and Sherer, Y.

Subjects
Epstein-Barr Virus Infections, Vaccines, Pregnancy, Stress, Physiological, Smoking, Humans, Female, Hormones, Stress, Psychological, Autoimmune Diseases, Circadian Rhythm
Published
2008

30. The Ped-APS Registry: the antiphospholipid syndrome in childhood

Author

Avcin, T., Cimaz, R., Rozman, B., Cervera, R., Ravelli, A., Martini, A., Meroni, P. l., Garay, S., Sztajnbok, F. r., Silva, C. a., Campos, L. m., Saad Magalhaes, C., de Oliveira, S. k., Silverman, E. d., Nielsen, S., Pruunsild, C., Dressler, F., Berkun, Y., Padeh, S., Barash, J., Uziel, Y., Harel, L., Mukamel, M., Revel Vilk, S., Kenet, G., Gattorno, M., Rigante, Donato, Zulian, F., Falcini, F., Kuzmanovska, D. b., Susic, G., Buyukgebiz, A., Ozisik, K., Gozdasoglu, S., Rodriguez, V., Butani, L., Rigante, Donato (ORCID:0000-0001-7032-7779), Avcin, T., Cimaz, R., Rozman, B., Cervera, R., Ravelli, A., Martini, A., Meroni, P. l., Garay, S., Sztajnbok, F. r., Silva, C. a., Campos, L. m., Saad Magalhaes, C., de Oliveira, S. k., Silverman, E. d., Nielsen, S., Pruunsild, C., Dressler, F., Berkun, Y., Padeh, S., Barash, J., Uziel, Y., Harel, L., Mukamel, M., Revel Vilk, S., Kenet, G., Gattorno, M., Rigante, Donato, Zulian, F., Falcini, F., Kuzmanovska, D. b., Susic, G., Buyukgebiz, A., Ozisik, K., Gozdasoglu, S., Rodriguez, V., Butani, L., and Rigante, Donato (ORCID:0000-0001-7032-7779)

Abstract

In recent years, antiphospholipid syndrome (APS) has been increasingly recognised in various paediatric autoimmune and nonautoimmune diseases, but the relatively low prevalence and heterogeneity of APS in childhood made it very difficult to study in a systematic way. The project of an international registry of paediatric patients with APS (the Ped-APS Registry) was initiated in 2004 to foster and conduct multicentre, controlled studies with large number of paediatric APS patients. The Ped-APS Registry is organised as a collaborative project of the European Forum on Antiphospholipid Antibodies and Juvenile Systemic Lupus Erythematosus Working Group of the Paediatric Rheumatology European Society. Currently, it documents a standardised clinical, laboratory and therapeutic data of 133 children with antiphospholipid antibodies (aPL)-related thrombosis from 14 countries. The priority projects for future research of the Ped-APS Registry include prospective enrollment of new patients with aPL-related thrombosis, assessment of differences between the paediatric and adult APS, evaluation of proinflammatory genotype as a risk factor for APS manifestations in childhood and evaluation of patients with isolated nonthrombotic aPL-related manifestations.

Published
2009

33. AB1182 Efficacy and safety of canakinumab, fully human anti-interleukin-1beta antibody, in systemic juvenile idiopathic arthritis

Author

Ruperto, N., primary, Brunner, H., additional, Quartier, P., additional, Constantin, T., additional, Wulffraat, N., additional, Horneff, G., additional, Brik, R., additional, McCann, L., additional, Kasapcopur, O., additional, Rutkowska-Sak, L., additional, Schneider, R., additional, Berkun, Y., additional, Calvo, I., additional, Erguven, M., additional, Goffin, L., additional, Hofer, M., additional, Kallinich, T., additional, Knupp, S., additional, Uziel, Y., additional, Viola, S., additional, Nistala, K., additional, Wouters, C., additional, Cimaz, R., additional, Ferrandiz, M., additional, Flato, B., additional, Luz Gamir, M., additional, Kone-Paut, I., additional, Grom, A., additional, Magnusson, B., additional, Ozen, S., additional, Sztajnbok, F., additional, Lheritier, K., additional, Kim, D., additional, Abrams, K., additional, Martini, A., additional, and Lovell, D., additional

Published
2013
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37. Common infectious agents prevalence in antiphospholipid syndrome

Author

Zinger, H., primary, Sherer, Y., additional, Goddard, G., additional, Berkun, Y., additional, Barzilai, O., additional, Agmon-Levin, N., additional, Ram, M., additional, Blank, M., additional, Tincani, A., additional, Rozman, B., additional, Cervera, R., additional, and Shoenfeld, Y., additional

Published
2009
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41. Lupus around the World

Author

Uziel, Y, primary, Gorodnitski, N, additional, Mukamel, M, additional, Padeh, S, additional, Brik, R, additional, Barash, J, additional, Mevorach, D, additional, Berkun, Y, additional, Tauber, T, additional, Press, J, additional, Harel, L, additional, Navon, P, additional, Rubenstein, M, additional, Naparstek, Y, additional, and Hashkes, PJ, additional

Published
2007
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47. Clinical disease among patients heterozygous for familial mediterranean fever.

Author

Marek-Yagel D, Berkun Y, Padeh S, Abu A, Reznik-Wolf H, Livneh A, Pras M, and Pras E

Abstract

OBJECTIVE: To define the molecular basis of familial Mediterranean fever (FMF) in patients with only 1 mutation in the MEFV gene. METHODS: Genetic analysis was performed in 20 FMF patients, including full sequencing of complementary DNA (cDNA) samples and multiplex ligation-dependent probe amplification analysis. In patients with first-degree relatives with FMF, haplotype analysis was also performed. RESULTS: A second mutation was found in 2 patients. In the other 18 patients, we could not identify additional mutations, large genomic deletions, or duplications. Analysis of single-nucleotide polymorphisms along the cDNA ruled out a lack of expression of 1 of the alleles. In 2 of the 3 families in which more than 1 sibling had FMF, we showed that the affected siblings inherited a different MEFV allele from the parent who did not have the MEFV mutation. CONCLUSION: These findings are highly consistent with the existence of a clinical phenotype among some patients who are heterozygous for FMF and could explain the vertical transmission in some families. A single mutation in the MEFV gene may be much more common than was previously thought and may include up to 25% of patients who are diagnosed as having FMF. [ABSTRACT FROM AUTHOR]

Published
2009
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49. Peritoneal adhesions and intestinal obstructions in patients with familial Mediterranean fever--are they more frequent?

Author

Berkun Y, Ben-Chetrit E, and Klar A

Abstract

OBJECTIVE: Familial Mediterranean fever (FMF) is characterized by recurrent episodes of peritonitis. A controversy exists as to whether intestinal obstruction due to peritoneal adhesions is more common among FMF patients compared with healthy controls. The aim of the study was to estimate the rate of spontaneous or postsurgical small-bowel obstruction (SBO) in FMF patients. METHODS: We reviewed the charts of 560 FMF patients followed in our clinic for the occurrence of spontaneous SBO. We also assessed the occurrence of postappendectomy intestinal obstruction among 89 FMF patients compared with 417 individuals without FMF who underwent an appendectomy without other abdominal surgery in the same medical center. RESULTS: Ten of 471 FMF patients (2.1%) developed spontaneous SBO, 8 of whom required laparotomy and adhesiolysis. Six of 89 FMF patients (6.7%) who underwent appendectomy developed SBO. None of the non-FMF patients developed SBO. CONCLUSIONS: Our retrospective study showed that FMF patients are at a higher risk than healthy individuals for developing SBO either spontaneously or as a postsurgical complication. Physicians should be alert to this possible complication when FMF patients arrive at the emergency room. Copyright © 2007 by Elsevier Inc. [ABSTRACT FROM AUTHOR]

Published
2007
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50. Outcome of a national Israeli cohort of pediatric systemic lupus erythematosus.

Author

Uziel, Y., Gorodnitski, N., Mukamel, M., Padeh, S., Brik, R., Barash, J., Mevorach, D., Berkun, Y., Tauber, T., Press, J., Harel, L., Navon, P., Rubenstein, M., Naparstek, Y., and Hashkes, P. J.

Subjects
SYSTEMIC lupus erythematosus, AUTOIMMUNE diseases, PEDIATRIC therapy, CHRONIC kidney failure, KIDNEY diseases, RHEUMATOLOGY, JOINT diseases
Abstract

The aim of this study was to describe the clinical manifestations and outcomes of a national cohort of childhood systemic lupus erythematosus (cSLE). All cases of cSLE registered in the Israeli national registry of children with rheumatic diseases between 1987–2003 were examined for disease activity and damage by the SLE disease activity index (SLEDAI) and SLE collaborating clinics/American College of Rheumatology (SLICC/ACR) damage index. Demographic, clinical, laboratory and treatment factors were analysed for their effect on the outcome. One-hundred and two patients were identified, 81% females, with a mean age at diagnosis of 13.3 ± 2.6 years. The mean SLEDAI score was 17.2 ± 9.0 (range 2–60). Fifty four patients were followed for at least five years. The mean SLEDAI decreased to 7.6 ± 6.3 (0–29) and the mean SLICC/ACR damage index was 0.7 ± 1.6 (0–8). Five patients developed chronic renal failure. No patients died. No factors were found to be significantly associated with the outcome except the initial SLEDAI score. The five-year outcome of our national cSLE cohort was good; with relatively low activity and minimal damage in most patients. The initial SLEDAI predicted the development of late damage. [ABSTRACT FROM AUTHOR]

Published
2007
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