Results 191 to 200 of about 3,059,732 (298)
A Pragmatic Trial of a Shared Decision‐Making Intervention to Improve Medication Adherence and Outcomes in Systemic Lupus Erythematosus: The HCQ‐SAFE Study
Arthritis &Rheumatology, EarlyView.Objective
Hydroxychloroquine (HCQ) nonadherence in systemic lupus erythematosus (SLE) stemming from decision complexities can be improved with shared decision‐making (SDM) tools clarifying benefits and harms. This study aimed to develop and evaluate HCQ‐SAFE, a pictogram‐based SDM tool during SLE visits.Caroline Packee, Jay J. Patel, Jessica Kent, Betty Chewning, Sancia Ferguson, Patricia Tellez‐Giron, David Gazeley, Christie M. Bartels, Shivani Garg +8 morewiley +1 more sourceDistinct Molecular Pathways Supporting Sjögren Disease Clusters and Disease Progression
Arthritis &Rheumatology, EarlyView.Objective
Sjögren disease (SjD) is a heterogeneous autoimmune disease. We aimed to investigate blood transcriptomic signatures and disease progression among three recently defined clusters of patients with SjD: (1) B cell active disease with low symptom burden (BALS), (2) high systemic activity (HSA), and (3) low systemic activity with high symptom ...Sacha E. Silva‐Saffar, Yann Nguyen, Raphaèle Seror, Jacques‐Eric Gottenberg, Anna Niarakis, Xavier Mariette, Gaetane Nocturne +6 morewiley +1 more sourcePharmacokinetics, Effectiveness and Safety of Certolizumab Pegol in Children and Adolescents With Active Juvenile Idiopathic Arthritis: 9+‐Year Results From a Multicenter, Open‐Label Study
Arthritis &Rheumatology, EarlyView.Objective
The purpose of this study was to assess the pharmacokinetics, effectiveness, safety, and immunogenicity of certolizumab pegol (CZP) in polyarticular‐course juvenile idiopathic arthritis (pcJIA). Methods
Pediatric Arthritis Study of Certolizumab Pegol (NCT01550003), a multicenter, open‐label study, enrolled patients aged 2 to 17 years with ...Hermine I. Brunner, Lyudmila Grebenkina, Irina Nikishina, Ekaterina Alexeeva, Vyacheslav Chasnyk, Carlos Abud‐Mendoza, Nadina Rubio‐Pérez, Heinrike Schmeling, María del Rocio Maldonado‐Velázquez, Diane Brown, Andrew Zeft, Esi Morgan, C. Egla Rabinovich, Daniel Kingsbury, Hulya Bukulmez, Beth Gottlieb, Thomas Griffin, Lisa Imundo, Stacey Tarvin, Earl Silverman, Laura Shaughnessy, Saori Shimizu, Paulette Williams, Rocío Lledó‐García, Gauri Utturkar, Baran Ufuktepe, Alberto Martini, Daniel J. Lovell, Nicolino Ruperto, the Paediatric Rheumatology International Trials Organisation (PRINTO); the Pediatric Rheumatology Collaborative Study Group (PRCSG), Hermine I. Brunner, Lyudmila Grebenkina, Irina Nikishina, Ekaterina Alexeeva, Vyacheslav Chasnyk, Carlos Abud‐Mendoza, Nadina Rubio‐Pérez, Heinrike Schmeling, María del Rocio Maldonado‐Velázquez, Diane Brown, Andrew Zeft, Esi Morgan, C. Egla Rabinovich, Daniel Kingsbury, Hulya Bukulmez, Beth Gottlieb, Thomas Griffin, Lisa Imundo, Stacey Tarvin, Earl Silverman, Alberto Martini, Daniel L. Lovell, Nicolino Ruperto +52 morewiley +1 more sourceComplement Activation Linked to Type II Interferon Signaling in Still Disease
Arthritis &Rheumatology, EarlyView.Objective
Still disease (SD) is an autoinflammatory syndrome characterized by innate immune dysregulation. Although complement can drive inflammation, its involvement in SD remains to be defined. Thus, we aimed to assess complement activation in SD. Methods
Complement was assessed using transcriptomic, proteomic, and in vitro approaches. RNA sequencing Freya M. C. H. Huijsmans, Tabea Thalheim, Alejandra Bodelón, Greta Rogani, Lyanne J. P. M. Sijbers, Remco G. A. Erkens, Aafke de Ligt, Rianne Scholman, Aron Brinker, Gisella B. Beretta, Nienke M. Ter Haar, Thomas Vogl, Johannes Roth, Trang T. Duong, Sytze de Roock, Joost F. Swart, Deborah A. Marshall, Susanne M. Benseler, Rae S. M. Yeung, Christoph Kessel, Sebastiaan J. Vastert, Emely L. Verweyen, Jorg van Loosdregt, on behalf of the UCAN CAN‐DU/UCAN CURE Consortia and the One Child Every Child Initiative, Adam Huber, Bianca Lang, Chelsea DeCoste, Elizabeth Stringer, Suzanne Ramsey, Alan Rosenberg, Kate Neufeld, Mehul Jariwala, Tristan Kerr, Alexander Mosoiu, Alisa Rachlis, Amy Xu, Arthur Cheng, Brenleigh Jebb, Brian Feldman, Bruno Pereira, Deborah Levy, Dilan Dissanayake, Elizaveta Limenis, Evelyn Rozenblyum, Harper Cheng, Jennifer Ji Young Lee, Lynn Spiegel, Rayfel Schneider, Ronald Laxer, Ruud Verstegen, Shirley Tse, Andrea Human, David Cabral, Herman Tam, Jaime Guzman, Kim Morishita, Kristin Houghton, Lori Tucker, Mercedes Chan, Ross Petty, Tommy Gerschman, Annet van Royen‐Kerkhof, Berent Prakken, Erika Van Nieuwenhove, Marc Jansen, Nico Wulffraat, Ciarán Duffy, Nadia Luca, Roman Jurencak, Tala El Tal, Claire LeBlanc, Gaëlle Chédeville, Piya Lahiry, Rosie Scuccimarri, Sarah Campillo, Clare Hutchinson, Daniah Basodan, Dax G Rumsey, Hon Yan Ng, Jeanine McColl, Lillian Lim, Tara McGrath, Danielle Brinkman, Petra Hissink Muller, Elizabeth Legger, Wineke Armbrust, Ellen Schatorje, Esther Hoppenreijs, Elodie Boudes, Gillian Currie, Heinrike Schmeling, Muhammed Dhalla, Nicole Johnson, Paivi Miettunen, Ravneet Sran, Rebeka Stevenson, Erkan Demirkaya, Jonathan Park, Roberta Berard, Giske Biesbroek, Mariken Gruppen, Gordon Soon, Joseph Cafazzo, Liane Heale, Michelle Batthish, Tania Cellucci, Lily Lim, Maarten IJzerman, Marinka Twilt, Marleen Verkaaik, Philomine van Pelt, Sylvia Kamphuis, Michelle Kip, Nicholas Blanchette, Paul Dancey, Regina de Geus +115 morewiley +1 more sourcePersistent Interleukin‐18 Fuels Expansion of CD38+HLA‐DR+CD8+ T Cells in Still Disease and Macrophage Activation Syndrome
Arthritis &Rheumatology, EarlyView.Objective
Still disease (SD) is an autoinflammatory disorder characterized by remarkably high interleukin‐18 (IL‐18) levels. Increasing evidence suggests that adaptive immunity also contributes to its pathogenesis, particularly in refractory courses. Macrophage activation syndrome (MAS), one of SD's most severe complications, is associated with further Greta Rogani, Remco G. A. Erkens, Alejandra Bodelón, Tim R. Mocking, Marein T. M. Putmans, Freya M. C. H. Huijsmans, Lyanne J. P. M. Sijbers, Aafke M. De Ligt, Maurice J. H. Van Haaren, Rianne C. Scholman, Noël M. M. Dautzenberg, Joyce I. Meesters‐Ensing, Martina Rossano, Laura Porretti, Stefan Nierkens, Francesca S. Minoia, Sebastiaan J. Vastert, Jorg van Loosdregt +17 morewiley +1 more sourceHuman Monocytic Models Reveal Genotype‐Dependent Inflammatory Programs in VEXAS Syndrome
Arthritis &Rheumatology, EarlyView.Objective
VEXAS syndrome is a severe X‐linked autoinflammatory disorder caused by somatic mutations in ubiquitin‐like modifier activating enzyme 1 (UBA1), with clinical outcomes that vary by UBA1 genotype. We aimed to elucidate genotype‐specific inflammatory programs and identify potential therapeutic targets.Kana Higashitani, Tatsuma Ban, Yohei Kirino, Go R. Sato, Soichiro Adachi, Yuki Iizuka, Kayo Harita, Ayaka Maeda, Osamu Ohara, Hideaki Nakajima, Tomohiko Tamura +10 morewiley +1 more source