Search

Your search keyword '"Choy, Ernest"' showing total 1,203 results
Start Over Author "Choy, Ernest"
1,203 results on '"Choy, Ernest"'

206. BHPR research: qualitative1. Complex reasoning determines patients' perception of outcome following foot surgery in rheumatoid arhtritis

Author

Backhouse, Michael R., Vinall, Karen A., Redmond, Anthony, Helliwell, Philip, Keenan, Anne-Maree, Dale, Rebecca M., Thomas, Amanda, Aronson, Diane, Turner-Cobb, Julie, Sengupta, Raj, France, Brisa, Hill, Ingrid, Flurey, Caroline A., Morris, Marianne, Pollock, Jon, Hughes, Rod, Richards, Pam, Hewlett, Sarah, Ryan, Sarah, Lille, Kate, Adams, Jo, Haq, Inam, McArthur, Margaret, Goodacre, Lynne, Birt, Linda, Wilson, Oonagh, Kirwan, John, Dures, Emma, Quest, Enid, Rajak, Rizwan, Thomas, Tasmin, Lawson, Tom, Petford, Sharon, Hale, Elizabeth, Kitas, George D., Gooberman-Hill, Rachael, Jinks, Clare, Dziedzic, Krysia, Bouças, Sofia Barbosa, Hislop, Kelly, Rhodes, Carol, Ali, Fizzah, Ong, Bie Nio, White, Derrick, Hensor, Elizabeth, Ferguson, Anna M., Douiri, Abdel, Scott, David L., Lempp, Heidi, Halls, Serena, Law, Rebecca-Jane, Jones, Jeremy, Markland, David, Maddison, Peter, Thom, Jeanette, Thom, Jeanette M., Breslin, Anne, Kraus, Alexandra, Gordhan, Chandrika, Dennis, Sean, Connor, John, Chowdhary, Bhavani, Lottay, Neena, Juneja, Parmjit, Bacon, Paul A., Isaacs, David, Jack, James, Keller, Majella, Tibble, Jeremy, Hammond, Alison, Gill, Rachel, Tyson, Sarah, Tennant, Alan, Nordenskiold, Ulla, Pease, Emily E., Pease, Colin T., Trehane, Anne, Rahmeh, Fouz, Cornell, Patricia, Westlake, Sarah L., Rose, Katy, Alber, Catherine Fouad, Watson, Liam, Stratton, Richard, Lazarus, Mark, McNeilly, Natasha E., Waterfield, Jackie, Hurley, Mike, Greenwood, James, Clayton, Ann M., Lynch, Michael, Clewes, Adrian, Dawson, Julie, Abernethy, Veronica, Griffiths, Ann E., Chamberlain, Victoria A., McLoughlin, YokeMei, Campbell, Sophie, Hayes, Janita, Moffat, Claire, McKenna, Frank, Shah, Preeti, Williams, Ann, Rhys-Dillon, Ceril, Goodfellow, Rhian, Martin, James C., Bari, Farhan, Hughes, Gwenan, Thomas, Eleri, Baker, Sarah, Collins, David, Price, Elizabeth, Williamson, Lyn, Dunkley, Lisa, Youll, Matthew J., Rodziewicz, Mia, Reynolds, John A., Berry, Jacqueline, Pavey, Chee, Hyrich, Kimme, Gorodkin, Rachel, Wilkinson, Kate, Bruce, Ian, Barton, Anne, Silman, Alan, Ho, Pauline, Cornell, Tricia, Richards, Selwyn, Holmes, A., Parker, S., Smith, H., Briggs, N., Arthanari, S., Nisar, M., Thwaites, Catharine, Kamath, Sanjeet, Price, Shyra, Robinson, Sandra M., Walker, David, Coop, Hazel, Al-Allaf, Wahab, Charleton, Rebecca C., Griffiths, Bridget, Edwards, Elizabeth A., Partlett, Rosamund, Martin, Keith, Tarzi, Mike, Panthakalam, Sathianathan, Freeman, Tanya, Ainley, Louise, Turner, Michael, Hughes, Lyndsay, Russell, Bridget, Jenkins, Suzanne, Done, John, Young, Adam, Jones, Tadeusz, Gaywood, Ian C., Pande, Ira, Pradère, Marie-Josèphe, Bhaduri, Mahua, Smith, Angela, Cook, Haley, Abraham, Sonya, Ngcozana, Tanaka, Denton, Christopher P., Parker, Louise, Black, Carol M., Ong, Voon, Thompson, Nicola, White, Catherine, Duddy, Martin, Jobanputra, Paresh, Bacon, Pauline, Smith, Jacqueline, Richardson, Ann, Giancola, Giorgio, Soh, Vicky, Spencer, Simon, Greenhalgh, Ann, Hanson, Mark, De Lord, Denise, Lloyd, Mark, Wong, Henna, Wren, Damian, Grover, Bob, Hall, John, Neville, Cai, Alton, Peter, Kelly, Stephen, Bombardieri, Michele, Humby, Fran, Ng, Nora, Di Cicco, Maria, Hands, Rebecca, Epis, Oscar, Filer, Andrew, Buckley, Christopher, McInnes, Iain, Taylor, Peter, Pitzalis, Costantino, Freeston, Jane, Conaghan, Philip, Grainger, Andrew, O'Connor, Philip J., Evans, Rob, Emery, Paul, Hodgson, Richard, Fleischmann, Roy, Han, Chenglong, van der Heijde, Desiree, Xu, Weichun, Hsia, Elizabeth, Kavanaugh, Arthur, Gladman, Dafna, Chattopadhyay, Chandrabhusan, Beutler, Anna, Zayat, Ahmed S., Ellegard, Karen, Terslev, Lene, Wakefield, Richard J., Ciurtin, Coziana, Leandro, Maria, Dey, Dzifa, Nandagudi, Anupama, Giles, Ian, Shipley, Mike, Morris, Vanessa, Ioannou, John, Ehrenstein, Michael, Sen, Debajit, Chan, Marian, Quinlan, Tim M., Brophy, Richard, Mewar, Devesh, Patel, Dipti, Wilby, M. J., Pellegrini, Vincent, Eyes, Brian, Crooks, Daniel, Anderson, Marina, Ball, Elisabeth, McKeeman, Helen, Burns, James, Yau, Wing Hoi, Moore, Owen, Foo, Joanne, Benson, Claire, Patterson, Chris, Wright, Gary, Taggart, Allister, Drew, Sarah, Tanner, Lorraine, Sanyal, Kaushik, Bourke, Brian E., Alston, Claire, Baqai, Charlotte, Chard, Michael, Sandhu, Virinderjit, Jordan, Kelsey, Munns, Catherine, Zouita, Louisa, Shattles, Warren, Davies, Ursula, Makadsi, Raad, Griffith, Sian, Kiely, Patrick D., Dimofte, Ionela, Dabu, Mihaela, Dabu, Bogdan, Dobarro, David, Schreiber, Benjamin E., Warrell, Clare, Handler, Clive, Coghlan, Gerry, Denton, Chris, Ishorari, Jasmine, Bunn, Chris, Beynon, Huw, George Malal, Joby J., Boton-Maggs, Ben, Leung, Alexander, Farewell, Daniel, Choy, Ernest, Gullick, Nicola J., Choy, Ernest H., Wincup, Chris, Fisher, Ben, Charles, Peter, Pollard, Louise C., Kirkham, Bruce W., Ma, Margaret H., Ramanujan, Saroja, Cavet, Guy, Haney, Doug, Kingsley, Gabrielle H., Scott, David, Cope, Andrew, Singh, Animesh, Wilson, Jo, Isaacs, Anthony, Wing, Charlotte, McLaughlin, Maeve, Penn, Henry, Genovese, Mark C., Sebba, Anthony, Rubbert-Roth, Andrea, Scali, Juan, Zilberstein, Moshe, Thompson, Liz, Van Vollenhoven, Ronald, De Benedetti, Fabrizio, Brunner, Hermine, Allen, Roger, Brown, Diane, Chaitow, Jeffrey, Pardeo, Manuela, Espada, Graciela, Flato, Berit, Horneff, Gerd, Devlin, Clare, Kenwright, Andrew, Schneider, Rayfel, Woo, Patricia, Martini, Alberto, Lovell, Daniel, Ruperto, Nicola, John, Holly, Hale, Elizabeth D., Treharne, Gareth J., Carroll, Douglas, Mercer, Louise, Low, Audrey, Galloway, James, Watson, Kath, Lunt, Mark, Symmons, Deborah, Davies, Rebecca, Dixon, William, Balarajah, Sharmili, Sandhu, Amrita, Ariyo, Mercy, Rankin, Elizabeth, Sandoo, Aamer, van Zanten, Jet J. Veldhuijzen, Toms, Tracey E., Smith, Jacqueline P., Malik, Saadia, Toberty, Elizabeth, Thalayasingam, Nishanthi, Hamilton, Jennifer, Kelly, Clive, Puntis, Daniel, Saravanan, Vadivelu, Rynne, Martin, Heycock, Carol, Winter, Richard, Wardle, Phil, Toms, Tracey, Cadman, Susan, Nightingale, Peter, Kitas, George, Alhusain, Awal Z., Verstappen, Suzanne M., Mirjafari, Hoda, Charlton-Menys, Valentine, Bunn, Diane, Durrington, Paul, Cooney, Jennifer K., Moore, Jonathan P., Lemmey, Andrew, Jones, Jeremy G., Maddison, Peter J., Ahmad, Yasmeen A., Ahmed, Tazeen J., Leone, Francesca, Browne, Hannah K., Wig, Surabhi, Chevance, Aurelie, Moore, Tonia, Manning, Joanne, Vail, Andy, Herrick, Ariane L., Derrett-Smith, Emma, Hoyles, Rachel, Moinzadeh, Pia, Chighizola, Cecilia, Khan, Korsa, Abraham, David, Warrell, Clare E., Sykes, Rebecca, Muir, Lindsay, Ennis, Holly, Shiwen, Xu, Thompson, Katherine, Liu, Shangxi, Leask, Andrew, Abraham, David J., Strickland, Gemma, Pauling, John, Betteridge, Zoe, Dunphy, Juliet, Owen, Pat, McHugh, Neil, Abignano, Giuseppina, Cuomo, Giovanna, Buch, Maya H., Rosenberg, William M., Valentini, Gabriele, Del Galdo, Francesco, Jenkins, Jessica, Pauling, John D., Howell, Kevin, Nihtyanova, Svetlana, Fonseca, Carmen, Malaviya, Anshuman P., Hadjinicolaou, Andreas V., Nisar, Muhammad K., Ruddlesden, Michael, Furlong, Anita, Baker, Sharon, Hall, Frances C., Raut-Roy, Dominique, Peluso, Rosario, Dario Di Minno, M. N., Iervolino, Salvatore, Costa, Luisa, Atteno, Mariangela, Lofrano, Mariana, Soscia, Ernesto, Castiglione, Fabiana, Foglia, Francesca, Scarpa, Raffaele, Wallis, Dinny, Dougados, Maxime, Keystone, Edward, Heckaman, Michele, Mease, Philip, Landewé, Robert, Nguyen, Dianne, Winfield, Rachel A., Dyke, Claire, Clemence, Mark, Mackay, Kirsten, Haywood, Kirstie L., Packham, Jon, Jordan, Kelvin P., Davies, Helen, Brophy, Sinead, Irvine, Elizabeth, Cooksey, Roxanne, Dennis, Michael S., Siebert, Stefan, Ibrahim, Fowzia, Krueger, Gerald, Gathany, Tim, Mudivarthy, Surekha, Mack, Michael, Tandon, Neeta, Sieper, Joachim, Braun, Jürgen, van der Heijde, Désirée, Isaacs, John, Dahmen, Georg, Wollenhaupt, Jürgen, Schulze-Koops, Hendrik, Gsteiger, Sandro, Bertolino, Arthur, Hueber, Wolfgang, Tak, Paul P., Cohen, Carla J., Karaderi, Tugce, Pointon, Jennifer J., Wordsworth, Bryan P., Keidel, Sarah, Farrar, Claire, Appleton, Louise H., Adshead, Rebecca, Tahir, Hasan, Greenwood, Mandy, Donnelly, Simon P., Wajed, Julekha, Kirkham, Bruce, Backhouse, Michael R., Vinall, Karen A., Redmond, Anthony, Helliwell, Philip, Keenan, Anne-Maree, Dale, Rebecca M., Thomas, Amanda, Aronson, Diane, Turner-Cobb, Julie, Sengupta, Raj, France, Brisa, Hill, Ingrid, Flurey, Caroline A., Morris, Marianne, Pollock, Jon, Hughes, Rod, Richards, Pam, Hewlett, Sarah, Ryan, Sarah, Lille, Kate, Adams, Jo, Haq, Inam, McArthur, Margaret, Goodacre, Lynne, Birt, Linda, Wilson, Oonagh, Kirwan, John, Dures, Emma, Quest, Enid, Rajak, Rizwan, Thomas, Tasmin, Lawson, Tom, Petford, Sharon, Hale, Elizabeth, Kitas, George D., Gooberman-Hill, Rachael, Jinks, Clare, Dziedzic, Krysia, Bouças, Sofia Barbosa, Hislop, Kelly, Rhodes, Carol, Ali, Fizzah, Ong, Bie Nio, White, Derrick, Hensor, Elizabeth, Ferguson, Anna M., Douiri, Abdel, Scott, David L., Lempp, Heidi, Halls, Serena, Law, Rebecca-Jane, Jones, Jeremy, Markland, David, Maddison, Peter, Thom, Jeanette, Thom, Jeanette M., Breslin, Anne, Kraus, Alexandra, Gordhan, Chandrika, Dennis, Sean, Connor, John, Chowdhary, Bhavani, Lottay, Neena, Juneja, Parmjit, Bacon, Paul A., Isaacs, David, Jack, James, Keller, Majella, Tibble, Jeremy, Hammond, Alison, Gill, Rachel, Tyson, Sarah, Tennant, Alan, Nordenskiold, Ulla, Pease, Emily E., Pease, Colin T., Trehane, Anne, Rahmeh, Fouz, Cornell, Patricia, Westlake, Sarah L., Rose, Katy, Alber, Catherine Fouad, Watson, Liam, Stratton, Richard, Lazarus, Mark, McNeilly, Natasha E., Waterfield, Jackie, Hurley, Mike, Greenwood, James, Clayton, Ann M., Lynch, Michael, Clewes, Adrian, Dawson, Julie, Abernethy, Veronica, Griffiths, Ann E., Chamberlain, Victoria A., McLoughlin, YokeMei, Campbell, Sophie, Hayes, Janita, Moffat, Claire, McKenna, Frank, Shah, Preeti, Williams, Ann, Rhys-Dillon, Ceril, Goodfellow, Rhian, Martin, James C., Bari, Farhan, Hughes, Gwenan, Thomas, Eleri, Baker, Sarah, Collins, David, Price, Elizabeth, Williamson, Lyn, Dunkley, Lisa, Youll, Matthew J., Rodziewicz, Mia, Reynolds, John A., Berry, Jacqueline, Pavey, Chee, Hyrich, Kimme, Gorodkin, Rachel, Wilkinson, Kate, Bruce, Ian, Barton, Anne, Silman, Alan, Ho, Pauline, Cornell, Tricia, Richards, Selwyn, Holmes, A., Parker, S., Smith, H., Briggs, N., Arthanari, S., Nisar, M., Thwaites, Catharine, Kamath, Sanjeet, Price, Shyra, Robinson, Sandra M., Walker, David, Coop, Hazel, Al-Allaf, Wahab, Charleton, Rebecca C., Griffiths, Bridget, Edwards, Elizabeth A., Partlett, Rosamund, Martin, Keith, Tarzi, Mike, Panthakalam, Sathianathan, Freeman, Tanya, Ainley, Louise, Turner, Michael, Hughes, Lyndsay, Russell, Bridget, Jenkins, Suzanne, Done, John, Young, Adam, Jones, Tadeusz, Gaywood, Ian C., Pande, Ira, Pradère, Marie-Josèphe, Bhaduri, Mahua, Smith, Angela, Cook, Haley, Abraham, Sonya, Ngcozana, Tanaka, Denton, Christopher P., Parker, Louise, Black, Carol M., Ong, Voon, Thompson, Nicola, White, Catherine, Duddy, Martin, Jobanputra, Paresh, Bacon, Pauline, Smith, Jacqueline, Richardson, Ann, Giancola, Giorgio, Soh, Vicky, Spencer, Simon, Greenhalgh, Ann, Hanson, Mark, De Lord, Denise, Lloyd, Mark, Wong, Henna, Wren, Damian, Grover, Bob, Hall, John, Neville, Cai, Alton, Peter, Kelly, Stephen, Bombardieri, Michele, Humby, Fran, Ng, Nora, Di Cicco, Maria, Hands, Rebecca, Epis, Oscar, Filer, Andrew, Buckley, Christopher, McInnes, Iain, Taylor, Peter, Pitzalis, Costantino, Freeston, Jane, Conaghan, Philip, Grainger, Andrew, O'Connor, Philip J., Evans, Rob, Emery, Paul, Hodgson, Richard, Fleischmann, Roy, Han, Chenglong, van der Heijde, Desiree, Xu, Weichun, Hsia, Elizabeth, Kavanaugh, Arthur, Gladman, Dafna, Chattopadhyay, Chandrabhusan, Beutler, Anna, Zayat, Ahmed S., Ellegard, Karen, Terslev, Lene, Wakefield, Richard J., Ciurtin, Coziana, Leandro, Maria, Dey, Dzifa, Nandagudi, Anupama, Giles, Ian, Shipley, Mike, Morris, Vanessa, Ioannou, John, Ehrenstein, Michael, Sen, Debajit, Chan, Marian, Quinlan, Tim M., Brophy, Richard, Mewar, Devesh, Patel, Dipti, Wilby, M. J., Pellegrini, Vincent, Eyes, Brian, Crooks, Daniel, Anderson, Marina, Ball, Elisabeth, McKeeman, Helen, Burns, James, Yau, Wing Hoi, Moore, Owen, Foo, Joanne, Benson, Claire, Patterson, Chris, Wright, Gary, Taggart, Allister, Drew, Sarah, Tanner, Lorraine, Sanyal, Kaushik, Bourke, Brian E., Alston, Claire, Baqai, Charlotte, Chard, Michael, Sandhu, Virinderjit, Jordan, Kelsey, Munns, Catherine, Zouita, Louisa, Shattles, Warren, Davies, Ursula, Makadsi, Raad, Griffith, Sian, Kiely, Patrick D., Dimofte, Ionela, Dabu, Mihaela, Dabu, Bogdan, Dobarro, David, Schreiber, Benjamin E., Warrell, Clare, Handler, Clive, Coghlan, Gerry, Denton, Chris, Ishorari, Jasmine, Bunn, Chris, Beynon, Huw, George Malal, Joby J., Boton-Maggs, Ben, Leung, Alexander, Farewell, Daniel, Choy, Ernest, Gullick, Nicola J., Choy, Ernest H., Wincup, Chris, Fisher, Ben, Charles, Peter, Pollard, Louise C., Kirkham, Bruce W., Ma, Margaret H., Ramanujan, Saroja, Cavet, Guy, Haney, Doug, Kingsley, Gabrielle H., Scott, David, Cope, Andrew, Singh, Animesh, Wilson, Jo, Isaacs, Anthony, Wing, Charlotte, McLaughlin, Maeve, Penn, Henry, Genovese, Mark C., Sebba, Anthony, Rubbert-Roth, Andrea, Scali, Juan, Zilberstein, Moshe, Thompson, Liz, Van Vollenhoven, Ronald, De Benedetti, Fabrizio, Brunner, Hermine, Allen, Roger, Brown, Diane, Chaitow, Jeffrey, Pardeo, Manuela, Espada, Graciela, Flato, Berit, Horneff, Gerd, Devlin, Clare, Kenwright, Andrew, Schneider, Rayfel, Woo, Patricia, Martini, Alberto, Lovell, Daniel, Ruperto, Nicola, John, Holly, Hale, Elizabeth D., Treharne, Gareth J., Carroll, Douglas, Mercer, Louise, Low, Audrey, Galloway, James, Watson, Kath, Lunt, Mark, Symmons, Deborah, Davies, Rebecca, Dixon, William, Balarajah, Sharmili, Sandhu, Amrita, Ariyo, Mercy, Rankin, Elizabeth, Sandoo, Aamer, van Zanten, Jet J. Veldhuijzen, Toms, Tracey E., Smith, Jacqueline P., Malik, Saadia, Toberty, Elizabeth, Thalayasingam, Nishanthi, Hamilton, Jennifer, Kelly, Clive, Puntis, Daniel, Saravanan, Vadivelu, Rynne, Martin, Heycock, Carol, Winter, Richard, Wardle, Phil, Toms, Tracey, Cadman, Susan, Nightingale, Peter, Kitas, George, Alhusain, Awal Z., Verstappen, Suzanne M., Mirjafari, Hoda, Charlton-Menys, Valentine, Bunn, Diane, Durrington, Paul, Cooney, Jennifer K., Moore, Jonathan P., Lemmey, Andrew, Jones, Jeremy G., Maddison, Peter J., Ahmad, Yasmeen A., Ahmed, Tazeen J., Leone, Francesca, Browne, Hannah K., Wig, Surabhi, Chevance, Aurelie, Moore, Tonia, Manning, Joanne, Vail, Andy, Herrick, Ariane L., Derrett-Smith, Emma, Hoyles, Rachel, Moinzadeh, Pia, Chighizola, Cecilia, Khan, Korsa, Abraham, David, Warrell, Clare E., Sykes, Rebecca, Muir, Lindsay, Ennis, Holly, Shiwen, Xu, Thompson, Katherine, Liu, Shangxi, Leask, Andrew, Abraham, David J., Strickland, Gemma, Pauling, John, Betteridge, Zoe, Dunphy, Juliet, Owen, Pat, McHugh, Neil, Abignano, Giuseppina, Cuomo, Giovanna, Buch, Maya H., Rosenberg, William M., Valentini, Gabriele, Del Galdo, Francesco, Jenkins, Jessica, Pauling, John D., Howell, Kevin, Nihtyanova, Svetlana, Fonseca, Carmen, Malaviya, Anshuman P., Hadjinicolaou, Andreas V., Nisar, Muhammad K., Ruddlesden, Michael, Furlong, Anita, Baker, Sharon, Hall, Frances C., Raut-Roy, Dominique, Peluso, Rosario, Dario Di Minno, M. N., Iervolino, Salvatore, Costa, Luisa, Atteno, Mariangela, Lofrano, Mariana, Soscia, Ernesto, Castiglione, Fabiana, Foglia, Francesca, Scarpa, Raffaele, Wallis, Dinny, Dougados, Maxime, Keystone, Edward, Heckaman, Michele, Mease, Philip, Landewé, Robert, Nguyen, Dianne, Winfield, Rachel A., Dyke, Claire, Clemence, Mark, Mackay, Kirsten, Haywood, Kirstie L., Packham, Jon, Jordan, Kelvin P., Davies, Helen, Brophy, Sinead, Irvine, Elizabeth, Cooksey, Roxanne, Dennis, Michael S., Siebert, Stefan, Ibrahim, Fowzia, Krueger, Gerald, Gathany, Tim, Mudivarthy, Surekha, Mack, Michael, Tandon, Neeta, Sieper, Joachim, Braun, Jürgen, van der Heijde, Désirée, Isaacs, John, Dahmen, Georg, Wollenhaupt, Jürgen, Schulze-Koops, Hendrik, Gsteiger, Sandro, Bertolino, Arthur, Hueber, Wolfgang, Tak, Paul P., Cohen, Carla J., Karaderi, Tugce, Pointon, Jennifer J., Wordsworth, Bryan P., Keidel, Sarah, Farrar, Claire, Appleton, Louise H., Adshead, Rebecca, Tahir, Hasan, Greenwood, Mandy, Donnelly, Simon P., Wajed, Julekha, and Kirkham, Bruce

Abstract

Background: Foot surgery is common in patients with RA but research into surgical outcomes is limited and conceptually flawed as current outcome measures lack face validity: to date no one has asked patients what is important to them. This study aimed to determine which factors are important to patients when evaluating the success of foot surgery in RA Methods: Semi structured interviews of RA patients who had undergone foot surgery were conducted and transcribed verbatim. Thematic analysis of interviews was conducted to explore issues that were important to patients. Results: 11 RA patients (9 ♂, mean age 59, dis dur = 22yrs, mean of 3 yrs post op) with mixed experiences of foot surgery were interviewed. Patients interpreted outcome in respect to a multitude of factors, frequently positive change in one aspect contrasted with negative opinions about another. Overall, four major themes emerged. Function: Functional ability & participation in valued activities were very important to patients. Walking ability was a key concern but patients interpreted levels of activity in light of other aspects of their disease, reflecting on change in functional ability more than overall level. Positive feelings of improved mobility were often moderated by negative self perception ("I mean, I still walk like a waddling duck”). Appearance: Appearance was important to almost all patients but perhaps the most complex theme of all. Physical appearance, foot shape, and footwear were closely interlinked, yet patients saw these as distinct separate concepts. Patients need to legitimize these feelings was clear and they frequently entered into a defensive repertoire ("it's not cosmetic surgery; it's something that's more important than that, you know?”). Clinician opinion: Surgeons' post operative evaluation of the procedure was very influential. The impact of this appraisal continued to affect patients' lasting impression irrespective of how the outcome compared to their initial goals ("wh

Published
2017

211. Alterations to adipose tissue morphology during inflammatory arthritis is indicative of vasculopathology in DBA/1 mice

Author

Sime, Katie, Choy, Ernest H., and Williams, Anwen S.

Subjects
Inflammation, Male, vasculature, Adipose Tissue, White, Arthritis, Galectin 3, Macrophages, Adipose tissue, macrophage, Arthritis, Experimental, Disease Models, Animal, Mice, Adipose Tissue, Brown, Mice, Inbred DBA, perivascular adipose tissue, galectin-3, Animals, inflammatory arthritis, Research Paper, Signal Transduction
Abstract

The physiologic function of adipose tissue is altered by the host's inflammatory response; the implications for maintaining human health and regulating inflammation-associated disease progression are ill defined. However, this cannot be investigated in humans, therefore the use of animal models is required. With the aim to determine morphological and molecular alterations to perivascular and organ-associated adipose tissues during inflammatory arthritis, collagen-induced arthritis (CIA) was established in male DBA/1 mice. Emerging evidence from this study signposts CIA in the DBA/1 mouse as a model that is relevant to study the development and treatment of early cardiovascular pathology associated with inflammatory arthritis. Here, we show global morphological changes in adipose tissue and the thoracic aorta in animals induced with CIA compared with the non-immunized controls. In CIA, we concluded that the increased cell count in PVAT was, at least in part, caused by an ingress and/or expansion of macrophages that had a mixed phenotype. A substantial increase of galectin-3 was expressed in PVAT from mice with CIA. Galectin-3 is elevated in the blood of patients with CVDs, however, it has never before been measured in PVAT in rodents or humans. Here, PVAT-associated galectin-3 is identified as a potential biomarker for detecting early vascular pathology in CIA and a promising candidate for translation to RA.

Published
2017

213. EULAR points to consider for the management of difficult-to-treat rheumatoid arthritis.

Author

Nagy, György, Roodenrijs, Nadia M. T., Welsing, Paco M. J., Kedves, Melinda, Hamar, Attila, van der Goes, Marlies C., Kent, Alison, Bakkers, Margot, Pchelnikova, Polina, Blaas, Etienne, Senolt, Ladislav, Szekanecz, Zoltan, Choy, Ernest H., Dougados, Maxime, Jacobs, Johannes W. G., Geenen, Rinie, Bijlsma, Johannes W. J., Zink, Angela, Aletaha, Daniel, and Schoneveld, Leonard

Subjects
RHEUMATOID arthritis treatment, RHEUMATOID arthritis diagnosis, HEPATITIS B, RESEARCH, RESEARCH methodology, HEPATITIS C, EVALUATION research, ANTIRHEUMATIC agents, COMPARATIVE studies, RHEUMATOID arthritis, DRUGS, SYMPTOMS, EXERCISE, PATIENT compliance, PATIENT education, COMORBIDITY, DISEASE complications
Abstract

Objective: To develop evidence-based European Alliance of Associations for Rheumatology (EULAR) points to consider (PtCs) for the management of difficult-to-treat rheumatoid arthritis (D2T RA).Methods: An EULAR Task Force was established comprising 34 individuals: 26 rheumatologists, patient partners and rheumatology experienced health professionals. Two systematic literature reviews addressed clinical questions around diagnostic challenges, and pharmacological and non-pharmacological therapeutic strategies in D2T RA. PtCs were formulated based on the identified evidence and expert opinion. Strength of recommendations (SoR, scale A-D: A typically consistent level 1 studies and D level 5 evidence or inconsistent studies) and level of agreement (LoA, scale 0-10: 0 completely disagree and 10 completely agree) of the PtCs were determined by the Task Force members.Results: Two overarching principles and 11 PtCs were defined concerning diagnostic confirmation of RA, evaluation of inflammatory disease activity, pharmacological and non-pharmacological interventions, treatment adherence, functional disability, pain, fatigue, goal setting and self-efficacy and the impact of comorbidities. The SoR varied from level C to level D. The mean LoA with the overarching principles and PtCs was generally high (8.4-9.6).Conclusions: These PtCs for D2T RA can serve as a clinical roadmap to support healthcare professionals and patients to deliver holistic management and more personalised pharmacological and non-pharmacological therapeutic strategies. High-quality evidence was scarce. A research agenda was created to guide future research. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

215. Remission and Rheumatoid Arthritis: Data on Patients Receiving Usual Care in Twenty-Four Countries

Author

Sokka, Tuulikki, Hetland, Merete Lund, Mäkinen, Heidi, Kautiainen, Hannu, Hørslev-Petersen, Kim, Luukkainen, Reijo K., Combe, Bernard, Badsha, Humeira, Drosos, Alexandros A., Devlin, Joe, Ferraccioli, Gianfranco, Morelli, Alessia, Hoekstra, Monique, Majdan, Maria, Sadkiewicz, Stefan, Belmonte, Miguel, Holmqvist, Ann-Carin, Choy, Ernest, Burmester, Gerd R., Tunc, Recep, Dimić, Aleksander, Nedović, Jovan, Stanković, Aleksandra, Bergman, Martin, Toloza, Sergio, and Pincus, Theodore

Published
2008

217. Effect of biologics and targeted synthetic disease-modifying anti-rheumatic drugs on fatigue in rheumatoid arthritis

Author

Choy, Ernest H

Subjects
rheumatoid arthritis, medicine.medical_specialty, Reviews, Disease, Antibodies, Monoclonal, Humanized, DMARDs, Arthritis, Rheumatoid, outcome measures, systematic review, Piperidines, Rheumatology, biologic therapies, Internal medicine, medicine, Humans, Pyrroles, Pharmacology (medical), Fatigue, Biological Products, Sulfonamides, Tofacitinib, business.industry, Confounding, medicine.disease, Clinical trial, Antirheumatic Agents, Sarilumab, Pyrimidines, Purines, Rheumatoid arthritis, Azetidines, Pyrazoles, Janus kinase, business
Abstract

Fatigue is a common and debilitating symptom in patients with RA. Since 2007, fatigue has been included as one of the core outcome measures in RA. Clinical trials of biologic DMARDs (bDMARDs) and targeted synthetic DMARDs (tsDMARDs) have included fatigue as a secondary endpoint. A Cochrane review in 2016 concluded that the bDMARDs have a moderate effect on improving fatigue in RA. More recent clinical trials of the new biologic agent sarilumab and the Janus kinase inhibitors tofacitinib and baricitinib showed similar benefits. It remains unclear whether the effect of bDMARDs and tsDMARDs on fatigue is mediated by direct effects or through a reduction in inflammation. As fatigue was a secondary endpoint, many analyses did not adjust for potential confounding factors, including pain, mood and anaemia, which is a significant limitation.

Published
2019

218. Synovial cellular and molecular signatures stratify clinical response to csDMARD therapy and predict radiographic progression in early rheumatoid arthritis patients

Author

Humby, Frances, Lewis, Myles, Ramamoorthi, Nandhini, Hackney, Jason A, Barnes, Michael R, Bombardieri, Michele, Setiadi, A. Francesca, Kelly, Stephen, Bene, Fabiola, DiCicco, Maria, Riahi, Sudeh, Rocher, Vidalba, Ng, Nora, Lazarou, Ilias, Hands, Rebecca, van der Heijde, Désirée, Landewé, Robert B M, van der Helm-van Mil, Annette, Cauli, Alberto, McInnes, Iain, Buckley, Christopher Dominic, Choy, Ernest H, Taylor, Peter C, Townsend, Michael J, Pitzalis, Costantino, Clinical Immunology and Rheumatology, and AII - Inflammatory diseases

Subjects
dmards (synthetic), inflammation, early rheumatoid arthritis, Rheumatoid Arthritis, synovitis
Abstract

Objectives To unravel the hierarchy of cellular/molecular pathways in the disease tissue of early, treatment-naïve rheumatoid arthritis (RA) patients and determine their relationship with clinical phenotypes and treatment response/outcomes longitudinally. Methods 144 consecutive treatment-naïve early RA patients ( Results Cellular and molecular analyses of synovial tissue demonstrated for the first time in early RA the presence of three pathology groups: (1) lympho-myeloid dominated by the presence of B cells in addition to myeloid cells; (2) diffuse-myeloid with myeloid lineage predominance but poor in B cells nd (3) pauci-immune characterised by scanty immune cells and prevalent stromal cells. Longitudinal correlation of molecular signatures demonstrated that elevation of myeloid- and lymphoid-associated gene expression strongly correlated with disease activity, acute phase reactants and DMARD response at 6 months. Furthermore, elevation of synovial lymphoid-associated genes correlated with autoantibody positivity and elevation of osteoclast-targeting genes predicting radiographic joint damage progression at 12 months. Patients with predominant pauci-immune pathology showed less severe disease activity and radiographic progression. Conclusions We demonstrate at disease presentation, prior to pathology modulation by therapy, the presence of specific cellular/molecular synovial signatures that delineate disease severity/progression and therapeutic response and may pave the way to more precise definition of RA taxonomy, therapeutic targeting and improved outcomes.

Published
2019

219. Clinical outcomes according to PD-L1 status and age in the prospective international SAUL study of atezolizumab (atezo) for locally advanced or metastatic urothelial carcinoma (UC) or non-UC of the urinary tract

Author

Sternberg, Cora N. Merseburger, Axel Stuart Choy, Ernest and Castellano, Daniel E. Lopez-Rios, Fernando James, Nicholas and Banna, Giuseppe Luigi De Giorgi, Ugo Masini, Cristina and Bamias, Aristotelis del Muro, Xavier Garcia Powles, Thomas and Duran, Ignacio Gedye, Craig Gamulin, Marija Zengerling, Friedemann Geczi, Lajos de Ducla, Sabine Fear, Simon and Loriot, Yohann

Published
2019

229. Nonserious Infections in Patients With Rheumatoid Arthritis: Results From the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis.

Author

Bechman, Katie, Halai, Kapil, Yates, Mark, Norton, Sam, Cope, Andrew P., Hyrich, Kimme L., Galloway, James B., Maiden, Nicola, Price, Tom, Hopkinson, Neil, O'Reilly, Sheila, Hordon, Lesley, Griffiths, Ian, Porter, Duncan, Capell, Hilary, Hassell, Andy, Benitha, Romela, Choy, Ernest, Walsh, David, and Emery, Paul

Subjects
THERAPEUTIC use of glucocorticoids, INFECTION risk factors, REPORTING of diseases, INTERLEUKINS, RITUXIMAB, SCIENTIFIC observation, CONFIDENCE intervals, AGE distribution, ANTI-inflammatory agents, BIOTHERAPY, INFECTION, RISK assessment, SEX distribution, RHEUMATOID arthritis, DESCRIPTIVE statistics, QUESTIONNAIRES, ADALIMUMAB, LONGITUDINAL method, PROPORTIONAL hazards models, COMORBIDITY, ETANERCEPT, CHEMICAL inhibitors
Abstract

Objective: To describe the frequency and predictors of nonserious infections (NSI) and compare incidence across biologic agents within the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis (BSRBR‐RA). Methods: The BSRBR‐RA is a prospective observational cohort study. An NSI was defined as an infection that did not require hospitalization or intravenous therapy. Infections were captured from clinician questionnaires and patient diaries. Individuals were considered "at risk" from the date of initiation of biologic treatment for up to 3 years. Drug exposure was defined by agent: tumor necrosis factor inhibitor (TNFi), interleukin‐6 (IL‐6) inhibitor, B cell depletion (rituximab), or conventional synthetic disease‐modifying antirheumatic drugs (csDMARDs) alone. A multiple‐failure Cox model was used with multivariable adjustment. Missing data were addressed using multiple imputation. Results: There were 17,304 NSI in 8,145 patients, with an event rate of 27.0 per person per year (95% confidence interval [95% CI] 26.6–27.4). Increasing age, female sex, comorbidity burden, glucocorticoid therapy, higher Disease Activity Score in 28 joints, and higher Health Assessment Questionnaire disability index were associated with an increased risk of NSI. There was a significant reduction in NSI risk with csDMARDs compared to biologic treatments. Compared to TNFi, IL‐6 inhibition and rituximab were associated with a higher NSI risk (adjusted hazard ratio 1.45 [95% CI 1.29–1.63] and adjusted hazard ratio 1.28 [95% CI 1.14–1.45], respectively), while the csDMARD cohort had a lower risk (adjusted hazard ratio 0.64 [95% CI 0.59–0.70]). Within the TNFi class, adalimumab was associated with a higher NSI risk than etanercept (adjusted hazard ratio 1.11 [95% CI 1.05–1.17]). Conclusion: NSI occur frequently in RA, and predictors mirror those reported with serious infections. All biologics are associated with a greater risk of NSI, with differences observed between agents. While unmeasured confounding must be considered, the magnitude of effect is large, and a relationship between NSI and targeted immunomodulatory therapy likely exists. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

230. Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Author

Heathfield, Sarah, Parker, Ben, Zeef, Leo, Bruce, Ian, Alexander, Yvonne, Collins, Fraser, Stone, Michael, Wang, Edward, Williams, Anwen S., Wright, Helen L., Thomas, Huw B., Moots, Robert J., Edwards, Steven W., Bullock, Craig, Chapman, Victoria, Walsh, David A., Mobasheri, Ali, Kendall, David, Kelly, Sara, Bayley, Rachel, Buckley, Chris D., Young, Stephen P., Rump-Goodrich, Lisa, Middleton, Jim, Chen, Liye, Fisher, Roman, Kollnberger, Simon, Shastri, Nilabh, Kessler, Benedikt M., Bowness, Paul, Nazeer Moideen, Abdul, Evans, Laura, Osgood, Louise, Jones, Simon A., Nowell, Mari A., Mahadik, Younis, Young, Stephen, Morgan, Matthew, Gordon, Caroline, Harper, Lorraine, Giles, Joanna L., Paul Morgan, B., Harris, Claire L., Rysnik, Oliwia J., McHugh, Kirsty, Payeli, Sravan, Marroquin, Osiris, Shaw, Jacqueline, Renner, Christoph, Nayar, Saba, Cloake, Tom, Bombardieri, Michele, Pitzalis, Costantino, Buckley, Chris, Barone, Francesca, Lane, Peter, Coles, Mark, Williams, Emma L., Edwards, Christopher J., Cooper, Cyrus, Oreffo, Richard O., Dunn, Sara, Crawford, Aileen, Wilkinson, Mark, Le Maitre, Christine, Bunning, Rowena, Daniels, Jodie, Phillips, Kate L. E., Chiverton, Neil, Le Maitre, Christine L., Shaw, Jackie, Ridley, Anna, Wong-Baeza, Isabel, Keidel, Sarah, Chan, Antoni, Gullick, Nicola J., Abozaid, Hanan S., Jayaraj, David M., Evans, Hayley G., Scott, David L., Choy, Ernest H., Taams, Leonie S., Hickling, M., Golor, G., Jullion, A., Shaw, S., Kretsos, K., Bari, Syed F., Rhys-Dillon, Brian, Amos, Nicholson, Siebert, Stefan, Bunning, Rowena D., Haddock, Gail, Cross, Alison K., Kate, I., Phillips, E., Cross, Alison, Bunning, Rowena A. D., Ceeraz, Sabrina, Spencer, Jo, Choy, Ernest, Corrigall, Valerie, Crilly, Anne, Palmer, Helen, Lockhart, John, Plevin, Robin, Ferrell, William R., McInnes, Iain, Hutchinson, David, Perry, Liz, DiCicco, Maria, Humby, Frances, Kelly, Stephen, Hands, Rebecca, McInnes, Ian, Taylor, Peter, Mehta, Puja, Mitchell, Adam, Tysoe, Carolyn, Caswell, Richard, Owens, Martina, Vincent, Tonia, Hashmi, Tahir M., Price-Forbes, Alec, Sharp, Charlotte A., Murphy, Helen, Wood, Elizabeth F., Doherty, Teresa, Sheldon, Jo, Sofat, Nidhi, Goff, Iain, Platt, Philip N., Abdulkader, Rita, Clunie, Gavin, Ismajli, Mediola, Nikiphorou, Elena, Young, Adam, Tugnet, Nicola, Dixey, Josh, Banik, Snehashish, Alcorn, Desmond, Hunter, John, Win Maw, Win, Patil, Pravin, Hayes, Fiona, Main Wong, Way, Borg, Frances A., Dasgupta, Bhaskar, Malaviya, Anshuman P., Ostor, Andrew J., Chana, Jasroop K., Ahmed, Azeem A., Edmonds, Sally, Coward, Lucy, Borg, Frances, Heaney, Jonathan, Amft, Nicole, Simpson, John, Dhillon, Veena, Ayalew, Yezenash, Khattak, Fazlihakim, Gayed, Mary, Amarasena, Roshan I., McKenna, Frank, Mc Laughlin, Maeve, Baburaj, Krishnan, Fattah, Zozik, Ng, Nora, Wilson, Jo, Colaco, Bernard, Williams, Mark R., Adizie, Tochukwu, Casey, Matthew, Lip, Stefanie, Tan, Shaun, Anderson, David, Robertson, Calum, Devanny, Ian, Field, Max, Walker, David, Robinson, Sandra, Ryan, Sarah, Hassell, Andrew, Bateman, James, Allen, Maggie, Davies, David, Crouch, Carina, Walker-Bone, Karen, Gainsborough, Nicola, Lutalo, Pamela M., Davies, Ursula M., Mckew, Jennifer R., Millar, Auleen M., Wright, Stephen A., Bell, Aubrey L., Thapper, Muryum, Roussou, Thalia, Cumming, Jo, Hull, Richard G., McKeogh, John, O'Connor, Mortimer B., Hassan, Ahmed I., Bond, Ursula, Swan, Joan, Phelan, Mark J., Coady, David, Kumar, Namita, Farrow, Luke, Bukhari, Marwan, Oldroyd, Alexander G., Greenbank, Cathi, McBeth, John, Duncan, Rosie, Brown, Deborah, Horan, Michael, Pendleton, Neil, Littlewood, Alison, Cordingley, Lis, Mulvey, Matthew, Curtis, Elizabeth M., Cole, Zoe A., Crozier, Sarah R., Georgia, Ntani, Robinson, Siân M., Godfrey, Keith M., Sayer, Avan A., Inskip, Hazel M., Harvey, Nicholas C., Davies, Rebecca, Mercer, Louise, Galloway, James, Low, Audrey, Watson, Kath, Lunt, Mark, Symmons, Deborah, Hyrich, Kimme, Chitale, Sarang, Estrach, Cristina, Goodson, Nicola J., Rankin, Elizabeth, Jiang, C. Q., Cheng, K. K., Lam, T. H., Adab, Peymané, Ling, Stephanie, Humphreys, Jennifer, Ellis, Corrinne, Bunn, Diane, Verstappen, Suzanne M., Fluess, Elisa, Macfarlane, Gary J., Bond, Christine, Jones, Gareth T., Scott, Ian C., Steer, Sophia, Lewis, Cathryn M., Cope, Andrew, Mulvey, Matthew R., Lovell, Karina, Keeley, Philip, Woby, Steve, Beasley, Marcus, Viatte, Sebastien, Plant, Darren, Fu, Bo, Solymossy, Csilla, Worthington, Jane, Barton, Anne, Williams, Frances M., Osei-Bordom, Daniel-Clement, Popham, Maria, MacGregor, Alex, Spector, Tim, Little, Jayne, Herrick, Ariane, Pushpakom, S., Ennis, H., McBurney, H., Worthington, J., Newman, W., Ibrahim, Ibrahim, Morgan, Anne, Wilson, Anthony, Isaacs, John, Sanderson, Tessa, Hewlett, Sarah, Calnan, Michael, Morris, Marianne, Raza, Karim, Kumar, Kanta, Cardy, Caroline M., Pauling, John D., Jenkins, Jessica, Brown, Sue J., McHugh, Neil, Mugford, Miranda, Davies, Charlotte, Cooper, Nicola, Brooksby, Alan, Dures, Emma, Ambler, Nick, Fletcher, Debbie, Pope, Denise, Robinson, Frances, Rooke, Royston, Gorman, Claire L., Reynolds, Piero, Hakim, Alan J., Bosworth, Ailsa, Weaver, Dan, Kiely, Patrick D., Skeoch, Sarah, Jani, Meghna, Amarasena, Roshan, Rao, Chandini, Macphie, Elizabeth, McLoughlin, Yokemei, Shah, Preeti, Else, Sara, Semenova, Olga, Thompson, Helen, Ogunbambi, Olabambo, Kallankara, Sathish, Patel, Yusuf, Baguley, Elaine, Halsey, John, Severn, Andrew, Selvan, Shilpa, Price, Elizabeth, Husain, Muhammad J., Brophy, Sinead, Phillips, Ceri J., Cooksey, Roxanne, Irvine, Elizabeth, Lendrem, Dennis, Mitchell, Sheryl, Bowman, Simon, Pease, Colin T., Emery, Paul, Andrews, Jacqueline, Sutcliffe, Nurhan, Lanyon, Peter, Gupta, Monica, McLaren, John, Regan, Marian, Cooper, Annie, Giles, Ian, Isenberg, David, Griffiths, Bridget, Foggo, Heather, Edgar, Suzanne, Vadivelu, Saravanan, Ng, Wan-Fai, Iqbal, Itrat, Heron, Louise, Pilling, Claire, Marks, Jonathan, Hull, Richard, Ledingham, Jo, Han, Chenglong, Gathany, Tim, Tandon, Neeta, Hsia, Elizabeth, Taylor, P., Strand, V., Sensky, T., Harta, N., Fleming, S., Kay, Lesley, Rutherford, Michelle, Nicholl, Karl, Eyre, Tracey, Wilson, Gillian, Johnson, Phil, Russell, M., Timoshanko, J., Duncan, G., Spandley, A., Roskell, S., West, Louise, Adshead, Rebecca, Donnelly, Simon P., Ashton, Simon, Tahir, Hasan, Patel, Dipti, Darroch, James, Boulton, John, Ellis, Benjamin, Finlay, Ron, Murray-Brown, William, Priori, R., Tappuni, T., Vartoukian, S., Seoudi, N., Picarelli, G., Fortune, F., Valesini, G., Pitzalis, C., Bombardieri, M., Ball, Elisabeth, Rooney, Madeleine, Bell, Aubrey, Mérida, Angeles Acosta, Tarelli, Edward, Axford, John, Pericleous, Charis, Pierangeli, Silvia S., Ioannou, John, Rahman, Anisur, Alavi, Azita, Hughes, Michael, Evans, Bronwen, Zaki, Awal, Hui, Michelle, Garner, Rozeena, Rees, Frances, Bavakunji, Riaz, Daniel, Priya, Varughese, Sneha, Srikanth, Asha, Andres, Mariano, Pearce, Fiona, Leung, Jansen, Lim, Ken, Oomatia, Amin, Petri, Michelle, Fang, Hong, Birnbaum, Julius, Amissah-Arthur, Maame, Stewart, Kirsty, Jennens, Hannah, Braude, Simon, Sutton, Emily J., Watson, Kath D., Yee, Chee-Seng, Jayne, David, Akil, Mohammed, Ahmad, Yasmeen, D'Cruz, David, Khamashta, Munther, Teh, Lee-Suan, Zoma, Asad, Dey, Ida D., Kenu, Ernest, Garza-Garcia, Acely, Murfitt, Lucy, Driscoll, Paul C., Pierangeli, Silvia, Ioannou, Yiannis, Reynolds, John A., Ray, David W., O'Neill, Terence, Segeda, Iuliia, Shevchuk, Sergii, Kuvikova, Inna, Brown, Nina, Venning, Michael, Dhanjal, Mandish, Mason, Justin, Nelson-Piercy, Catherine, Basu, Neil, Paudyal, Priya, Stockton, Marie, Lawton, Sally, Dent, Caroline, Kindness, Kathy, Meldrum, Gillian, John, Elizabeth, Arthur, Catherine, West, Lucy, Macfarlane, Matthew V., Reid, David M., Yates, Max, Loke, Yoon, Watts, Richard, Christidis, Dimitrios, Williams, Mark, Sivakumar, Rajappa, Misra, Ramnath, Danda, Debashish, Mahendranath, K. M., Bacon, Paul A., and Mackie, Sarah L.

Abstract

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q < 0.00005). This was supported by qPCR analysis at 6 hrs (E-selectin and VCAM-1; 208.5 fold and 40.5, respectively above control) and also at 1, 3 and 24 hrs (E-selectin; 25.6, 93.5, 12.7 fold, respectively) (VCAM-1; 4.7, 47.2, 17.6 fold) (n = 3; p < 0.05). In contrast, HAoECs treated with TNF in combination with CZP exhibited control levels of E-selectin and VCAM-1 transcript (p > 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interest

Published
2017

233. Fibromyalgia and Chronic Pain Syndromes

Author

Arnold, Lesley M., Choy, Ernest, Clauw, Daniel J., Goldenberg, Don L., Harris, Richard E., Helfenstein, Milton, Jensen, Troels Staehelin, Noguchi, Koichi, Silverman, Stuart L., Ushida, Takahiro, and Wang, Guochun

Subjects
unified diagnostic guidelines, neuroimaging, Fibromyalgia, chronic widespread pain, interprofessional collaboration, Original Articles, central amplification, ComputingMethodologies_DOCUMENTANDTEXTPROCESSING, regulatory pathway, Humans, central sensitivity syndromes, Chronic Pain, central pain, sensory hypersensitivity
Abstract

Supplemental Digital Content is available in the text., This manuscript, developed by a group of chronic pain researchers and clinicians from around the world, aims to address the state of knowledge about fibromyalgia (FM) and identify ongoing challenges in the field of FM and other chronic pain syndromes that may be characterized by pain centralization/amplification/hypersensitivity. There have been many exciting developments in research studies of the pathophysiology and treatment of FM and related syndromes that have the potential to improve the recognition and management of patients with FM and other conditions with FM-like pain. However, much of the new information has not reached all clinicians, especially primary care clinicians, who have the greatest potential to use this new knowledge to positively impact their patients’ lives. Furthermore, there are persistent misconceptions about FM and a lack of consensus regarding the diagnosis and treatment of FM. This paper presents a framework for future global efforts to improve the understanding and treatment of FM and other associated chronic pain syndromes, disseminate research findings, identify ways to enhance advocacy for these patients, and improve global efforts to collaborate and reach consensus about key issues related to FM and chronic pain in general.

Published
2016

234. The role of interleukin-6 trans-signalling on cardiovascular dysfunction in inflammatory arthritis.

Author

Davies, Ruth, Williams, Jessica, Sime, Katie, Jin, Hyun-Sun, Thompson, Charlotte, Jordan, Lauren, Lang, Derek, Halcox, Julian P, Ellins, Elizabeth, Jones, Gareth W, Jones, Simon A, Rose-John, Stefan, Williams, Anwen, and Choy, Ernest

Subjects
INTERLEUKINS, BIOMARKERS, DISEASE progression, INFECTIOUS arthritis, SCIENTIFIC observation, CAROTID intima-media thickness, ANIMAL experimentation, MUSCLES, CROSS-sectional method, CARDIOVASCULAR diseases, CELLULAR signal transduction, ATHEROSCLEROSIS, DIAGNOSIS, MICE, LONGITUDINAL method, CHEMICAL inhibitors
Abstract

Objectives Cardiovascular (CV) mortality in RA patients is 50% higher than in the general population. There is increasing recognition that systemic inflammation is a major driver of this. IL-6 is implicated in cardiovascular disease (CVD) in the general population but its role in CVD in RA is undefined. Of the two modes of IL-6 signalling, trans-signalling is pro-inflammatory whereas classical signalling is linked with inflammation resolution. This study examines the role of IL-6 trans-signalling in CVD in a mouse model and patients with RA. Methods Myography determined the effect of IL-6 trans-signalling blockade, using sgp130Fc, on aortic constriction in murine collagen-induced arthritis. Serum CCL2 and sVCAM-1 as soluble biomarkers of sIL-6R trans-signalling were investigated in a human cross-sectional study. An observational longitudinal study investigated the association between these biomarkers and progression of subclinical atherosclerosis in early RA by measuring carotid intima-media thickness (CIMT). Results sgp130Fc reduced arthritis severity, serum CCL2 and sVCAM-1 and restored vascular function in collagen-induced arthritis (CIA). In established RA, sVCAM-1 correlated with the 28-joint DAS (DAS28) and CV risk. In early RA, baseline DAS28 was associated with CIMT change at 6 months. CIMT 'rapid progressors' at 12 months had higher baseline sVCAM-1, haemoglobin A1c, cholesterol:high-density lipoprotein cholesterol ratio and LDL cholesterol. Conclusions IL-6 trans-signalling plays a pivotal role in vascular dysfunction in CIA. In early RA, sVCAM-1 was associated with progression of subclinical atherosclerosis. Inflammation from RA onset in CVD-susceptible individuals may accelerate atherosclerosis. IL-6 trans-signalling blockade may be beneficial to RA patients and perhaps for atherosclerosis in the general population. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

235. Survey of physician experiences and perceptions about the diagnosis and treatment of fibromyalgia

Author

Perrot Serge, Choy Ernest, Petersel Danielle, Ginovker Anna, and Kramer Erich

Subjects
Public aspects of medicine, RA1-1270
Abstract

Abstract Background Fibromyalgia (FM) is a condition characterized by widespread pain and is estimated to affect 0.5-5% of the general population. Historically, it has been classified as a rheumatologic disorder, but patients consult physicians from a variety of specialties in seeking diagnosis and ultimately treatment. Patients report considerable delay in receiving a diagnosis after initial presentation, suggesting diagnosis and management of FM might be a challenge to physicians. Methods A questionnaire survey of 1622 physicians in six European countries, Mexico and South Korea was conducted. Specialties surveyed included primary care physicians (PCPs; n=809) and equal numbers of rheumatologists, neurologists, psychiatrists and pain specialists. Results The sample included experienced doctors, with an expected clinical caseload for their specialty. Most (>80%) had seen a patient with FM in the last 2 years. Overall, 53% of physicians reported difficulty with diagnosing FM, 54% reported their training in FM was inadequate, and 32% considered themselves not knowledgeable about FM. Awareness of American College of Rheumatology classification criteria ranged from 32% for psychiatrists to 83% for rheumatologists. Sixty-four percent agreed patients found it difficult to communicate FM symptoms, and 79% said they needed to spend more time to identify FM. Thirty-eight percent were not confident in recognizing the symptoms of FM, and 48% were not confident in differentiating FM from conditions with similar symptoms. Thirty-seven percent were not confident developing an FM treatment plan, and 37% were not confident managing FM patients long-term. In general, rheumatologists reported least difficulties/greatest confidence, and PCPs and psychiatrists reported greatest difficulties/least confidence. Conclusions Diagnosis and managing FM is challenging for physicians, especially PCPs and psychiatrists, but other specialties, including rheumatologists, also express difficulties. Improved training in FM and initiatives to improve patient-doctor communication are needed and may help the management of this condition.

Published
2012
Full Text
View/download PDF

236. Patients with fibromyalgia display less functional connectivity in the brain’s pain inhibitory network

Author

Jensen Karin B, Loitoile Rita, Kosek Eva, Petzke Frank, Carville Serena, Fransson Peter, Marcus Hanke, Williams Steven CR, Choy Ernest, Mainguy Yves, Vitton Olivier, Gracely Richard H, Gollub Randy, Ingvar Martin, and Kong Jian

Subjects
Pathology, RB1-214
Abstract

Abstract Background There is evidence for augmented processing of pain and impaired endogenous pain inhibition in Fibromyalgia syndrome (FM). In order to fully understand the mechanisms involved in FM pathology, there is a need for closer investigation of endogenous pain modulation. In the present study, we compared the functional connectivity of the descending pain inhibitory network in age-matched FM patients and healthy controls (HC). We performed functional magnetic resonance imaging (fMRI) in 42 subjects; 14 healthy and 28 age-matched FM patients (2 patients per HC), during randomly presented, subjectively calibrated pressure pain stimuli. A seed-based functional connectivity analysis of brain activity was performed. The seed coordinates were based on the findings from our previous study, comparing the fMRI signal during calibrated pressure pain in FM and HC: the rostral anterior cingulate cortex (rACC) and thalamus. Results FM patients required significantly less pressure (kPa) to reach calibrated pain at 50 mm on a 0–100 visual analogue scale (p Conclusion Patients with FM displayed less connectivity within the brain’s pain inhibitory network during calibrated pressure pain, compared to healthy controls. The present study provides brain-imaging evidence on how brain regions involved in homeostatic control of pain are less connected in FM patients. It is possible that the dysfunction of the descending pain modulatory network plays an important role in maintenance of FM pain and our results may translate into clinical implications by using the functional connectivity of the pain modulatory network as an objective measure of pain dysregulation.

Published
2012
Full Text
View/download PDF

237. Influence of co-morbid fibromyalgia on disease activity measures and response to tumour necrosis factor inhibitors in axial spondyloarthritis: results from a UK national register

Author

Macfarlane, Gary J, MacDonald, Ross I R, Pathan, Ejaz, Siebert, Stefan, Gaffney, Karl, Choy, Ernest, Packham, Jon, Martin, Kathryn R, Haywood, Kirstie, Sengupta, Raj, Atzeni, Fabiola, and Jones, Gareth T

Subjects
Adult, Male, disease register, response, Fibromyalgia, United Nations, Tumor Necrosis Factor-alpha, axial spondyloarthritis, Clinical Science, Middle Aged, Severity of Illness Index, Treatment Outcome, Antirheumatic Agents, Spondylarthritis, cohort study, outcome, Humans, epidemiology, Female, biologic therapy, Registries, co-morbidity, disease activity, Axial spondyloarthritis, Biologic therapy, Co-morbidity, Cohort study, Disease activity, Disease register, Epidemiology, Outcome, Response, Aged
Abstract

Objective:\ud \ud To quantify the extent to which co-morbid FM is associated with higher disease activity, worse quality of life (QoL) and poorer response to TNF inhibitors (TNFis) in patients with axial SpA.\ud Methods:\ud \ud A prospective study recruiting across 83 centres in the UK. Clinical information and patient-reported measures were available, including 2011 criteria for FM. Multivariable linear regression was used to model the effect of meeting the FM criteria on disease activity, QoL and response to TNFis.\ud Results:\ud \ud A total of 1757 participants were eligible for analyses, of whom 22.1% met criteria for FM. Those with co-morbid FM criteria had higher disease activity [BASDAI average difference FM+ − FM− 1.04 (95% CI 0.75, 1.33)] and worse QoL [Ankylosing Spondylitis Quality of Life score difference 1.42 (95% CI 0.88, 1.96)] after adjusting for demographic, clinical and lifestyle factors. Among 291 participants who commenced biologic therapy, BASDAI scores in those with co-morbid FM were 2.0 higher at baseline but decreased to 1.1 higher at 12 months. There was no significant difference in the likelihood of meeting Assessment of SpondyloArthritis international Society 20 criteria at 12 months. Less improvement in disease activity and QoL over 3 months of TNFi therapy was most strongly related to high scores on the FM criteria symptom severity scale component.\ud Conclusion:\ud \ud Fulfilling criteria for FM has a modest impact on the assessment of axial SpA disease activity and QoL and does not significantly influence response to biologic therapy. Those with a high symptom severity scale on FM assessment may benefit from additional specific management for FM.

Published
2018

238. Influence of co-morbid fibromyalgia on disease activity measures and response to TNF inhibitors in axial spondyloarthritis : results from a UK national register

Author

Macfarlane, Gary J., MacDonald, Ross I. R., Pathan, Ejaz, Siebert, Stefan, Gaffney, Karl, Choy, Ernest, Packham, Jon, Martin, Kathryn R., Haywood, Kirstie L., Sengupta, Raj, Atzeni, Fabiola, and Jones, Gareth T.

Subjects
RC
Abstract

Objective \ud \ud To quantify the extent to which co-morbid fibromyalgia (FM) is associated with higher disease activity, worse quality of life and poorer response to TNF inhibition (TNFi) in patients with axSpa.\ud \ud Method\ud \ud A prospective study recruiting across 83 centres in the United Kingdom. Clinical information and patient reported measures were available, including 2011 criteria for FM. Multivariable linear regression was used to model the effect of meeting the FM criteria on disease activity, quality of life and response to TNFi.\ud \ud Results \ud \ud 1757 participants were eligible for analyses of whom 22.1% met criteria for FM. Those with comorbid FM criteria had higher disease activity (BASDAI average difference FM+ve - FM-ve 1.04; 95% CI 0.75, 1.33) and worse quality of life (ASQoL difference 1.42; 95% CI 0.88, 1.96) after adjusting for demographic, clinical and lifestyle factors. Amongst 291 participants who commenced biologic therapy, higher BASDAI scores in those with co-morbid FM reduced from 2.0 at baseline to 1.1 at 12 months and there was only a 3% difference (not significant) in likelihood of meeting ASAS20 criteria at 12 months. Less improvement in disease activity and quality of life over three months of TNFi therapy was most strongly related to high scores on the FM criteria symptom severity (SSS) component.\ud \ud Conclusion \ud \ud Fulfilling criteria for FM has a modest impact on assessment of axSpa disease activity and quality of life, and does not significantly influence response to biologic therapy. Those with high SSS on FM assessment, may benefit from specific management for FM.\ud

Published
2018

243. Synovial tissue signatures enhance clinical classification and prognostic/treatment response algorithms in early inflammatory arthritis and predict requirement for subsequent biological therapy: results from the pathobiology of early arthritis cohort (PEAC)

Author

Lliso-Ribera, Gloria, primary, Humby, Frances, additional, Lewis, Myles, additional, Nerviani, Alessandra, additional, Mauro, Daniele, additional, Rivellese, Felice, additional, Kelly, Stephen, additional, Hands, Rebecca, additional, Bene, Fabiola, additional, Ramamoorthi, Nandhini, additional, Hackney, Jason A, additional, Cauli, Alberto, additional, Choy, Ernest H, additional, Filer, Andrew, additional, Taylor, Peter C, additional, McInnes, Iain, additional, Townsend, Michael J, additional, and Pitzalis, Costantino, additional

Published
2019
Full Text
View/download PDF

244. Group cognitive–behavioural programme to reduce the impact of rheumatoid arthritis fatigue: the RAFT RCT with economic and qualitative evaluations

Author

Hewlett, Sarah, primary, Almeida, Celia, additional, Ambler, Nicholas, additional, Blair, Peter S, additional, Choy, Ernest, additional, Dures, Emma, additional, Hammond, Alison, additional, Hollingworth, William, additional, Kadir, Bryar, additional, Kirwan, John, additional, Plummer, Zoe, additional, Rooke, Clive, additional, Thorn, Joanna, additional, Turner, Nicholas, additional, and Pollock, Jonathan, additional

Published
2019
Full Text
View/download PDF

245. Molecular Portraits of Early Rheumatoid Arthritis Identify Clinical and Treatment Response Phenotypes

Author

Lewis, Myles J., primary, Barnes, Michael R., additional, Blighe, Kevin, additional, Goldmann, Katriona, additional, Rana, Sharmila, additional, Hackney, Jason A., additional, Ramamoorthi, Nandhini, additional, John, Christopher R., additional, Watson, David S., additional, Kummerfeld, Sarah K., additional, Hands, Rebecca, additional, Riahi, Sudeh, additional, Rocher-Ros, Vidalba, additional, Rivellese, Felice, additional, Humby, Frances, additional, Kelly, Stephen, additional, Bombardieri, Michele, additional, Ng, Nora, additional, DiCicco, Maria, additional, van der Heijde, Désirée, additional, Landewé, Robert, additional, van der Helm-van Mil, Annette, additional, Cauli, Alberto, additional, McInnes, Iain B., additional, Buckley, Christopher D., additional, Choy, Ernest, additional, Taylor, Peter C., additional, Townsend, Michael J., additional, and Pitzalis, Costantino, additional

Published
2019
Full Text
View/download PDF

246. Primary Results from SAUL, a Multinational Single-arm Safety Study of Atezolizumab Therapy for Locally Advanced or Metastatic Urothelial or Nonurothelial Carcinoma of the Urinary Tract

Author

Sternberg, Cora N., primary, Loriot, Yohann, additional, James, Nicholas, additional, Choy, Ernest, additional, Castellano, Daniel, additional, Lopez-Rios, Fernando, additional, Banna, Giuseppe L., additional, De Giorgi, Ugo, additional, Masini, Cristina, additional, Bamias, Aristotelis, additional, Garcia del Muro, Xavier, additional, Duran, Ignacio, additional, Powles, Thomas, additional, Gamulin, Marija, additional, Zengerling, Friedemann, additional, Geczi, Lajos, additional, Gedye, Craig, additional, de Ducla, Sabine, additional, Fear, Simon, additional, and Merseburger, Axel S., additional

Published
2019
Full Text
View/download PDF

249. FRI0106 SARILUMAB AND TOCILIZUMAB RECEPTOR OCCUPANCY (RO), AND EFFECTS ON C-REACTIVE PROTEIN (CRP) LEVELS, IN PATIENTS WITH RHEUMATOID ARTHRITIS (RA)

Author

Xu, Christine, primary, Nolain, Patrick, additional, Lu, Qiang, additional, Paccaly, Anne, additional, Iglesias-Rodriguez, Melitza, additional, John, Gregory St, additional, Nivens, Chad, additional, Maldonado, Rafael, additional, Ishii, Tomonori, additional, Choy, Ernest, additional, and Kanamaluru, Vanaja, additional

Published
2019
Full Text
View/download PDF

250. OP0165 EULAR RECOMMENDATIONS FOR THE DIAGNOSIS AND THE MANAGEMENT OF RHEUMATIC IMMUNE-RELATED ADVERSE EVENTS DUE TO CANCER IMMUNOTHERAPY

Author

Kostine, Marie, primary, Finckh, Axel, additional, Bingham, Clifton, additional, Visser, Karen, additional, Leipe, Jan, additional, Schulze-Koops, Hendrik, additional, Choy, Ernest, additional, Benesova, Karolina, additional, Radstake, Timothy R., additional, Cope, Andrew, additional, Lambotte, Oliver, additional, Gottenberg, Jacques-Eric, additional, Allenbach, Yves, additional, Visser, Marianne, additional, Rusthoven, Cindy, additional, Thomasen, Lone, additional, Jamal, Shahin, additional, Marabelle, Aurélien, additional, Larkin, James, additional, Haanen, John, additional, Calabrese, Leonard, additional, Mariette, Xavier, additional, and Schaeverbeke, Thierry, additional

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results