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9. A Multicenter, Randomized, Placebo-Controlled Trial of Atorvastatin for the Primary Prevention of Cardiovascular Events in Patients With Rheumatoid Arthritis

Author

Kitas, George D, Nightingale, Peter, Armitage, Jane, Sattar, Naveed, Belch, Jill JF, Symmons, Deborah PM, Williams, Hawys, Vasishta, Shobna, Storey, Rebecca, Bruce, Ian, Durrington, Paul, McInnes, Iain, Situnayake, Deva, Struthers, Allan, Lowe, Gordon, Fox, Keith, Haskard, Dorian, Dore, Caroline, Bosworth, Ailsa, Frenneaux, Michael, Edwards, Christopher, Emberson, Jonathan, Bax, Deborah, Cobbe, Stuart, Stott, David, Sturrock, Roger, Macfarlane, Peter, Klocke, Rainer, Pullar, Tom, Tan, Su, Knight, Susan, Rowe, Iain, Kumar, Pradeep, Goodson, Nicky, Mulherin, Diarmuid, Brzeski, Micheal, Gardiner, Philip, Walker, David, Callaghan, Rob, Allen, Margaret, McCarey, David, George, Emmanuel, Deighton, Chris, Kirkham, Bruce, Teh, Lee-Suan, Luqmani, Raashid, Chakravarty, Kuntal, Roussou, Euthalia, Nixon, Jenny, Richards, Selwyn, Scott, David, Woolf, Tony, Prouse, Peter, Packham, Jonathan, Davies, Martin, DeLord, Denise, O'Neill, Terence, Pande, Ira, Watts, Richard, Rankin, Elizabeth, Papasawas, George, Emery, Paul, Morgan, Ann, Sinha, Arvind, Dasgupta, Bhaskar, Creamer, Paul, Zoma, Asad, Walsh, David, Van-Laar, Jaap, Capps, Nigel, Cairns, Andrew, Marguerie, Christopher, Kumar, Namita, Abernethy, Rikki, Lillicrap, Mark, Ralston, Stuart, Makadsi, Raad, Hopkinson, Neil, Akil, Mohammed, Ahmad, Yasmeen, Adler, Matthew, Bukhari, Marwan, Sanders, Paul, Binymin, Khalid, Hassan, Alaa, Hughes, Rod, Irani, Mike, O'Reilly, David, Sainsbury, Paul, Richmond, Ruth, Malgorzata, Magliano, Nisar, Mohammed, McEntergart, Ann, Roy, Dipak, Marks, Jeffrey, Batley, Michael, Mahmud, Taher, McKenna, Frank, Harris, Helen, Smyth, Anita, Tunn, Eddie, Young, Adam, Baburaj, Krishnan, Thomas, Joegi, Hall, Frances, Marshall, Tarnya, Rao, Chandini, Dixey, Josh, Gendi, Nagui, Birrell, Fraser, Chelliah, Gladstone, Fishman, Daniel, Knights, Sally, Coady, David, Smith, Bill, Harrison, Beverley, Naz, Sophia, Siebert, Stefan, Chan, Anthony, Putchakayala, Kiran, Al-Ansari, Atheer, Gough, Andrew, Pyne, Dev, Patel, Yusaf, Isdale, Amanda, Harvie, John, Consortium, TRACERA, Comm, Trial Management, Comm, Trial Steering, Comm, Data Monitoring, Comm, Endpoints, and Principal, TRACERA Recruiting Ctr

Published
2019

10. A multicenter, randomized, placebo‐controlled trial of atorvastatin for the primary prevention of cardiovascular events in patients with rheumatoid arthritis

Author

Kitas, George D., Nightingale, Peter, Armitage, Jane, Sattar, Naveed, Belch, Jill J. F., Symmons, Deborah P. M., Kitas, George, Belch, Jill, Symmons, Deborah, Williams, Hawys, Vasishta, Shobna, Storey, Rebecca, Bruce, Ian, Durrington, Paul, McInnes, Iain, Situnayake, Deva, Struthers, Allan, Lowe, Gordon, Fox, Keith, Haskard, Dorian, Dore, Caroline, Bosworth, Ailsa, Frenneaux, Michael, Edwards, Christopher, Emberson, Jonathan, Bax, Deborah, Cobbe, Stuart, Stott, David, Sturrock, Roger, Macfarlane, Peter, Klocke, Rainer, Pullar, Tom, Knight, Susan, Rowe, Iain, Kumar, Pradeep, Goodson, Nicky, Mulherin, Diarmuid, Brzeski, Micheal, Gardiner, Philip, Walker, David, Callaghan, Rob, Allen, Margaret, McCarey, David, George, Emmanuel, Deighton, Chris, Kirkham, Bruce, Teh, Lee‐Suan, Luqmani, Raashid, Chakravarty, Kuntal, Nixon, Jenny, Richards, Selwyn, Scott, David, Woolf, Tony, Prouse, Peter, Packham, Jonathan, Davies, Martin, DeLord, Denise, O’Neill, Terence, Pande, Ira, Harvie, John, Watts, Richard, Rankin, Elizabeth, Papasavvas, George, Emery, Paul, Sinha, Arvind, Dasgupta, Bhaskar, Creamer, Paul, Zoma, Asad, Walsh, David, Van‐Laar, Jaap, Capps, Nigel, Cairns, Andrew, Marguerie, Christopher, Kumar, Namita, Abernethy, Rikki, Lillicrap, Mark, Ralston, Stuart, Makadsi, Raad, Hopkinson, Neil, Tan, Su, Akil, Mohammed, Ahmad, Yasmeen, Adler, Matthew, Bukhari, Marwan, Sanders, Paul, Roussou, Euthalia, Binymin, Khalid, Hassan, Alaa, Hughes, Rod, O’Reilly, David, Sainsbury, Paul, Richmond, Ruth, Malgorzata, Magliano, Nisar, Mohammed, McEntergart, Ann, Roy, Dipak, Marks, Jeffrey, Batley, Michael, McKenna, Frank, Irani, Mike, Harris, Helen, Smyth, Anita, Tunn, Eddie, Young, Adam, Thomas, Joegi, Hall, Frances, Marshall, Tarnya, Rao, Chandini, Baburaj, Krishnan, Dixey, Josh, Gendi, Nagui, Birrell, Fraser, Chelliah, Gladstone, Morgan, Ann, Fishman, Daniel, Knights, Sally, Coady, David, Smith, Bill, Harrison, Beverley, Siebert, Stefan, Chan, Anthony, Putchakayala, Kiran, Al‐Ansari, Atheer, Gough, Andrew, Naz, Sophia, Pyne, Dev, Mahmud, Taher, Patel, Yusaf, and Isdale, Amanda

Abstract

Objective:\ud \ud Rheumatoid arthritis (RA) is associated with increased cardiovascular event (CVE) risk. The impact of statins in RA is not established. We assessed whether atorvastatin is superior to placebo for the primary prevention of CVEs in RA patients.\ud Methods:\ud \ud A randomized, double‐blind, placebo‐controlled trial was designed to detect a 32% CVE risk reduction based on an estimated 1.6% per annum event rate with 80% power at P < 0.05. RA patients age >50 years or with a disease duration of >10 years who did not have clinical atherosclerosis, diabetes, or myopathy received atorvastatin 40 mg daily or matching placebo. The primary end point was a composite of cardiovascular death, myocardial infarction, stroke, transient ischemic attack, or any arterial revascularization. Secondary and tertiary end points included plasma lipids and safety.\ud Results:\ud \ud A total of 3,002 patients (mean age 61 years; 74% female) were followed up for a median of 2.51 years (interquartile range [IQR] 1.90, 3.49 years) (7,827 patient‐years). The study was terminated early due to a lower than expected event rate (0.70% per annum). Of the 1,504 patients receiving atorvastatin, 24 (1.6%) experienced a primary end point, compared with 36 (2.4%) of the 1,498 receiving placebo (hazard ratio [HR] 0.66 [95% confidence interval (95% CI) 0.39, 1.11]; P = 0.115 and adjusted HR 0.60 [95% CI 0.32, 1.15]; P = 0.127). At trial end, patients receiving atorvastatin had a mean ± SD low‐density lipoprotein (LDL) cholesterol level 0.77 ± 0.04 mmoles/liter lower than those receiving placebo (P < 0.0001). C‐reactive protein level was also significantly lower in the atorvastatin group than the placebo group (median 2.59 mg/liter [IQR 0.94, 6.08] versus 3.60 mg/liter [IQR 1.47, 7.49]; P < 0.0001). CVE risk reduction per mmole/liter reduction in LDL cholesterol was 42% (95% CI −14%, 70%). The rates of adverse events in the atorvastatin group (n = 298 [19.8%]) and placebo group (n = 292 [19.5%]) were similar.\ud Conclusion:\ud \ud Atorvastatin 40 mg daily is safe and results in a significantly greater reduction of LDL cholesterol level than placebo in patients with RA. The 34% CVE risk reduction is consistent with the Cholesterol Treatment Trialists’ Collaboration meta‐analysis of statin effects in other populations.

Published
2019

14. 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

15. 067 A regional survey and audit of service provision for giant cell arteritis

Author

Sharp, Charlotte A, primary, Little, Jayne, additional, Davies, Edward, additional, Bruce, Ellen S, additional, Chinoy, Hector, additional, Coates, Lucy, additional, MacPhie, Elizabeth, additional, Naz, Sophia, additional, Ottewell, Lesley, additional, Rao, Chandini, additional, Snowden, Neil, additional, Teh, Lee-Suan, additional, Watson, Pippa, additional, Wig, Surabhi, additional, Wood, E F, additional, Shah, Preeti, additional, and Mercer, Louise, additional

Published
2018
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16. Potential drug–drug interactions in the pediatric intensive care unit of a tertiary care hospital.

Author

Rao, Chandini, Shenoy, Varadaraj, and Udaykumar, Padmaja

Subjects
*PEDIATRIC intensive care, *INTENSIVE care units, *TERTIARY care, *HOSPITAL care, *INTENSIVE care patients, *DRUG interactions
Abstract

Aim: To identify and evaluate the potential drug–drug interactions (PDDI) in hospitalized patients in a pediatric intensive care unit (PICU). Materials and Methods: In this cross-sectional observational study, we analyzed prescriptions of children aged 1 month–15 years admitted to PICU for PDDIs, and categorized them based on the severity (mild, moderate, and severe), underlying mechanisms, number of concomitant drugs used and potential outcomes of these PDDIs, using a drug interaction checking software. Results: Of the 122 prescriptions, we found 175 PDDIs in 77 prescriptions, of which 75.43% were of moderate, 17.71% minor, 6.86% major severity, and none was contraindicated.. The number of PDDIs increased with the number of medications per prescription. The average number of PDDIs per prescription was the highest in those that had >10 drugs (4.29). Pharmacodynamic interactions constituted the majority (73.71%) compared to pharmacokinetic interactions (23.43%). Common PDDIs encountered were between salbutamol and phenylephrine (11.43%), between anti-epileptic drugs (10.86%) and 3rd generation cephalosporins and aminoglycosides (10.29%). The most common potential outcome of these DDIs was hypokalemia (13.71%). Conclusion: There is a high prevalence of PDDIs in PICUs, mostly of moderate severity, with a significant relationship with the number of concomitant medications prescribed. Precaution is required while implementing polypharmacy in children. [ABSTRACT FROM AUTHOR]

Published
2019
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18. Switching patients with inflammatory arthritis from Etanercept (Enbrel ® ) to the biosimilar drug, SB4 (Benepali ® ): A single-centre retrospective observational study in the UK and a review of the literature.

Author

Madenidou AV, Jeffries A, Varughese S, Jones S, Sari-Kouzel H, Veevers H, and Rao C

Abstract

Objective/aim: SB4 (Benepali ® ), the Etanercept biosimilar, is licenced in the UK for the same indications as the reference product, Enbrel ® . In 2016, the Rheumatology Department at Blackpool Teaching Hospitals switched the Etanercept patients, who gave consent, to SB4. A proportion of these patients switched back to Etanercept and therefore we aimed to investigate the reasons of SB4 withdrawal and compare our results with the current evidence., Methods: We included all the patients switched to SB4 until April 2018, identified from the departmental biologics database. We also searched the published and grey literature through November 2018 for similar articles., Results: 72 Etanercept patients switched to SB4, of which 19 (26.4%) switched back to Etanercept within 6 months on the biosimilar product. All the 19 patients remained on Etanercept until the time of data analysis. The main reason of withdrawal was loss of effect (LOE, 58%). In RA, the duration on Etanercept was associated with SB4 withdrawal (OR 1.43 [95% CI 1.02, 2.00]) and LOE was reflected in the DAS- 28, PGS and CRP increase and in the number of tender joints (all p <0.05). We found ten observational studies reporting 3184 patients, who switched from Etanercept to SB4 and 432 of them (14%) stopped SB4., Conclusion: The majority (73.6%) stayed on SB4, which is consistent with the current evidence. Taking also into consideration the results of the other studies, it is unclear if this withdrawal is a true failure on SB4, nocebo effect or spontaneous disease flare., (© 2019 The Mediterranean Journal of Rheumatology (MJR).)

Published
2019
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