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3. There is No Fast Track to Identify Fast Decliners in Alpha-1 Antitrypsin Deficiency by Spirometry: A Longitudinal Study of Repeated Measurements

Author

Stockley, James A, Stockley, Robert A, and Sapey, Elizabeth

Subjects
Spirometry, Longitudinal study, medicine.medical_specialty, International Journal of Chronic Obstructive Pulmonary Disease, decline, Pulmonary Disease, Chronic Obstructive, 03 medical and health sciences, 0302 clinical medicine, alpha 1-Antitrypsin Deficiency, Internal medicine, medicine, Humans, Longitudinal Studies, 030212 general & internal medicine, Mild disease, Lung function, Original Research, Retrospective Studies, alpha-1 antitrypsin deficiency, COPD, Alpha 1-antitrypsin deficiency, medicine.diagnostic_test, business.industry, lung function, General Medicine, obstructive airways disease, medicine.disease, Predictive value, 030228 respiratory system, alpha 1-Antitrypsin, Fast track, business
Abstract

James A Stockley,1 Robert A Stockley,2 Elizabeth Sapey3 1Lung Function & Sleep Department, University Hospitals Birmingham NHS Foundation Trust, Birmingham, B15 2GW, UK; 2Respiratory Department, University Hospitals Birmingham NHS Foundation Trust, Birmingham, B15 2GW, UK; 3PIONEER Health Data Hub in Acute Care, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, B15 2GW, UKCorrespondence: Elizabeth SapeyPIONEER Health Data Hub in Acute Care, Institute of Inflammation and Ageing, University of Birmingham, Edgbaston, Birmingham, B15 2GW, UKEmail E.sapey@bham.ac.ukBackground: It is known that lung function decline in Alpha-1 Antitrypsin Deficiency (AATD) varies. Those with a rapid decline are at highest risk of poorer outcomes but may benefit most from targeted treatments including augmentation therapy. Current evidence suggests rapid decliners can be identified after 3 years of serial follow-up. It would be advantageous to identify these patients over a shorter time period, especially in mild disease.Methods: Post-bronchodilator spirometry was performed every 6 months for a total of 18 months (4 measurements) by PiZZ AATD patients (ex- or never-smokers) either without spirometric COPD or with mild COPD. Where possible, retrospective spirometry data were included. Decline was assessed using 2 (baseline and 6 month) or four measurements (including baseline, 6, 12 and 18 months) and compared to retrospective decline rates using annual measurements over 3 years.Results: Seventy-two PiZZ AATD patients were included, with 27 having at least three years of retrospective, annual spirometry. 18-month progression obtained by linear regression showed variable degrees of change with 29 showing no decline, 8 showing slow decline and 35 showing rapid decline. Bland-Altman plots showed that there was no overall agreement between predicted rate of decline using data obtained over 6 months and that obtained over 18 months. Furthermore, there was no agreement between rate of decline from either 6 or 18 months’ data when compared to data collected over 3 years. The positive predictive value for rapid decline with 18 months of data compared to 3 years was only 50.0%.Conclusion: This study suggests serial lung function over 18 months cannot identify AATD patients who have rapidly declining lung function. There is an urgent need for different biomarkers to help identify these patients at the earliest opportunity.Keywords: lung function, decline, obstructive airways disease, alpha-1 antitrypsin deficiency

Published
2021
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4. Hypoxia increases the potential for neutrophil-mediated endothelial damage in COPD

Author

Lodge, Katharine M, Vassallo, Arlette, Liu, Bin, Long, Merete, Newby, Paul R, Agha-Jaffar, Danya, Paschalaki, Koralia, Green, Clara E, Belchamber, Kylie BR, Ridger, Victoria C, Stockley, Robert A, Sapey, Elizabeth, Summers, Charlotte, Cowburn, Andrew S, Chilvers, Edwin R, Li, Wei, Condliffe, Alison M, Lodge, Katharine M [0000-0002-3203-9941], and Apollo - University of Cambridge Repository

Subjects
Pulmonary Disease, Chronic Obstructive, cardiovascular disease, Neutrophils, Endothelial Cells, Humans, cell degranulation, Vascular System Injuries, Hypoxia, Leukocyte Elastase, neutrophil elastase, vascular endothelium, respiratory tract diseases
Abstract

Rationale: Chronic obstructive pulmonary disease (COPD) patients experience excess cardiovascular morbidity and mortality, and exacerbations further increase the risk of such events. COPD is associated with persistent blood and airway neutrophilia, and systemic and tissue hypoxia. Hypoxia augments neutrophil elastase release, enhancing capacity for tissue injury. Objective: To determine whether hypoxia-driven neutrophil protein secretion contributes to endothelial damage in COPD. Methods: The healthy human neutrophil secretome generated under normoxic or hypoxic conditions was characterised by quantitative mass spectrometry, and the capacity for neutrophil-mediated endothelial damage assessed. Histotoxic protein levels were measured in normoxic versus hypoxic neutrophil supernatants and plasma from exacerbating COPD patients and healthy controls. Main results: Hypoxia promoted PI3Kγ-dependent neutrophil elastase secretion, with greater release seen in neutrophils from COPD patients. Supernatants from neutrophils incubated under hypoxia caused pulmonary endothelial cell damage and identical supernatants from COPD neutrophils increased neutrophil adherence to endothelial cells. Proteomics revealed differential neutrophil protein secretion under hypoxia and normoxia; hypoxia augmented secretion of a subset of histotoxic granule and cytosolic proteins, with significantly greater release seen in COPD neutrophils. The plasma of COPD patients had higher content of hypoxia-upregulated neutrophil-derived proteins and protease activity, and vascular injury markers. Conclusions: Hypoxia drives a destructive ‘hyper-secretory’ neutrophil phenotype conferring enhanced capacity for endothelial injury, with a corresponding signature of 5 neutrophil degranulation and vascular injury identified in COPD patient plasma. Thus, hypoxic enhancement of neutrophil degranulation may contribute to increased cardiovascular risk in COPD. These insights may identify new therapeutic opportunities for endothelial damage in COPD.

Published
2022

5. Additional file 1: of Health status decline in Îą-1 antitrypsin deficiency: a feasible outcome for disease modifying therapies?

Author

Stockley, Robert, Edgar, Ross, Starkey, Sian, and Turner, Alice

Subjects
respiratory system, respiratory tract diseases
Abstract

Table S1. Demographics of patients without COPD. Table S2. Demographics of patients with COPD. Tables S3. a-c FEV1 and Kco decline including annual change in absolute units. Table S4. SGRQ domains and total scores for non COPD cohort split by those with normal age related decline in Kco and those with rapid decline. Table S5. SGRQ deterioration for COPD cohort split by normal age related Kco decline and rapid Kco decline. (DOCX 35 kb)

Published
2018
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6. Children must be protected from the tobacco industry's marketing tactics

Author

Hopkinson, Nicholas, Wallis, Colin, Higgins, Bernard, Gaduzo, Stephen, Sherrington, Rebecca, Keilty, Sarah, Stern, Myra, Britton, John, Bush, Andrew, Moxham, John, Sylvester, Karl, Griffiths, Valerie, Sutherland, Tim, Crossingham, Iain, Raju, Raghu, Spencer, Charlotte, Safavi, Shahideh, Deegan, Paul, Seymour, John, Hickman, Katherine, Hughes, John, Wieboldt, Jason, Shaheen, Fizah, Peedell, Clive, Mackenzie, Nesta, Nicholl, David, Jolley, Caroline, Crooks, Gillian, Dow, Claire, Deveson, Pete, Bintcliffe, Oliver, Gray, Barry, Kumar, Sanjay, Haney, Sarah, Docherty, Marianne, Thomas, Angela, Chua, Felix, Dwarakanath, Akshay, Summers, Geoffrey, Prowse, Keith, Lytton, Stephen, Ong, Yee Ean, Graves, Jennifer, Banerjee, Tushar, English, Peter, Leonard, Andrew, Brunet, Martin, Chaudhry, Nauman, Ketchell, Robert Ian, Cummings, Natalie, Lebus, Jenny, Sharp, Charles, Meadows, Chris, Harle, Amelie, Stewart, Tara, Parry, Diane, Templeton-Wright, Suzanne, Moore-Gillon, John, Stratford- Martin, James, Saini, Sarvesh, Matusiewicz, Simon, Merritt, Simon, Dowson, Lee, Satkunam, Karnan, Hodgson, Luke, Suh, Eui-Sik, Durrington, Hannah, Browne, Emma, Walters, Nicola, Steier, Joerg, Barry, Simon, Griffiths, Mark, Hart, Nicholas, Nikolic, Marko, Berry, Matthew, Thomas, Ajit, Miller, Joy, McNicholl, Diarmuid, Marsden, Paul, Warwick, Geoffrey, Barr, Laura, Adeboyeku, David, Mohd Noh, Mohd Shahrin, Griffiths, Paul, Davies, Lisa, Quint, Jennifer, Lyall, Rebecca, Shribman, Jonathan, Collins, Andrea, Goldman, Jon, Bloch, Susannah, Gill, Alison, Man, William, Christopher, Anne, Yasso, Razouqi, Rajhan, Ashwin, Shrikrishna, Dinesh, Moore, Caroline, Absalom, Gareth, Booton, Richard, Fowler, Robert William, Mackinlay, Carolyn, Sapey, Elizabeth, Lock, Sara, Walker, Paul, Jha, Akhilesh, Satia, Imran, Bradley, Bethia, Mustfa, Naveed, Haqqee, Raana, Thomas, Matt, Patel, Anant, Redington, Anthony, Pillai, Anilkumar, Keaney, Niall, Fowler, Stephen, Lowe, Lesley, Brennan, Amanda, Morrison, Douglas, Murray, Clare, Hankinson, Jenny, Dutta, P, Maddocks, Matthew, Pengo, Martino, Curtis, Katrina, Rafferty, Gerrard, Hutchinson, John, Whitfield, Ruth, Turner, Steve, Breen, Ronan, Naveed, Shams-un-nisa, Goode, Chris, Esterbrook, Georgina, Ahmed, Liju, Walker, Woolf, Ford, David, Connett, Gary, Davidson, Philip, Elston, Will, Stanton, Andrew, Morgan, David, Myerson, James, Maxwell, David, Harrris, Ann, Parmar, Sonia, Houghton, Catherine, Winter, Robert, Puthucheary, Zudin, Thomson, Fiona, Sturney, Sharon, Harvey, John, Haslam, Patricia L, Patel, Irem, Jennings, David, Range, Simon, Mallia-Milanes, Brendan, Collett, Anne, Tate, Paul, Russell, Richard, Feary, Johanna, O'Driscoll, Ronan, Eaden, James, Round, Jonathan, Sharkey, Emma, Montgomery, Mary, Vaughan, Sophie, Scheele, Kate, Lithgow, Anna, Partridge, Samuel, Chavasse, Richard, Restrick, Louise, Agrawal, Sanjay, Abdallah, Said, Lacy-Colson, Amruta, Adams, Nick, Mitchell, Sally, Haja Mydin, Helmy, Ward, Ann, Denniston, Sarah, Steel, Mark, Ghosh, Dipansu, Connellan, Stephen, Rigge, Lucy, Williams, Ruth, Grove, Alison, Anwar, Sadia, Dobson, Lee, Hosker, Harold, Stableforth, David, Greening, Neil, Howell, Tim, Casswell, Georgina, Davies, Sarah, Tunnicliffe, Georgia, Mitchelmore, Philip, Phitidis, Elpida, Robinson, Louise, Bafadhel, Mona, Robinson, Grace, Boland, Alison, Lipman, Marc, Bourke, Stephen, Kaul, Sundeep, Cowie, Calvin, Forrest, Ian, Starren, Elizabeth, Burke, Hannah, Furness, John, Bhowmik, Angshu, Everett, Caroline, Seaton, Douglas, Holmes, Steve, Doe, Simon, Parker, Samuel, Graham, Annika, Paterson, Ian, Maqsood, Usman, Ohri, Chandra, Iles, Peter, Kemp, Samuel, Iftikhar, Ahsan, Carlin, Chris, Fletcher, Tim, Emerson, Peter, Beasley, Victoria, Ramsay, Michelle, Buttery, Robert, Mungall, Sarah, Crooks, Stephen, Ridyard, John, Ross, David, Guadagno, Alison, Holden, Emma, Coutts, Ian, Cullen, Kathy, O'Connor, Sally, Barker, Jack, Sloper, Katherine, Watson, John, Smith, Peter, Anderson, Paul, Brown, Louise, Nyman, Cyril, Milburn, Heather, Clive, Amelia, Serlin, Matthew, Bolton, Charlotte, Fuld, Jonathan, Powell, Helen, Dayer, Mark, Woolhouse, Ian, Georgiadi, Adamantia, Leonard, Helen, Dodd, James, Campbell, Ian, Ruiz, Gary, Zurek, Andrew, Paton, James Y, Malin, Adam, Wood, Fraser, Hynes, Gareth, Connell, David, Spencer, David, Brown, Sarah, Smith, David, Cooper, David, O'Kane, Cecilia, Hicks, Alex, Creagh-Brown, Ben, Lordan, James, Nickol, Annabel, Primhak, Robert, Fleming, Louise, Powrie, Duncan, Brown, Joanna, Zoumot, Zaid, Elkin, Sarah, Szram, Joanna, Scaffardi, Anthony, Marshall, Robert, Macdonald, Ian, Lightbody, Darren, Farmer, Ray, Wheatley, Iain, Radnan, Paul, Lane, Ian, Booth, Andrew, Tilbrook, Sean, Capstick, Toby, Hewitt, Lee, McHugh, Martin, Nelson, Christopher, Wilson, Patrick, Padmanaban, Vijay, White, John, Davison, John, O'Callaghan, Una, Hodson, Matthew, Edwards, John, Campbell, Colin, Ward, Simon, Wooler, Edwina, Ringrose, Elizabeth, Bridges, Diana, Matthew Hodson, John Edwards, Colin Campbell, Simon Ward, Edwina Wooler, Elizabeth Ringrose, Diana Bridges, Rosalind Backham, Kim Randall, Tracey Mathieson, Long, Alex, Parkes, Marilyn, Clarke, Sarah, Allen, Bev, Connelly, Carol, Forster, Georgia, Hoadley, Jacky, Martin, Katharine, Barnham, Kate, Khan, Katie, Munday, Maureen, Edwards, Catherine, O'Hara, Doreen, Turner, Sally, Pieri-Davies, Sue, Ford, Kate, Daniels, Tracey, Wright, Joanne, Towns, Rebecca, Fern, Karen, Butcher, Jane, Burgin, Karen, Winter, Barbara, Freeman, Debbie, Olive, Sandra, Gray, Linda, Pye, Kathy, Roots, Debbie, Cox, Nicola, Davies, Carol-Anne, Wicker, Jacquelyne, Hilton, Kay, Lloyd, Jananee, MacBean, Vicky, Wood, Marion, Kowal, Julia, Downs, Janis, Ryan, Helen, Guyatt, Fran, Nicoll, Debby, Lyons, Elizabeth, Narasimhan, Divya, Rodman, Anne, Walmsley, Sandy, Newey, Alison, Buxton, Maria, Dewar, Maria, Cooper, Angela, Reilly, Jacqui, Lloyd, Julie, Macmillan, Alison Bennett, Olley, Amy, Voase, Nia, Martin, Sarah, McCarvill, Iona, Christensen, Anne, Agate, Rowan, Heslop, Karen, Timlett, Amber, Hailes, Karen, Davey, Claire, Pawulska, Barbara, Lane, Amber, Ioakim, Shona, Hough, Alexandra, Treharne, Jo, Jones, Helen, Winter-Burke, Alice, Miller, Lauren, Connolly, Bronwen, Bingham, Lyn, Fraser, Una, Bott, Julia, Johnston, Carol, Graham, Alison, Curry, Denise, Sumner, Helen, Costello, Carol Ann, Bartoszewicz, Charlotte, Badman, Ros, Williamson, Kathryn, Taylor, Amy, Purcell, Helen, Barnett, Emma, Molloy, Alanna, Crawfurd, Laura, Collins, Nicola, Monaghan, Valerie, Mir, Misbah, Lord, Victoria, Stocks, Janet, Edwards, Adrian, Greenhalgh, Trish, Lenney, Warren, McKee, Martin, McAuley, Danny, Majeed, Azeem, Cookson, John, Baker, Emma, Janes, Sam, Wedzicha, Wisia, Lomas Dean, David, Harrison, Brian, Davison, Tony, Calverley, Peter, Wilson, Robert, Stockley, Robert, Ayres, Jon, Gibson, John, Simpson, John, Burge, Sherwood, Warner, John, Thomson, Neil, Davies, Peter, Woodcock, Ashley, Woodhead, Mark, Spiro, Stephen, Ormerod, Lawrence, Bothamley, Graham, Partridge, Martyn, Shields, Michael, Montgomery, Hugh, Simonds, Anita, Barnes, Peter, Durham, Stephen, Malone, Sarah, Arabnia, Gilda, Olivier, Sharon, Gardiner, Karen, and Edwards, Sheila

Subjects
Marketing, Tobacco harm reduction, Government, Adolescent, Health professionals, business.industry, MEDLINE, Tobacco Industry, Tobacco Products, General Medicine, Tobacco industry, United Kingdom, Lung disease, Environmental health, Tobacco in Alabama, Product Packaging, Humans, Medicine, Packaging and labeling, Child, business
Abstract

Every day in the UK, hundreds of children aged 11-15 years start smoking for the first time,1 2 and there is compelling evidence that children’s perceptions of cigarettes are influenced by branding.3 4 As health professionals working to prevent and treat lung disease caused by smoking, we welcome the government’s …

7. Protocol for the EARCO Registry: a pan-European observational study in patients with α1-antitrypsin deficiency

Author

Greulich, Timm, Altraja, Alan, Barrecheguren, Miriam, Bals, Robert, Chlumsky, Jan, Chorostowska-Wynimko, Joanna, Clarenbach, Christian, Corda, Luciano, Corsico, Angelo Guido, Ferrarotti, Ilaria, Esquinas, Cristina, Gouder, Caroline, Hećimović, Ana, Ilic, Aleksandra, Ivanov, Yavor, Janciauskiene, Sabina, Janssens, Wim, Kohler, Malcolm, Krams, Alvils, Lara, Beatriz, Mahadeva, Ravi, McElvaney, Gerry, Mornex, Jean-François, O'Hara, Karen, Parr, David, Piitulainen, Eava, Schmid-Scherzer, Karin, Seersholm, Niels, Stockley, Robert A, Stolk, Jan, Sucena, Maria, Tanash, Hanan, Turner, Alice, Ulmeanu, Ruxandra, Wilkens, Marion, Yorgancioğlu, Arzu, Zaharie, Ana, and Miravitlles, Marc

Subjects
Emphysema, Rare Diseases, Clinical Research, Chronic Obstructive Pulmonary Disease, FOS: Biological sciences, Prevention, Genetics, 32 Biomedical and Clinical Sciences, 3202 Clinical Sciences, Lung, 3. Good health
Abstract

RATIONALE AND OBJECTIVES: Alpha-1 antitrypsin deficiency (AATD) is a genetic condition that leads to an increased risk of emphysema and liver disease. Despite extensive investigation, there remain unanswered questions concerning the natural history, pathophysiology, genetics and the prognosis of the lung disease in association with AATD. The European Alpha-1 Clinical Research Collaboration (EARCO) is designed to bring together researchers from European countries and to create a standardised database for the follow-up of patients with AATD. STUDY DESIGN AND POPULATION: The EARCO Registry is a non-interventional, multicentre, pan-European, longitudinal observational cohort study enrolling patients with AATD. Data will be collected prospectively without interference/modification of patient's management by the study team. The major inclusion criterion is diagnosed severe AATD, defined by an AAT serum level

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