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1. Prevalence and prognostic ability of the GOLD 2017 classification compared to the GOLD 2011 classification in a Norwegian COPD cohort

Author

Le LAK, Johannessen A, Hardie JA, Johansen OE, Gulsvik A, Vikse BE, and Bakke P

Subjects
Prevalence, prognostic ability, GOLD 2017, GOLD 2011, COPD, Diseases of the respiratory system, RC705-779
Abstract

Lan Ai Kieu Le,1 Ane Johannessen,2,3 Jon Andrew Hardie,2 Odd Erik Johansen,4,5 Amund Gulsvik,2 Bjørn Egil Vikse,1,2 Per Bakke21Department of Medicine, Haugesund Hospital, Haugesund, Norway; 2Department of Clinical Medicine, University of Bergen, Bergen, Norway; 3Centre for International Health, Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway; 4Department of Medicine, Bærum Hospital, Gjettum, Norway; 5Boehringer Ingelheim Norway KS, Asker, NorwayRationale: The Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 is based on an ABCD assessment tool of symptoms and exacerbation history and grade 1–4 of airflow limitation severity, facilitating classification either into 4 groups (ABCD) or 16 groups (1A-4D). We aimed to compare the GOLD 2011, GOLD 2017 ABCD, and GOLD 2017 1A-4D classifications in terms of their distribution and prediction of mortality and hospitalizations.Methods: In the GenKOLS study, 912 COPD patients with FEV1 less than 80% of the predicted answered questionnaires and performed lung function testing in 2003–2005. The patients were recruited from a hospital patient registry (n=662) and from the general population (n=250), followed up until 2011 with respect to all-cause and respiratory mortality, and all-cause and respiratory hospitalizations. We performed logistic regression and receiver operating curve (ROC) analyses for the different classifications with estimations of area under the curve (AUC) for comparisons.Results: Mean age at baseline was 60 years (SD 11), 55% were male. Mean duration of follow-up was 91 months. By GOLD 2011, 21% were classified as group A, 29% group B, 6% group C, and 43% as group D, corresponding percentages for GOLD 2017 were: 25%, 52%, 3%, and 20%. The GOLD 2011 classification had higher AUC values than the GOLD 2017 group ABCD classification for respiratory mortality and hospitalization, but after inclusion of airflow limitation severity in GOLD 2017 groups 2A–4D, AUC values were significantly higher with GOLD 2017.Conclusion: In a clinically relevant sample of COPD patients, the GOLD 2017 classification doubles the prevalence of group B and halves the prevalence of groups C and D as compared to the GOLD 2011 classification. The prediction of respiratory mortality and respiratory hospitalization was better for GOLD 2017 2A–4D taking airflow limitation severity into account, as compared to GOLD 2017 ABCD and GOLD 2011.Keywords: respiratory, hospitalization, mortality, Cox regression, ABCD classification, airflow limitation

Published
2019

2. Incidence of utilization- and symptom-defined COPD exacerbations in hospital- and population-recruited patients

Author

Erdal M, Johannessen A, Eagan TM, Bakke P, Gulsvik A, and Grønseth R

Subjects
Chronic obstructive pulmonary disease, exacerbations, general population, predictors, Diseases of the respiratory system, RC705-779
Abstract

Marta Erdal1,2 Ane Johannessen3 Tomas Mikal Eagan1,2 Per Bakke2 Amund Gulsvik2 Rune Grønseth1,2 1Department of Thoracic Medicine, Haukeland University Hospital, 2Department of Clinical Science, University of Bergen, 3Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway Objectives: The objectives of this study were to estimate the impact of recruitment source and outcome definition on the incidence of acute exacerbations of COPD (AECOPD) and explore possible predictors of AECOPD.Patients and methods: During a 1-year follow-up, we performed a baseline visit and four telephone interviews of 81 COPD patients and 132 controls recruited from a population-based survey and 205 hospital-recruited COPD patients. Both a definition based on health care utilization and a symptom-based definition of AECOPD were applied. For multivariate analyses, we chose a negative binomial regression model.Results: COPD patients from the population- and hospital-based samples experienced on average 0.4 utilization-defined and 2.9 symptom-defined versus 1.0 and 5.9 annual exacerbations, respectively. The incidence rate ratios for utilization-defined AECOPD were 2.45 (95% CI 1.22–4.95), 3.43 (95% CI 1.59–7.38), and 5.67 (95% CI 2.58–12.48) with Global Initiative on Obstructive Lung Disease spirometric stages II, III, and IV, respectively. The corresponding incidence rate ratios for the symptom-based definition were 3.08 (95% CI 1.96–4.84), 3.45 (95% CI 1.92–6.18), and 4.00 (95% CI 2.09–7.66). Maintenance therapy (regular long-acting muscarinic antagonists, long-acting beta-2 agonists, inhaled corticosteroids, or theophylline) also increased the risk of AECOPD with both exacerbation definitions (incidence rate ratios 1.65 and 1.73, respectively). The risk of AECOPD was 59%–78% higher in the hospital sample than in the population sample.Conclusion: If externally valid conclusions are to be made regarding incidence and predictors of AECOPD, studies should be based on general population samples or adjustments should be made on account of a likely higher incidence in other samples. Likewise, the effect of different AECOPD definitions should be taken into consideration. Keywords: COPD, exacerbations, general population, predictors

Published
2016

4. Author Correction: New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries

Author

Shrine, Nick, Guyatt, Anna L., Erzurumluoglu, A. Mesut, Jackson, Victoria E., Hobbs, Brian D., Melbourne, Carl A., Batini, Chiara, Fawcett, Katherine A., Song, Kijoung, Sakornsakolpat, Phuwanat, Li, Xingnan, Boxall, Ruth, Reeve, Nicola F., Obeidat, Ma’en, Zhao, Jing Hua, Wielscher, Matthias, Weiss, Stefan, Kentistou, Katherine A., Cook, James P., Sun, Benjamin B., Zhou, Jian, Hui, Jennie, Karrasch, Stefan, Imboden, Medea, Harris, Sarah E., Marten, Jonathan, Enroth, Stefan, Kerr, Shona M., Surakka, Ida, Vitart, Veronique, Lehtimäki, Terho, Allen, Richard J., Bakke, Per S., Beaty, Terri H., Bleecker, Eugene R., Bossé, Yohan, Brandsma, Corry-Anke, Chen, Zhengming, Crapo, James D., Danesh, John, DeMeo, Dawn L., Dudbridge, Frank, Ewert, Ralf, Gieger, Christian, Gulsvik, Amund, Hansell, Anna L., Hao, Ke, Hoffman, Joshua D., Hokanson, John E., Homuth, Georg, Joshi, Peter K., Joubert, Philippe, Langenberg, Claudia, Li, Xuan, Li, Liming, Lin, Kuang, Lind, Lars, Locantore, Nicholas, Luan, Jian’an, Mahajan, Anubha, Maranville, Joseph C., Murray, Alison, Nickle, David C., Packer, Richard, Parker, Margaret M., Paynton, Megan L., Porteous, David J., Prokopenko, Dmitry, Qiao, Dandi, Rawal, Rajesh, Runz, Heiko, Sayers, Ian, Sin, Don D., Smith, Blair H., Artigas, María Soler, Sparrow, David, Tal-Singer, Ruth, Timmers, Paul R. H. J., Van den Berge, Maarten, Whittaker, John C., Woodruff, Prescott G., Yerges-Armstrong, Laura M., Troyanskaya, Olga G., Raitakari, Olli T., Kähönen, Mika, Polašek, Ozren, Gyllensten, Ulf, Rudan, Igor, Deary, Ian J., Probst-Hensch, Nicole M., Schulz, Holger, James, Alan L., Wilson, James F., Stubbe, Beate, Zeggini, Eleftheria, Jarvelin, Marjo-Riitta, Wareham, Nick, Silverman, Edwin K., Hayward, Caroline, Morris, Andrew P., Butterworth, Adam S., Scott, Robert A., Walters, Robin G., Meyers, Deborah A., Cho, Michael H., Strachan, David P., Hall, Ian P., Tobin, Martin D., and Wain, Louise V.

Published
2024
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6. Underlying causes of cryptogenic stroke and TIA in the nordic atrial fibrillation and stroke (NOR-FIB) study – the importance of comprehensive clinical evaluation

Author

Ratajczak-Tretel, B., Lambert, A. Tancin, Al-Ani, R., Arntzen, K., Bakkejord, G. K., Bekkeseth, H. M.O., Bjerkeli, V., Eldøen, G., Gulsvik, A. K., Halvorsen, B., Høie, G. A., Ihle-Hansen, H., Ingebrigtsen, S., Kremer, C., Krogseth, S. B., Kruuse, C., Kurz, M., Nakstad, I., Novotny, V., Naess, H., Qazi, R., Rezaj, M. K., Rørholt, D. M., Steffensen, L. H., Sømark, J., Tobro, H., Truelsen, T. C., Wassvik, L., Ægidius, K. L., Atar, D., and Aamodt, A. H.

Published
2023
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7. Prediction of underlying atrial fibrillation in patients with a cryptogenic stroke: results from the NOR-FIB Study

Author

Ratajczak-Tretel, B., Lambert, A. Tancin, Al-Ani, R., Arntzen, K., Bakkejord, G. K., Bekkeseth, H. M. O., Bjerkeli, V., Eldøen, G., Gulsvik, A. K., Halvorsen, B., Høie, G. A., Ihle-Hansen, H., Ihle-Hansen, H., Ingebrigtsen, S., Kremer, C., Krogseth, S. B., Kruuse, C., Kurz, M., Nakstad, I., Novotny, V., Næss, H., Qazi, R., Rezaj, M. K., Rørholt, D. M., Steffensen, L. H., Sømark, J., Tobro, H., Truelsen, T. C., Wassvik, L., Ægidius, K. L., Atar, D., and Aamodt, Anne Hege

Published
2023
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8. Prevalence of chronic cough, its risk factors and population attributable risk in the Burden of Obstructive Lung Disease (BOLD) study: a multinational cross-sectional study

Author

Hafizi, Hasan, Aliko, Anila, Bardhi, Donika, Tafa, Holta, Thanasi, Natasha, Mezini, Arian, Teferici, Alma, Todri, Dafina, Nikolla, Jolanda, Kazasi, Rezarta, Cherkaski, Hamid Hacene, Bengrait, Amira, Haddad, Tabarek, Zgaoula, Ibtissem, Ghit, Maamar, Roubhia, Abdelhamid, Boudra, Soumaya, Atoui, Feryal, Yakoubi, Randa, Benali, Rachid, Bencheikh, Abdelghani, Ait-Khaled, Nadia, Jenkins, Christine, Marks, Guy, Bird, Tessa, Espinel, Paola, Hardaker, Kate, Toelle, Brett, Studnicka, Michael, Dawes, Torkil, Lamprecht, Bernd, Schirhofer, Lea, Islam, Akramul, Ahmed, Syed Masud, Islam, Shayla, Islam, Qazi Shafayetul, Mesbah-Ul-Haque, Chowdhury, Tridib Roy, Chatterjee, Sukantha Kumar, Mia, Dulal, Chandra Das, Shyamal, Rahman, Mizanur, Islam, Nazrul, Uddin, Shahaz, Islam, Nurul, Khatun, Luiza, Parvin, Monira, Khan, Abdul Awal, Islam, Maidul, Lawin, Herve, Kpangon, Arsene, Kpossou, Karl, Agodokpessi, Gildas, Ayelo, Paul, Fayomi, Benjamin, Mbatchou, Bertrand, Ashu, Atongno Humphrey, Tan, Wan C., Wang, Wen, Zhong, NanShan, Liu, Shengming, Lu, Jiachun, Ran, Pixin, Wang, Dali, Zheng, Jin-ping, Zhou, Yumin, Jogi, Rain, Laja, Hendrik, Ulst, Katrin, Zobel, Vappu, Lill, Toomas-Julius, Adegnika, Ayola Akim, Welte, Tobias, Bodemann, Isabelle, Geldmacher, Henning, SchwedaLinow, Alexandra, Gislason, Thorarinn, Benedikdtsdottir, Bryndis, Jorundsdottir, Kristin, Lovisa Gudmundsdottir, Gudmundsdottir, Sigrun, Gudmundsson, Gunnar, Rao, Mahesh, Koul, Parvaiz A., Malik, Sajjad, Hakim, Nissar A., Khan, Umar Hafiz, Chowgule, Rohini, Shetye, Vasant, Raphael, Jonelle, Almeda, Rosel, Tawde, Mahesh, Tadvi, Rafiq, Katkar, Sunil, Kadam, Milind, Dhanawade, Rupesh, Ghurup, Umesh, Juvekar, Sanjay, Hirve, Siddhi, Sambhudas, Somnath, Chaidhary, Bharat, Tambe, Meera, Pingale, Savita, Umap, Arati, Umap, Archana, Shelar, Nitin, Devchakke, Sampada, Chaudhary, Sharda, Bondre, Suvarna, Walke, Savita, Gawhane, Ashleshsa, Sapkal, Anil, Argade, Rupali, Gaikwad, Vijay, Salvi, Sundeep, Brashier, Bill, Londhe, Jyoti, Madas, Sapna, Aquart-Stewart, Althea, Aikman, Akosua Francia, Sooronbaev, Talant M., Estebesova, Bermet M., Akmatalieva, Meerim, Usenbaeva, Saadat, Kydyrova, Jypara, Bostonova, Eliza, Sheraliev, Ulan, Marajapov, Nuridin, Toktogulova, Nurgul, Emilov, Berik, Azilova, Toktogul, Beishekeeva, Gulnara, Dononbaeva, Nasyikat, Tabyshova, Aijamal, Mortimer, Kevin, Nyapigoti, Wezzie, Mwangoka, Ernest, Kambwili, Mayamiko, Chipeta, Martha, Banda, Gloria, Mkandawire, Suzgo, Banda, Justice, Loh, Li-Cher, Rashid, Abdul, Sholehah, Siti, Benjelloun, Mohamed C., Nejjari, Chakib, Elbiaze, Mohamed, El Rhazi, Karima, Wouters, E.F.M., Wesseling, G.J., Obaseki, Daniel, Erhabor, Gregory, Awopeju, Olayemi, Adewole, Olufemi, Gulsvik, Amund, Endresen, Tina, Svendsen, Lene, Nafees, Asaad A., Irfan, Muhammad, Fatmi, Zafar, Zahidie, Aysha, Shaukat, Natasha, Iqbal, Meesha, Idolor, Luisito F., de Guia, Teresita S., Francisco, Norberto A., Roa, Camilo C., Ayuyao, Fernando G., Tady, Cecil Z., Tan, Daniel T., Banal-Yang, Sylvia, Balanag, Vincent M., Jr., Reyes, Maria Teresita N., Dantes, Renato B., Amarillo, Lourdes, Berratio, Lakan U., Fernandez, Lenora C., Garcia, Gerard S., Naval, Sullian S., Reyes, Thessa, Roa, Camilo C., Jr., Sanchez, Flordeliza, Simpao, Leander P., Nizankowska-Mogilnicka, Ewa, Frey, Jakub, Harat, Rafal, Mejza, Filip, Nastalek, Pawel, Pajak, Andrzej, Skucha, Wojciech, Szczeklik, Andrzej, Twardowska, Magda, Barbara, Cristina, Rodrigues, Fatima, Dias, Herminia, Cardoso, Joao, Almeida, João, Matos, Maria Joao, Simão, Paula, Santos, Moutinho, Ferreira, Reis, Al Ghobain, M., Alorainy, H., El-Hamad, E., Al Hajjaj, M., Hashi, A., Dela, R., Fanuncio, R., Doloriel, E., Marciano, I., Safia, L., Bateman, Eric, Jithoo, Anamika, Adams, Desiree, Barnes, Edward, Freeman, Jasper, Hayes, Anton, Hlengwa, Sipho, Johannisen, Christine, Koopman, Mariana, Louw, Innocentia, Ludick, Ina, Olckers, Alta, Ryck, Johanna, Storbeck, Janita, Gunasekera, Kirthi, Wickremasinghe, Rajitha, Elsony, Asma, Elsadig, Hana A., Osman, Nada Bakery, Noory, Bandar Salah, Mohamed, Monjda Awad, Akasha Ahmed Osman, Hasab Alrasoul, Moham ed Elhassan, Namarig, El Zain, Abdel Mu’is, Mohamaden, Marwa Mohamed, Khalifa, Suhaiba, Elhadi, Mahmoud, Hassan, Mohand, Abdelmonam, Dalia, Janson, Christer, Olafsdottir, Inga Sif, Nisser, Katarina, SpetzNystrom, Ulrike, Hagg, Gunilla, Lund, GunMarie, Seemungal, Terence, Lutchmansingh, Fallon, Conyette, Liane, Harrabi, Imed, Denguezli, Myriam, Tabka, Zouhair, Daldoul, Hager, Boukheroufa, Zaki, Chouikha, Firas, Khalifa, Wahbi Belhaj, Kocabas, Ali, Hancioglu, Attila, Hanta, Ismail, Kuleci, Sedat, Turkyilmaz, Ahmet Sinan, Umut, Sema, Unalan, Turgay, Burney, Peter G.J., Gnatiuc, Louisa, Azar, Hadia, Patel, Jaymini, Amor, Caron, Potts, James, Tumilty, Michael, McLean, Fiona, Dudhaiya, Risha, Buist, A. Sonia, McBurnie, Mary Ann, Vollmer, William M., Gillespie, Suzanne, Sullivan, Sean, Lee, Todd A., Weiss, Kevin B., Jensen, Robert L., Crapo, Robert, Enright, Paul, Mannino, David M., Cain, John, Copeland, Rebecca, Hazen, Dana, Methvin, Jennifer, Abozid, Hazim, Burney, Peter, Hartl, Sylvia, Breyer-Kohansal, Robab, Al Ghobain, Mohammed, Denguezli, Meriam, Loh, Li Cher, Paraguas, Stefanni Nonna, Franssen, Frits M.E., Mannino, David, Anand, Mahesh Padukudru, Buist, Sonia, El Sony, Asma, Breyer, Marie-Kathrin, Burghuber, Otto C., Wouters, Emiel F.M., and Amaral, Andre F.S.

Published
2024
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10. Prevalence of chronic cough, its risk factors and population attributable risk in the Burden of Obstructive Lung Disease (BOLD) study: a multinational cross-sectional studyResearch in context

Author

Hazim Abozid, Jaymini Patel, Peter Burney, Sylvia Hartl, Robab Breyer-Kohansal, Kevin Mortimer, Asaad A. Nafees, Mohammed Al Ghobain, Tobias Welte, Imed Harrabi, Meriam Denguezli, Li Cher Loh, Abdul Rashid, Thorarinn Gislason, Cristina Barbara, Joao Cardoso, Fatima Rodrigues, Terence Seemungal, Daniel Obaseki, Sanjay Juvekar, Stefanni Nonna Paraguas, Wan C. Tan, Frits M.E. Franssen, Filip Mejza, David Mannino, Christer Janson, Hamid Hacene Cherkaski, Mahesh Padukudru Anand, Hasan Hafizi, Sonia Buist, Parvaiz A. Koul, Asma El Sony, Marie-Kathrin Breyer, Otto C. Burghuber, Emiel F.M. Wouters, Andre F.S. Amaral, Anila Aliko, Donika Bardhi, Holta Tafa, Natasha Thanasi, Arian Mezini, Alma Teferici, Dafina Todri, Jolanda Nikolla, Rezarta Kazasi, Amira Bengrait, Tabarek Haddad, Ibtissem Zgaoula, Maamar Ghit, Abdelhamid Roubhia, Soumaya Boudra, Feryal Atoui, Randa Yakoubi, Rachid Benali, Abdelghani Bencheikh, Nadia Ait-Khaled, Christine Jenkins, Guy Marks, Tessa Bird, Paola Espinel, Kate Hardaker, Brett Toelle, Michael Studnicka, Torkil Dawes, Bernd Lamprecht, Lea Schirhofer, Akramul Islam, Syed Masud Ahmed, Shayla Islam, Qazi Shafayetul Islam, Mesbah-Ul-Haque, Tridib Roy Chowdhury, Sukantha Kumar Chatterjee, Dulal Mia, Shyamal Chandra Das, Mizanur Rahman, Nazrul Islam, Shahaz Uddin, Nurul Islam, Luiza Khatun, Monira Parvin, Abdul Awal Khan, Maidul Islam, Herve Lawin, Arsene Kpangon, Karl Kpossou, Gildas Agodokpessi, Paul Ayelo, Benjamin Fayomi, Bertrand Mbatchou, Atongno Humphrey Ashu, Wen Wang, NanShan Zhong, Shengming Liu, Jiachun Lu, Pixin Ran, Dali Wang, Jin-ping Zheng, Yumin Zhou, Rain Jogi, Hendrik Laja, Katrin Ulst, Vappu Zobel, Toomas-Julius Lill, Ayola Akim Adegnika, Isabelle Bodemann, Henning Geldmacher, Alexandra SchwedaLinow, Bryndis Benedikdtsdottir, Kristin Jorundsdottir, Lovisa Gudmundsdottir, Sigrun Gudmundsdottir, Gunnar Gudmundsson, Mahesh Rao, Sajjad Malik, Nissar A. Hakim, Umar Hafiz Khan, Rohini Chowgule, Vasant Shetye, Jonelle Raphael, Rosel Almeda, Mahesh Tawde, Rafiq Tadvi, Sunil Katkar, Milind Kadam, Rupesh Dhanawade, Umesh Ghurup, Siddhi Hirve, Somnath Sambhudas, Bharat Chaidhary, Meera Tambe, Savita Pingale, Arati Umap, Archana Umap, Nitin Shelar, Sampada Devchakke, Sharda Chaudhary, Suvarna Bondre, Savita Walke, Ashleshsa Gawhane, Anil Sapkal, Rupali Argade, Vijay Gaikwad, Sundeep Salvi, Bill Brashier, Jyoti Londhe, Sapna Madas, Althea Aquart-Stewart, Akosua Francia Aikman, Talant M. Sooronbaev, Bermet M. Estebesova, Meerim Akmatalieva, Saadat Usenbaeva, Jypara Kydyrova, Eliza Bostonova, Ulan Sheraliev, Nuridin Marajapov, Nurgul Toktogulova, Berik Emilov, Toktogul Azilova, Gulnara Beishekeeva, Nasyikat Dononbaeva, Aijamal Tabyshova, Wezzie Nyapigoti, Ernest Mwangoka, Mayamiko Kambwili, Martha Chipeta, Gloria Banda, Suzgo Mkandawire, Justice Banda, Li-Cher Loh, Siti Sholehah, Mohamed C. Benjelloun, Chakib Nejjari, Mohamed Elbiaze, Karima El Rhazi, E.F.M. Wouters, G.J. Wesseling, Gregory Erhabor, Olayemi Awopeju, Olufemi Adewole, Amund Gulsvik, Tina Endresen, Lene Svendsen, Muhammad Irfan, Zafar Fatmi, Aysha Zahidie, Natasha Shaukat, Meesha Iqbal, Luisito F. Idolor, Teresita S. de Guia, Norberto A. Francisco, Camilo C. Roa, Fernando G. Ayuyao, Cecil Z. Tady, Daniel T. Tan, Sylvia Banal-Yang, Vincent M. Balanag, Jr., Maria Teresita N. Reyes, Renato B. Dantes, Lourdes Amarillo, Lakan U. Berratio, Lenora C. Fernandez, Gerard S. Garcia, Sullian S. Naval, Thessa Reyes, Camilo C. Roa, Jr., Flordeliza Sanchez, Leander P. Simpao, Ewa Nizankowska-Mogilnicka, Jakub Frey, Rafal Harat, Pawel Nastalek, Andrzej Pajak, Wojciech Skucha, Andrzej Szczeklik, Magda Twardowska, Herminia Dias, João Almeida, Maria Joao Matos, Paula Simão, Moutinho Santos, Reis Ferreira, M. Al Ghobain, H. Alorainy, E. El-Hamad, M. Al Hajjaj, A. Hashi, R. Dela, R. Fanuncio, E. Doloriel, I. Marciano, L. Safia, Eric Bateman, Anamika Jithoo, Desiree Adams, Edward Barnes, Jasper Freeman, Anton Hayes, Sipho Hlengwa, Christine Johannisen, Mariana Koopman, Innocentia Louw, Ina Ludick, Alta Olckers, Johanna Ryck, Janita Storbeck, Kirthi Gunasekera, Rajitha Wickremasinghe, Asma Elsony, Hana A. Elsadig, Nada Bakery Osman, Bandar Salah Noory, Monjda Awad Mohamed, Hasab Alrasoul Akasha Ahmed Osman, Namarig Moham ed Elhassan, Abdel Mu’is El Zain, Marwa Mohamed Mohamaden, Suhaiba Khalifa, Mahmoud Elhadi, Mohand Hassan, Dalia Abdelmonam, Inga Sif Olafsdottir, Katarina Nisser, Ulrike SpetzNystrom, Gunilla Hagg, GunMarie Lund, Fallon Lutchmansingh, Liane Conyette, Myriam Denguezli, Zouhair Tabka, Hager Daldoul, Zaki Boukheroufa, Firas Chouikha, Wahbi Belhaj Khalifa, Ali Kocabas, Attila Hancioglu, Ismail Hanta, Sedat Kuleci, Ahmet Sinan Turkyilmaz, Sema Umut, Turgay Unalan, Peter G.J. Burney, Louisa Gnatiuc, Hadia Azar, Caron Amor, James Potts, Michael Tumilty, Fiona McLean, Risha Dudhaiya, A. Sonia Buist, Mary Ann McBurnie, William M. Vollmer, Suzanne Gillespie, Sean Sullivan, Todd A. Lee, Kevin B. Weiss, Robert L. Jensen, Robert Crapo, Paul Enright, David M. Mannino, John Cain, Rebecca Copeland, Dana Hazen, and Jennifer Methvin

Subjects
Chronic cough, Epidemiology, Global health, Excess risk, Medicine (General), R5-920
Abstract

Summary: Background: Chronic cough is a common respiratory symptom with an impact on daily activities and quality of life. Global prevalence data are scarce and derive mainly from European and Asian countries and studies with outcomes other than chronic cough. In this study, we aimed to estimate the prevalence of chronic cough across a large number of study sites as well as to identify its main risk factors using a standardised protocol and definition. Methods: We analysed cross-sectional data from 33,983 adults (≥40 years), recruited between Jan 2, 2003 and Dec 26, 2016, in 41 sites (34 countries) from the Burden of Obstructive Lung Disease (BOLD) study. We estimated the prevalence of chronic cough for each site accounting for sampling design. To identify risk factors, we conducted multivariable logistic regression analysis within each site and then pooled estimates using random-effects meta-analysis. We also calculated the population attributable risk (PAR) associated with each of the identifed risk factors. Findings: The prevalence of chronic cough varied from 3% in India (rural Pune) to 24% in the United States of America (Lexington,KY). Chronic cough was more common among females, both current and passive smokers, those working in a dusty job, those with a history of tuberculosis, those who were obese, those with a low level of education and those with hypertension or airflow limitation. The most influential risk factors were current smoking and working in a dusty job. Interpretation: Our findings suggested that the prevalence of chronic cough varies widely across sites in different world regions. Cigarette smoking and exposure to dust in the workplace are its major risk factors. Funding: Wellcome Trust.

Published
2024
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11. Polygenic risk scores identify heterogeneity in asthma and chronic obstructive pulmonary disease

Author

Moll, Matthew, Sordillo, Joanne E., Ghosh, Auyon J., Hayden, Lystra P., McDermott, Gregory, McGeachie, Michael J., Dahlin, Amber, Tiwari, Anshul, Manmadkar, Monica G., Abston, Eric D., Pavuluri, Chandan, Saferali, Aabida, Begum, Sofina, Ziniti, John P., Gulsvik, Amund, Bakke, Per S., Aschard, Hugues, Iribarren, Carlos, Hersh, Craig P., Sparks, Jeffrey A., Hobbs, Brian D., Lasky-Su, Jessica A., Silverman, Edwin K., Weiss, Scott T., Wu, Ann Chen, and Cho, Michael H.

Published
2023
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12. Can spirometric norms be set using pre- or post- bronchodilator test results in older people?

Author

Kato Bernet, Gulsvik Amund, Vollmer William, Janson Christer, Studnika Michael, Buist Sonia, and Burney Peter

Subjects
Normal values, BOLD study, European population, Diseases of the respiratory system, RC705-779
Abstract

Abstract Background Chronic Obstructive Pulmonary Disease (COPD) is defined by post-bronchodilator spirometry. Data on “normal values” come predominantly from pre-bronchodilator spirometry. The effects of this on diagnosis are unknown. Methods Lower limits of normal (LLN) were estimated from “normal” participants in the Burden of Obstructive Lung Disease (BOLD) programme. Values separately derived using pre- and post-bronchodilator spirometry were compared. Sensitivity and specificity of criteria derived from pre-bronchodilator spirometry and pre-bronchodilator spirometry adjusted by a constant were assessed in the remaining population. The “gold standard” was the LLN for the post-bronchodilator spirometry in the “normal population”. For FEV1/FVC, sensitivity and specificity of criteria were also assessed when a fixed value of < 70% was used rather than LLN. Results Of 6,600 participants with full data, 1,354 were defined as “normal”. Mean differences between pre- and post- bronchodilator measurements were small and the Bland-Altman plots showed no association between difference and mean value. Compared with using the gold standard, however, tests using pre-bronchodilator spirometry had a sensitivity and specificity of detecting a low FEV1 of 78.4% and 100%, a low FVC of 99.8% and 99.1% and a low FEV1/FVC ratio of 65% and 100%. Adjusting this by a constant improved the sensitivity without substantially altering the specificity for FEV1 (99%, 99.8%), FVC (97.4%, 99.9%) and FEV1/FVC (98.7%, 99.5%). Conclusions Using pre-bronchodilator spirometry to derive norms for lung function reduces sensitivity compared to a post-bronchodilator gold standard. Adjustment of these values by a constant can improve validity of the test.

Published
2012
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13. Underlying causes of cryptogenic stroke and TIA in The Nordic Atrial Fibrillation and Stroke (NOR-FIB) Study – the importance of comprehensive clinical evaluation

Author

B. Ratajczak-Tretel, A. Tancin Lambert, R. Al-Ani, K. Arntzen, G. K. Bakkejord, H. M.O. Bekkeseth, V. Bjerkeli, G. Eldøen, A. K. Gulsvik, B. Halvorsen, G. A. Høie, H. Ihle-Hansen, S. Ingebrigtsen, C. Kremer, S. B. Krogseth, C. Kruuse, M. Kurz, I. Nakstad, V. Novotny, H. Naess, R. Qazi, M. K. Rezaj, D. M. Rørholt, L. H. Steffensen, J. Sømark, H. Tobro, T. C. Truelsen, L. Wassvik, K. L. Ægidius, D. Atar, and A. H. Aamodt

Subjects
Cryptogenic stroke, Stroke cause, Atrial fibrillation, Insertable cardiac monitor, Guidelines, Secondary prevention, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Cryptogenic stroke is a heterogeneous condition, with a wide spectrum of possible underlying causes for which the optimal secondary prevention may differ substantially. Attempting a correct etiological diagnosis to reduce the stroke recurrence should be the fundamental goal of modern stroke management. Methods Prospective observational international multicenter study of cryptogenic stroke and cryptogenic transient ischemic attack (TIA) patients clinically monitored for 12 months to assign the underlying etiology. For atrial fibrillation (AF) detection continuous cardiac rhythm monitoring with insertable cardiac monitor (Reveal LINQ, Medtronic) was performed. The 12-month follow-up data for 250 of 259 initially included NOR-FIB patients were available for analysis. Results After 12 months follow-up probable stroke causes were revealed in 43% patients, while 57% still remained cryptogenic. AF and atrial flutter was most prevalent (29%). In 14% patients other possible causes were revealed (small vessel disease, large-artery atherosclerosis, hypercoagulable states, other cardioembolism). Patients remaining cryptogenic were younger (p

Published
2023
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15. Early life environment and snoring in adulthood

Author

Franklin Karl A, Janson Christer, Gíslason Thórarinn, Gulsvik Amund, Gunnbjörnsdottir Maria, Laerum Birger N, Lindberg Eva, Norrman Eva, Nyström Lennarth, Omenaas Ernst, Torén Kjell, and Svanes Cecilie

Subjects
Diseases of the respiratory system, RC705-779
Abstract

Abstract Background To our knowledge, no studies of the possible association of early life environment with snoring in adulthood have been published. We aimed to investigate whether early life environment is associated with snoring later in life. Methods A questionnaire including snoring frequency in adulthood and environmental factors in early life was obtained from 16,190 randomly selected men and women, aged 25–54 years, in Sweden, Norway, Iceland, Denmark and Estonia (response rate 74%). Results A total of 15,556 subjects answered the questions on snoring. Habitual snoring, defined as loud and disturbing snoring at least 3 nights a week, was reported by 18%. Being hospitalized for a respiratory infection before the age of two years (adjusted odds ratio (OR) = 1.27; 95% confidence interval (CI) 1.01–1.59), suffering from recurrent otitis as a child (OR = 1.18; 95%CI 1.05–1.33), growing up in a large family (OR = 1.04; 95%CI 1.002–1.07) and being exposed to a dog at home as a newborn (OR = 1.26; 95%CI 1.12–1.42) were independently related to snoring later in life and independent of a number of possible confounders in adulthood. The same childhood environmental factors except household size were also related with snoring and daytime sleepiness combined. Conclusion The predisposition for adult snoring may be partly established early in life. Having had severe airway infections or recurrent otitis in childhood, being exposed to a dog as a newborn and growing up in a large family are environmental factors associated with snoring in adulthood.

Published
2008
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16. X chromosome associations with chronic obstructive pulmonary disease and related phenotypes: an X chromosome-wide association study

Author

Lystra P. Hayden, Brian D. Hobbs, Robert Busch, Michael H. Cho, Ming Liu, Camila M. Lopes-Ramos, David A. Lomas, Per Bakke, Amund Gulsvik, Edwin K. Silverman, James D. Crapo, Terri H. Beaty, Nan M. Laird, Christoph Lange, and Dawn L. DeMeo

Subjects
COPD, Lung function, Emphysema, X chromosome-wide association study, Sex differences, X chromosome inactivation, Diseases of the respiratory system, RC705-779
Abstract

Abstract Background The association between genetic variants on the X chromosome to risk of COPD has not been fully explored. We hypothesize that the X chromosome harbors variants important in determining risk of COPD related phenotypes and may drive sex differences in COPD manifestations. Methods Using X chromosome data from three COPD-enriched cohorts of adult smokers, we performed X chromosome specific quality control, imputation, and testing for association with COPD case–control status, lung function, and quantitative emphysema. Analyses were performed among all subjects, then stratified by sex, and subsequently combined in meta-analyses. Results Among 10,193 subjects of non-Hispanic white or European ancestry, a variant near TMSB4X, rs5979771, reached genome-wide significance for association with lung function measured by FEV1/FVC ( $$\beta$$ β 0.020, SE 0.004, p 4.97 × 10–08), with suggestive evidence of association with FEV1 ( $$\beta$$ β 0.092, SE 0.018, p 3.40 × 10–07). Sex-stratified analyses revealed X chromosome variants that were differentially trending in one sex, with significantly different effect sizes or directions. Conclusions This investigation identified loci influencing lung function, COPD, and emphysema in a comprehensive genetic association meta-analysis of X chromosome genetic markers from multiple COPD-related datasets. Sex differences play an important role in the pathobiology of complex lung disease, including X chromosome variants that demonstrate differential effects by sex and variants that may be relevant through escape from X chromosome inactivation. Comprehensive interrogation of the X chromosome to better understand genetic control of COPD and lung function is important to further understanding of disease pathology. Trial registration Genetic Epidemiology of COPD Study (COPDGene) is registered at ClinicalTrials.gov, NCT00608764 (Active since January 28, 2008). Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints Study (ECLIPSE), GlaxoSmithKline study code SCO104960, is registered at ClinicalTrials.gov, NCT00292552 (Active since February 16, 2006). Genetics of COPD in Norway Study (GenKOLS) holds GlaxoSmithKline study code RES11080, Genetics of Chronic Obstructive Lung Disease.

Published
2023
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17. Genetic Associations and Architecture of Asthma-COPD Overlap

Author

John, Catherine, Guyatt, Anna L., Shrine, Nick, Packer, Richard, Olafsdottir, Thorunn A., Liu, Jiangyuan, Hayden, Lystra P., Chu, Su H., Koskela, Jukka T., Luan, Jian’an, Li, Xingnan, Terzikhan, Natalie, Xu, Hanfei, Bartz, Traci M., Petersen, Hans, Leng, Shuguang, Belinsky, Steven A., Cepelis, Aivaras, Hernández Cordero, Ana I., Obeidat, Ma’en, Thorleifsson, Gudmar, Meyers, Deborah A., Bleecker, Eugene R., Sakoda, Lori C., Iribarren, Carlos, Tesfaigzi, Yohannes, Gharib, Sina A., Dupuis, Josée, Brusselle, Guy, Lahousse, Lies, Ortega, Victor E., Jonsdottir, Ingileif, Sin, Don D., Bossé, Yohan, van den Berge, Maarten, Nickle, David, Quint, Jennifer K., Sayers, Ian, Hall, Ian P., Langenberg, Claudia, Ripatti, Samuli, Laitinen, Tarja, Wu, Ann C., Lasky-Su, Jessica, Bakke, Per, Gulsvik, Amund, Hersh, Craig P., Hayward, Caroline, Langhammer, Arnulf, Brumpton, Ben, Stefansson, Kari, Cho, Michael H., Wain, Louise V., and Tobin, Martin D.

Published
2022
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18. Outcome-based Definition of the Lower Limit of Normal in Spirometry: A Study of 26,000 Young Adult Men.

Author

Cestelli, Lucia, Stavem, Knut, Johannessen, Ane, Gulsvik, Amund, and Nielsen, Rune

Subjects
YOUNG adults, DEMOGRAPHIC surveys, SPIROMETRY, BODY mass index, YOUNG men, VITAL capacity (Respiration)
Abstract

Rationale: The definition of the lower limit of normal (LLN) of spirometric variables is not well established. Objectives: To investigate the relationship between spirometric abnormalities defined with different thresholds of the LLN and clinical outcomes and to explore the possibility of using different LLN thresholds according to the pretest probability of disease. Methods: We studied the associations between prebronchodilator spirometric abnormalities (forced expiratory volume in the first second [FEV1] < LLN, forced vital capacity [FVC] < LLN, airflow obstruction, spirometric restriction) defined with different thresholds of the LLN (10th, 5th, 2.5th, 1st percentile) and multiple outcomes (prevalence of spirometric abnormalities, respiratory symptoms, all-cause and respiratory mortality) in 26,091 30- to 46-year-old men who participated in a general population survey in Norway in 1988–1990 and were followed for 26 years. Analyses were performed with both local and Global Lung Function Initiative (GLI)-2012 reference equations, stratified by pretest risk (presence or absence of respiratory symptoms), and adjusted for age, body mass index, smoking, and education. Results: In the total population, the prevalence of airflow obstruction was 11.6% with GLI-LLN10, 11.0% with Local-LLN5, 6.1% with GLI-LLN5, 7.6% with Local-LLN2.5, and 3.5% with GLI-LLN2.5. The prevalence of spirometric restriction was 5.9% with GLI-LLN10, 5.2% with Local-LLN5, and 2.8% with GLI-LLN5. Increasingly lower thresholds of the LLN were associated with increasingly higher odds of respiratory symptoms and hazard of mortality for all spirometric abnormalities with both reference equations. Spirometric abnormalities defined with Local-LLN2.5 in asymptomatic subjects were associated with lower hazard of all-cause mortality (hazard ratio [HR], 1.50; 95% confidence interval [CI], 1.15–1.95 for FEV1 < LLN) than those defined with Local-LLN5 in the general population (HR, 1.67; 95% CI, 1.50–1.87 for FEV1 < LLN) and symptomatic subjects (HR, 1.67; 95% CI, 1.46–1.91 for FEV1 < LLN). Overall, the prevalence of spirometric abnormalities and associations with outcomes obtained with Local-LLN5 were comparable to those obtained with GLI-LLN10 and those obtained with Local-LLN2.5 to GLI-LLN5. Conclusions: There is a relationship between statistically based thresholds of the LLN of spirometric variables and clinical outcomes. Different thresholds of the LLN may be used in different risk subgroups of subjects, but the choice of the threshold needs to be evaluated together with the choice of reference equations. [ABSTRACT FROM AUTHOR]

Published
2024
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19. Period and cohort effects: consequences on spirometric lung function in Norway during the 20th century

Author

Lucia Cestelli, Ane Johannessen, Knut Stavem, Amund Gulsvik, and Rune Nielsen

Subjects
Medicine
Abstract

Background and aim Several factors can influence measured lung function over time. The aim of this study was to investigate period and cohort effects on spirometric measures in a large general population sample in Norway during the 20th century, using Global Lung Function Initiative (GLI-2012) equations as a reference. Methods 36 466 subjects (born 1894–1969) from four cross-sectional surveys conducted between 1965 and 1999 were included, with harmonised data on smoking habits, respiratory symptoms, lung diseases, education and spirometry. Changes in forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) z-scores in healthy subjects across surveys were explored to investigate period effects. Linear mixed-effects models of FEV1 and FVC z-scores on birth cohort, with survey as random effect, were used to investigate cohort effects, both in subjects of the total population and in healthy ones. Results Relatively higher FEV1 and FVC z-scores in healthy subjects were found in the first survey (1965–1970) compared to the more recent ones (1988–1999), suggesting period effects. FEV1 and FVC z-scores increased significantly with birth cohort from 1894 to 1935, after adjustment for covariates. A more stable trend of FEV1 and FVC z-scores with birth cohort was evidenced for subjects born more recently (1945–1969). Conclusions An increase of lung function with year of birth was observed in Norwegian subjects during the first half of the 20th century. The impact of period effects on lung function decreased from 1965 to 1999.

Published
2022
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20. Genetic Association and Risk Scores in a Chronic Obstructive Pulmonary Disease Meta-analysis of 16,707 Subjects.

Author

Busch, Robert, Hobbs, Brian D, Zhou, Jin, Castaldi, Peter J, McGeachie, Michael J, Hardin, Megan E, Hawrylkiewicz, Iwona, Sliwinski, Pawel, Yim, Jae-Joon, Kim, Woo Jin, Kim, Deog K, Agusti, Alvar, Make, Barry J, Crapo, James D, Calverley, Peter M, Donner, Claudio F, Lomas, David A, Wouters, Emiel F, Vestbo, Jørgen, Tal-Singer, Ruth, Bakke, Per, Gulsvik, Amund, Litonjua, Augusto A, Sparrow, David, Paré, Peter D, Levy, Robert D, Rennard, Stephen I, Beaty, Terri H, Hokanson, John, Silverman, Edwin K, Cho, Michael H, National Emphysema Treatment Trial Genetics, Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-Points, International COPD Genetics Network, and COPDGene Investigators

Subjects
National Emphysema Treatment Trial Genetics, Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-Points, International COPD Genetics Network, COPDGene Investigators, Humans, Pulmonary Disease, Chronic Obstructive, Genetic Predisposition to Disease, Respiratory Function Tests, Risk Factors, Aged, Middle Aged, Female, Male, Genome-Wide Association Study, alpha-1 antitrypsin, chronic obstructive pulmonary disease, genetic epidemiology, genetic risk factors, genetic risk score, Chronic Obstructive Pulmonary Disease, Lung, Clinical Research, Genetics, Prevention, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Respiratory, Cardiorespiratory Medicine and Haematology, Respiratory System
Abstract

The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving genome-wide significance. In addition, the combined contribution of genetic variation to COPD risk has not been fully explored. We sought to determine: (1) whether studies of variants from previous studies of COPD or lung function in a larger sample could identify additional associated variants, particularly for severe COPD; and (2) the impact of genetic risk scores on COPD. We genotyped 3,346 single-nucleotide polymorphisms (SNPs) in 2,588 cases (1,803 severe COPD) and 1,782 control subjects from four cohorts, and performed association testing with COPD, combining these results with existing genotyping data from 6,633 cases (3,497 severe COPD) and 5,704 control subjects. In addition, we developed genetic risk scores from SNPs associated with lung function and COPD and tested their discriminatory power for COPD-related measures. We identified significant associations between SNPs near PPIC (P = 1.28 × 10-8) and PPP4R4/SERPINA1 (P = 1.01 × 10-8) and severe COPD; the latter association may be driven by recognized variants in SERPINA1. Genetic risk scores based on SNPs previously associated with COPD and lung function had a modest ability to discriminate COPD (area under the curve, ∼0.6), and accounted for a mean 0.9-1.9% lower forced expiratory volume in 1 second percent predicted for each additional risk allele. In a large genetic association analysis, we identified associations with severe COPD near PPIC and SERPINA1. A risk score based on combining genetic variants had modest, but significant, effects on risk of COPD and lung function.

Published
2017

21. Genetic loci associated with chronic obstructive pulmonary disease overlap with loci for lung function and pulmonary fibrosis

Author

Hobbs, Brian D, de Jong, Kim, Lamontagne, Maxime, Bossé, Yohan, Shrine, Nick, Artigas, María Soler, Wain, Louise V, Hall, Ian P, Jackson, Victoria E, Wyss, Annah B, London, Stephanie J, North, Kari E, Franceschini, Nora, Strachan, David P, Beaty, Terri H, Hokanson, John E, Crapo, James D, Castaldi, Peter J, Chase, Robert P, Bartz, Traci M, Heckbert, Susan R, Psaty, Bruce M, Gharib, Sina A, Zanen, Pieter, Lammers, Jan W, Oudkerk, Matthijs, Groen, HJ, Locantore, Nicholas, Tal-Singer, Ruth, Rennard, Stephen I, Vestbo, Jørgen, Timens, Wim, Paré, Peter D, Latourelle, Jeanne C, Dupuis, Josée, O'Connor, George T, Wilk, Jemma B, Kim, Woo Jin, Lee, Mi Kyeong, Oh, Yeon-Mok, Vonk, Judith M, de Koning, Harry J, Leng, Shuguang, Belinsky, Steven A, Tesfaigzi, Yohannes, Manichaikul, Ani, Wang, Xin-Qun, Rich, Stephen S, Barr, R Graham, Sparrow, David, Litonjua, Augusto A, Bakke, Per, Gulsvik, Amund, Lahousse, Lies, Brusselle, Guy G, Stricker, Bruno H, Uitterlinden, André G, Ampleford, Elizabeth J, Bleecker, Eugene R, Woodruff, Prescott G, Meyers, Deborah A, Qiao, Dandi, Lomas, David A, Yim, Jae-Joon, Kim, Deog Kyeom, Hawrylkiewicz, Iwona, Sliwinski, Pawel, Hardin, Megan, Fingerlin, Tasha E, Schwartz, David A, Postma, Dirkje S, MacNee, William, Tobin, Martin D, Silverman, Edwin K, Boezen, H Marike, and Cho, Michael H

Subjects
Biological Sciences, Genetics, Chronic Obstructive Pulmonary Disease, Lung, Human Genome, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Respiratory, Adult, Aged, Aged, 80 and over, Alleles, Asthma, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Middle Aged, Phenotype, Polymorphism, Single Nucleotide, Pulmonary Disease, Chronic Obstructive, Pulmonary Fibrosis, Risk Factors, Smoking, COPDGene Investigators, ECLIPSE Investigators, LifeLines Investigators, SPIROMICS Research Group, International COPD Genetics Network Investigators, UK BiLEVE Investigators, International COPD Genetics Consortium, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality worldwide. We performed a genetic association study in 15,256 cases and 47,936 controls, with replication of select top results (P < 5 × 10-6) in 9,498 cases and 9,748 controls. In the combined meta-analysis, we identified 22 loci associated at genome-wide significance, including 13 new associations with COPD. Nine of these 13 loci have been associated with lung function in general population samples, while 4 (EEFSEC, DSP, MTCL1, and SFTPD) are new. We noted two loci shared with pulmonary fibrosis (FAM13A and DSP) but that had opposite risk alleles for COPD. None of our loci overlapped with genome-wide associations for asthma, although one locus has been implicated in joint susceptibility to asthma and obesity. We also identified genetic correlation between COPD and asthma. Our findings highlight new loci associated with COPD, demonstrate the importance of specific loci associated with lung function to COPD, and identify potential regions of genetic overlap between COPD and other respiratory diseases.

Published
2017

22. Sex-Based Genetic Association Study Identifies CELSR1 as a Possible Chronic Obstructive Pulmonary Disease Risk Locus among Women

Author

Hardin, Megan, Cho, Michael H, Sharma, Sunita, Glass, Kimberly, Castaldi, Peter J, McDonald, Merry-Lynn, Aschard, Hugues, Senter-Sylvia, Jody, Tantisira, Kelan, Weiss, Scott T, Hersh, Craig P, Morrow, Jarrett D, Lomas, David, Agusti, Alvar, Bakke, Per, Gulsvik, Amund, O'Connor, George T, Dupuis, Josée, Hokanson, John, Crapo, James D, Beaty, Terri H, Laird, Nan, Silverman, Edwin K, and DeMeo, Dawn L

Subjects
Biological Sciences, Genetics, Chronic Obstructive Pulmonary Disease, Tobacco Smoke and Health, Prevention, Clinical Research, Lung, Tobacco, Human Genome, Respiratory, Aged, Alleles, Cadherins, Demography, Female, Gene Expression Regulation, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Pulmonary Disease, Chronic Obstructive, Risk Factors, chronic obstructive pulmonary disease, genetics, growth and development, sex, genome-wide association study, COPDGene and Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-Points Investigators, Cardiorespiratory Medicine and Haematology, Respiratory System, Biochemistry and cell biology, Cardiovascular medicine and haematology
Abstract

Chronic obstructive pulmonary disease (COPD) is a complex disease with strong environmental and genetic influences and sexually dimorphic features. Although genetic risk factors for COPD have been identified, much of the heritability remains unexplained. Sex-based genetic association studies may uncover additional COPD genetic risk factors. We studied current and former smokers from COPD case-control cohorts (COPDGene non-Hispanic whites and African Americans, Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-Points, and Genetics of Chronic Obstructive Lung Disease). COPD was defined as post-bronchodilator forced expiratory volume in 1 second/forced vital capacity less than 0.70 and forced expiratory volume in 1 second percent predicted less than 80. Testing was performed across all cohorts and combined in a meta-analysis adjusted for age, pack-years, and genetic ancestry. We first performed genome-wide single-nucleotide polymorphism (SNP)-by-sex interaction testing on the outcome of COPD affection status. We performed sex-stratified association testing for SNPs with interaction P less than 10-6. We examined over 8 million SNPs in four populations, including 6,260 subjects with COPD (40.6% female) and 5,269 smoking control subjects (47.3% female). The SNP rs9615358 in the cadherin gene CELSR1 approached genome-wide significance for an interaction with sex (P = 1.24 × 10-7). In the sex-stratified meta-analysis, this SNP was associated with COPD among females (odds ratio, 1.37 [95% confidence interval, 1.25-1.49]; P = 3.32 × 10-7) but not males (odds ratio, 0.90 [95% confidence interval, 0.79-1.01]; P = 0.06). CELSR1 is involved in fetal lung development. In a human fetal lung tissue dataset, we observed greater CELSR1 expression in female compared with male samples. This SNP-by-sex genome-wide association analysis identified the fetal lung development gene, CELSR1, as a potential sex-specific risk factor for COPD. Identifying sex-specific genetic risk factors may reveal new insights into sexually dimorphic features of COPD.

Published
2017

23. A genome-wide association study of bronchodilator response in participants of European and African ancestry from six independent cohorts

Author

Jessica D. Gereige, Hanfei Xu, Victor E. Ortega, Michael H. Cho, Ming Liu, Phuwanat Sakornsakolpat, Edwin K. Silverman, Terri H. Beaty, Bruce E. Miller, Per Bakke, Amund Gulsvik, Craig P. Hersh, Jarrett D. Morrow, Elizabeth J. Ampleford, Gregory A. Hawkins, Eugene R. Bleecker, Deborah A. Meyers, Stephen P. Peters, Juan C. Celedón, Kelan Tantisira, Jiang Li, Josée Dupuis, and George T. O'Connor

Subjects
Medicine
Abstract

Introduction Bronchodilator response (BDR) is a measurement of acute bronchodilation in response to short-acting β2-agonists, with a heritability between 10 and 40%. Identifying genetic variants associated with BDR may lead to a better understanding of its complex pathophysiology. Methods We performed a genome-wide association study (GWAS) of BDR in six adult cohorts with participants of European ancestry (EA) and African ancestry (AA) including community cohorts and cohorts ascertained on the basis of obstructive pulmonary disease. Validation analysis was carried out in two paediatric asthma cohorts. Results A total of 10 623 EA and 3597 AA participants were included in the analyses. No single nucleotide polymorphism (SNP) was associated with BDR at the conventional genome-wide significance threshold (p

Published
2022
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27. Chronic obstructive pulmonary disease and related phenotypes: polygenic risk scores in population-based and case-control cohorts

Author

Soler Artigas, María, Jackson, Victoria E, Strachan, David P, Hui, Jennie, James, Alan L, Kerr, Shona M, Polasek, Ozren, Vitart, Veronique, Marten, Jonathan, Rudan, Igor, Kähönen, Mika, Surakka, Ida, Gieger, Christian, Karrasch, Stefan, Rawal, Rajesh, Schulz, Holger, Deary, Ian J, Harris, Sarah E, Enroth, Stefan, Gyllensten, Ulf, Imboden, Medea, Probst-Hensch, Nicole M, Lehtimäki, Terho, Raitakari, Olli T, Langenberg, Claudia, Luan, Jian'an, Wareham, Nick, Zhao, Jing Hua, Hayward, Caroline, Murray, Alison, Porteous, David J, Smith, Blair H, Jarvelin, Marjo-Riitta, Wielscher, Matthias, Joshi, Peter K, Kentistou, Katherine A, Timmers, Paul RHJ, Wilson, James F, Cook, James P, Lind, Lars, Mahajan, Anubha, Morris, Andrew P, Ewert, Ralf, Homuth, Georg, Stubbe, Beate, Weiss, Stefan, Zeggini, Eleftheria, Moll, Matthew, Sakornsakolpat, Phuwanat, Shrine, Nick, Hobbs, Brian D, DeMeo, Dawn L, John, Catherine, Guyatt, Anna L, McGeachie, Michael J, Gharib, Sina A, Obeidat, Ma'en, Lahousse, Lies, Wijnant, Sara R A, Brusselle, Guy, Meyers, Deborah A, Bleecker, Eugene R, Li, Xingnan, Tal-Singer, Ruth, Manichaikul, Ani, Rich, Stephen S, Won, Sungho, Kim, Woo Jin, Do, Ah Ra, Washko, George R, Barr, R Graham, Psaty, Bruce M, Bartz, Traci M, Hansel, Nadia N, Barnes, Kathleen, Hokanson, John E, Crapo, James D, Lynch, David, Bakke, Per, Gulsvik, Amund, Hall, Ian P, Wain, Louise, Weiss, Scott T, Silverman, Edwin K, Dudbridge, Frank, Tobin, Martin D, and Cho, Michael H

Published
2020
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28. Common and Rare Variants Genetic Association Analysis of Cigarettes per Day Among Ever-Smokers in Chronic Obstructive Pulmonary Disease Cases and Controls

Author

ECLIPSE and COPDGene Investigators, Lutz, Sharon M., Frederiksen, Brittni, Begum, Ferdouse, McDonald, Merry-Lynn N., Cho, Michael H., Hobbs, Brian D., Parker, Margaret M., DeMeo, Dawn L., Hersh, Craig P., Ehringer, Marissa A., Young, Kendra, Jiang, Lai, Foreman, Marilyn G., Kinney, Greg L., Make, Barry J., Lomas, David A., Bakke, Per, Gulsvik, Amund, Crapo, James D., Silverman, Edwin K., Beaty, Terri H., and Hokanson, John E.

Published
2019

29. A genome-wide association study identifies risk loci for spirometric measures among smokers of European and African ancestry.

Author

Lutz, Sharon M, Cho, Michael H, Young, Kendra, Hersh, Craig P, Castaldi, Peter J, McDonald, Merry-Lynn, Regan, Elizabeth, Mattheisen, Manuel, DeMeo, Dawn L, Parker, Margaret, Foreman, Marilyn, Make, Barry J, Jensen, Robert L, Casaburi, Richard, Lomas, David A, Bhatt, Surya P, Bakke, Per, Gulsvik, Amund, Crapo, James D, Beaty, Terri H, Laird, Nan M, Lange, Christoph, Hokanson, John E, Silverman, Edwin K, ECLIPSE Investigators, and COPDGene Investigators

Subjects
ECLIPSE Investigators, COPDGene Investigators, Chromosomes, Human, Pair 4, Chromosomes, Human, Pair 15, Humans, Genetic Predisposition to Disease, Bronchodilator Agents, Forced Expiratory Volume, Spirometry, Risk Factors, Cohort Studies, Smoking, Genome, Human, Middle Aged, African Continental Ancestry Group, European Continental Ancestry Group, Female, Male, Meta-Analysis as Topic, Genome-Wide Association Study, Genetic Loci, Chronic obstructive pulmonary disease, DBH, FEV1, FEV1/FVC, Genome-wide association study, Chromosomes, Human, Pair 4, Pair 15, Genome, Genetics & Heredity, Genetics
Abstract

BackgroundPulmonary function decline is a major contributor to morbidity and mortality among smokers. Post bronchodilator FEV1 and FEV1/FVC ratio are considered the standard assessment of airflow obstruction. We performed a genome-wide association study (GWAS) in 9919 current and former smokers in the COPDGene study (6659 non-Hispanic Whites [NHW] and 3260 African Americans [AA]) to identify associations with spirometric measures (post-bronchodilator FEV1 and FEV1/FVC). We also conducted meta-analysis of FEV1 and FEV1/FVC GWAS in the COPDGene, ECLIPSE, and GenKOLS cohorts (total n = 13,532).ResultsAmong NHW in the COPDGene cohort, both measures of pulmonary function were significantly associated with SNPs at the 15q25 locus [containing CHRNA3/5, AGPHD1, IREB2, CHRNB4] (lowest p-value = 2.17 × 10(-11)), and FEV1/FVC was associated with a genomic region on chromosome 4 [upstream of HHIP] (lowest p-value = 5.94 × 10(-10)); both regions have been previously associated with COPD. For the meta-analysis, in addition to confirming associations to the regions near CHRNA3/5 and HHIP, genome-wide significant associations were identified for FEV1 on chromosome 1 [TGFB2] (p-value = 8.99 × 10(-9)), 9 [DBH] (p-value = 9.69 × 10(-9)) and 19 [CYP2A6/7] (p-value = 3.49 × 10(-8)) and for FEV1/FVC on chromosome 1 [TGFB2] (p-value = 8.99 × 10(-9)), 4 [FAM13A] (p-value = 3.88 × 10(-12)), 11 [MMP3/12] (p-value = 3.29 × 10(-10)) and 14 [RIN3] (p-value = 5.64 × 10(-9)).ConclusionsIn a large genome-wide association study of lung function in smokers, we found genome-wide significant associations at several previously described loci with lung function or COPD. We additionally identified a novel genome-wide significant locus with FEV1 on chromosome 9 [DBH] in a meta-analysis of three study populations.

Published
2015

31. Overdiagnosis of COPD in Subjects With Unobstructed Spirometry: A BOLD Analysis

Author

Zhong, NanShan, Liu, Shengming, Lu, Jiachun, Ran, Pixin, Wang, Dali, Zheng, Jingping, Zhou, Yumin, Kocabaş, Ali, Hancioglu, Attila, Hanta, Ismail, Kuleci, Sedat, Turkyilmaz, Ahmet Sinan, Umut, Sema, Unalan, Turgay, Studnicka, Michael, Dawes, Torkil, Lamprecht, Bernd, Sator, Lea, Bateman, Eric, Jithoo, Anamika, Adams, Desiree, Barnes, Edward, Freeman, Jasper, Hayes, Anton, Hlengwa, Sipho, Johannisen, Christine, Koopman, Mariana, Louw, Innocentia, Ludick, Ina, Olckers, Alta, Ryck, Johanna, Storbeck, Janita, Gislason, Thorarinn, Benedikdtsdottir, Bryndis, Jörundsdottir, Kristin, Gudmundsdottir, Lovisa, Gudmundsdottir, Sigrun, Gundmundsson, Gunnar, Nizankowska-Mogilnicka, Ewa, Frey, Jakub, Harat, Rafal, Mejza, Filip, Nastalek, Pawel, Pajak, Andrzej, Skucha, Wojciech, Szczeklik, Andrzej, Twardowska, Magda, Welte, Tobias, Bodemann, Isabelle, Geldmacher, Henning, Schweda-Linow, Alexandra, Gulsvik, Amund, Endresen, Tina, Svendsen, Lene, Tan, Wan C., Wang, Wen, Mannino, David M., Cain, John, Copeland, Rebecca, Hazen, Dana, Methvin, Jennifer, Dantes, Renato B., Amarillo, Lourdes, Berratio, Lakan U., Fernandez, Lenora C., Francisco, Norberto A., Garcia, Gerard S., de Guia, Teresita S., Idolor, Luisito F., Naval, Sullian S., Reyes, Thessa, Roa, Camilo C., Jr., Sanchez, Ma. Flordeliza, Simpao, Leander P., Jenkins, Christine, Marks, Guy, Bird, Tessa, Espinel, Paola, Hardaker, Kate, Toelle, Brett, Burney, Peter G.J., Amor, Caron, Potts, James, Tumilty, Michael, McLean, Fiona, Wouters, E.F.M., Wesseling, G.J., Bárbara, Cristina, Rodrigues, Fátima, Dias, Hermínia, Cardoso, João, Almeida, João, Matos, Maria João, Simão, Paula, Santos, Moutinho, Ferreira, Reis, Janson, Christer, Olafsdottir, Inga Sif, Nisser, Katarina, Spetz-Nyström, Ulrike, Hägg, Gunilla, Lund, Gun-Marie, Jõgi, Rain, Laja, Hendrik, Ulst, Katrin, Zobel, Vappu, Lill, Toomas-Julius, Koul, Parvaiz A., Malik, Sajjad, Hakim, Nissar A., Khan, Umar Hafiz, Chowgule, Rohini, Shetye, Vasant, Raphael, Jonelle, Almeda, Rosel, Tawde, Mahesh, Tadvi, Rafiq, Katkar, Sunil, Kadam, Milind, Dhanawade, Rupesh, Ghurup, Umesh, Harrabi, Imed, Denguezli, Myriam, Tabka, Zouhair, Daldoul, Hager, Boukheroufa, Zaki, Chouikha, Firas, Khalifa, Wahbi Belhaj, Roa, Camilo C., Ayuyao, Fernando G., Tady, Cecil Z., Tan, Daniel T., Banal-Yang, Sylvia, Balanag, Vincent M., Jr., Reyes, Maria Teresita N., Juvekar, Sanjay, Hirve, Siddhi, Sambhudas, Somnath, Chaidhary, Bharat, Tambe, Meera, Pingale, Savita, Umap, Arati, Umap, Archana, Shelar, Nitin, Devchakke, Sampada, Chaudhary, Sharda, Bondre, Suvarna, Walke, Savita, Gawhane, Ashleshsa, Sapkal, Anil, Argade, Rupali, Gaikwad, Vijay, Salvi, Sundeep, Brashier, Bill, Londhe, Jyoti, Madas, Sapna, Obaseki, Daniel, Erhabor, Gregory, Awopeju, Olayemi, Adewole, Olufemi, Horner, Andreas, Kaiser, Bernhard, McBurnie, Mary Ann, Buist, A. Sonia, Gnatiuc, Luisa, Bateman, Eric D., and Burney, Peter

Published
2019
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32. Common Genetic Variants Associated with Resting Oxygenation in Chronic Obstructive Pulmonary Disease

Author

McDonald, Merry-Lynn N, Cho, Michael H, Sørheim, Inga-Cecilie, Lutz, Sharon M, Castaldi, Peter J, Lomas, David A, Coxson, Harvey O, Edwards, Lisa D, MacNee, William, Vestbo, Jørgen, Yates, Julie C, Agusti, Alvar, Calverley, Peter MA, Celli, Bartolome, Crim, Courtney, Rennard, Stephen I, Wouters, Emiel FM, Bakke, Per, Tal-Singer, Ruth, Miller, Bruce E, Gulsvik, Amund, Casaburi, Richard, Wells, J Michael, Regan, Elizabeth A, Make, Barry J, Hokanson, John E, Lange, Christoph, Crapo, James D, Beaty, Terri H, Silverman, Edwin K, and Hersh, Craig P

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Lung, Prevention, Clinical Research, Chronic Obstructive Pulmonary Disease, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Black or African American, Aged, Aged, 80 and over, Chromosomes, Human, Pair 15, Female, Genetic Predisposition to Disease, Genetic Variation, Genome-Wide Association Study, Humans, Hypoxia, Male, Middle Aged, Oximetry, Oxygen, Polymorphism, Single Nucleotide, Prognosis, Pulmonary Disease, Chronic Obstructive, Rest, White People, chronic obstructive pulmonary disease, hypoxemia, pulse oximetry, genome-wide association study, oxygen saturation, Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints and COPDGene Investigators, Cardiorespiratory Medicine and Haematology, Respiratory System, Biochemistry and cell biology, Cardiovascular medicine and haematology
Abstract

Hypoxemia is a major complication of chronic obstructive pulmonary disease (COPD) that correlates with disease prognosis. Identifying genetic variants associated with oxygenation may provide clues for deciphering the heterogeneity in prognosis among patients with COPD. However, previous genetic studies have been restricted to investigating COPD candidate genes for association with hypoxemia. To report results from the first genome-wide association study (GWAS) of resting oxygen saturation (as measured by pulse oximetry [Spo2]) in subjects with COPD, we performed a GWAS of Spo2 in two large, well characterized COPD populations: COPDGene, including both the non-Hispanic white (NHW) and African American (AA) groups, and Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE). We identified several suggestive loci (P < 1 × 10(-5)) associated with Spo2 in COPDGene in the NHW (n = 2810) and ECLIPSE (n = 1758) groups, and two loci on chromosomes 14 and 15 in the AA group (n = 820) from COPDGene achieving a level of genome-wide significance (P < 5 × 10(-8)). The chromosome 14 single-nucleotide polymorphism, rs6576132, located in an intergenic region, was nominally replicated (P < 0.05) in the NHW group from COPDGene. The chromosome 15 single-nucleotide polymorphisms were rare in subjects of European ancestry, so the results could not be replicated. The chromosome 15 region contains several genes, including TICRR and KIF7, and is proximal to RHCG (Rh family C glyocoprotein gene). We have identified two loci associated with resting oxygen saturation in AA subjects with COPD, and several suggestive regions in subjects of European descent with COPD. Our study highlights the importance of investigating the genetics of complex traits in different racial groups.

Published
2014

33. Risk loci for chronic obstructive pulmonary disease: a genome-wide association study and meta-analysis

Author

Cho, Michael H, McDonald, Merry-Lynn N, Zhou, Xiaobo, Mattheisen, Manuel, Castaldi, Peter J, Hersh, Craig P, DeMeo, Dawn L, Sylvia, Jody S, Ziniti, John, Laird, Nan M, Lange, Christoph, Litonjua, Augusto A, Sparrow, David, Casaburi, Richard, Barr, R Graham, Regan, Elizabeth A, Make, Barry J, Hokanson, John E, Lutz, Sharon, Dudenkov, Tanda Murray, Farzadegan, Homayoon, Hetmanski, Jacqueline B, Tal-Singer, Ruth, Lomas, David A, Bakke, Per, Gulsvik, Amund, Crapo, James D, Silverman, Edwin K, Beaty, Terri H, and on behalf of the NETT Genetics, ICGN

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Chronic Obstructive Pulmonary Disease, Genetics, Prevention, Lung, Human Genome, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Pulmonary Disease, Chronic Obstructive, NETT Genetics, ICGN, ECLIPSE and COPDGene Investigators, Public Health and Health Services, Other Medical and Health Sciences, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundThe genetic risk factors for susceptibility to chronic obstructive pulmonary disease (COPD) are still largely unknown. Additional genetic variants are likely to be identified by genome-wide association studies in larger cohorts or specific subgroups. We sought to identify risk loci for moderate to severe and severe COPD with data from several cohort studies.MethodsWe combined genome-wide association analysis data from participants in the COPDGene study (non-Hispanic white and African-American ethnic origin) and the ECLIPSE, NETT/NAS, and Norway GenKOLS studies (self-described white ethnic origin). We did analyses comparing control individuals with individuals with moderate to severe COPD and with a subset of individuals with severe COPD. Single nucleotide polymorphisms yielding a p value of less than 5 × 10(-7) in the meta-analysis at loci not previously described were genotyped in individuals from the family-based ICGN study. We combined results in a joint meta-analysis (threshold for significance p

Published
2014

36. New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries

Author

Shrine, Nick, Guyatt, Anna L., Erzurumluoglu, A. Mesut, Jackson, Victoria E., Hobbs, Brian D., Melbourne, Carl A., Batini, Chiara, Fawcett, Katherine A., Song, Kijoung, Sakornsakolpat, Phuwanat, Li, Xingnan, Boxall, Ruth, Reeve, Nicola F., Obeidat, Ma’en, Zhao, Jing Hua, Wielscher, Matthias, Weiss, Stefan, Kentistou, Katherine A., Cook, James P., Sun, Benjamin B., Zhou, Jian, Hui, Jennie, Karrasch, Stefan, Imboden, Medea, Harris, Sarah E, Marten, Jonathan, Enroth, Stefan, Kerr, Shona M., Surakka, Ida, Vitart, Veronique, Lehtimäki, Terho, Allen, Richard J., Bakke, Per S., Beaty, Terri H., Bleecker, Eugene R., Bossé, Yohan, Brandsma, Corry-Anke, Chen, Zhengming, Crapo, James D., Danesh, John, DeMeo, Dawn L., Dudbridge, Frank, Ewert, Ralf, Gieger, Christian, Gulsvik, Amund, Hansell, Anna L., Hao, Ke, Hoffman, Joshua D., Hokanson, John E., Homuth, Georg, Joshi, Peter K., Joubert, Philippe, Langenberg, Claudia, Li, Xuan, Li, Liming, Lin, Kuang, Lind, Lars, Locantore, Nicholas, Luan, Jian’an, Mahajan, Anubha, Maranville, Joseph C., Murray, Alison, Nickle, David C., Packer, Richard, Parker, Margaret M., Paynton, Megan L., Porteous, David J., Prokopenko, Dmitry, Qiao, Dandi, Rawal, Rajesh, Runz, Heiko, Sayers, Ian, Sin, Don D, Smith, Blair H, Soler Artigas, María, Sparrow, David, Tal-Singer, Ruth, Timmers, Paul R. H. J., Van den Berge, Maarten, Whittaker, John C., Woodruff, Prescott G., Yerges-Armstrong, Laura M., Troyanskaya, Olga G., Raitakari, Olli T., Kähönen, Mika, Polašek, Ozren, Gyllensten, Ulf, Rudan, Igor, Deary, Ian J., Probst-Hensch, Nicole M., Schulz, Holger, James, Alan L, Wilson, James F., Stubbe, Beate, Zeggini, Eleftheria, Jarvelin, Marjo-Riitta, Wareham, Nick, Silverman, Edwin K., Hayward, Caroline, Morris, Andrew P., Butterworth, Adam S., Scott, Robert A., Walters, Robin G., Meyers, Deborah A., Cho, Michael H., Strachan, David P., Hall, Ian P., Tobin, Martin D., and Wain, Louise V.

Published
2019
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37. Genetic landscape of chronic obstructive pulmonary disease identifies heterogeneous cell-type and phenotype associations

Author

Sakornsakolpat, Phuwanat, Prokopenko, Dmitry, Lamontagne, Maxime, Reeve, Nicola F., Guyatt, Anna L., Jackson, Victoria E., Shrine, Nick, Qiao, Dandi, Bartz, Traci M., Kim, Deog Kyeom, Lee, Mi Kyeong, Latourelle, Jeanne C., Li, Xingnan, Morrow, Jarrett D., Obeidat, Ma’en, Wyss, Annah B., Bakke, Per, Barr, R. Graham, Beaty, Terri H., Belinsky, Steven A., Brusselle, Guy G., Crapo, James D., de Jong, Kim, DeMeo, Dawn L., Fingerlin, Tasha E., Gharib, Sina A., Gulsvik, Amund, Hall, Ian P., Hokanson, John E., Kim, Woo Jin, Lomas, David A., London, Stephanie J., Meyers, Deborah A., O’Connor, George T., Rennard, Stephen I., Schwartz, David A., Sliwinski, Pawel, Sparrow, David, Strachan, David P., Tal-Singer, Ruth, Tesfaigzi, Yohannes, Vestbo, Jørgen, Vonk, Judith M., Yim, Jae-Joon, Zhou, Xiaobo, Bossé, Yohan, Manichaikul, Ani, Lahousse, Lies, Silverman, Edwin K., Boezen, H. Marike, Wain, Louise V., Tobin, Martin D., Hobbs, Brian D., and Cho, Michael H.

Published
2019
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38. Atrial fibrillation in cryptogenic stroke and TIA patients in The Nordic Atrial Fibrillation and Stroke (NOR-FIB) Study: Main results

Author

Ratajczak-Tretel, B., Tancin Lambert, A., Al-Ani, R., Arntzen, K., Bakkejord, G. K., Bekkeseth, H. M. O., Bjerkeli, V., Eldøen, G., Gulsvik, A., Halvorsen, B., Høie, G. A., Ihle-Hansen, H., Ingebrigtsen, S., Johansen, H., Kremer, C., Krogseth, S. B., Kruuse, C., Kurz, M., Nakstad, I., Novotny, V., Næss, H., Qazi, R., Rezaj, M. K., Rørholt, D. M., Steffensen, L. H., Sømark, J., Tobro, H., Truelsen, T. C., Wassvik, L., Ægidius, K. L., Atar, D., and Aamodt, A. H.

Subjects
biomarkers, atrial fibrillation, Cryptogenic stroke, Neurology (clinical), anticoagulation, arrhythmia monitoring, Cardiology and Cardiovascular Medicine, insertable cardiac monitor, secondary prevention
Abstract

Introduction: Secondary stroke prevention depends on proper identification of the underlying etiology and initiation of optimal treatment after the index event. The aim of the NOR-FIB study was to detect and quantify underlying atrial fibrillation (AF) in patients with cryptogenic stroke (CS) or transient ischaemic attack (TIA) using insertable cardiac monitor (ICM), to optimise secondary prevention, and to test the feasibility of ICM usage for stroke physicians. Patients and methods: Prospective observational international multicenter real-life study of CS and TIA patients monitored for 12 months with ICM (Reveal LINQ) for AF detection. Results: ICM insertion was performed in 91.5% by stroke physicians, within median 9 days after index event. Paroxysmal AF was diagnosed in 74 out of 259 patients (28.6%), detected early after ICM insertion (mean 48 ± 52 days) in 86.5% of patients. AF patients were older (72.6 vs 62.2; p Discussion and conclusions: ICM was an effective tool for diagnosing underlying AF, capturing AF in 29% of the CS and TIA patients. AF was asymptomatic in most cases and would mainly have gone undiagnosed without ICM. The insertion and use of ICM was feasible for stroke physicians in stroke units.

Published
2022

40. Prediction of underlying atrial fibrillation in patients with a cryptogenic stroke:results from the NOR-FIB Study

Author

Ratajczak-Tretel, B., Lambert, A. Tancin, Al-Ani, R., Arntzen, K., Bakkejord, G. K., Bekkeseth, H. M. O., Bjerkeli, V., Eldøen, G., Gulsvik, A. K., Halvorsen, B., Høie, G. A., Ihle-Hansen, H., Ingebrigtsen, S., Kremer, C., Krogseth, S. B., Kruuse, C., Kurz, M., Nakstad, I., Novotny, V., Næss, H., Qazi, R., Rezaj, M. K., Rørholt, D. M., Steffensen, L. H., Sømark, J., Tobro, H., Truelsen, T. C., Wassvik, L., Ægidius, K. L., Atar, D., Aamodt, Anne Hege, Ratajczak-Tretel, B., Lambert, A. Tancin, Al-Ani, R., Arntzen, K., Bakkejord, G. K., Bekkeseth, H. M. O., Bjerkeli, V., Eldøen, G., Gulsvik, A. K., Halvorsen, B., Høie, G. A., Ihle-Hansen, H., Ingebrigtsen, S., Kremer, C., Krogseth, S. B., Kruuse, C., Kurz, M., Nakstad, I., Novotny, V., Næss, H., Qazi, R., Rezaj, M. K., Rørholt, D. M., Steffensen, L. H., Sømark, J., Tobro, H., Truelsen, T. C., Wassvik, L., Ægidius, K. L., Atar, D., and Aamodt, Anne Hege

Abstract

Background: Atrial fibrillation (AF) detection and treatment are key elements to reduce recurrence risk in cryptogenic stroke (CS) with underlying arrhythmia. The purpose of the present study was to assess the predictors of AF in CS and the utility of existing AF-predicting scores in The Nordic Atrial Fibrillation and Stroke (NOR-FIB) Study. Method: The NOR-FIB study was an international prospective observational multicenter study designed to detect and quantify AF in CS and cryptogenic transient ischaemic attack (TIA) patients monitored by the insertable cardiac monitor (ICM), and to identify AF-predicting biomarkers. The utility of the following AF-predicting scores was tested: AS5F, Brown ESUS-AF, CHA2DS2-VASc, CHASE-LESS, HATCH, HAVOC, STAF and SURF. Results: In univariate analyses increasing age, hypertension, left ventricle hypertrophy, dyslipidaemia, antiarrhythmic drugs usage, valvular heart disease, and neuroimaging findings of stroke due to intracranial vessel occlusions and previous ischemic lesions were associated with a higher likelihood of detected AF. In multivariate analysis, age was the only independent predictor of AF. All the AF-predicting scores showed significantly higher score levels for AF than non-AF patients. The STAF and the SURF scores provided the highest sensitivity and negative predictive values, while the AS5F and SURF reached an area under the receiver operating curve (AUC) > 0.7. Conclusion: Clinical risk scores may guide a personalized evaluation approach in CS patients. Increasing awareness of the usage of available AF-predicting scores may optimize the arrhythmia detection pathway in stroke units.

Published
2023

41. Atrial fibrillation in cryptogenic stroke and TIA patients in The Nordic Atrial Fibrillation and Stroke (NOR-FIB) Study:Main results

Author

Ratajczak-Tretel, B., Tancin Lambert, A., Al-Ani, R., Arntzen, K., Bakkejord, G. K., Bekkeseth, H. M. O., Bjerkeli, V., Eldøen, G., Gulsvik, A., Halvorsen, B., Høie, G. A., Ihle-Hansen, H., Ingebrigtsen, S., Johansen, H., Kremer, C., Krogseth, S. B., Kruuse, C., Kurz, M., Nakstad, I., Novotny, V., Næss, H., Qazi, R., Rezaj, M. K., Rørholt, D. M., Steffensen, L. H., Sømark, J., Tobro, H., Truelsen, T. C., Wassvik, L., Ægidius, K. L., Atar, D., Aamodt, A. H., Ratajczak-Tretel, B., Tancin Lambert, A., Al-Ani, R., Arntzen, K., Bakkejord, G. K., Bekkeseth, H. M. O., Bjerkeli, V., Eldøen, G., Gulsvik, A., Halvorsen, B., Høie, G. A., Ihle-Hansen, H., Ingebrigtsen, S., Johansen, H., Kremer, C., Krogseth, S. B., Kruuse, C., Kurz, M., Nakstad, I., Novotny, V., Næss, H., Qazi, R., Rezaj, M. K., Rørholt, D. M., Steffensen, L. H., Sømark, J., Tobro, H., Truelsen, T. C., Wassvik, L., Ægidius, K. L., Atar, D., and Aamodt, A. H.

Abstract

Introduction: Secondary stroke prevention depends on proper identification of the underlying etiology and initiation of optimal treatment after the index event. The aim of the NOR-FIB study was to detect and quantify underlying atrial fibrillation (AF) in patients with cryptogenic stroke (CS) or transient ischaemic attack (TIA) using insertable cardiac monitor (ICM), to optimise secondary prevention, and to test the feasibility of ICM usage for stroke physicians. Patients and methods: Prospective observational international multicenter real-life study of CS and TIA patients monitored for 12 months with ICM (Reveal LINQ) for AF detection. Results: ICM insertion was performed in 91.5% by stroke physicians, within median 9 days after index event. Paroxysmal AF was diagnosed in 74 out of 259 patients (28.6%), detected early after ICM insertion (mean 48 ± 52 days) in 86.5% of patients. AF patients were older (72.6 vs 62.2; p < 0.001), had higher pre-stroke CHA₂DS₂-VASc score (median 3 vs 2; p < 0.001) and admission NIHSS (median 2 vs 1; p = 0.001); and more often hypertension (p = 0.045) and dyslipidaemia (p = 0.005) than non-AF patients. The arrhythmia was recurrent in 91.9% and asymptomatic in 93.2%. At 12-month follow-up anticoagulants usage was 97.3%. Discussion and conclusions: ICM was an effective tool for diagnosing underlying AF, capturing AF in 29% of the CS and TIA patients. AF was asymptomatic in most cases and would mainly have gone undiagnosed without ICM. The insertion and use of ICM was feasible for stroke physicians in stroke units.

Published
2023

43. Barn som pårørende til psykisk syke foreldre

Author

Gulsvik, Nora Margrethe Østdahl, Haugli, Marie Bakken, and Sollid, May Ingvild Volungholen

Abstract

Bakgrunn: Barn som pårørende til foreldre med psykiske lidelser er en særdeles utsatt gruppe, og vil i større grad bli utsatt for risikofaktorer som kan medføre utvikling av atferdsforstyrrelser, emosjonelle vansker eller kognitive utviklingsforstyrrelser. Sykepleiere er lovpålagt å kartlegge og følge opp barna, men forskning og personlige erfaringer viser at barn i møte med sykepleiere ofte ikke blir sett, hørt eller involvert, selv om vi gjerne tror det motsatte. Hensikt: Hensikten med oppgaven var å undersøke sykepleieres kunnskap og holdninger til arbeidet med barn som pårørende, samt innhente kunnskap om barns erfaringer i møte med sykepleiere, og hvilke intervensjoner og tiltak som kan hjelpe barn til å mestre egen livssituasjon. Metode: Det er anvendt litteraturstudie som metode for å besvare problemstillingen. Teori og kunnskap er dermed basert på allerede eksisterende faglitteratur og forskning. Resultater: I studiene kom det frem at sykepleiere manglet klare rutiner og retningslinjer i arbeidet med barn som pårørende. Sykepleiers individuelle kompetanse og erfaring hadde betydning for kartleggingen og oppfølgingen av barna, og barns behov for informasjon var fremtredende. Familiesentrert omsorg og tydeliggjøring av barneansvarliges rolle viste seg å være viktige tiltak for å styrke barnas resiliens og mestring av egen livssituasjon. Konklusjon: Sykepleiere har en viktig rolle i kartlegging og oppfølging av barn som pårørende, men manglende rutiner og retningslinjer gjør at dette arbeidet blir gjort i varierende grad. For å fremme mestring hos barna må behovet for informasjon ivaretas, samt implementering av familiesentrert omsorg i utøvelsen av sykepleie. Nøkkelord: barn som pårørende, sykepleier, mestring, familiesentrert omsorg Background: Children as relatives to mentally ill parents are particularly vulnerable and will be exposed to a greater extent of risk factors that can lead to the development of behavioral disorders, emotional difficulties, or cognitive developmental disorders. Nurses are required by law to survey and follow up the children, but research and personal experiences show that children are often not seen, heard, and involved, even if we like to think the opposite. Aim: The aim of this thesis was to explore nurses’ knowledge and attitude towards working with children as relatives, as well as to obtain knowledge about children’s experiences with nurses, and which interventions and measures that can help children in coping with their life situation. Method: A literature study has been used as a method to answer the issue. Theory and knowledge are based on already existing literature and research. Results: The studies revealed that nurses lacked clear practices and guidelines in their work with children as relatives. Nurses' individual competence and experience were important for mapping and follow-up of the children, and children's need for information was prominent. Family-focused care and clarifying the role of childcare providers proved to be important measures to support the children’s resilience and coping skills. Conclusion: Nurses have an important role in mapping and following up children as relatives, but lack of routines and guidelines means that this work is done to varying degrees. In order to promote coping in the children, their need for information must be taken care of, as well as the implementation of family-centered care in the practice of nursing. Key words: children as relatives, nurse, coping, family-focused care

Published
2023

44. Additional file 1 of X chromosome associations with chronic obstructive pulmonary disease and related phenotypes: an X chromosome-wide association study

Author

Hayden, Lystra P., Hobbs, Brian D., Busch, Robert, Cho, Michael H., Liu, Ming, Lopes-Ramos, Camila M., Lomas, David A., Bakke, Per, Gulsvik, Amund, Silverman, Edwin K., Crapo, James D., Beaty, Terri H., Laird, Nan M., Lange, Christoph, and DeMeo, Dawn L.

Abstract

Additional file 1: Text and Figures S1–S5. Supplementary text for the methods (study phenotype, quality control, imputation, significance and suggestive thresholds, annotation), results (power to detect associations, annotation of rs142755000), and discussion (suggestive associations) as well as related references. Figure S1. a: COPDGene XWAS in Stratified Populations All Subjects. b: COPDGene XWAS in Stratified Populations Males. c: COPDGene XWAS in Stratified Populations Females. Figure S2. Meta-analysis XWAS in Stratified Population. Figure S3. Meta-analysis Locus Plots of Top Suggested Associations in COPD Related Phenotypes. Figure S4. Meta-analysis Quantile–Quantile and Manhattan Plots. Figure S5. Sex differential edge weights connecting the transcription factor POU3F4 in GTEx Lung Tissue.

Published
2023
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45. Chronic airflow obstruction and ambient particulate air pollution

Author

Hamid Hacene Cherkaski, Rain Jõgi, Peter Burney, Eric D. Bateman, Terence A. R. Seemungal, Rune Nielsen, Gregory E. Erhabor, Filip Mejza, Padukudru Anand Mahesh, David M. Mannino, Asaad Ahmed Nafees, Amund Gulsvik, Guy B. Marks, Cosetta Minelli, Louisa Gnatiuc, Cristina Bárbara, Thorarinn Gislason, Mohammed Al Ghobain, Althea Aquart-Stewart, Meriam Denguezli, Ali Kocabas, Tobias Welte, Christer Janson, Kevin Mortimer, Herve Lawin, Andre F.S. Amaral, Emiel F.M. Wouters, Imed Harrabi, A. Sonia Buist, Jaymini Patel, O.F. Awopeju, Michael Studnicka, Talant Sooronbaev, Li Cher Lo, Daniel O. Obaseki, Elaine Fuertes, Sanjay Juvekar, Bertrand Hugo Mbatchou Ngahane, Asma El Sony, Parvaiz A Koul, Wan C. Tan, RS: NUTRIM - R3 - Respiratory & Age-related Health, Pulmonologie, MUMC+: MA Longziekten (3), Repositório da Universidade de Lisboa, Group, The BOLD (Burden of Obstructive Lung Disease) Collaborative Research, and Wellcome Trust

Subjects
Pulmonary and Respiratory Medicine, wa_754, Male, Passive smoking, Respiratory Medicine and Allergy, Respiratory System, wa_750a, 010501 environmental sciences, Airflow obstruction, medicine.disease_cause, Brief Communication, 01 natural sciences, 03 medical and health sciences, Arbetsmedicin och miljömedicin, Pulmonary Disease, Chronic Obstructive, 0302 clinical medicine, Environmental health, BOLD (Burden of Obstructive Lung Disease) Collaborative Research Group members, Air Pollution, Medicine, Humans, 0105 earth and related environmental sciences, Lungmedicin och allergi, Air Pollutants, Science & Technology, Poverty, business.industry, Tobacco control, 1103 Clinical Sciences, Dust, Occupational Health and Environmental Health, Environmental Exposure, Particulates, Particulate air pollution, medicine.disease, Obstructive lung disease, BOLD (Burden of Obstructive Lung Disease) Collaborative Research Group, PREVALENCE, Gross national income, 030228 respiratory system, wf_140, Female, Particulate Matter, business, COPD epidemiology, Life Sciences & Biomedicine, wf_600
Abstract

© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ. This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/., Smoking is the most well-established cause of chronic airflow obstruction (CAO) but particulate air pollution and poverty have also been implicated. We regressed sex-specific prevalence of CAO from 41 Burden of Obstructive Lung Disease study sites against smoking prevalence from the same study, the gross national income per capita and the local annual mean level of ambient particulate matter (PM2.5) using negative binomial regression. The prevalence of CAO was not independently associated with PM2.5 but was strongly associated with smoking and was also associated with poverty. Strengthening tobacco control and improved understanding of the link between CAO and poverty should be prioritised., Supported by Wellcome Trust grant 085790/Z/08/Z for the BOLD (Burden of Obstructive Lung Disease) Study. The initial BOLD programprogramme was funded in part by unrestricted educational grants to the Operations CenterCentre in Portland, Oregon from Altana, Aventis, AstraZeneca, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Merck, Novartis, Pfizer, Schering-Plough, Sepracor, and the University of Kentucky (Lexington, KY). A full list of local funders can be found at https://www.boldstudy.org.

Published
2021

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