Inflammatory Bowel Diseases Before and After 1990
Background and Aims: Inflammatory bowel disease (IBD) is caused by interaction of genetic and environmental risk factors. We evaluated potential determinants of the post-1990 increased incidence in North America. Methods: Using fitted generalized linear models, we assessed clinical features, smoking...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-01-01
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| Series: | Gastro Hep Advances |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2772572322001388 |
| _version_ | 1828189396395884544 |
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| author | Brindusa Truta Ferdouse Begum Lisa Wu Datta Steven R. Brant Steven R. Brant Judy H. Cho Richard H. Duerr Dermot B.P. McGovern John R. Rioux Mark S. Silverberg |
| author_facet | Brindusa Truta Ferdouse Begum Lisa Wu Datta Steven R. Brant Steven R. Brant Judy H. Cho Richard H. Duerr Dermot B.P. McGovern John R. Rioux Mark S. Silverberg |
| author_sort | Brindusa Truta |
| collection | DOAJ |
| description | Background and Aims: Inflammatory bowel disease (IBD) is caused by interaction of genetic and environmental risk factors. We evaluated potential determinants of the post-1990 increased incidence in North America. Methods: Using fitted generalized linear models, we assessed clinical features, smoking and genetic risk scores (GRS) for Crohn’s disease (CD) and ulcerative colitis (UC) in the National Institutes of Diabetes, Digestion and Kidney Diseases IBD Genetics Consortium database, before and post 1990. Results: Among 2744 patients (55% CD, 42.2% UC), smoking status and GRS were the main determinants of diagnosis age. After 1990, smoking at diagnosis declined significantly in both UC and CD (34.1% vs 20.8%, P < .001, and 14.7% vs 8.7%, P = .06, respectively). In UC, ex-smoking increased (9% vs 15%, P < .001), and nonsmoking rates remained unchanged, whereas in CD, ex-smoking remained unchanged. CD-GRS and IBD-GRS were significantly associated with young diagnosis age, Jewish ethnicity, IBD family history, and surgery. CD-GRS showed a borderline significant decrease (P = .058) in multivariate analysis post 1990 but only when excluding surgery in the model; surgery significantly decreased post 1990 in both CD and UC. CD-GRS inversely correlated with smoking at diagnosis (P < .001) suggesting that, in the presence of smoking, CD may only require a low genetic risk to develop. Conclusion: Significantly increase in ex-smoking correlates with UC incidence post 1990. Conversely, smoking risk decreased significantly post 1990 despite rising CD incidence. CD-GRS likewise trended to decrease post 1990 only when not accounting for a significant decrease in CD surgery. We therefore deduce that unaccounted risk factors (eg, dietary, obesity, antibiotic use, improved hygiene, etc.) or greater detection or presence of mild CD may underlie post-1990 increased CD incidence. |
| first_indexed | 2024-04-12T08:04:55Z |
| format | Article |
| id | doaj.art-dd85c3f4ae8a48deb59f327504bffcdd |
| institution | Directory Open Access Journal |
| issn | 2772-5723 |
| language | English |
| last_indexed | 2024-04-12T08:04:55Z |
| publishDate | 2023-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Gastro Hep Advances |
| spelling | doaj.art-dd85c3f4ae8a48deb59f327504bffcdd2022-12-22T03:41:12ZengElsevierGastro Hep Advances2772-57232023-01-01212232Inflammatory Bowel Diseases Before and After 1990Brindusa Truta0Ferdouse Begum1Lisa Wu Datta2Steven R. Brant3Steven R. BrantJudy H. ChoRichard H. DuerrDermot B.P. McGovernJohn R. RiouxMark S. SilverbergDivision of Gastroenterology, Harvey M. and Lyn P. Meyerhoff Inflammatory Bowel Disease Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; Correspondence: Address correspondence to: Brindusa Truta, MD, 1830 E Monument Street, Room 426, Baltimore, Maryland 21205.Division of Gastroenterology, Harvey M. and Lyn P. Meyerhoff Inflammatory Bowel Disease Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MarylandDivision of Gastroenterology, Harvey M. and Lyn P. Meyerhoff Inflammatory Bowel Disease Center, Johns Hopkins University School of Medicine, Baltimore, MarylandDivision of Gastroenterology, Harvey M. and Lyn P. Meyerhoff Inflammatory Bowel Disease Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland; Division of Gastroenterology and Hepatology, Department of Medicine, Rutgers Robert Wood Johnson Medical School, The Rutgers Crohns and Colitis Center of New Jersey, New Brunswick, New Jersey; Department of Genetics and the Human Genetics Institute of New Jersey, Rutgers University, New Brunswick, New JerseyBackground and Aims: Inflammatory bowel disease (IBD) is caused by interaction of genetic and environmental risk factors. We evaluated potential determinants of the post-1990 increased incidence in North America. Methods: Using fitted generalized linear models, we assessed clinical features, smoking and genetic risk scores (GRS) for Crohn’s disease (CD) and ulcerative colitis (UC) in the National Institutes of Diabetes, Digestion and Kidney Diseases IBD Genetics Consortium database, before and post 1990. Results: Among 2744 patients (55% CD, 42.2% UC), smoking status and GRS were the main determinants of diagnosis age. After 1990, smoking at diagnosis declined significantly in both UC and CD (34.1% vs 20.8%, P < .001, and 14.7% vs 8.7%, P = .06, respectively). In UC, ex-smoking increased (9% vs 15%, P < .001), and nonsmoking rates remained unchanged, whereas in CD, ex-smoking remained unchanged. CD-GRS and IBD-GRS were significantly associated with young diagnosis age, Jewish ethnicity, IBD family history, and surgery. CD-GRS showed a borderline significant decrease (P = .058) in multivariate analysis post 1990 but only when excluding surgery in the model; surgery significantly decreased post 1990 in both CD and UC. CD-GRS inversely correlated with smoking at diagnosis (P < .001) suggesting that, in the presence of smoking, CD may only require a low genetic risk to develop. Conclusion: Significantly increase in ex-smoking correlates with UC incidence post 1990. Conversely, smoking risk decreased significantly post 1990 despite rising CD incidence. CD-GRS likewise trended to decrease post 1990 only when not accounting for a significant decrease in CD surgery. We therefore deduce that unaccounted risk factors (eg, dietary, obesity, antibiotic use, improved hygiene, etc.) or greater detection or presence of mild CD may underlie post-1990 increased CD incidence.http://www.sciencedirect.com/science/article/pii/S2772572322001388IBDGeneticSmokingEnvironmental Risks |
| spellingShingle | Brindusa Truta Ferdouse Begum Lisa Wu Datta Steven R. Brant Steven R. Brant Judy H. Cho Richard H. Duerr Dermot B.P. McGovern John R. Rioux Mark S. Silverberg Inflammatory Bowel Diseases Before and After 1990 Gastro Hep Advances IBD Genetic Smoking Environmental Risks |
| title | Inflammatory Bowel Diseases Before and After 1990 |
| title_full | Inflammatory Bowel Diseases Before and After 1990 |
| title_fullStr | Inflammatory Bowel Diseases Before and After 1990 |
| title_full_unstemmed | Inflammatory Bowel Diseases Before and After 1990 |
| title_short | Inflammatory Bowel Diseases Before and After 1990 |
| title_sort | inflammatory bowel diseases before and after 1990 |
| topic | IBD Genetic Smoking Environmental Risks |
| url | http://www.sciencedirect.com/science/article/pii/S2772572322001388 |
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