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Modifiable risk factors for RA: prevention, better than cure?
Objective. To perform a meta-synthesis of the evidence for modifiable lifestyle risk factors for inflammatory polyarthritis (IP) and RA. Methods. We performed a MEDLINE literature search. Case–control and cohort studies and systematic reviews published from 1948 through February 2011 and studying mo...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3281496/ https://www.ncbi.nlm.nih.gov/pubmed/22120459 http://dx.doi.org/10.1093/rheumatology/ker299 |
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author | Lahiri, Manjari Morgan, Catharine Symmons, Deborah P. M. Bruce, Ian N. |
author_facet | Lahiri, Manjari Morgan, Catharine Symmons, Deborah P. M. Bruce, Ian N. |
author_sort | Lahiri, Manjari |
collection | PubMed |
description | Objective. To perform a meta-synthesis of the evidence for modifiable lifestyle risk factors for inflammatory polyarthritis (IP) and RA. Methods. We performed a MEDLINE literature search. Case–control and cohort studies and systematic reviews published from 1948 through February 2011 and studying modifiable risk factors for RA were retrieved. The main outcome measure was diagnosis of RA according to the standard criteria. Results. Smoking contributes up to 25% of the population burden of RA. The risk is dose related, stronger in males and especially strong for anti-citrullinated peptide antibody positive (ACPA(+)) RA through an interaction with the shared epitope. After smoking cessation, there is, however, a latency of up to 20 years to return to baseline risk. Other associations are less definitive; however, prospective studies suggest that dietary antioxidants and breastfeeding may be protective and that high coffee consumption may increase RA risk. An inverse association with alcohol intake (especially in smokers) and with education/social class (especially seropositive RA) and an increased risk with obesity (seronegative RA) is also noted. Conclusion. There is a need for further large-scale prospective studies with a consistent definition of RA phenotype (undifferentiated IP through to ACPA(+)/RF(+) disease). This will ultimately afford the opportunity to evaluate preventative population strategies for RA akin to the well-established programmes for cardiovascular disease and cancer, targeting common risk factors. |
format | Online Article Text |
id | pubmed-3281496 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-32814962012-02-17 Modifiable risk factors for RA: prevention, better than cure? Lahiri, Manjari Morgan, Catharine Symmons, Deborah P. M. Bruce, Ian N. Rheumatology (Oxford) Clinical Science Objective. To perform a meta-synthesis of the evidence for modifiable lifestyle risk factors for inflammatory polyarthritis (IP) and RA. Methods. We performed a MEDLINE literature search. Case–control and cohort studies and systematic reviews published from 1948 through February 2011 and studying modifiable risk factors for RA were retrieved. The main outcome measure was diagnosis of RA according to the standard criteria. Results. Smoking contributes up to 25% of the population burden of RA. The risk is dose related, stronger in males and especially strong for anti-citrullinated peptide antibody positive (ACPA(+)) RA through an interaction with the shared epitope. After smoking cessation, there is, however, a latency of up to 20 years to return to baseline risk. Other associations are less definitive; however, prospective studies suggest that dietary antioxidants and breastfeeding may be protective and that high coffee consumption may increase RA risk. An inverse association with alcohol intake (especially in smokers) and with education/social class (especially seropositive RA) and an increased risk with obesity (seronegative RA) is also noted. Conclusion. There is a need for further large-scale prospective studies with a consistent definition of RA phenotype (undifferentiated IP through to ACPA(+)/RF(+) disease). This will ultimately afford the opportunity to evaluate preventative population strategies for RA akin to the well-established programmes for cardiovascular disease and cancer, targeting common risk factors. Oxford University Press 2012-03 2011-11-24 /pmc/articles/PMC3281496/ /pubmed/22120459 http://dx.doi.org/10.1093/rheumatology/ker299 Text en The Author(s) 2011. Published by Oxford University Press on behalf of The British Society for Rheumatology. http://creativecommons.org/licenses/by-nc/2.5 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Clinical Science Lahiri, Manjari Morgan, Catharine Symmons, Deborah P. M. Bruce, Ian N. Modifiable risk factors for RA: prevention, better than cure? |
title | Modifiable risk factors for RA: prevention, better than cure? |
title_full | Modifiable risk factors for RA: prevention, better than cure? |
title_fullStr | Modifiable risk factors for RA: prevention, better than cure? |
title_full_unstemmed | Modifiable risk factors for RA: prevention, better than cure? |
title_short | Modifiable risk factors for RA: prevention, better than cure? |
title_sort | modifiable risk factors for ra: prevention, better than cure? |
topic | Clinical Science |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3281496/ https://www.ncbi.nlm.nih.gov/pubmed/22120459 http://dx.doi.org/10.1093/rheumatology/ker299 |
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