Published by Oxford University Press on behalf of the International Epidemiological Association
International Journal of Epidemiology
© The Author 2005; all rights reserved.
doi:10.1093/ije/dyi082
Commentary: Juvenile idiopathic arthritis—
issues of definition and causation
Deborah Symmons
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immunological abnormality in the child, which later leads to
arthritis. Second the role of maternal smoking could be via low
birth weight and small-for-gestational age. This in turn might
lead to an increased susceptibility to childhood infections,
which might trigger arthritis. Jaakola and Gissler considered this
possibility but felt it could not explain the size of the observed
effect. Third the maternal smoking might be a marker for what
is actually the true risk factor. For example, if a mother smokes
during pregnancy she is also likely to smoke after pregnancy—
and it may be the exposure to environmental smoke as an
infant that is the true culprit. Smoking is an important
contributor to autoimmunity.6 Smokers have been reported to
have abnormalities in T-lymphocyte function, a reduction in the
number of natural killer cells and abnormalities in humoral and
cellular immunity. This might be conveyed to the child in utero
or might be acquired by passive smoking. Finally, an earlier
study showed that the risk of JIA was 40% lower in breast-fed
than in non-breast-fed children.7 It is possible that mothers
who smoke are less likely to breast-feed and so this might be the
link between smoking and arthritis onset.
In conclusion further studies are needed to confirm these
results in other populations and to try and understand the
mechanism underlying the association.
References
1 Foeldvari I, Bidde M. Validation of the proposed ILAR classification
criteria for juvenile idiopathic arthritis. J Rheumatol 2000;27:1069–72.
2 Jaakola JJK, Gissler M. Maternal smoking in pregnancy as a
determinant of rheumaotid arthritis and other inflammatory
polyarthropathies during the first 7 years of life. Int J Epidemiol
doi:10.1093/ije/dyi006.
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