Parental rheumatoid arthritis and childhood epilepsy

Ane Lilleøre Rom; Chun Sen Wu; Jørn Olsen; Damini Jawaheer; Merete Lund Hetland; Jakob Christensen; Bent Ottesen; Lina Steinrud Mørch

doi:10.1212/WNL.0000000000003424

Parental rheumatoid arthritis and childhood epilepsy

Ane Lilleøre Rom^*, Chun Sen Wu, Jørn Olsen, Damini Jawaheer, Merete Lund Hetland, Jakob Christensen, Bent Ottesen, Lina Steinrud Mørch

^*Corresponding author af dette arbejde

11 Citationer (Scopus)

Abstract

Objective: To assess the influence of parental rheumatoid arthritis (RA) on risk of epilepsy. Methods: We performed a nationwide cohort study including all singletons born in Denmark from 1977 to 2008 (n = 1,917,723) through individual linkage to nationwide Danish registries. The children were followed for an average of 16 years. Main outcome measures were adjusted hazard ratios (HRs) for epilepsy with onset in early childhood (29 days-4 years), late childhood (5-15 years), adolescence/adulthood (≥15 years), and at any age until the end of follow-up (December 31, 2010). Results: Compared to unexposed children, children exposed to maternal RA had an increased risk of early and late childhood epilepsy (adjusted HRs 1.34 [95% confidence interval (CI) 1.13-1.60] and 1.26 [95% CI 1.13-1.41]), while children exposed to maternal RA had no increased risk of epilepsy in adolescence/adulthood (HR 1.15 [95% CI 0.92-1.45]). Paternal RA was not associated with an overall risk of epilepsy in the offspring (HR 0.96 [95% CI 0.81-1.15]) or at any age. Children exposed to maternal RA in utero had a more pronounced increased risk of early childhood epilepsy than children exposed to mothers who were diagnosed with RA after childbirth (HR 1.90 [95% CI 1.26-2.86] vs HR 1.26 [95% CI 1.03-1.52], respectively [p = 0.16]). Conclusions: Exposure to maternal RA was associated with an increased risk of childhood epilepsy, while exposure to paternal RA was not, which indicates that changes in the intrauterine environment may play a role.

Originalsprog	Engelsk
Tidsskrift	Neurology
Vol/bind	87
Udgave nummer	24
Sider (fra-til)	2510-2516
Antal sider	7
ISSN	0028-3878
DOI	https://doi.org/10.1212/WNL.0000000000003424
Status	Udgivet - 2016

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10.1212/WNL.0000000000003424

Citationsformater

@article{9c77f446298f42ba9cc40135478a2138,

title = "Parental rheumatoid arthritis and childhood epilepsy",

abstract = "Objective: To assess the influence of parental rheumatoid arthritis (RA) on risk of epilepsy. Methods: We performed a nationwide cohort study including all singletons born in Denmark from 1977 to 2008 (n = 1,917,723) through individual linkage to nationwide Danish registries. The children were followed for an average of 16 years. Main outcome measures were adjusted hazard ratios (HRs) for epilepsy with onset in early childhood (29 days-4 years), late childhood (5-15 years), adolescence/adulthood (≥15 years), and at any age until the end of follow-up (December 31, 2010). Results: Compared to unexposed children, children exposed to maternal RA had an increased risk of early and late childhood epilepsy (adjusted HRs 1.34 [95% confidence interval (CI) 1.13-1.60] and 1.26 [95% CI 1.13-1.41]), while children exposed to maternal RA had no increased risk of epilepsy in adolescence/adulthood (HR 1.15 [95% CI 0.92-1.45]). Paternal RA was not associated with an overall risk of epilepsy in the offspring (HR 0.96 [95% CI 0.81-1.15]) or at any age. Children exposed to maternal RA in utero had a more pronounced increased risk of early childhood epilepsy than children exposed to mothers who were diagnosed with RA after childbirth (HR 1.90 [95% CI 1.26-2.86] vs HR 1.26 [95% CI 1.03-1.52], respectively [p = 0.16]). Conclusions: Exposure to maternal RA was associated with an increased risk of childhood epilepsy, while exposure to paternal RA was not, which indicates that changes in the intrauterine environment may play a role.",

author = "Rom, {Ane Lille{\o}re} and Wu, {Chun Sen} and J{\o}rn Olsen and Damini Jawaheer and Hetland, {Merete Lund} and Jakob Christensen and Bent Ottesen and M{\o}rch, {Lina Steinrud}",

year = "2016",

doi = "10.1212/WNL.0000000000003424",

language = "English",

volume = "87",

pages = "2510--2516",

journal = "Neurology",

issn = "0028-3878",

publisher = "Lippincott Williams & Wilkins",

number = "24",

}

TY - JOUR

T1 - Parental rheumatoid arthritis and childhood epilepsy

AU - Rom, Ane Lilleøre

AU - Wu, Chun Sen

AU - Olsen, Jørn

AU - Jawaheer, Damini

AU - Hetland, Merete Lund

AU - Christensen, Jakob

AU - Ottesen, Bent

AU - Mørch, Lina Steinrud

PY - 2016

Y1 - 2016

N2 - Objective: To assess the influence of parental rheumatoid arthritis (RA) on risk of epilepsy. Methods: We performed a nationwide cohort study including all singletons born in Denmark from 1977 to 2008 (n = 1,917,723) through individual linkage to nationwide Danish registries. The children were followed for an average of 16 years. Main outcome measures were adjusted hazard ratios (HRs) for epilepsy with onset in early childhood (29 days-4 years), late childhood (5-15 years), adolescence/adulthood (≥15 years), and at any age until the end of follow-up (December 31, 2010). Results: Compared to unexposed children, children exposed to maternal RA had an increased risk of early and late childhood epilepsy (adjusted HRs 1.34 [95% confidence interval (CI) 1.13-1.60] and 1.26 [95% CI 1.13-1.41]), while children exposed to maternal RA had no increased risk of epilepsy in adolescence/adulthood (HR 1.15 [95% CI 0.92-1.45]). Paternal RA was not associated with an overall risk of epilepsy in the offspring (HR 0.96 [95% CI 0.81-1.15]) or at any age. Children exposed to maternal RA in utero had a more pronounced increased risk of early childhood epilepsy than children exposed to mothers who were diagnosed with RA after childbirth (HR 1.90 [95% CI 1.26-2.86] vs HR 1.26 [95% CI 1.03-1.52], respectively [p = 0.16]). Conclusions: Exposure to maternal RA was associated with an increased risk of childhood epilepsy, while exposure to paternal RA was not, which indicates that changes in the intrauterine environment may play a role.

AB - Objective: To assess the influence of parental rheumatoid arthritis (RA) on risk of epilepsy. Methods: We performed a nationwide cohort study including all singletons born in Denmark from 1977 to 2008 (n = 1,917,723) through individual linkage to nationwide Danish registries. The children were followed for an average of 16 years. Main outcome measures were adjusted hazard ratios (HRs) for epilepsy with onset in early childhood (29 days-4 years), late childhood (5-15 years), adolescence/adulthood (≥15 years), and at any age until the end of follow-up (December 31, 2010). Results: Compared to unexposed children, children exposed to maternal RA had an increased risk of early and late childhood epilepsy (adjusted HRs 1.34 [95% confidence interval (CI) 1.13-1.60] and 1.26 [95% CI 1.13-1.41]), while children exposed to maternal RA had no increased risk of epilepsy in adolescence/adulthood (HR 1.15 [95% CI 0.92-1.45]). Paternal RA was not associated with an overall risk of epilepsy in the offspring (HR 0.96 [95% CI 0.81-1.15]) or at any age. Children exposed to maternal RA in utero had a more pronounced increased risk of early childhood epilepsy than children exposed to mothers who were diagnosed with RA after childbirth (HR 1.90 [95% CI 1.26-2.86] vs HR 1.26 [95% CI 1.03-1.52], respectively [p = 0.16]). Conclusions: Exposure to maternal RA was associated with an increased risk of childhood epilepsy, while exposure to paternal RA was not, which indicates that changes in the intrauterine environment may play a role.

U2 - 10.1212/WNL.0000000000003424

DO - 10.1212/WNL.0000000000003424

M3 - Journal article

C2 - 27856781

AN - SCOPUS:85005953157

SN - 0028-3878

VL - 87

SP - 2510

EP - 2516

JO - Neurology

JF - Neurology

IS - 24

ER -

Parental rheumatoid arthritis and childhood epilepsy

Abstract

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