Luis O Rustveld1, Sheryl F Kelsey, Ravi Sharma. 1. Department of Family and Community Medicine, Baylor College of Medicine, 3701 Kirby Drive, Suite 600, Houston, TX 77098-3926, USA. rustveld@bcm.edu
Abstract
OBJECTIVES: A growing body of evidence suggests an association between maternal infection and preeclampsia. To examine the strength of this association, we conducted a comprehensive review of studies published in peer-reviewed journals. METHODS: Data collection for this review involved Medline, Embase, and Cochrane data base searches of published studies since 1964 on the relationship between maternal infection and preeclampsia. Data were abstracted according to predefined inclusion and exclusion criteria. Study population included women with preeclampsia and normotensive mothers with and without bacterial or viral infections. Altogether, thirty two original studies were identified and evaluated for methodological quality, preeclampsia diagnosis and adjustment for well-known preeclampsia confounders. Pooled odds ratios and 95% confidence intervals, according to infection status, were calculated using DerSimonian-Laird random-effects models. Publication bias was assessed with a funnel plot and Egger's regression asymmetry test. RESULTS: Sixteen of the 32 studies evaluated were selected for inclusion in the meta-analysis. These studies showed that women with either a bacterial or viral infection were at higher risk of developing preeclampsia, compared to women without infection. Combined results for the 16 studies yielded an OR of 2.1 (95% CI 1.6-2.7). Separate pooled estimates for prospective (OR 2.3, 95% CI 1.7-3.0), case control and retrospective studies combined (OR 2.0, 95% CI 1.4-2.9) yielded similar results. Heterogeneity was significant across overall pooled estimates, case control and retrospective studies (Q(df=20) of 45.7, P = .001; Q(df=10) of 38.7, P < .005, respectively), but not prospective studies (Q(df=9) of 6.5 P = .69). CONCLUSIONS: In our analysis, any infection (bacterial or viral) was associated with a two-fold higher risk of preeclampsia. This association may provide a potential explanation for preeclampsia-related inflammation.
OBJECTIVES: A growing body of evidence suggests an association between maternal infection and preeclampsia. To examine the strength of this association, we conducted a comprehensive review of studies published in peer-reviewed journals. METHODS: Data collection for this review involved Medline, Embase, and Cochrane data base searches of published studies since 1964 on the relationship between maternal infection and preeclampsia. Data were abstracted according to predefined inclusion and exclusion criteria. Study population included women with preeclampsia and normotensive mothers with and without bacterial or viral infections. Altogether, thirty two original studies were identified and evaluated for methodological quality, preeclampsia diagnosis and adjustment for well-known preeclampsia confounders. Pooled odds ratios and 95% confidence intervals, according to infection status, were calculated using DerSimonian-Laird random-effects models. Publication bias was assessed with a funnel plot and Egger's regression asymmetry test. RESULTS: Sixteen of the 32 studies evaluated were selected for inclusion in the meta-analysis. These studies showed that women with either a bacterial or viral infection were at higher risk of developing preeclampsia, compared to women without infection. Combined results for the 16 studies yielded an OR of 2.1 (95% CI 1.6-2.7). Separate pooled estimates for prospective (OR 2.3, 95% CI 1.7-3.0), case control and retrospective studies combined (OR 2.0, 95% CI 1.4-2.9) yielded similar results. Heterogeneity was significant across overall pooled estimates, case control and retrospective studies (Q(df=20) of 45.7, P = .001; Q(df=10) of 38.7, P < .005, respectively), but not prospective studies (Q(df=9) of 6.5 P = .69). CONCLUSIONS: In our analysis, any infection (bacterial or viral) was associated with a two-fold higher risk of preeclampsia. This association may provide a potential explanation for preeclampsia-related inflammation.
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