Apo E isoforms, insulin output and plasma lipid levels in essential hypertension

Dembińska‐Kieć,; Kawecka‐Jaszcz,; Kwaśniak,; Guevara, Jose; Pankiewicz,; Malczewska‐Malec,; Iwanejko,; Hartwich,; Zdzienicka,; Stochmal,; Leszczyńska‐Goľˇląbek,

doi:10.1046/j.1365-2362.1998.00259.x

Cited by 4 publications

(2 citation statements)

References 28 publications

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“…In the influential analysis of E4 carriers versus non-carriers, there was evidence for two studies that had a greater effect to the overall significance of the estimates. The first study was that of Niu et al, 32 which if removed produced an overall estimate of 1.09 (95% CI: 0.98, 1.21) and the second one was that of Dembinska-Kiec et al, 33 which, if removed produced an overall estimate of 1.12 (95% CI: 0.99, 1.25). The same studies influenced the analysis of E4 allele versus the others and produced an overall estimate of 1.24 (95% CI: 1.04, 1.49) and 1.30 (95% CI: 1.06, 1.59), respectively, when removed.…”

Section: Resultsmentioning

confidence: 99%

“…We have shown that the E4 allele is associated with an increased risk for hypertension. We identified two influential studies (Niu et al 32 and Dembinska-Kiec et al 33 ) both of which were performed in 'normal' populations with essential hypertension (Chinese and Polish, respectively) and, in the cumulative meta-analysis of both contrasts they were clearly responsible for more significant evidence favoring the association. The common feature of these studies is the significant discordance in the E4 allele frequency between controls and cases (5.72% in controls versus 20.07% in cases and 15.38% versus 40.83%, respectively).…”

Section: Discussionmentioning

confidence: 99%

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The association between apolipoprotein E gene polymorphisms and essential hypertension: a meta-analysis of 45 studies including 13 940 cases and 16 364 controls

et al. 2012

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The apolipoprotein E single-nucleotide polymorphisms are among the potential candidate genes that may serve as modulators in susceptibility to essential hypertension. In an effort to clarify earlier inconclusive results, we performed a meta-analysis of population-based case-control genetic association studies. Random-effects methods were applied on summary data in order to combine the results of the individual studies. We identified in total 45 studies, including 13 940 hypertensive cases and 16 364 controls. The contrast of E4 carriers versus non-carriers yielded an overall odds ratio (OR) of 1.16 (95% confidence interval (CI): 1.02, 1.31), whereas the contrast of E4 allele versus the others in a subtotal of 6617 cases and 7330 controls, yielded an OR of 1.39 (95% CI: 1.12, 1.72). There was moderate evidence of publication bias in both contrasts, which was eliminated after excluding studies not in Hardy-Weinberg equilibrium. Subgroup analyses revealed that significant estimates arose from studies on Asian populations, as opposed to the Caucasian ones. Furthermore, no evidence of publication bias was demonstrated in the comparisons within this subgroup. Our results are consistent with recent meta-analyses but show that the association is weaker than that has been previously demonstrated. Further studies are needed in order to fully address questions about the etiological mechanism of the particular association, as well as to study the effect in populations of African descent.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%