Association of Apolipoprotein E With Intracerebral Hemorrhage Risk by Race/Ethnicity: A Meta-analysis.
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Marini Sandro, Crawford Katherine, Morotti Andrea, Lee Myung J, Pezzini Alessandro, Moomaw Charles J, Flaherty Matthew L, Montaner Joan, Roquer Jaume, Jimenez-Conde Jordi, Giralt-Steinhauer Eva, Elosua Roberto, Cuadrado-Godia Elisa, Soriano-Tarraga Carolina, Slowik Agnieszka, Jagiella Jeremiasz M, Pera Joanna, Urbanik Andrzej, Pichler Alexander, Hansen Björn M, McCauley Jacob L, Tirschwell David L, Selim Magdy, Brown Devin L, Silliman Scott L, Worrall Bradford B, Meschia James F, Kidwell Chelsea S, Testai Fernando D, Kittner Steven J, Schmidt Helena, Enzinger Christian, Deary Ian J, Rannikmae Kristiina, Samarasekera Neshika, Al-Shahi Salman Rustam, Sudlow Catherine L, Klijn Catharina J M, van Nieuwenhuizen Koen M, Fernandez-Cadenas Israel, Delgado Pilar, Norrving Bo, Lindgren Arne, Goldstein Joshua N, Viswanathan Anand, Greenberg Steven M, Falcone Guido J, Biffi Alessandro, Langefeld Carl D, Woo Daniel, Rosand Jonathan, Anderson Christopher D, International Stroke Genetics Consortium
Аннотация
OBJECTIVE: To evaluate associations between established differences in ICH risk by race/ethnicity and the variability in the risks of apolipoprotein E (APOE) ε4 alleles, the most potent genetic risk factor for ICH.
DESIGN, SETTING, AND PARTICIPANTS: This case-control study of primary ICH meta-analyzed the association of APOE allele status on ICH risk, applying a 2-stage clustering approach based on race/ethnicity and stratified by a contributing study. A propensity score analysis was used to model the association of APOE with the burden of hypertension across race/ethnic groups. Primary ICH cases and controls were collected from 3 hospital- and population-based studies in the United States and 8 in European sites in the International Stroke Genetic Consortium. Participants were enrolled from January 1, 1999, to December 31, 2017. Participants with secondary causes of ICH were excluded from enrollment. Controls were regionally matched within each participating study.
MAIN OUTCOMES AND MEASURES: Clinical variables were systematically obtained from structured interviews within each site. APOE genotype was centrally determined for all studies.
RESULTS: In total, 13 124 participants (7153 [54.5%] male with a median [interquartile range] age of 66 [56-76] years) were included. In white participants, APOE ε2 (odds ratio [OR], 1.49; 95% CI, 1.24-1.80; P < .001) and APOE ε4 (OR, 1.51; 95% CI, 1.23-1.85; P < .001) were associated with lobar ICH risk; however, within self-identified Hispanic and black participants, no associations were found. After propensity score matching for hypertension burden, APOE ε4 was associated with lobar ICH risk among Hispanic (OR, 1.14; 95% CI, 1.03-1.28; P = .01) but not in black (OR, 1.02; 95% CI, 0.98-1.07; P = .25) participants. APOE ε2 and ε4 did not show an association with nonlobar ICH risk in any race/ethnicity.
CONCLUSIONS AND RELEVANCE: APOE ε4 and ε2 alleles appear to affect lobar ICH risk variably by race/ethnicity, associations that are confirmed in white individuals but can be shown in Hispanic individuals only when the excess burden of hypertension is propensity score-matched; further studies are needed to explore the interactions between APOE alleles and environmental exposures that vary by race/ethnicity in representative populations at risk for ICH.