Clinical nutrition ESPEN · 2025
Maternal metabolic dysfunction-associated steatotic liver disease during pregnancy and its impact on offspring steatosis.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
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.
Klepper Corie M, Trout Andrew T, Dong Shun, Fei Lin, Stankiewicz Traci E, Wayland Jennifer, Moreno-Fernandez Maria E, Divanovic Senad, Xanthakos Stavra A, DeFranco Emily, Woo Jessica G, Mouzaki Marialena
Аннотация
BACKGROUND & AIM: To investigate the yet unexplored links between maternal and offspring outcomes of pregnancy metabolic dysfunction-associated steatotic liver disease (MASLD).
METHODS: Prospective observational study using magnetic resonance imaging with proton density fat fraction (MRI-PDFF) to determine the presence of maternal and offspring liver steatosis during gestation (3rd trimester) and in the first year postpartum. Women were deemed at high or low risk for MASLD if they had risk factors (pre-pregnancy obesity or MASLD, gestational diabetes, rapid weight gain during pregnancy). Multivariable regression and longitudinal mixed models assessed associations and changes in MRI-derived fat measures.
RESULTS: We recruited 57 pregnant women; 47 (82 %) were high-risk for MASLD. MASLD was seen in 18 % (n = 10) of women (and 15 % [n = 7/47] of those high-risk), with a median PDFF of 5.9 % (IQR: 5.6-12.0 %). Maternal weight, BMI and HDL-C differed between groups. The fetal liver and placental PDFF of offspring of women with and without MASLD were not different. N = 7 (12 %) infants had clinically significant steatosis in utero, all offspring of mothers without gestational MASLD. Of the 30 mothers with repeat liver MRI-PDFF at 9 months postpartum, ten (33 %)had MASLD. N = 44 infants followed up at either 3 or 9 months of age, with only one still demonstrating significant steatosis 9 months. No infant exposed to gestational MASLD had significant steatosis in the first year.
CONCLUSIONS: Gestational MASLD is generally mild, but hepatic fat fraction increases postpartum. Clinically significant hepatic steatosis occurs as early as in utero but is not associated with maternal MASLD.
METHODS: Prospective observational study using magnetic resonance imaging with proton density fat fraction (MRI-PDFF) to determine the presence of maternal and offspring liver steatosis during gestation (3rd trimester) and in the first year postpartum. Women were deemed at high or low risk for MASLD if they had risk factors (pre-pregnancy obesity or MASLD, gestational diabetes, rapid weight gain during pregnancy). Multivariable regression and longitudinal mixed models assessed associations and changes in MRI-derived fat measures.
RESULTS: We recruited 57 pregnant women; 47 (82 %) were high-risk for MASLD. MASLD was seen in 18 % (n = 10) of women (and 15 % [n = 7/47] of those high-risk), with a median PDFF of 5.9 % (IQR: 5.6-12.0 %). Maternal weight, BMI and HDL-C differed between groups. The fetal liver and placental PDFF of offspring of women with and without MASLD were not different. N = 7 (12 %) infants had clinically significant steatosis in utero, all offspring of mothers without gestational MASLD. Of the 30 mothers with repeat liver MRI-PDFF at 9 months postpartum, ten (33 %)had MASLD. N = 44 infants followed up at either 3 or 9 months of age, with only one still demonstrating significant steatosis 9 months. No infant exposed to gestational MASLD had significant steatosis in the first year.
CONCLUSIONS: Gestational MASLD is generally mild, but hepatic fat fraction increases postpartum. Clinically significant hepatic steatosis occurs as early as in utero but is not associated with maternal MASLD.