Relationship between Dietary Fatty Acid Intake with Nonalcoholic Fatty Liver Disease and Liver Fibrosis in People with HIV.

Relationship between Dietary Fatty Acid Intake with Nonalcoholic Fatty Liver Disease and Liver Fibrosis in People with HIV.
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DOI:
10.3390/nu13103462
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发表时间:
2021-09-29
期刊:
影响因子:
5.9
通讯作者:
Perazzo H
Perazzo H
中科院分区:
医学2区
文献类型:
--
作者:
de Almeida CF;da Silva PS;Cardoso CSA;Moreira NG;Antunes JC;de Andrade MM;Silva J;Araujo MC;Peres WAF;do Brasil PEAA;Moreira RI;Cardoso SW;Veloso VG;Grinsztejn B;de Brito PD;Perazzo H

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我们的目的是评估艾滋病毒/艾滋病患者 (PLWHA) 中脂质食物摄入量与非酒精性脂肪性肝病 (NAFLD) 和/或肝纤维化之间的关系。在这项横断面研究中,使用瞬时弹性成像来检测 NAFLD 和/或肝纤维化的存在。通过两次 24 小时饮食回忆 (24-HDR) 评估饮食中脂肪和脂肪酸 (FA) 的摄入量 (n = 451)。进行了多变量逻辑回归模型。与摄入量较低的参与者相比,总脂肪摄入量较高的参与者患 NAFLD 的几率较高[调整后比值比 (aOR) = 1.91(95% 置信区间 (95% CI) 1.06–3.44)]。此外,n6-PUFA(n6-多不饱和 FA)和月桂酸 FA 摄入量中等的参与者患 NAFLD 的几率较低,分别为 aOR = 0.54 (95% CI 0.3–0.98) 和 aOR = 0.42 (95% CI 0.22–0.78)。此外,较高的肉豆蔻脑脂肪酸摄入量(第四个四分位数)是 NAFLD 的重要保护因素 [aOR = 0.56 (95% CI 0.32–0.99)]。月桂酸 FA [0.38 (95% CI 0.18–0.80)]、肉豆蔻酸 FA [0.38 (0.17–0.89)]、棕榈油酸 FA [0.40 (0.19–0.82)] 和油酸 FA [0.35 (0.16–0.79)] 摄入量较高的参与者患肝纤维化的几率明显较低。另一方面,较高的 n-6 PUFA 摄入量与纤维化显着相关 [aOR = 2.45 (95% CI 1.12–5.32)]。总脂肪和 FA 的膳食评估应纳入 HIV 护理中,作为预防 PLWHA 中 NAFLD 和纤维化的工具。
We aimed to evaluate the relationship between food intake of lipids with nonalcoholic fatty liver disease (NAFLD) and/or liver fibrosis in people living with HIV/AIDS (PLWHA). In this cross-sectional study, transient elastography was used to detect the presence of NAFLD and/or liver fibrosis. The dietary intake of fats and fatty acids (FA) were assessed by two 24 h dietary recalls (24-HDR) (n = 451). Multivariate logistic regression models were performed. Participants with higher intake of total fat were associated with higher odds for NAFLD compared to those with lower consumption [adjusted odds ratio (aOR) = 1.91 (95% confidence interval (95% CI) 1.06–3.44)]. Furthermore, participants with intermediate intake of n6-PUFA (n6-poly-unsaturated FA) and lauric FA had lower odds for NAFLD, respectively aOR = 0.54 (95% CI 0.3–0.98) and aOR = 0.42 (95% CI 0.22–0.78). Additionally, a higher intake of myristoleic FA (fourth quartile) was a significant protective factor for NAFLD [aOR = 0.56 (95% CI 0.32–0.99)]. Participants with higher intake of lauric FA [0.38 (95% CI 0.18–0.80)], myristic FA [0.38 (0.17–0.89)], palmitoleic FA [0.40 (0.19–0.82)] and oleic FA [0.35 (0.16–0.79)] had positively less odds of having liver fibrosis. On the other hand, higher intake of n-6 PUFA was significantly associated with fibrosis [aOR = 2.45 (95% CI 1.12–5.32)]. Dietary assessment of total fat and FA should be incorporated into HIV care as a tool for preventing NAFLD and fibrosis in PLWHA.
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