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标题: 肥胖增加了脂肪肝疾病中纤维化进展的风险 [打印本页]

作者: StephenW    时间: 2018-7-25 18:19     标题: 肥胖增加了脂肪肝疾病中纤维化进展的风险

Obesity increases risk for fibrosis progression in fatty liver disease

Kim Y, et al. Clin Gastroenterol Hepatol. 2018;doi:10.1016/j.cgh.2018.07.006.
July 24, 2018

Obesity and weight gain correlated with an increased risk for fibrosis progression based on aspartate aminotransferase-to-platelet ratio in a large cohort study of adults with nonalcoholic fatty liver disease.

“Weight gain during adulthood is associated with higher leptin and lower adiponectin levels, possibly leading to the development of NASH,” Yejin Kim, MD, from the Kangbuk Samsung Hospital in South Korea, and colleagues wrote. “The protective effect of weight loss against fibrosis progression may relate to fat loss, by which the adverse impacts of excess adiposity may be diminished.”

Among a cohort of 40,700 Korean patients with NAFLD and low APRI, factors positively associated with weight change categories were male sex, current smoking, alcohol use and education level.

In contrast, factors inversely associated with weight change categories included hypertension, diabetes, history of cardiovascular disease, systolic and diastolic blood pressure, glucose, total cholesterol, triglycerides and homeostatic model assessment of insulin resistance (HOMA-IR).

In a multivariate analysis for APRI progression, the researchers compared weight loss and weight gain with weight stability through weight change quintiles. Researchers observed less APRI progression among patients in the first (HR = 0.68; 95% CI, 0.62-0.74) and second quintiles (HR = 0.86; 95% CI, 0.78-0.94) than in the fourth (HR = 1.17; 95% CI, 1.07-1.28) and fifth quintiles (HR = 1.71; 95% CI, 1.58-1.85). The significance did not change after adjusting for high sensitive C-reactive protein (hsCRP) and HOMA-IR.

Additionally, the researchers found that other metabolic factors such as increasing quintiles of triglyceride, uric acid and HOMA-IR, as well as decreasing quintiles of HDL cholesterol correlated with an increased risk for worsening APRI in a dose-response manner (P < .001).

“Although the mechanisms underlying the association between excessive adiposity or fat gain and the fibrosis progression are not yet fully understood, insulin resistance and inflammation are thought to be involved,” the researchers wrote. “However, after adjustment for HOMA-IR and hsCRP, the association between obesity, weight gain and fibrosis progression remained significant.”

Kim and colleagues also noted that weight change reflects a patient’s muscle structure and that sarcopenia has been shown to correlate with significant liver fibrosis in NAFLD. Therefore, they advise that other factors besides BMI should be considered in NAFLD cases, such as fat distribution and body composition. – by Talitha Bennett

Disclosure: The authors report no relevant financial disclosures.

作者: StephenW    时间: 2018-7-25 18:19

肥胖增加了脂肪肝疾病中纤维化进展的风险

Kim Y,et al。 Clin Gastroenterol Hepatol。 2018; DOI:10.1016 / j.cgh.2018.07.006。
2018年7月24日

在一项针对非酒精性脂肪性肝病成人的大型队列研究中,肥胖和体重增加与基于天冬氨酸氨基转移酶与血小板比率的纤维化进展风险增加相关。

“成年期体重增加与瘦素水平升高和脂联素水平降低有关,可能导致NASH的发展,”来自韩国Kangbuk三星医院的医学博士Yejin Kim及其同事写道。 “减肥对纤维化进展的保护作用可能与脂肪减少有关,过度肥胖的不利影响可能会减少。”

在一组40,700名患有NAFLD和低APRI的韩国患者中,与体重变化类别正相关的因素是男性,当前吸烟,饮酒和教育水平。

相反,与体重变化类别成反比的因素包括高血压,糖尿病,心血管疾病史,收缩压和舒张压,葡萄糖,总胆固醇,甘油三酯和胰岛素抵抗的稳态模型评估(HOMA-IR)。

在APRI进展的多变量分析中,研究人员通过体重变化的五分位数比较体重减轻和体重增加与体重稳定性。研究人员观察到,第一(HR = 0.68; 95%CI,0.62-0.74)和第二五分之一(HR = 0.86; 95%CI,0.78-0.94)患者的APRI进展较第四(HR = 1.17; 95%) CI,1.07-1.28)和第五个五分位数(HR = 1.71; 95%CI,1.58-1.85)。调整高敏C-反应蛋白(hsCRP)和HOMA-IR后,显着性没有变化。

此外,研究人员发现,其他代谢因素,如增加五分位数,尿酸和HOMA-IR的五分位数,以及降低高密度脂蛋白胆固醇的五分之一,与剂量反应方式恶化APRI的风险增加相关(P <.001 )。

研究人员写道:“虽然过度肥胖或脂肪增加与纤维化进展之间关联的机制尚未完全了解,但人们认为胰岛素抵抗和炎症是有关的。” “然而,在调整HOMA-IR和hsCRP后,肥胖,体重增加和纤维化进展之间的关联仍然很显着。”

Kim及其同事还指出,体重变化反映了患者的肌肉结构,并且肌肉减少症已显示与NAFLD中的显着肝纤维化相关。因此,他们建议在NAFLD病例中应考虑除BMI之外的其他因素,如脂肪分布和身体成分。 - Talitha Bennett

披露:作者报告没有相关的财务披露。




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