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阿托伐他汀通过降低肿瘤坏死因子-α活性部分改善非酒精性脂肪性肝炎的疾病活动度。

Atorvastatin improves disease activity of nonalcoholic steatohepatitis partly through its tumour necrosis factor-α-lowering property.

机构信息

Department of Medicine and Molecular Sciences, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.

出版信息

Dig Liver Dis. 2012 Jun;44(6):492-6. doi: 10.1016/j.dld.2011.12.013. Epub 2012 Jan 20.

DOI:10.1016/j.dld.2011.12.013
PMID:22265683
Abstract

BACKGROUND

We have previously found that atorvastatin decreases liver injury markers in patients with nonalcoholic steatohepatitis. However, how atorvastatin treatment ameliorates the disease activity in nonalcoholic steatohepatitis patients remains unknown.

AIMS

We examined here which anthropometric, metabolic and inflammatory variables were improved and related with amelioration of disease activity in atorvastatin-treated nonalcoholic steatohepatitis patients.

METHODS

Forty-two biopsy-proven nonalcoholic steatohepatitis patients with dyslipidemia were enrolled. Patients were treated with atorvastatin (10mg/day) for 12 months.

RESULTS

Atorvastatin significantly decreased liver transaminase, γ-glutamyl transpeptidase, low-density lipoprotein-cholesterol, triglycerides, type IV collagen, and tumour necrosis factor-α levels, whilst it increased adiponectin and high-density lipoprotein-cholesterol. Atorvastatin improved nonalcoholic fatty liver disease activity score and increased liver to spleen density ratio. Multiple stepwise regression analysis revealed that γ-glutamyl transpeptidase, tumour necrosis factor-α and liver to spleen density ratio (inversely) were independently associated with nonalcoholic fatty liver disease activity score. Aspartate aminotransferase, low-density lipoprotein-cholesterol and nonalcoholic fatty liver disease activity score were independent determinants of decreased liver to spleen density ratio.

CONCLUSION

The present study suggests that atorvastatin improves the disease activity of nonalcoholic steatohepatitis partly via its tumour necrosis factor-α-lowering property.

摘要

背景

我们之前发现阿托伐他汀可降低非酒精性脂肪性肝炎患者的肝损伤标志物。然而,阿托伐他汀治疗如何改善非酒精性脂肪性肝炎患者的疾病活动度尚不清楚。

目的

我们在此检查了哪些人体测量、代谢和炎症变量得到改善,并与阿托伐他汀治疗的非酒精性脂肪性肝炎患者疾病活动度的改善相关。

方法

纳入 42 例经肝活检证实的非酒精性脂肪性肝炎合并血脂异常患者。患者接受阿托伐他汀(10mg/天)治疗 12 个月。

结果

阿托伐他汀显著降低了肝转氨酶、γ-谷氨酰转肽酶、低密度脂蛋白胆固醇、甘油三酯、IV 型胶原和肿瘤坏死因子-α水平,同时增加了脂联素和高密度脂蛋白胆固醇。阿托伐他汀改善了非酒精性脂肪性肝病活动评分,并增加了肝脾密度比。多元逐步回归分析显示,γ-谷氨酰转肽酶、肿瘤坏死因子-α和肝脾密度比(呈负相关)与非酒精性脂肪性肝病活动评分独立相关。天冬氨酸转氨酶、低密度脂蛋白胆固醇和非酒精性脂肪性肝病活动评分是降低肝脾密度比的独立决定因素。

结论

本研究表明,阿托伐他汀通过降低肿瘤坏死因子-α部分改善了非酒精性脂肪性肝炎的疾病活动度。

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