NAFLD之诊断及处置指引


  【24drs.com】根据一篇新的实务指引,非酒精性脂肪肝(NAFLD)患者的适当介入,包括减重、维他命E和/或pioglitazone。美国肝病研究协会(AASLD)、美国胃肠科学院(ACG)与美国胃肠科协会发表了新版的NAFLD诊断与处置建议,刊载于6月份的肝脏学期刊。
  
  印第安那大学医学院的Naga Chalasani医师等人写道,NAFLD的定义需要有影像或组织学脂肪肝证据,没有引起继发性肝脂肪堆积,如大量饮酒的原因,使用致脂性药物或遗传性疾病。多数病患中,NAFLD与肥胖、糖尿病、血脂异常等代谢风险因素有关。NAFLD在组织学上进一步分类为非酒精性脂肪肝(NAFL)和非酒精性脂性肝炎(NASH)。
  
  以下是指引重点:
  * 减重一般可减轻脂肪肝,但是须减重达10%才可改善坏死性炎症。
  * NAFLD病患不应大量饮酒。
  * 每天800 IU维他命E(a-tocopherol)可改善切片证实NASH之非糖尿病成人的肝脏组织;因此可将它考虑作为这类病患的第一线用药,但是其它病患则否,仍有待进一步的证据支持其疗效。
  * Omega-3脂肪酸可以考虑作为NAFLD病患高三酸甘油脂血症的第一线治疗,但是还无法建议用于NAFLD或NASH的特定治疗。
  * Metformin不建议用于NASH之肝病患者的特定治疗。
  * Pioglitazone可以用来治疗切片证实NASH病患的脂性肝炎,但是长期安全性和效果尚未建立。
  * 对于其它方面符合之肥胖NAFLD或NASH病患但无肝硬化者,前肠减重手术不是禁忌。不过,还无法将前肠减重手术考虑作为治疗NASH的特定治疗选项。
  * Statins类药物可以用来治疗NAFLD和NASH病患的血脂异常,但是不应用为特定治疗NASH,还需要随机控制试验的证据。
  * 医师应检视其它类型慢性肝病以及有脂肪肝和脂性肝炎之肝脏脂肪肝患者的代谢风险因素与其它病因。
  * 根据AASLD/ACG实务指引,NASH肝硬化病患应筛检食道静脉曲张,应考虑肝细胞肿瘤筛检。
  * 因为不确定周边的诊断检测、治疗选项、长期效果与成本效益,不建议对一线照护诊所的成年病患或糖尿病/肥胖门诊的高风险对象进行NAFLD筛检。
  * 目前未建议全面筛检NAFLD病患的家庭成员。
  * 疑似NAFLD患者必须排除脂肪肝的竞争病因和共同存在的一般慢性肝病。
  * 持续地高血清铁浓度及铁饱和度增加时可能需要肝脏切片,特别是C282Y HFE基因突变同型合子或异型合子者。
  * 高血清抗体效价以及有其它自体免疫肝病特征(例如转胺酶相当高或球蛋白值高)的病患,应接受更完整的自体免疫肝病检查。
  * 代谢症状可预测NAFLD病患出现脂性肝炎,因此也可以用在特定病患的肝切片。
  * NAFLD纤维化分数可帮助辨识发生桥接纤维化和/或肝硬化之可能性较高的NAFLD病患。
  * 肝脏脂肪肝之竞争病因和共有慢性肝病无法排除其它原因的疑似NAFLD病患,应考虑进行肝切片。
  
  这篇临床实务指引也提供孩童NAFLD的处置和治疗建议。
  
  资料来源:http://www.24drs.com/professional/list/content.asp?x_idno=6869&x_classno=0&x_chkdelpoint=Y
  

NAFLD Diagnosis and Management Guidelines Issued

By Laurie Barclay, MD
Medscape Medical News

June 27, 2012 — Suitable interventions in some patients with nonalcoholic fatty liver disease (NAFLD) may include weight loss, vitamin E, and/or pioglitazone, according to a new practice guideline. The American Association for the Study of Liver Diseases (AASLD), American College of Gastroenterology (ACG), and American Gastroenterological Association issued the new recommendations for NAFLD diagnosis and management, which are published in the June issue of Hepatology.

"The definition of [NAFLD] requires that (a) there is evidence of hepatic steatosis, either by imaging or by histology and (b) there are no causes for secondary hepatic fat accumulation such as significant alcohol consumption, use of steatogenic medication or hereditary disorders," write Naga Chalasani, MD, FACG, from the Indiana University School of Medicine in Indianapolis, and colleagues. "In the majority of patients, NAFLD is associated with metabolic risk factors such as obesity, diabetes mellitus, and dyslipidemia. NAFLD is histologically further categorized into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH)."

Highlights of the recommendations in adults include the following:

  • Weight loss generally reduces hepatic steatosis, but up to 10% weight loss may be needed to improve necroinflammation.
  • Patients with NAFLD should not consume heavy amounts of alcohol.
  • Vitamin E (a-tocopherol), 800 IU/day, improves liver histology in nondiabetic adults with biopsy-proven NASH. It should therefore be considered as a first-line pharmacotherapy for this patient population, but not in other patients, pending further evidence supporting its efficacy.
  • Omega-3 fatty acids may be considered as first-line therapy for hypertriglyceridemia in patients with NAFLD, but it is premature to recommend them for the specific treatment of NAFLD or NASH.
  • Metformin is not recommended as a specific treatment for liver disease in adults with NASH.
  • Pioglitazone may be used to treat steatohepatitis in patients with biopsy-proven NASH, but long-term safety and efficacy have not been established.
  • Foregut bariatric surgery is not contraindicated in otherwise eligible obese individuals with NAFLD or NASH but without established cirrhosis. However, it is premature to consider foregut bariatric surgery as an established option to specifically treat NASH.
  • Statins can be used to treat dyslipidemia in patients with NAFLD and NASH, but they should not be used to specifically treat NASH, pending evidence from randomized controlled trials.
  • Clinicians should look for metabolic risk factors and alternate etiologies for hepatic steatosis in patients who have other types of chronic liver disease and who also have steatosis and steatohepatitis.
  • Patients with NASH cirrhosis should be screened for gastroesophageal varices and should be considered for hepatocellular carcinoma screening according to the AASLD/ACG practice guidelines.
  • Because of uncertainties surrounding diagnostic tests, treatment options, long-term benefits, and cost-effectiveness, screening for NAFLD is not advised among adults attending primary care clinics or high-risk groups attending diabetes or obesity clinics.
  • Systematic screening of family members of patients with NAFLD is currently not recommended.
  • Competing etiologies for steatosis and coexisting common chronic liver disease must be excluded in patients with suspected NAFLD.
  • Persistently high serum ferritin and increased iron saturation may warrant a liver biopsy, especially in patients with homozygous or heterozygous C282Y HFE (hemochromatosis) gene mutations.
  • Patients with high serum titers of autoantibodies and other features suggesting autoimmune liver disease (eg, very high aminotransferases or high globulin levels) should undergo a more thorough work-up for autoimmune liver disease.
  • Metabolic syndrome predicts the presence of steatohepatitis in patients with NAFLD and can therefore be used to target patients for a liver biopsy.
  • The NAFLD Fibrosis Score helps to identify patients with NAFLD who have a higher likelihood of having bridging fibrosis and/or cirrhosis.
  • Liver biopsy should be considered in patients with suspected NAFLD in whom competing etiologies for hepatic steatosis and coexisting chronic liver diseases cannot be otherwise excluded.

This clinical practice guideline also provides recommendations for the management and treatment of NAFLD in children.

Some of the guideline authors and reviewers report various financial relationships involving Gilead, Genentech, Mochida, Amylin, Eli Lilly, Ikaria, Intercept, Cumberland Pharmaceuticals, J & J, Merck, GlaxoSmithKline, Karo Bio, Salix, Advanced Life Sciences, Bristol Meyers Squibb, Teva Pharmaceuticals, Abbott, Biolex, Sanofi-Aventis, Vertex, Tibotec, Vertex, Norgine, Celgene, Pfizer, Geneva Foundation, Daichi-Sankyo, Roche, Quark Pharmaceuticals, Synageva BioPharma, Raptor Pharmaceuticals, Takeda, Astella, Exhalenz, Immuron, Schering-Plough, and/or Rottapharm.

Hepatology. 2012;55:2005-2023.

    
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