NAFLD之診斷及處置指引


  【24drs.com】根據一篇新的實務指引,非酒精性脂肪肝(NAFLD)患者的適當介入,包括減重、維他命E和/或pioglitazone。美國肝病研究協會(AASLD)、美國胃腸科學院(ACG)與美國胃腸科協會發表了新版的NAFLD診斷與處置建議,刊載於6月份的肝臟學期刊。
  
  印第安那大學醫學院的Naga Chalasani醫師等人寫道,NAFLD的定義需要有影像或組織學脂肪肝證據,沒有引起繼發性肝脂肪堆積,如大量飲酒的原因,使用致脂性藥物或遺傳性疾病。多數病患中,NAFLD與肥胖、糖尿病、血脂異常等代謝風險因素有關。NAFLD在組織學上進一步分類為非酒精性脂肪肝(NAFL)和非酒精性脂性肝炎(NASH)。
  
  以下是指引重點:
  * 減重一般可減輕脂肪肝,但是須減重達10%才可改善壞死性炎症。
  * NAFLD病患不應大量飲酒。
  * 每天800 IU維他命E(a-tocopherol)可改善切片證實NASH之非糖尿病成人的肝臟組織;因此可將它考慮作為這類病患的第一線用藥,但是其他病患則否,仍有待進一步的證據支持其療效。
  * Omega-3脂肪酸可以考慮作為NAFLD病患高三酸甘油脂血症的第一線治療,但是還無法建議用於NAFLD或NASH的特定治療。
  * Metformin不建議用於NASH之肝病患者的特定治療。
  * Pioglitazone可以用來治療切片證實NASH病患的脂性肝炎,但是長期安全性和效果尚未建立。
  * 對於其他方面符合之肥胖NAFLD或NASH病患但無肝硬化者,前腸減重手術不是禁忌。不過,還無法將前腸減重手術考慮作為治療NASH的特定治療選項。
  * Statins類藥物可以用來治療NAFLD和NASH病患的血脂異常,但是不應用為特定治療NASH,還需要隨機控制試驗的證據。
  * 醫師應檢視其他類型慢性肝病以及有脂肪肝和脂性肝炎之肝臟脂肪肝患者的代謝風險因素與其他病因。
  * 根據AASLD/ACG實務指引,NASH肝硬化病患應篩檢食道靜脈曲張,應考慮肝細胞腫瘤篩檢。
  * 因為不確定周邊的診斷檢測、治療選項、長期效果與成本效益,不建議對一線照護診所的成年病患或糖尿病/肥胖門診的高風險對象進行NAFLD篩檢。
  * 目前未建議全面篩檢NAFLD病患的家庭成員。
  * 疑似NAFLD患者必須排除脂肪肝的競爭病因和共同存在的一般慢性肝病。
  * 持續地高血清鐵濃度及鐵飽和度增加時可能需要肝臟切片,特別是C282Y HFE基因突變同型合子或異型合子者。
  * 高血清抗體效價以及有其他自體免疫肝病特徵(例如轉胺酶相當高或球蛋白值高)的病患,應接受更完整的自體免疫肝病檢查。
  * 代謝症狀可預測NAFLD病患出現脂性肝炎,因此也可以用在特定病患的肝切片。
  * NAFLD纖維化分數可幫助辨識發生橋接纖維化和/或肝硬化之可能性較高的NAFLD病患。
  * 肝臟脂肪肝之競爭病因和共有慢性肝病無法排除其他原因的疑似NAFLD病患,應考慮進行肝切片。
  
  這篇臨床實務指引也提供孩童NAFLD的處置和治療建議。
  
  資料來源: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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