Propensity for non-alcoholic fatty liver disease: more evidence for ethnic susceptibility.
Propensity for non-alcoholic fatty liver disease: more evidence for ethnic susceptibility.
复制标题
非酒精性脂肪肝的倾向：种族易感性的更多证据。
DOI：
10.1111/j.1478-3231.2008.01959.x
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Caldwell,StephenH
中科院分区：
文献类型：
--
作者：
Harmon,RChristopher;Caldwell,StephenH
Non-alcoholic fatty liver disease (NAFLD) is a spectrum of disorders defined by excess accumulation of triglyceride in the liver that ranges from simple steatosis, which is often stable clinically, to non-alcoholic steatohepatitis, which can progress to cirrhosis (1). NAFLD has also been linked to other forms of liver disease such as hepatitis C manifesting as increased disease severity including rapid progression to cirrhosis (2). Although NAFLD usually occurs in association with obesity and insulin resistance, the relative prevalence of steatosis in different ethnic groups indicates that these associated conditions are often ‘essential but not sufficient’in the development of NAFLD. For example, we noted some years ago that African Americans represented a paucity of NAFLD patients in spite of high burdens of obesity and diabetes (3). These findings have since been confirmed and extended with the observations that US citizens of Hispanic descent represent a disproportionately high fraction of NAFLD patients although it remains unclear whether or not this might represent admixture of Native American groups (4–6). Such variation is important to understand as it holds clues for disease pathogenesis, variable target organ injury in metabolic syndrome and individualized treatment strategies.Riquelme et al.(7) now report the prevalence of NAFLD in South American individuals of primarily Hispanic descent. Subjects underwent an interview for documentation of ethnicity (also supported by mitochondrial-based genetic analysis) and alcohol consumption as well as anthropometric determinations, blood collection and liver ultrasound. The homoeostasis model assessment-insulin resistance (HOMA-IR) was utilized to provide an objective measurement of the degree of insulin resistance. Their results showed that the prevalence of ultrasound-based ‘presumed’NAFLD was 23.4% in this population. This prevalence increased with age and correlated to alanine aminotransferase (ALT), body mass index, HOMA-IR and CRP. Several comments are warranted. Firstly, this was a large study with 832 subjects and consisted of a relatively homogeneous population defined epidemiologically and genetically. The authors also utilized what many feel to be a more appropriate upper limit of normal (30 and 19 for men and women, respectively) for ALT determination (8). One shortcoming of the paper was that the diagnosis of NAFLD was made by ultrasound, which is an imperfect test. Sadeeh et al.(9) showed that> 33% hepatic steatosis was required for accurate determination by ultrasound. In addition, it may have been more instructive to compare the Hispanic group to other ethnic groups and to have examined the relationships to lipoproteins and serum lipids.
