الفهرس 
Nonalcoholic Fatty Liver Disease (NAFLD)Only 14 pages are availabe for public view
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Abstract
Paralleling the increasing prevalence of obesity in the pediatric population, nonalcoholic fatty liver disease (NAFLD) become one of the most common causes of liver disease in obese children and young adults. NAFLD is a disease in which excessive fat accumulates in the liver of patients without history of alcohol abuse. Pathogenesis of NAFLD is associated with many factors such as inflammatory cytokines/adipokines, mitochondrial dysfunction and oxidative stress which lead to steatohepatitis and / or fibrosis. NAFLD is closely associated with obesity and linked with disorders of insulin action and insulin resistance (IR). There are two types of NAFLD: simple benign steatosis demonstrating only fat deposition in hepatocytes and nonalcoholic steatohepatitis (NASH) demonstrating not only steatosis but also progressive necro-inflammatory reaction. NASH can progress to liver cirrhosis and results in complications that include hepatocelluar carcinoma. There appears to be a close relationship between hepatic steatosis and high serum uric-acid (SUA) levels, as uric acid may play a role in insulin resistance. However, the association between SUA and hepatic steatosis remains controversial, and differs according to weight status. Most studies that have controlled for other metabolic risk factors suggest a positive relationship between SUA and hepatic steatosis in obese individuals while, in non-obese individuals, SUA is not consistently associated with the presence of hepatic steatosis. Moreover, some studies have examined this difference in association with other metabolic abnormalities and demonstrated a close relationship between high SUA levels and the presence of hepatic steatosis, regardless of weight status and the presence of the MetS and concluded that high SUA can be considered an independent indicator of hepatic steatosis. Recently, SUA level was reported to be significantly associated with NAFLD, and the prevalence rate of NAFLD increased with progressively higher SUA levels. A recent population based study from United States (US) reported that elevated SUA level was independently associated with ultrasound-diagnosed NAFLD in a nationally representative sample of US nondiabetic adults and increasing SUA was associated with increasing severity of NAFLD on ultrasonography. Additionally, hyperuricemia was reported to be a common finding in patients with NAFLD and is independently associated with early histological findings in this clinically relevant condition that necessitate further longitudinal studies to characterize the role of SUA in the natural history of NAFLD. Also, SUA level was found to be elevated in MetS and was strongly associated with IR and NAFLD and the rate of production of uric acid by hepatocytes was a sensitive index of compromised cell ATP homeostasis. These findings warrant further studies on the role of uric acid in NAFLD. Moreover, data on the relationship between SUA and pediatric NAFLD are few. Therefore, we performed this prospective case-control study.