Nonalcoholic Fatty Liver Diseases
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Obesity in childhood influences the quality of a person’s life throughout his/her lifespan. It is followed by a variety of inconvenient psycho-social and medical problems. The main cause of nonalcoholic fatty liver disease (NAFLD) development is obesity and overweight. It is a kind of epidemic in modern children. Obesity and overweight are usually resulted from poor dietetic behavior and sedentary lifestyle. It is possible to define somatic and visceral obesity that are predisposing factors for the development of cardiovascular and endocrine pathology in adulthood. Visceral obesity is usually associated with steatic liver impairment. Nowadays, there is a significant problem of NAFLDs in children (Della Corte et al., 2012; Sagi et al., 2007; Mathur, Das, & Arora, 2007).
NAFLD was firstly described by Ludwig in 1980 (Della Corte et al., 2012). NAFLD is a liver pathology; it varies from uncomplicated hepatic steatosis which has a positive clinical prognosis to nonalcoholic steatohepatitis which prognosis depends on the degree of impairment of liver tissue. NAFLD may be characterized by various forms of fibrosis (from mild to moderate one) and inflammation. Nowadays, in Western countries, NAFLD turns to take one of the leading positions among chronic diseases of the liver both in children and adolescents. 15-20% of obese adults have NAFLD (Mathur, Das, & Arora, 2007); NAFLD was detected in 20-77% of obese children (Mathur, Das, & Arora, 2007). A high level of serum aminotransferases was found in 10-25% of obese Italian children (Mathur, Das, & Arora, 2007). According to the data obtained from ultrasonography, NAFLD was detected in 42% of obese children. It was determined that diagnosis of liver steatosis correlated with Body Mass Index (Mathur, Das, & Arora, 2007). In 77% of obese Chinese children steatosis was shown by ultrasonography. Both high levels of aminotransferases and steatosis were detected in 24% of obese children. In those children, higher waist-hip ratios were decreased in comparison with children with simple steatosis (Mathur, Das, & Arora, 2007).
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Etiology and Pathogenesis of NAFLD
All the causes of NAFLD in children may be divided into two main groups: hepatic (metabolic liver diseases and syndromes, chronic hepatitis) and non-hepatic (nutritional, infections, drugs, diabetes mellitus, and inflammatory diseases of alimentary tract) (Mathur, Das, & Arora, 2007).
Inheritance also plays a crucial role in NAFLD development. A family history of type 2 diabetes mellitus, obesity, hyperlipidemia, and coronary heart diseases is common for children with NAFLD (Sagi et al., 2007). On the basis of the genetic background, some trigger factors such as hyperinsulinemia provoke impairment of fat and fatty acids metabolism. It promotes the steatosis development that leads to oxidative stress, mitochondrial dysfunction of hepatocytes, pro-inflammatory cytokine imbalance, and activation of Kupfer cells (Mathur, Das, & Arora, 2007). All these result in necrosis of the liver tissue, inflammation, and at last in fibrosis of the liver (Della Corte et al., 2012).
Steatosis of the liver may be a result of the increased de novo synthesis of fatty acids and triglycerides, the increased delivery of free fatty acids to the liver or impaired metabolism of fatty acids by hepatocytes (Della Corte et al., 2012).
Pathological changes vary from simple steatosis to fibrosis and rarely to cirrhosis. The “gold standard” in NAFLD diagnosis is a liver biopsy. The minimum criterion for NAFLD diagnosis is the detection of macrovacuolar steatosis. Its extension varies from 5% of parenchyma to the total impairment of the liver, especially in association with inflammatory lympho-hystiocytes infiltrates, apoptotic bodies and balloon dystrophy of the hepatocytes are the crucial features of NAFLD.
In contrast to adults, in children macrovacuolar steatosis is usually detected in the periportal region (in adults, it is generally localized in perivenular region (Della Corte et al., 2012)). As for fibrosis in children, it is usually localized in the portal-periportal tract while in adults it is predominantly pericellular and perisinusoidal. According to localization of fibrosis, Schwimneer et al. (2005) proposed a classification of children’s NAFLD. Type 1 is characterized by steatosis of the zone 3, ballooning, and perisinusoidal fibrosis; type 2 of NAFLD is distinguished by steatosis of the zone 1, or panacinar steatosis, portal inflammation and fibrosis without ballooning and perisinusoidal fibrosis. However, mixed types of NAFLD are common in children (Della Corte et al., 2012).
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NAFLD in children is usually declared without any symptoms of liver impairment; it commonly appears as unexpected finding during incidental ultrasonography performed for any other clinical testimonies (Sagi et al., 2007). Rarely, some patients complain of discomfort in the right hypochondriac region or fatigue. Objectively, hepatomegaly, hyperinsulinemia, and acanthosis nigricans are typical for NAFLD. Children with NAFLD are usually overweight or even obese.
Hypertransaminasemia is typical but not obligatory for NAFLD; its level correlates with the degree of histological impairment of the liver.
It is important to diagnose NAFLD at the early stages because untreated NAFLD in reversible stage results in poor prognosis. Therefore, it is a crucial idea that all the obese children or children with overweight have to be screened for early revealing of NAFLD in order to start the treatment as early as possible. Liver biopsy is the best diagnostic tool, which can set the diagnosis of NAFLD, determine the grade of severity, and even provide a prognosis of the disease (Sagi et al., 2007). Conducting of liver biopsy examinations in children has numerous contradictions from parents’ side; that is why strict testimonies for this manipulation have to be established. Therefore, the most effective noninvasive diagnostic methods for revealing NAFLD are MRI and ultrosonography. Transient elastography of the liver by FibroScan helps measure the stiffness of the liver tissue which aids to confirm the diagnosis of NAFLD (Della Corte et al., 2012).