NAFLD – stem the root before it’s too late

A distinct group of liver diseases is attributed to disorders of metabolism, either acquired or inherited. The most common acquired metabolic disorder is non – alcoholic fatty liver disease. Non-alcoholic fatty liver disease (NAFLD) represents a range of disorders that have in common the presence of fatty liver in individuals who do not consume alcohol or do so in very small quantities. NAFLD has become the most common cause of chronic liver disease. NAFLD contributes to the progression of other liver diseases such as HCV and HBV infection. Increasingly, NAFLD is found to increase the risk of hepatocellular carcinoma, although, unlike in chronic viral hepatitis and alcoholic liver disease, it may often do so in the absence of significant scarring. NAFLD is the most common metabolic disorder associated with :rn1. Metabolic syndrome rn2. Obesity rn3. Type 2 diabetes mellitus rn4. Other impairments of insulin responsivenessrn5. Dyslipidemiarn6. Hypertension NAFLD may show all the changes associated with alcoholic liver disease :rn1. Steatosis rn2. Steatohepatitis rn3. Steatofibrosis Steatofibrosis in NAFLD shows precisely the same features and progression as it does in alcoholic liver disease, although portal fibrosis may he more prominent. Cirrhosis may develop, is often subclinical for years, and when established, the steatosis or steatohepatitis may be reduced or absent. Pathogenesisrn1. Insulin resistance gives rise to hepatic steatosis.rn2. Hepatocellular oxidative injury resulting in liver cell necrosis and the inflammatory reactions to it. Hepatic steatosis, like obesity in general, arises from an overabundance of calorie rich food, diminished exercise, and genetic / epigenetic mechanisms. It is found that individuals with NAFLD eat more fast food and exercise less. High fructose corn syrup, a nearly ubiquitous, inexpensive sweetener in manufactured foods, also appears to promote insulin resistance. In individuals with established insulin resistance and metabolic syndrome, the visceral adipose tissue not only increases, but also become dysfunctional, with reduced production of the lipid hormone, adiponectin, and increased production of inflammatory cytokines such as TNF – alpha and IL – 6. These changes in turn promote hepatocyte apoptosis (cell death). Fat laden cells are highly sensitive to lipid peroxidation products generated by oxidative stress which can damage mitochondrial and plasma membranes, causing apoptosis. Diminished autography also contribute to mitochondrial injury and formation of Mallory- Denk bodies. rnPaediatrics NAFLD is being increasingly recognition as the obesity epidemic spreads to Paediatrics age groups, although its histologic features differ somewhat from that seen in adults. Typically children show more diffuse steatosis, and portal and parenchymal mononuclear infiltration, rather than parenchymal neutrophils. SymptomsrnIndividuals with simple steatosis are generally asymptomatic. Clinical presentation is often related to other signs and symptoms of the metabolic syndrome, in particular insulin resistance or diabetes mellitus. rnImaging studies may reveal fat accumulation in the liver. However, liver biopsy is the most reliable diagnostic tool for NAFLD. The goal of treating individuals with NAFLD is to reverse the steatosis and prevent cirrhosis by correcting the underlying risk factors, such as obesity and hyperlipidemia, and to treat insulin resistance. The prevalence of NAFLD varies among ethnic groups and probably relates, at least in part, to genetic differences. rnTo know more about your specific condition, please visit an Hepatotologist in a a trusted hospital close to you.