NAFLD and NASH
People usually associate liver disorders with alcoholism or viral hepatitis. The facts reveal that non-alcoholic fatty liver disease is the evildoer that will most likely attack your liver.
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease that can progress to cirrhosis and hepatocellular carcinoma. NAFLD is associated with the metabolic syndrome and its features, including obesity, insulin resistance, impaired glucose tolerance, and dyslipidemia.
Non-Alcoholic Fatty Liver Disease (NAFLD) is present in up to one-third of the general population and virtually in all of patients after fifties with metabolic risk factors such as obesity and diabetes. NAFLD used to be almost exclusively a disease of adults.
What's even more frightening is that, like diabetes and hypertension, this silent liver condition sneaks up and can cause life-threatening health problems years down the line.
Obesity and its associated comorbidities are among the most prevalent and challenging conditions in the 21st century. A major metabolic consequence of obesity is insulin resistance, which is a key pathogenic factor resulting in hepatic fat accumulation, namely build up of triglycerides (fat) in the liver cells which results in non-alcoholic fatty liver disease (NAFLD).
Fat cells (adipocytes) are the only specialized cells to store triglycerides (fat) without harm for themselves. All other cell types including liver cells may store only a limited quantity of fat for their current fuel needs without detriment to their condition. Excess of fat in liver cells results in lipotoxicity
(lipid-induced cellular injury) and some time later it eventually results in lipoapoptosis of liver cells (apoptosis - cell death, accordingly lipoapoptosis is death of a cell as a result of lipotoxicity.)
Excess hepatic triglyceride accumulation is associated with various medications, nutritional factors, and multiple genetic defects in energy metabolism. However, the most common disorder which results in hepatic steatosis is the metabolic syndrome. So the NAFLD is the hepatic component of the metabolic syndrome - insulin resistance, obesity, type 2 diabetes mellitus, dyslipidemia, and hypertension.
Non-alcoholic fatty liver disease is a clinicopathological term that comprises a succession of liver damage stages, ranging from simple hepatic steatosis to non-alcoholic steatohepatitis (NASH), and cirrhosis (see the Figure).
Hepatic steatosis can either be a benign, noninflammatory condition that appears to have no adverse consequences for decades or can progress and be associated with steatohepatitis: a condition that can result in end-stage liver disease, so NAFLD is an important public health problem.
In other words there are two patterns of NAFLD: fatty liver alone (hepatic steatosis) and nonalcoholic steatohepatitis (NASH). In any case hepatic steatosis is a prerequisite for all subsequent events that lead to liver injury.
The NASH represents a shift from simple steatosis to an inflammatory condition. In patients with NASH progression to cirrhosis is most rapid. Studies show that as many as 10-15% of patients with nonalcoholic steatohepatitis may progress to cirrhosis within a 7-year period, and 3% may progress to liver failure (decompensated cirrhosis), eventually requiring liver transplantation
(up to 16% of liver transplants in the US are due to NASH.) Most worrisome is evidence that nonalcoholic steatohepatitis can progress to hepatocellular carcinoma (liver cancer) (see the Figure) even without cirrhosis stage and HCC is the most common cause of death in patients with NASH with advanced fibrosis.
Mortality among NAFLD patients is higher than the general population. Liver-related death is a leading cause of mortality.
How to stop disease progression from simple steatosis (hepatosteatosis) to Non-Alcoholic SteatoHepatitis (NASH)?
Our clinical experience has shown that cell therapy with cultured hepatoblsats stops liver damage in its tracks and even accelerates its regression, especially when it is combined with adjuvant therapies to correct metabolic syndrome. So this common killer is largely preventable, and can even be reversed if caught in time.
Treatment of Fatty Liver Disease (hepatosteatosis) is successful if all underlying factors and components of metabolic syndrome are treated. However transplantation of cultured hepatoblasts and hepatocytes is a key treatment component to stop progression and reverse liver fibrosis (scarring, which is always present with the Fatty Liver Disease).
Synonyms and related keywords: insulin resistance, steatosis, hepatic steatosis, liver steatosis steatohepatitis, alcohol-related fatty liver, alcoholic steatohepatitis, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, NASH, liver fibrosis, cirrhosis, impaired glucose tolerance, dyslipidemia, hyperlipidemia,
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