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Complications of liver disease for obesity
Complications of liver disease for obesity
Obesity leads to disruption of the liver, which is manifested in the increase of its size, an increase in hepatic biochemical parameters and changes at the cellular level (Large-steatosis, fatty steatosis, fibrosis and cirrhosis). Although these conditions are presented in the review, as a number of special cases, most likely, such violations can be attributed to the signs of the disease, known as Nonalcoholic fatty liver.
Due to the paucity of data, the breadth of the spread of this disease in obese patients is not known. The most characteristic feature is the increase in liver enzymes (alanine aminotransferase - ALT and aspartate aminotransferase - AST). But usually, these figures do not exceed twice the value of the upper limit of normal. In addition, the growth rate of liver enzymes does not correspond to the severity of histological changes. The diet itself can cause a temporary increase in liver enzyme concentrations during the first 6 weeks of weight loss.
Retrospective analysis of liver tissue samples taken for analysis from patients who had overweight or obese, showed that 30% of patients had hepatic fibrosis, connective tissue, and a third of them (10% of the entire group) was found hidden cirrhosis. In addition, many obese patients who show signs of fatty degeneration of the liver of nonalcoholic origin. From 40% to 100% of patients with nonalcoholic steatohepatitis (NSG), the combined data from several studies have obesity.
According to the autopsy (post-mortem examination) in patients suffering from obesity, in ~ 75% of the cases found steatosis in ~ 20% - and steatohepatitis in ~ 2% - cirrhosis of the liver. Although the clinical and laboratory signs of cellular and non-alcoholic fatty liver disease is identified, the nature and pathogenesis of this disease is still not well understood. Many disease is asymptomatic, or patients complain of fatigue, malaise or discomfort in the abdomen. Increasing the size of the liver is observed in 75% of patients. The ratio of AST / ALT patients are usually less than unity, in contrast to the values of this parameter in patients with alcoholic steatohepatitis.
In the observation of patients within 1-7 years, it was noted the progression of liver disease in 40% of patients, and 10% had developed cirrhosis. In addition, most patients with simple steatosis, a disease took a benign course, whereas steatohepatitis, fibrosis and cirrhosis often leads to complications and more severe disease. Although, ultimately, only a small number of patients with nonalcoholic fatty liver cirrhosis in countries with high incidence of obesity, this pathology is a major cause of liver cirrhosis.
In addition, obesity increases the risk of fibrosis and cirrhosis in patients with alcoholic liver disease and hepatitis C. It is not fully understood why people are obese, developing non-alcoholic fatty liver. There is reason to believe that the development of this pathology is often associated with intraabdominal obesity (defined by waist circumference), insulin resistance (increased fasting glucose and insulin in the blood), diabetes, elevated triglycerides, low concentrations of serum high-density lipoprotein (HDL) and hypertension.
There is a hypothesis that the development of this disease is associated with 2 or more damaging effects on the liver. This is primarily steatosis caused by the change is most often due to obesity of lipid metabolism, namely an increase in the splitting of triglycerides of adipose tissue, which in turn increases the supply of free fatty acids in the liver. Second, lipid peroxidation in the liver and release of cytokines may have a direct damaging effect on liver cells and promote inflammation and fibrosis.
Although weight loss is a common recommendation for obese patients with nonalcoholic fatty liver disease is not yet known whether such therapy affects the nature of the disease. The gradual weight loss of 10% or more can adjust the levels of liver enzymes and help to reduce the size of the liver, fat content in liver tissue and weakening of the manifestations of steatohepatitis. But the rapid weight loss during therapy with very low calorie diet or starvation can cause inflammation.
