Nonalcoholic fatty liver is a clinicopathologic syndrome characterized by fatty degeneration and fat accumulation in hepatic parenchymal cells without a history of excessive alcohol consumption. The spectrum of disease varies with the progression of the disease and includes simple fatty liver, steatohepatitis, fatty liver fibrosis and cirrhosis.
Nonalcoholic fatty liver is not only a liver lesion, but more importantly, as an important organ for substance metabolism in the body, its occurrence of fat deposition has serious and widespread effects on blood glucose and lipid metabolism, endangering human health. Nonalcoholic fatty liver is very closely related to diabetes mellitus and may be a precursor of early diabetes mellitus.
The risk of cardiovascular diseases such as glucose metabolism, hypertension, lipid metabolism disorders, coronary heart disease and stroke is significantly higher in patients with NAFLD. Abnormalities in glucose metabolism of varying degrees have been reported abroad to be about 50％ in the nonalcoholic fatty liver population. Patients with fatty liver in the normal stage of glucose metabolism are more likely to develop type 2 diabetes mellitus relative to those without fatty liver. Therefore, the prevention and treatment of NAFLD is of greater importance for the early diagnosis and active prevention and treatment of type 2 diabetes.
Once a diagnosis of fatty liver is made, it should not be overlooked that further clarification of the presence of abnormal glucose metabolism or diabetes mellitus, hypertension, coronary artery disease, and abnormal lipid metabolism is needed to assess the risk of diabetes mellitus and cardiovascular lesions. For patients with fatty liver whose glucose metabolism is still in a normal stage an oral glucose tolerance test is required to determine fasting and postprandial glucose. After these comprehensive assessments, a proper treatment plan can be formulated. Since ultrasound cannot accurately quantify liver fat content and classify the severity of fatty liver, liver fat can be accurately quantified, graded and staged by liver puncture pathology when the condition requires it, and this method is valuable in determining the degree of liver damage and fibrosis.
Treatment countermeasures.
1.Prevent and control the primary disease or related risk factors.
2.Basic treatment: develop reasonable energy intake as well as diet structure adjustment, moderate aerobic exercise, and correct poor lifestyle and behavior.
3.Avoid aggravation of liver damage: prevent drastic weight loss, drug abuse and other factors that may induce deterioration of liver disease.
4.Lose weight.
5.Insulin sensitizer: combined with type 2 diabetes, impaired glucose tolerance, increased fasting glucose and visceral obesity, consider applying metformin and thiazolidinediones with a view to improving insulin resistance and controlling blood glucose. Metformin and peroxisome proliferator-activated receptor (PPAR) γ agonists (thiazolidinediones) are both insulin receptor agonists and are used to treat fatty liver by improving insulin resistance. Animal experiments have found that metformin can reduce liver fat deposition, normalize transaminases and decrease blood lipids. The results of clinical application in several groups showed that patients lost weight and recovered liver function. Thiazolidinediones (rosiglitazone maleate) in animal experiments and the application of a few patients with fatty liver, can significantly improve insulin resistance, correct transaminase abnormalities, and some patients get better liver histology.
6.Lipid-lowering drugs: dyslipidemia after basic treatment and/or application of weight-loss and hypoglycemic drugs for more than 3-6 months, still showing mixed hyperlipidemia or hyperlipidemia combined with more than 2 risk factors, additional lipid-lowering drugs such as fibrates, statins or probucol need to be considered.
7, drugs for liver disease: NARLD with abnormal liver function, metabolic syndrome, after 3-6 months of basic treatment is still ineffective, as well as liver biopsy confirmed as NASH and the course of the disease is chronic progressive, can use drugs for liver disease adjuvant therapy, to antioxidant, anti-inflammatory, anti-fibrosis, according to drug performance and disease activity and disease stage reasonable choice of polyenyl phosphatidylcholine, vitamin E However, multiple drugs should not be applied simultaneously.
8. Liver transplantation: mainly used for the treatment of patients with NASH-related end-stage liver disease and partial cryptogenic cirrhosis with liver function loss, and the metabolic status should be screened before liver transplantation.
Monitoring of treatment
1, self-testing and monitoring, set up to enable patients to make simple charted records of their diet, exercise, sleep, weight and quality of life-related observations, for example, for evaluation between doctor and patient.
2. assessment of clinical signs and symptoms related to primary disease and liver disease, with the need to be alert to the possibility of subacute NASH and liver failure due to excessive weight loss (>5 kg per month).
3. observation of the components of the metabolic syndrome and their degree of practical goals and therapeutic control goals.
4. assessment of liver enzymology and hepatic functional reserve, the latter using the Child-Pugh classification and/or the MELD scoring system
5. imaging assessment of the extent and type of distribution of hepatic fatty infiltration.
6. dynamic observation of non-traumatic indicators of liver inflammation and progressive fibrosis, including serum fibrosis markers as well as other relevant laboratory indicators.
7. liver biopsy to assess changes in hepatic steatosis, inflammation and fibrosis, and to monitor the efficacy, safety and assess the prognosis of treatment.
8, clinical and laboratory-related tests for adverse drug reactions related to basic treatment.