After fatty liver is cured, will it become cancerous after many years?

Although the onset of nonalcoholic fatty liver disease (NAFLD) is hidden, it may eventually develop into cirrhosis or even hepatocellular carcinoma. Recently, The Lancet published a review article about NAFLD, detailing its epidemiology, natural history of diseases, and the latest progress of existing diagnosis and treatment methods and management concepts. In today's content, we will focus on na8edce1578e57a93174d5812d36 _ r.jpg "/> Screenshot Source: Summary of fatty liver diseases in The Lancet pointed out that the main cause of NAFLD is overnutrition, which will lead to abnormal accumulation of fat. In this case, the pro-inflammatory state of insulin resistance will be formed, leading to abnormal lipolysis, and the production of new lipids will continue to increase, while the transmission of fatty acids to the liver will not slow down. Over time, the metabolic capacity of the liver will be overwhelmed. The imbalance of lipid metabolism will lead to cell stress, inflammatory body activation and apoptotic cell death, followed by inflammatory stimulation, tissue regeneration and fibrosis. The pathogenesis of NAFLD is influenced by many metabolic, genetic and microbial factors. For example, genetic differences can affect about 20%-70% of the disease risk, and PNPLA3 gene is the most clear genetic variation related to NAFLD susceptibility. These gene variants may also affect NAFLD diseases, such as coronary artery disease and obesity. Other studies have shown that the composition of intestinal flora in patients with NAFLD has changed. How fast is the disease getting worse and how high is the risk? It needs to be clear that NAFLD includes a series of disease processes: from nonalcoholic simple hepatic steatosis (NAFL) to nonalcoholic steatohepatitis (NASH) which gradually causes liver fibrosis, and may eventually develop into cirrhosis, liver failure and even liver cancer. & ltimg src = "/v2-f0bfe 19 14984 BCF 73 aab 2 e 22 C2 b 7 1760 _ b . jpg " data-size = " normal " data-raw width = " 1 080 "data-rawheight =" 605 "data-default-watermark-src ="/v2-b78f67b3014d2f09f14 ▲ The disease spectrum of NAFLD: NAFL-NASH- compensated cirrhosis-decompensated cirrhosis. NASH and cirrhosis can progress to hepatocellular carcinoma. * Fibrosis subsided. (Image source: reference [1]) The study of matching liver biopsy samples provides important data for the disease progression rate. Although fibrosis may occur in the stage of nonalcoholic fatty liver or nonalcoholic steatohepatitis, it progresses faster in patients with nonalcoholic steatohepatitis, which may be caused by necrotizing necrotizing inflammation. Meta-analysis of matched liver biopsy samples showed that for NASH patients, the average fibrosis stage of 7. 1 year would be aggravated by one grade (from 0 [no fibrosis] to 4 [cirrhosis]); For NAFL patients, each step of fibrosis staging takes an average of 14.3 years. The natural development of NAFLD is reversible. In the three stages of the disease, from NAFLD to NASH to compensatory cirrhosis, the degree of fibrosis progress can change in both directions. However, fibrosis, especially advanced fibrosis (stage 3-4), will be a key prognostic indicator for the deterioration of liver-related results and the increase of total mortality. A meta-analysis of 4428 patients with NAFLD showed that the all-cause mortality of patients with stage 4 fibrosis (cirrhosis) was 3.42 times that of patients without fibrosis, and the liver-related mortality was 1 1. 13 times that of patients without fibrosis. From compensated cirrhosis to decompensated diseases (such as ascites, hepatic encephalopathy or gastroesophageal variceal bleeding), accompanied by portal hypertension or liver failure, the annual incidence of this progress is about 3%-4%. Liver cirrhosis is also the biggest risk factor for the development of hepatocellular carcinoma. The annual incidence of hepatocellular carcinoma (HCC) in patients with NASH cirrhosis is10.6 class = "content _ image" width = "404"/> Image source: 123RF It should be noted that it is not uncommon for NAFLD patients to be diagnosed after decades or even after developing cirrhosis. It is usually difficult to identify NAFLD unless the patient has evidence of portal hypertension (such as splenomegaly and thrombocytopenia) or liver-related complications. In addition, NASH and fibrosis usually have the same development trend, but in the stage of liver cirrhosis, the unique characteristics of steatosis or HASH will no longer be obvious. Therefore, most patients with cryptogenic cirrhosis (cirrhosis with unknown causes) may actually have NASH if they have metabolic diseases and no other known liver diseases, but their clinical features are no longer obvious. Because of its high prevalence, NAFLD has become the second leading cause of end-stage liver disease. NAFLD is also the second most common cause of primary liver cancer among adults waiting for liver transplantation in the United States. In Europe, NAFLD now accounts for 8.4% of the annual transplant reasons. The natural history and model studies of the disease also show that the total number of patients suffering from advanced liver disease and hepatocellular carcinoma due to NAFLD is increasing, and the proportion of NAFLD in all these diseases is also increasing. Risk factors that accelerate the development of the disease In most patients, liver disease is stable or slowly progressing, and will not lead to cirrhosis or liver-related death soon. However, a few patients will develop advanced liver fibrosis, and may develop advanced liver disease and hepatocellular carcinoma. The disease progression rate and clinical outcome of different patients are different, which may be due to different factors driving the development of the disease. For example, complications will accelerate the progress of the disease. In particular, the article points out that type 2 diabetes is related to advanced fibrosis, and the risk of complications related to cirrhosis and death from liver disease has increased by more than two times. Obesity (body mass index >; 30kg/m2), dyslipidemia (low HDL-C and high triglycerides) and hypertension are also associated with an increased risk of severe liver disease, although the impact is less than that of type 2 diabetes. In addition, insulin resistance and pituitary dysfunction are risk factors. Patients with NAFLD over 60 years old also have a higher risk of advanced fibrosis than younger patients. From the point of living habits, intake of fructose, cholesterol and alcohol will also promote the progress of the disease, while exercise and coffee have protective effects. In addition, some genes can also affect the development of diseases. Ppnla 3 gene is related to the severity of NAFLD, the development of hepatocellular carcinoma and mortality. Liver disease is not the main cause of death in patients with fatty liver. Although NAFLD patients are at risk of progressive liver disease, it is worth noting that the main cause of death in NAFLD patients is cardiovascular disease, followed by extrahepatic malignant tumors (such as colorectal cancer or breast cancer). Although it is not clear to what extent NAFLD directly affects the development of cardiovascular diseases, NAFLD and cardiovascular diseases * * * have some cardiac metabolic risk factors, which may lead to death. For example, NAFLD is associated with some metabolic diseases, especially type 2 diabetes and hypertension. Compared with the general population, NAFLD patients have a higher risk of cancer 1.9 times, especially liver cancer, gastrointestinal tumor and uterine cancer. The biological mechanism behind it may be that NAFLD is related to visceral obesity and chronic low-grade inflammation.