What Is Necrobiosis Lipoidica Diabeticorum?

Diabetes, especially type 2 diabetes, has prominent lipid metabolism disorders, and obesity or overweight are common. Total blood cholesterol, triglycerides, LDL, and VLDL are increased, while HDL is reduced, resulting in a large amount of lipid deposition in the liver and liver cell steatosis, formation. Fatty liver. The liver is an important digestive and endocrine organ of the human body, and plays an important role in the digestion, absorption, oxidation, decomposition, transformation and balance of lipids. Under normal circumstances, the liver contains a small amount of fat, which accounts for about 5% of the liver's weight. Fatty liver is when it contains more than 10% of the weight of the liver. When it exceeds 10% to 25%, it is called moderate fatty liver, and when it exceeds 25% to 50%, it is severe fatty liver.

Diabetes, especially type 2 diabetes, has prominent lipid metabolism disorders, and obesity or overweight are common. Total blood cholesterol, triglycerides, LDL, and VLDL are increased, while HDL is reduced, resulting in a large amount of lipid deposition in the liver and liver cell steatosis, formation. Fatty liver. The liver is an important digestive and endocrine organ of the human body, and plays an important role in the digestion, absorption, oxidation, decomposition, transformation and balance of lipids. Under normal circumstances, the liver contains a small amount of fat, which accounts for about 5% of the liver's weight. Fatty liver is when it contains more than 10% of the weight of the liver. When it exceeds 10% to 25%, it is called moderate fatty liver, and when it exceeds 25% to 50%, it is severe fatty liver.

Chinese name

Diabetic fatty liver

Foreign name

Diabetic fatty liver

Diabetic fatty liver I. Etiology and pathology:

The reason is that diabetes itself, fatty liver can occur at all ages, and it is related to the length of diabetes and the number of complications. The longer the disease, the more obvious the lipid metabolism disorder. Patients with endocrine abnormalities, physiological dysfunction, insufficient or relatively lack of insulin secretion cause liver lipid metabolism disorders. Because insulin resistance reduces the activity of insulin-suppressing fatty acids, the breakdown of peripheral adipose tissue increases, the hydrolysis of free fatty acids (FFA) increases, and a large amount of FFA is more likely to enter the liver through the portal vein system. In addition, the disease itself reduces the use of sugar and increases release, leading to abnormal accumulation of fat and fatty liver. Studies have found that hyperinsulinemia and impaired glucose tolerance can promote the occurrence of fatty liver, poorly controlled blood sugar for a long time, increased insulin promotes fat synthesis, inhibits lipolysis, liver protein synthesis is insufficient or synthesis disorders, liver cells The fat in it cannot be transported out of the liver in time, causing a large amount of fat to accumulate in liver cells, causing damage to liver function. Abnormal liver function affects normal glucose metabolism. It cannot convert excessively high blood sugar into liver glycogen storage, causing blood sugar to remain at a high level, which in turn worsens diabetes.

Diabetic fatty liver 2. Diagnosis:

The diagnostic criteria for fatty liver are usually based on laboratory and ultrasound examinations. Clinical manifestations are usually mild and nonspecific. Most patients do not have symptoms related to liver disease, which are mainly found during physical examinations or examinations for other diseases.

Diabetic fatty liver III. Ultrasound:

The maximum vertical diameter of the right lobe of diabetic fatty liver is mostly less than 14cm. The parenchymal echo particles are slightly thicker and stronger. The blood vessels in the liver are basically clear. The contrast between liver and kidney is large.

Diabetic fatty liver IV. Treatment:

(I) Basic treatment principles:

Treat diabetes early to prevent its complications. Measures include: treating diabetes; diet therapy to correct nutritional imbalances; maintaining the ideal weight and proper exercise necessary; behavior correction and self-care awareness education; preventing liver cell necrosis, inflammation and liver fibrosis.

(2) Non-drug treatment:

Avoid alcohol and correct malnutrition. The diet should be high in protein, low in sugar, low in fat, and multi-vitamin. Sufficient total calories and insufficient protein intake can promote the continued formation of fatty liver. Reduce sugar and polyvalent unsaturated fatty acids in the diet, but it is necessary to have essential fatty acids, and fat should not exceed 15% to 20% of total calories. Exercise therapy can reduce weight and correct obesity, thereby improving diabetes and its accompanying hyperinsulinemia, insulin resistance, hyperlipidemia, and regression of fatty liver.

(Three) drug treatment:

Drug-assisted treatment should be reasonable. Try to choose a hypoglycemic agent with minimal (or no) damage to the liver, with as little as possible. Disorders of lipoprotein metabolism involve multiple factors and multiple links, which are not only reflected at the level of blood circulation, but also at the level of tissues, cells and molecules. Especially after paying attention to the relationship between lipid peroxidation and inflammation and fibrosis, people try to find drug intervention Unfortunately, there are no satisfactory drugs so far in clinical practice. Lipid-lowering drugs: At present, there are still objections to the efficacy of lipid-lowering drugs, which need to be further verified. According to reports, many lipid-lowering drugs may tend to make blood lipids more concentrated in the liver for metabolism, but instead promote lipid storage and damage liver function. Polyvalent unsaturated lecithin: It is a stabilizer for liver sinusoidal endothelium and hepatocyte membrane, which can reduce lipid peroxidation, reduce lipid change of liver cells and its associated inflammation and fibrosis. Antioxidants: reduced glutathione, taurine, vitamin E, selenium organic compounds, etc., may reduce oxygen stress damage and liver fibrosis induced by lipid peroxidation.