Acquired hyperlipoproteinemia

Introduction to acquired hyperlipoproteinemia Secondary or acquired hyperlipoproteinemias are changes in lipid metabolism caused by organ diseases or drug reactions, and they are much more numerous than primary familial hyperlipoproteinemia, most of which are Does not cause skin lesions. Only forms with clinical manifestations similar to hyperlipidemia type IIb or IV may rapidly develop rash xanthomas, detailed medical history to rule out primary hyperlipoproteinemia. basic knowledge The proportion of sickness: 0.003%-0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: atherosclerosis, acute pancreatitis

Acquired hyperlipoproteinemia

Causes:

It is a change in lipid metabolism caused by organ disease or drug reaction.

Pathogenesis:

Low-density lipoprotein receptor, also known as ApoB, E receptor, is a cell surface glycoprotein with the highest amount of hepatocytes. The low-density lipoprotein receptor gene is located on human chromosome 19, and the cause of familial acquired hyperlipoproteinemia is natural mutations in the low-density lipoprotein receptor gene, including deletions, insertions, nonsense mutations, and missense mutations. . Dozens of low-density lipoprotein receptor gene mutations have been identified and can be divided into five categories.

Class I mutations: characterized by the fact that the mutant gene does not produce a measurable low-density lipoprotein receptor, and there is no low-density lipoprotein receptor on the cell membrane, which is the most common type of mutation.

Class II mutations: characterized by low-density lipoprotein receptors synthesized by mutant genes in cell maturation and transport disorders, and low-density lipoprotein receptors on the cell membrane are significantly reduced, and are also more common.

Class III mutations: characterized by a low-density lipoprotein receptor synthesized by a mutant gene that reaches the cell surface but does not bind to the ligand.

Class IV mutations: These mutations are mature low-density lipoprotein receptors that bind to low-density lipoproteins when they reach the cell surface, but do not undergo internal migration.

Class V mutations: characterized by the synthesis of low-density lipoprotein receptors, binding to low-density lipoproteins, and subsequent internal shifts, but receptors cannot be recycled to the cell membrane.

Different races, low-density lipoprotein receptor mutations occur differently. For example, in the heterozygous familial hypercholesterolemia of French-Canadians, the mutation caused by the deletion of the receptor gene accounts for 60%. The most prominent abnormality of the low-density lipoprotein receptor deficiency is the slowdown of low-density lipoprotein degradation from plasma. When the low-density lipoprotein receptor is normal, part of the intermediate density lipoprotein can be directly decomposed by the liver low-density lipoprotein receptor, but in familial hypercholesterolemia, low-density lipoprotein can not be decomposed, resulting in more Intermediate density lipoproteins are converted to low density lipoproteins, resulting in increased production of low density lipoproteins.

Acquired hyperlipoproteinemia prevention

1. Adjust a reasonable diet to reduce the intake of saturated fatty acids and cholesterol.

2. Adjust life and work styles Actively participate in sports activities, avoid sedentary, and control weight. Smoking cessation is limited to alcohol.

3. Patients with a family history of coronary heart disease, diabetes, and primary hyperlipidemia should be regularly examined for blood lipids, blood sugar, and liver function.

4. Men over 40 years of age, menopausal women should be regularly checked for blood lipids every year.

5. In order to be able to detect hyperlipidemia in an early and timely manner, it is recommended that all adults over the age of 20 should regularly check plasma total cholesterol levels. Plasma triglyceride levels should be measured in all patients with pancreatitis.

Acquired hyperlipoproteinemia complications Complications atherosclerosis acute pancreatitis

Complications of acquired hyperlipoproteinemia are atherosclerosis, hypertriglyceridemia, chylomicronemia, acute pancreatitis, and the like.

Acquired hyperlipoproteinemia symptoms common symptoms diabetes nodules hypoproteinemia

It is worth noting that diabetes, especially when it is not properly controlled, can cause rash xanthomas. In obstructive liver disease, there is hyperlipoproteinemia type IIa, which is mainly characterized by maculopathy, flat and nodular yellow. Tumors, generalized flat xanthoma often occur in atypical proteinemia.

Examination of acquired hyperlipoproteinemia

1. Determination of blood lipid profile Complete set including fasting TC, TG, LDL-C, HDL-C.

2. To determine the presence or absence of chylomicrons in plasma, a simple method is to place the plasma in a refrigerator at 4 ° C overnight, and then observe whether the plasma has a "creamy" top layer.

3. Plasma low density lipoprotein (LDL-C) concentration can be calculated using the Friedewald formula:

LDL-C (mg/dl) = TC-(HDL-CTG/5) or LDL-C (mmol/L) = TC-(HDL-C TG/2.2).

If the plasma triglyceride concentration is within 4.5 mmoL/L, the LDL-C concentration is calculated using this formula and the results are reliable. If the plasma triacylglycerol concentration exceeds 4.5 mmoL/L, this formula cannot be applied because the calculated LDL-C concentration will be significantly lower than the actual value.

The plasma cholesterol level may vary by ±10% within 1 to 2 weeks, and the laboratory variation is allowed to be within 3%. At least 2 records of blood specimen examination should be made before judging whether there is hyperlipidemia or determining prevention and treatment measures. .

Special examination about lipid metabolism

(1) Apolipoprotein assay: Determination of plasma Apo B and Apo AI levels is important for predicting the risk of coronary heart disease.

(2) In vivo lipoprotein metabolism test: In addition, gene DNA mutation analysis, lipoprotein-receptor interaction, and lipoprotein lipase and hepatic lipase, cholesterol lipase and synthetase can be measured.

Diagnosis and differentiation of acquired hyperlipoproteinemia

diagnosis

According to clinical manifestations, the characteristics of skin lesions and the characteristics of serum tests can be diagnosed.

Differential diagnosis

Detailed medical history to rule out primary hyperlipoproteinemia, diabetes, especially when not properly controlled can cause rash xanthomas, in obstructive liver disease, there is hyperlipoproteinemia type IIa, clinically the main performance For maculopathy, flat and nodular xanthomas, generalized flat xanthoma often occurs in atypical proteinemia.

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