Hyperlipidemia

Introduction to hyperlipidemia Hyperlipoidemia (hyperlipoidemia) refers to high blood lipid levels, which can directly cause diseases that seriously endanger human health, such as atherosclerosis, coronary heart disease, and pancreatitis. Most patients have no obvious symptoms and abnormal signs. Many people have found elevated levels of plasma lipoprotein when they have undergone blood biochemical tests for other reasons. basic knowledge Sickness ratio: 0.1% Susceptible people: no specific population Mode of infection: non-infectious Complications: myocardial infarction carotid stenosis

Cause of hyperlipidemia

Pathogenesis:

Low-density lipoprotein receptor, also known as Apo B, E receptor, is a cell surface glycoprotein with the highest content of hepatocytes. The low-density lipoprotein receptor gene is located on human chromosome 19, familial hypercholesterolemia. The cause of the disease is natural mutations in the low-density lipoprotein receptor gene, including deletions, insertions, nonsense mutations and missense mutations. Several dozen low-density lipoprotein receptor gene mutations have been identified and can be classified 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, such as French-Canadians heterozygous familial hypercholesterolemia, mutations caused by receptor gene deletion accounted for 60%, low-density lipoprotein receptor defects The most prominent abnormality is that the low-density lipoprotein is decomposed from plasma, and when the low-density lipoprotein receptor is normal, some of the intermediate-density lipoprotein can be directly taken up by the liver low-density lipoprotein receptor to be decomposed, but in the familial high. Cholesterolemia, low-density lipoprotein can not be broken down, causing more intermediate density lipoproteins to be converted to low-density lipoprotein, resulting in increased LDL production.

Hyperlipidemia prevention

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

2, adjust the life, work style actively participate in sports activities, to avoid sedentary, control weight, quit smoking and alcohol.

3, a family history of coronary heart disease, diabetes and primary hyperlipidemia should be regularly performed daily blood lipids, blood sugar, liver function and other comprehensive examination.

4, men over 40 years old, women after menopause should be regularly checked for blood lipids every year.

5. In order 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. For all patients with pancreatitis, plasma triglyceride levels should be measured.

Hyperlipidemia complications Complications myocardial infarction carotid stenosis

1. Early onset coronary heart disease is more common in familial hypercholesterolemia. The average age of onset is 45 years for males and 55 years for females. The youngest children develop myocardial infarction at 18 months, and other parts of the arteries can also develop porridge. Such sclerosis, such as carotid atherosclerosis can cause carotid stenosis, vascular murmurs can be heard in the carotid artery during physical examination.

2, obvious hypertriglyceridemia can cause acute pancreatitis.

Hyperlipidemia Symptoms Common Symptoms Arteriosclerosis Yellow Nodules High Blood Pressure Unstable Angina Glucose Obesity Kidney Globular Volume Increase Urine Oil

The clinical manifestations of hyperlipidemia are mainly the arteriosclerosis caused by the deposition of lipids in the dermis and the deposition of vascular endothelial cells. Although hyperlipidemia can cause yellow tumors, the incidence is not very high. High; and the occurrence and development of atherosclerosis is a slow and gradual process, so under normal circumstances, most patients have no obvious symptoms and abnormal signs, many people found it because of other reasons for blood biochemical tests. There is an increase in plasma lipoprotein levels.

1. Age of onset, gender and ethnicity:

Although homozygous familial hypercholesterolemia is very rare, its age of onset is earlier, patients can have clinical signs and symptoms of coronary heart disease before the age of 10, such as not getting timely and effective treatment, patients often around 20 years old Died of myocardial infarction, lipoprotein lipase deficiency can manifest as chylomicronemia syndrome from the time of infant or childhood.

Familial apolipoprotein B100 deficiency is mainly seen in Caucasian ethnic groups. It was not discovered until 1993 that a patient with Chinese descent had elevated LDL-cholesterol levels during childhood or adolescence. As time progressed, plasma totaled. Cholesterol and LDL-cholesterol levels will continue to rise.

Not all primary hyperlipidemia begins to develop from an early age. In addition to a small number of cases of familial mixed hyperlipidemia, most of them can develop hyperlipidemia after adulthood. In addition to sexually transmitted apolipoprotein E mutations, type III hyperlipoproteinemia is rarely seen in children and adolescents under the age of 20, and males are more common than females. Men are also older than women, and women usually only postmenopause. Onset, familial hypertriglyceridemia is also a disease in adulthood.

2, early onset cardiovascular disease:

There is often a family history of early onset coronary heart disease, familial apolipoprotein B100 deficiency, early onset of coronary heart disease is similar to heterozygous familial hypercholesterolemia, about 1 / year of coronary heart disease before the age of 60 3, patients with peripheral vascular disease often have hypertension, and 48% of patients have carotid atherosclerosis.

Early-onset vascular disease is more common in type III hyperlipoproteinemia. In addition to early-onset coronary heart disease, vascular lesions around the lower extremities are also common. See Table 2, familial lipoprotein lipase deficiency is rare. Early onset coronary heart disease.

3, pancreatitis:

Patients with familial lipoprotein lipase deficiency can block the capillaries of the pancreas due to chylomicron emboli, causing localized pancreatic cell necrosis leading to recurrent pancreatitis, and 1/3 to 1/2 of patients can develop acute pancreas Inflammation often occurs after eating a high-fat diet or after a meal. The degree of abdominal pain is positively correlated with plasma triglyceride levels. In addition, the performance of abdominal pain often varies from person to person, such as a diagnosis that is not easy to cause surgical errors.

Pancreatitis can also occur in patients with familial apolipoprotein CII deficiency, but the plasma VLDL-cholesterol level is relatively high, while the chylomicron concentration is relatively low, so the condition is relatively mild, and the symptoms are generally not obvious before the age of 20.

4, yellow tumor:

(1) flat yellow tumor: mainly seen around the eyelids, it is also known as eyelid xanthoma, which is more common in clinical practice. It is usually characterized by flat papules in the upper palate, which is orange-yellow, rice-to-soap-sized, oval-shaped. Clear borders, soft texture, usually slow development, the number can be gradually increased, a few can affect the face, neck, trunk and limbs, mainly in familial hypercholesterolemia, familial apolipoprotein B100 deficiency and type III hyperlipoprotein blood Symptoms; also seen in normal blood lipids, may be due to excessive intake of oxidized or modified lipoproteins by macrophages in tissues.

(2) palm wrinkle yellow tumor: distributed in the palm and finger wrinkles, orange-shaped line-like flat and slight convex, which is a characteristic manifestation of type III hyperlipoproteinemia, about 50% of patients can There is a palm wrinkle yellow tumor.

(3) Nodular xanthoma: occurs in the elbow, knee, knuckle and other extensions as well as sputum, hip, buttocks, etc., early scattered, is a round nodule of soybean to egg size, yellow, orange Or brownish red, clear boundary, soft texture, generally slow progress, increased nodules in the later stage, and merge into lobulated plaques of different sizes. Due to fibrosis, the texture gradually hardens and is not easy to subside, such as damage or merger. Infection can form ulcers. This type of yellow tumor is mainly found in type III hyperlipoproteinemia and is also characteristic.

(4) rash yellow tumor: a small papule with orange or brownish yellow color, its center is white, accompanied by an inflammatory base, similar to hemorrhoids, occurs in the abdominal wall, back, buttocks and other parts that are easily pressed, sometimes Oral mucosa can also be affected, mainly in the family of lipoprotein lipase deficiency and familial apolipoprotein CII deficiency caused by severe hypertriglyceridemia.

(5) nodular rash yellow tumor: more common in the extremities of the extremities, such as elbows and buttocks, orange-yellow nodular, can appear in batches in a short period of time, there is a fusion trend, surrounded by rash-like yellow tumors, Often accompanied by an inflammatory basal, mainly seen in type III hyperlipoproteinemia.

(6) Tendon yellow tumor: This is a special type of nodular yellow tumor, which occurs in the tendon, which is common in the Achilles tendon, the extensor tendon of the hand or the back of the foot, the rectus femoris and the deltoid tendon. Round or oval, hard subcutaneous nodules, adhesion to the skin, clear boundaries, about 58% of patients with familial hypercholesterolemia can develop tendon xanthomas, familial apolipoprotein B100 deficiency patients have 38 % can develop tendon xanthomas, can also be seen in some patients with type III hyperlipoproteinemia, if not carefully examined, some small tendon yellow tumors are easily missed, X-ray pictures can show the situation of Achilles tendon yellow tumor.

The above various yellow tumors can be seen in different types of hyperlipidemia, and various forms of xanthoma can also occur in the same type of hyperlipidemia, but familial mixed hyperlipidemia rarely has yellow tumors, usually, After effective lipid-lowering therapy, most yellow tumors can gradually subside.

5. Other performances:

The corneal arch is also known as the old ring. If it occurs in people under 40 years old, it is often accompanied by hyperlipidemia. Early-onset keratoconus is more common in familial hypercholesterolemia, but its specificity is not strong. About 28% of families Patients with apolipoprotein B100 deficiency may have corneal arches. In addition, they may also be seen in familial hypertriglyceridemia, and corneal opacity may occur in familial LCAT deficiency.

Severe hypertriglyceridemia (>22.6mmol/L or 2000mg/dl), the large granule lipoprotein rich in triacylglycerol is deposited on the small artery of the fundus to produce hyperlipidemia fundus; triacylglycerol is deposited on the net Endothelial cells can also cause hepatosplenomegaly; chylomicronemia can lead to dyspnea and neurological symptoms, homozygous familial hypercholesterolemia can occur migratory polyarthritis, but self-limiting, familial Patients with mixed hyperlipidemia and familial hypertriglyceridemia are mostly obese. Type III hyperlipoproteinemia is often accompanied by obesity, other metabolic disorders such as diabetes and hypothyroidism, which can lead to lipid levels in patients. Further elevated, patients with secondary hyperlipidemia may have clinical manifestations of various primary diseases.

Regarding the diagnostic criteria for hyperlipidemia, there is currently no uniform method at home and abroad. In order to prevent and treat atherosclerosis and coronary heart disease, the appropriate plasma cholesterol level is below 5.17mmol/L (200mg/dl). Cholesterol Education Program Committee developed by the adult treatment panel (ATP).

The new standard recommends starting treatment with LDL-C concentration >130mg/dl, with LDL-C concentration <100mg/dl as the treatment target, and more emphasis on low HDL-C concentration as a risk factor for coronary heart disease. The value <35mg/dl was modified to <40mg/dl, and it was suggested that when the concentration was >60mg/dl, it could offset a risk factor for coronary heart disease, reduce the classification of triacylglycerol, and pay more attention to the increase.

Most scholars in China believe that plasma total cholesterol concentration >5.17mmol / L (200mg / dl) can be determined as hypercholesterolemia, plasma triglyceride concentration >2.3mmol / L (200mg / dl) for hypertriglyceridemia, due to local The diagnostic criteria for hyperlipidemia were different due to factors such as differences in the population tested and differences in test methods used.

1. Classification of hyperlipidemia:

The commonly used classification of hyperlipidemia is not an etiological diagnosis. It can often change due to changes in diet, drugs or other environmental factors. The simple classification of hyperlipidemia has been included, and it is related to the incidence of coronary heart disease. Large type of hyperlipoproteinemia.

(1) It can be easily divided into the following four categories:

1 hypercholesterolemia: increased plasma TC levels.

2 mixed hyperlipidemia: increased plasma TC and TG levels.

3 hypertriglyceridemia: increased plasma TG levels.

4 low high density lipoproteinemia: plasma HDL-C levels decreased.

(2) According to the cause can be divided into:

1 Primary hyperlipidemia: abnormal lipid metabolism caused by genetic defects or gene mutations, eating habits, lifestyle and other natural environmental factors.

2 secondary hyperlipidemia: caused by a certain underlying disease, the common underlying diseases that can cause secondary hyperlipidemia, diabetes, hypothyroidism, chronic kidney disease and nephrotic syndrome, obstructive Hepatobiliary disorders, hepatic glycogen storage disorders, pancreatitis, alcoholism, idiopathic hypercalcemia, multiple myeloma, macroglobulinemia and lupus erythematosus, anorexia nervosa, etc. Some drugs such as thiazides Diuretics, oral contraceptives containing female hormones, thyroxine, anabolic steroids that promote anabolism, and certain beta-blockers, can also cause secondary hyperlipidemia, when these underlying conditions are cured or After control, or when the drug is discontinued, secondary hyperlipidemia can be corrected.

2. Identify risk factors and dangerous states of coronary heart disease other than high cholesterol:

(1) Positive risk factors:

1 Gender: The incidence rate of males is higher than that of females, which is 3-4 times higher in middle-aged women. The incidence of women after menopause increases, but the ratio of male to female is still about 1 time.

2 Age: With the increase of age, the incidence of coronary heart disease increases.

3 hypertension: regardless of the long-term increase in systolic or diastolic blood pressure, the risk of coronary heart disease increases.

4 Smoking: The degree of risk is related to the amount of smoking, and the risk of smokers is twice as high as that of non-smokers.

5 family history of coronary heart disease: a family history of coronary heart disease, especially early on coronary heart disease (referring to males before the age of 55, women before the age of 65), increased risk of coronary heart disease.

6 diabetes and impaired glucose tolerance: the risk of men is increased by 2 times, women are 3 to 4 times higher, regardless of insulin dependence or not, the risk is also increased.

7 premature menopause: women who go through early, and do not use estrogen replacement therapy, the risk of coronary heart disease increases.

8 Obesity: The distribution and degree of obesity are very important. The excessive increase of fat in the trunk and abdominal organs is definitely a risk factor for coronary heart disease. Other related risk factors include lifestyles with less activity, increased fibrinogen in the blood, and blood insulin. The importance of resistance, elevated blood lipoprotein (a) or hyperhomocysteinemia as a risk factor for coronary heart disease is under investigation.

(2) Negative risk factors: If the serum HDL-C level is >1.6mmol/L (60mg/dl), one risk factor can be subtracted, because high levels of HDL-C can reduce the risk factors of coronary heart disease.

Hyperlipidemia check

1. Determination of blood lipid profile:

Including fasting TC, TG, LDL-C, HDL-C.

2. Determine whether there are chylomicrons in the plasma:

An easy method is to place the plasma in a refrigerator at 4 ° C overnight and then observe if the plasma has a "creamy" top layer.

3. Plasma low density lipoprotein (LDL-C) concentration:

The calculation can be done using the Friedewald formula:

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

If the plasma triglyceride concentration is within 4.5mmoL/L, the LDL-C concentration is calculated by this formula. The result is reliable. If the plasma triacylglycerol concentration exceeds 4.5mmoL/L, this formula cannot be applied because the calculated LDL The -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. .

4. Special inspections on 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.

5. Other inspections:

Familial mixed hyperlipidemia and familial hypertriglyceridemia have insulin resistance, and plasma insulin levels are elevated, which can be clinically characterized as impaired glucose tolerance; type III hyperlipoproteinemia often has diabetes; familial Mixed hyperlipidemia may be associated with hyperuricemia; patients with type III hyperlipoproteinemia may be associated with hypothyroidism.

Diagnosis and diagnosis of hyperlipidemia

diagnosis

In the diagnosis of hyperlipidemia, it should be clear what type of abnormal lipid metabolism is in the patient, because the treatment of hyperlipidemia caused by different causes is different, so the primary hyperlipemia must be The disease is differentiated from secondary hyperlipidemia, and further determines its specific cause, which is helpful for the differential diagnosis of various hyperlipidemia.

Differential diagnosis

Sometimes type IIb hyperlipoproteinemia is easily confused with type IV hyperlipoproteinemia. At this time, plasma LDL-cholesterol levels can be measured. If LDL-cholesterol is >3.65mmol/L (130mg/dl), it is IIb. Type; vice versa.

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