What Is Hyperlipoproteinemia?

Hyperlipoproteinemia refers to elevated cholesterol (TC) and / or triacylglycerol (TG) levels in the plasma. It is actually a manifestation of elevated levels of one or more types of lipoproteins in the plasma. In recent years, it has been gradually recognized that the reduction of HDL-C (high density lipoprotein cholesterol) in plasma is also a disorder of blood lipid metabolism. Therefore, some people suggest the use of dyslipidemia, and believe that this name can more accurately reflect the state of dyslipidemia.

Basic Information

English name: Hyperlipoproteinemia
Visiting department: Endocrinology

Common symptoms: Xanthomas, fatty corneal arches, fundus changes, arteriosclerosis, etc.
Contagious: no

Causes of hyperlipoproteinemia

Cause of critical hypercholesterolemia

The causes of human critical hypercholesterolemia, in addition to its high base value, are mainly dietary factors such as high cholesterol and high saturated fatty acid intake and overweight caused by excessive calories, followed by age effects and women's menopause.

2. Causes of mild hypercholesterolemia

Mild hypercholesterolemia refers to a plasma TC (cholesterol) concentration of 6.21 to 7.49 mmol / L (240 to 289 mg / dl) or LDL 4.15 to 5.41 mmol / L (160 to 209 mg / dl). Most patients with mild hypercholesterolemia may be caused by the above-mentioned causes of critical hypercholesterolemia, and they also have genetic abnormalities. Due to the presence of abnormal genes, the rate of LDL catabolism is reduced, LDL synthesis is increased, or LDL structure is changed.

3. Causes of Severe Hypercholesterolemia

Severe hypercholesterolemia refers to a plasma cholesterol concentration exceeding 7.51mmol / L (290mg / dl) or LDL-C> 5.44mmol / L (210mg / dl). The best example of severe hypercholesterolemia is heterozygous familial hypercholesterolemia (FH). In the general population, the incidence of heterozygous FH is 1/500, while severe hypercholesterolemia is 5/100 in adults. Obviously, many severe hypercholesterolemias are caused by other genetic abnormalities.

In most cases, severe hypercholesterolemia is caused by a combination of the following factors: reduced catabolism of LDL, increased production of LDL, defective metabolism of LDL-Apo B, and LDL particles rich in cholesterol esters. There is also the above-mentioned cause of critical hypercholesterolemia. It can be seen that most severe hypercholesterolemia is likely to be caused by the interaction between polygenic defects and environmental factors.

4.Etiology of hypertriglyceridemia

The triacylglycerol content in medium chylomicron (CM) reaches about 90%, and the triacylglycerol content in very low density lipoprotein (VLDL) also reaches 60% to 65%. Therefore, these two types of lipoproteins are collectively referred to as rich in triacylglycerol. Of lipoprotein. Increased plasma triacylglycerol concentrations actually reflect increased CM and / or VLDL concentrations. Any cause of elevated CM and / or VLDL in plasma can cause hypertriglyceridemia.

(1) Secondary hypertriglyceridemia Many metabolic diseases and certain disease states, hormones and drugs can cause hypertriglyceridemia.

(2) Nutritional factors Many nutritional factors can cause elevated plasma triacylglycerol levels. Large intake of monosaccharides can also cause elevated plasma triacylglycerol levels. This may be related to concomitant insulin resistance; it may also be because monosaccharides can change the structure of VLDL and affect its clearance rate.

The structure of the diet also has an effect on elevated plasma triacylglycerol levels. The diet of our population is characterized by high sugar and low fat. Surveys have shown that sugar accounts for 76% to 79% of total calories, fat accounts for only 8.4% to 10.6%, and the incidence of hyperlipidemia reaches 11%. Endogenous high triacylglycerol plasma is the most common. Drinking alcohol also had a significant effect on plasma triacylglycerol levels.

(3) Lifestyle Plasma triacylglycerol concentration is higher in people who are accustomed to meditation than those who adhere to physical exercise. Both long-term and short-term physical exercise can reduce plasma triacylglycerol levels. Exercise can still increase LPL activity, increase HDL-C (high density lipoprotein cholesterol) levels, especially HDL2-C levels, and reduce liver lipase (HL) activity. Long-term adherence to exercise can also increase the clearance of exogenous triacylglycerols from plasma.

Smoking can also increase plasma triacylglycerol levels. Epidemiological studies have confirmed that smoking can increase plasma triacylglycerol levels by 9.1% compared to the normal average.

(4) Elevated plasma triacylglycerol levels caused by genetic abnormalities Genetic abnormalities of CM and VLDL assembly. LPL and Apo C (Apolipoprotein C) gene abnormalities. Apo E (Apolipoprotein E) gene is abnormal.

Clinical manifestations of hyperlipoproteinemia

The clinical manifestations of hyperlipidemia mainly include two aspects: on the one hand, xanthomas caused by lipid deposition in the dermis; on the other hand, atherosclerosis caused by lipid deposition on vascular endothelium, which produces coronary heart disease and peripheral Vascular disease and so on. Because the incidence of xanthomas is not very high in hyperlipidemia, and the occurrence and development of atherosclerosis takes a long time, most patients with hyperlipidemia have no symptoms or abnormal signs. Patients with hyperlipidemia are often found during blood biochemical tests (determining blood cholesterol and triacylglycerol).

1. Lipid deposition throughout the body

(1) Xanthomas is an abnormally limited bulge of the skin. Its color can be yellow, orange, or brownish red, with nodular, plaque, or pimples. The texture is generally soft. It is mainly due to the accumulation of lipid-phagocytic macrophages (foam cells), also known as yellow tumor cells, in the dermis.

(2) Lipid corneal arch The corneal arch is also known as the senile ring. If it is seen under 40 years of age, it is often accompanied by hyperlipidemia. Familial hypercholesterolemia is common, but the specificity is not very strong.

(3) Fundus changes in hyperlipidemia are caused by the deposition of large particles of triacylglycerol-rich large lipoproteins on the fundus arterioles, which cause light scattering. Often they are severe hypertriglyceridemia with chylomicronemia. Characteristic performance.

2. Atherosclerotic lesions

(1) Aortic atherosclerosis lesions are more common in the posterior wall of the aorta and its branch openings, with the abdominal aorta the heaviest, the thoracic aorta the second, and the ascending aorta the lightest.

(2) Coronary atherosclerosis.

(3) Carotid arteries and cerebral atherosclerosis are most common in the origin of the internal carotid artery, middle cerebral artery of the basilar artery, and Willis annulus fibrous plaques and atheromatous plaques, which often lead to stenosis of the lumen and can be caused by complex lesions Aggravated stenosis or even occlusion. Insufficient long-term blood supply can cause brain atrophy. Patients may have intellectual and memory loss, psychosis, and even dementia. Rapid interruption of blood supply can cause cerebral infarction (brain softening) of arteries and rupture of small aneurysms can cause cerebral hemorrhage and corresponding clinical manifestations.

(4) Renal atherosclerosis Lesions most commonly involve the opening of the renal artery and the proximal end of the main trunk, as well as the interlobular and arcuate arteries. Refractory renal vascular hypertension is often caused by plaque-induced narrowing of the lumen; it can also cause renal tissue infarction due to plaque combined with thrombosis, causing pain in the kidney area without anuria and fever. Larger scars remain after the infarct is mechanized. Multiple scars can cause the kidney to shrink, which is called AS-consolidated kidney.

(5) Atherosclerosis of the extremities The lower extremity arteries are the most severe. When the lumen of the larger artery is significantly narrowed, it can cause pain when the oxygen consumption is increased due to insufficient blood supply (such as walking), it improves after rest, and then severe pain occurs again when walking, which is called intermittent claudication. When the arterial lumen is completely blocked and the collateral circulation cannot be compensated, dry gangrene of the toes is caused.

(6) Mesenteric atherosclerosis When the mesenteric artery is narrowed or even blocked due to disease, the patient has severe abdominal pain, bloating and fever. If intestinal infarction is caused, there may be symptoms such as blood in the stool, paralytic intestinal obstruction, and shock.

Hyperlipoproteinemia test

1. Items for blood lipid examination

Serum TC, serum HDL-C, and serum TG serum LDL-C increased.

2. Review

If abnormality is found in the first test, the blood lipid level after 12 to 14 hours of fasting should be reviewed. There can be 10% variation in serum cholesterol levels within 1 to 2 weeks. Laboratory variation is allowed to be within 3%. At least 2 blood samples should be checked before judging the presence of hyperlipidemia or deciding on preventive measures.

Hyperlipoproteinemia diagnosis

Hyperlipidemia occurs when blood lipids are above the upper limit of normal people. Clinically, it can be divided into:

Hypercholesterolemia

Elevated serum TC levels.

2. Hypertriglyceridemia

Elevated serum TG levels.

3. Mixed hyperlipidemia

Serum TC and TG levels increased.

4. Low high density lipoproteinemia

Decreased serum HDL-C levels.

Hyperlipoproteinemia Treatment

Long-term comprehensive treatment should be adhered to, emphasizing the basis of diet control and physical exercise, combined with lipid-lowering medication. Secondary patients (such as diabetes and hypothyroidism) should actively treat the primary disease.

Diet and exercise therapy

The goal is to lower plasma cholesterol and maintain balanced nutrition. In addition to reducing cholesterol, exercise and weight loss can also reduce triglycerides and raise HDL cholesterol. Diet therapy and lifestyle improvement are the basic measures for the treatment of dyslipidemia. Regardless of whether or not to perform lipid-lowering therapy, you must adhere to diet control and lifestyle improvement.

2. Drug treatment

According to the type of dyslipidemia and the purpose to be achieved in the treatment, a suitable lipid-lowering drug is selected. Regular monitoring of lipid-lowering efficacy and adverse drug reactions is needed.

The main drugs for treating hyperlipidemia are:

(1) Hydroxyglutaryl coenzyme A reductase inhibitors (statins): That is hydroxyglutaryl coenzyme A reductase inhibitors, which are the most widely used drugs in clinical practice. The following statins are available: simvastatin, atorvastatin, rosuvastatin, generally recommended for evening use.

(2) Phenoxyacetic lipid-lowering drugs (fibrates);

(3) Niacin lipid-lowering drugs;

(4) Bile acid chelator;

(5) Cholesterol absorption inhibitor;

(6) Cholesterol synthesis inhibitor;

(7) n-3 fatty acids, n-3 (W-3) long-chain polyunsaturated fatty acids;

(8) Probkao.

Hyperlipoproteinemia prevention

Extensive and repeated health education through multiple channels, advocating scientific diet, balanced diet, regular physical exercise, preventing obesity, quitting smoking, limiting alcohol, and health education related to the prevention and treatment of chronic diseases such as cardiovascular disease, obesity and diabetes Combined to keep the blood lipids in the population at an appropriate level. In addition, regular health checkups also help early detection of people with abnormal blood lipids and should be treated promptly.