OVERVIEW
Hyperlipoproteinemia is defined as elevated plasma levels of cholesterol (TC) and/or triacylglycerol (TG). It is actually a manifestation of elevated plasma levels of one or more classes of lipoproteins. In recent years, it has been gradually recognized that decreased plasma HDL-C (high-density lipoprotein cholesterol) is also a disorder of lipid metabolism. It has been suggested that dyslipidemia should be used, and it is believed that this name is a more comprehensive and accurate reflection of the state of dyslipidemia.
Causes
1. Causes of critical hypercholesterolemia
The causes of critical hypercholesterolemia in humans, in addition to high basal values, are mainly dietary factors, i.e., overweight due to high cholesterol and saturated fatty acid intake and excess calories, and to a lesser extent, the effects of age and menopause in women.
2. Causes of mild hypercholesterolemia
Mild hypercholesterolemia is defined as a plasma TC (cholesterol) concentration of 6.21-7.49 mmol/L (240-289 mg/dl) or LDL 4.15-5.41 mmol/L (160-209 mg/dl). Most patients with mild hypercholesterolemia are probably due to the above causes of critical hypercholesterolemia in combination with an inherited genetic abnormality. Due to the presence of abnormal genes, the rate of LDL catabolism in the body is reduced, LDL synthesis is increased or LDL structure is altered.
3. Causes of severe hypercholesterolemia
Severe hypercholesterolemia is defined as a plasma cholesterol concentration of more than 7.51 mmol/L (290 mg/dl) or LDL-C > 5.44 mmol/L (210 mg/dl). The best example of severe hypercholesterolemia is heterozygous familial hypercholesterolemia (FH). The prevalence of heterozygous FH in the general population is 1/500, whereas severe hypercholesterolemia is 5/100 in adults.Clearly, many severe hypercholesterolemias are due to other genetic abnormalities.
In the vast majority of cases, severe hypercholesterolemia is the result of a combination of the following factors: reduced LDL catabolism, increased LDL production, defective LDL-Apo B metabolism, and cholesteryl ester-rich LDL particles. There are also the causes of critical hypercholesterolemia described above. It can be seen that most severe hypercholesterolemia is likely to be due to the interaction of polygenic defects and environmental factors.
4. Causes of hypertriglyceridemia
The triacylglycerol content of CM reaches about 90%, and the triacylglycerol content of VLDL reaches 60%-65%, thus these two types of lipoproteins are collectively called triacylglycerol-rich lipoproteins. Elevated plasma triacylglycerol concentrations actually reflect elevated CM and/or VLDL concentrations. Any cause of elevated plasma CM and/or VLDL can lead to hypertriglyceridemia.
(1) Secondary hypertriacylglycerolemia Many metabolic disorders certain disease states, hormones and drugs can cause hypertriacylglycerolemia.
(2) Nutritional factors Many nutritional factors can cause elevated plasma triacylglycerol levels. Plasma triacylglycerol levels can also be elevated by high intake of simple sugars. This may be related to concomitant insulin resistance; it may also be due to the fact that 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. China’s population diet is characterized by high sugar and low fat a survey showed that sugar accounted for 76% to 79% of the total calories, fat accounted for only 8.4% to lO.6%, while the incidence of hyperlipidemia up to 11% to endogenous high triacylglycerol plasma for the most common. Alcohol consumption also has a significant effect on plasma triacylglycerol levels.
(3) Lifestyle Plasma triacylglycerol concentrations are higher in sedentary individuals than in those who are physically active, and both long-term and short-term physical activity can reduce plasma triacylglycerol levels. Exercise also increases LPL activity, raises HDL-C (high-density lipoprotein cholesterol) levels, especially HDL2-C levels, and decreases hepatic lipase (HL) activity. Prolonged and consistent exercise also increases the removal of exogenous triacylglycerols from plasma.
Smoking also increases plasma triacylglycerol levels. Epidemiologic studies have confirmed that smoking increases plasma triacylglycerol levels by 9.1% compared to the average for normal subjects.
(4) Increased plasma triacylglycerol levels due to genetic abnormalities ① Genetic abnormalities in CM and VLDL assembly. ② Abnormalities in the genes for LPL and Apo CⅡ (apolipoprotein CⅡ). ③ Abnormalities in the Apo E (apolipoprotein E) gene.
Symptoms
The clinical manifestations of hyperlipidemia include two main aspects: on the one hand, yellow tumors caused by lipid deposition in the dermis; on the other hand, atherosclerosis caused by lipid deposition in the endothelium of blood vessels, resulting in coronary heart disease and peripheral vascular disease. Since the incidence of yellow tumors in hyperlipidemia is not very high, and the occurrence and development of atherosclerosis takes quite a long time, most patients with hyperlipidemia do not have any symptoms and abnormal signs found. Instead, hyperlipidemia is often detected during blood biochemical tests (measurement of blood cholesterol and triacylglycerols).
1. Lipid deposition throughout the body
(1) Xanthomas are abnormal, limited skin bumps that may be yellow, orange, or brownish-red in color and are often in the form of nodules, plaques, or papules, and are generally soft in texture. It is mainly due to the collection of lipid-phagocytizing macrophages (foam cells), also known as yellow tumor cells, in the dermis.
(2) Lipoatrophic corneal arches Corneal arches, also known as senile rings, are often associated with hyperlipidemia if seen in people under 40 years of age, with familial hypercholesterolemia being the most common, but the specificity is not very strong.
(3) Hyperlipidemic fundus changes are caused by the deposition of large triacylglycerol-rich lipoproteins on the small arteries of the fundus, causing light scattering, which is often a characteristic manifestation of severe hypertriglyceridemia with celiac disease.
2. Atherosclerotic lesions
(1) Atherosclerosis of the aorta The lesions are mostly found in the posterior wall of the aorta and the openings of its branches, with the abdominal aorta being the most serious, the thoracic aorta being the second, and the ascending aorta being the lightest.
(2) Coronary artery atherosclerosis
(3) Atherosclerosis of carotid artery and cerebral artery is most common in the beginning of internal carotid artery, basilar artery, middle cerebral artery and Willis ring fibrous plaque and atherosclerotic plaque, which often leads to narrowing of lumen and can be aggravated by compound lesions, stenosis or even formation of occlusion. Long-term insufficient blood supply can lead to atrophy of brain parenchyma. Patients may have intellectual and memory loss, psychopathy, or even dementia. Rapid interruption of blood supply can lead to cerebral infarction (cerebral softening), arterial and small aneurysm rupture can cause cerebral hemorrhage and the corresponding clinical manifestations.
(4) Renal artery atherosclerosis The lesion most often involves the opening of the renal artery and the proximal end of its main trunk, and can also involve the interlobular arteries and arteriovenous arteries. It often causes intractable renal vascular hypertension due to the narrowing of the lumen caused by plaques; it can also cause renal tissue infarction due to the combination of plaque thrombosis, resulting in renal pain, anuria and fever. After the infarction foci are mechanized, a large scar is left behind, and multiple scars can cause the kidney to shrink, which is called AS renal consolidation.
(5) Atherosclerosis of the limbs The lesions are more serious in the arteries of the lower limbs. When the lumen of the larger arteries is significantly narrowed, the lack of blood supply can lead to an increase in oxygen consumption (such as walking) can cause pain, which improves after resting, and then severe pain occurs again when walking, which is known as intermittent claudication. When the arterial lumen is completely blocked and the collateral circulation cannot compensate, it causes dry gangrene in the toe.
(6) Mesenteric artery atherosclerosis When the mesenteric artery is narrowed or even blocked due to lesions, the patient has severe abdominal pain, abdominal distension and fever. If it causes intestinal infarction, there may be symptoms such as blood in stool, paralytic intestinal obstruction and shock.
Examination
1. Items of blood lipid examination
Increased serum TC, serum HDL-C, serum TG serum LDL-C.
2.Re-check
If abnormalities are found in the first test, it is advisable to review the lipid levels after 12-14 hours of fasting. serum cholesterol levels may vary by 10% within 1-2 weeks, and laboratory variation is allowed to be within 3%. at least 2 blood specimens should be examined before determining the presence of hyperlipidemia or deciding on preventive and curative measures.
Diagnosis
Hyperlipidemia is defined as having blood lipids higher than the upper limit of normal. Clinically, it can be categorized into:
1. Hypercholesterolemia
Elevated serum TC level.
2. Hypertriglyceridemia
Elevated serum TG level.
3. Mixed hyperlipidemia
Elevated serum TC and TG levels.
4. Low HDL anemia
Decreased serum HDL-C level.
Treatment
Long-term comprehensive treatment should be adhered to, emphasizing on the basis of diet control and physical exercise, and combined with lipid-regulating drugs. For secondary cases (e.g. diabetes mellitus, hypothyroidism), the primary disease should be actively treated.
1. Diet and exercise therapy
The aim is to lower plasma cholesterol and maintain balanced nutrition. In addition to lowering cholesterol, exercise and lowering body weight can also lower triglycerides and raise HDL cholesterol. Dietary treatment and lifestyle improvement are the basic measures for dyslipidemia treatment. Regardless of whether or not medication is used to regulate lipids, dietary control and lifestyle improvement must be maintained.
2. Drug therapy
Depending on the type of dyslipidemia and the goal of treatment, appropriate lipid-regulating drugs should be selected. Regular monitoring of the efficacy of lipid regulation and adverse drug reactions is required.
The main drugs used to treat hyperlipidemia are:
(1) Hydroxyglutaryl coenzyme A reductase inhibitors (statins): i.e. hydroxyglutaryl coenzyme A reductase inhibitors, the most widely used class of drugs in clinical practice. The following statin drugs are now available: simvastatin, atorvastatin, resuvastatin, and are generally recommended to be taken at night.
(2) Phenoxyacetic acid lipid regulating drugs (Betaine);
(3) Niacin lipid regulating drugs;
(4) Bile acid chelators;
(5) Cholesterol absorption inhibitors;
(6) Cholesterol synthesis inhibitors;
(7) n-3 fatty acids, n-3 (W-3) long chain polyunsaturated fatty acids;
(8) Probucol.
Prevention
Extensive and repeated health education through a variety of channels, advocating scientific and balanced diets, regular physical exercise, prevention of obesity, smoking cessation and alcohol restriction, and combining with health promotion and education on the prevention and treatment of chronic diseases such as cardiovascular disease, obesity, and diabetes mellitus, so as to keep blood lipids in the population at an appropriate level. In addition, regular health checkups can help to detect dyslipidemia early, which should be treated in a timely manner.