Hypertriglyceridemia

Introduction to hypertriglyceridemia Hypertriglyceridemia (HTG) is an obstacle to the synthesis or degradation of heterologous triglyceride proteins. Triglyceride in blood refers to the highest content of chylomicrons and pre--lipoprotein, which has a great relationship with the formation of atherosclerosis. The rise of triglycerides is important for the occurrence of coronary heart disease. The value of elevated serum triglycerides is greater than that of cholesterol, especially myocardial infarction, 82% of patients with myocardial infarction have hypertriglyceridemia, and high Cholesterol is only 47%. Primary hyperlipidemia, obesity, arteriosclerosis, obstructive jaundice, diabetes, extreme anemia, nephrotic syndrome, pancreatitis, hypothyroidism, long-term hunger and high-fat diet can increase. Triglycerides can be pseudo-elevated after drinking. All patients with elevated serum triglyceride levels should undergo non-pharmacological treatments that alter dietary structure, control weight, quit smoking, and increase physical activity. Drug therapy should be used when elevated serum triglyceride levels combined with lipid disorders leading to atherosclerosis such as familial complex hyperlipidemia. basic knowledge The proportion of the disease: the incidence rate of the elderly over 60 years old is about 45% Susceptible people: no specific population Mode of infection: non-infectious Complications: hyperuricemia diabetes

Causes of hypertriglyceridemia

Common causes are diabetes, hypothyroidism, obesity, alcohol consumption, nephrotic syndrome, and taking certain drugs such as beta blockers, diuretics, estrogens, glucocorticoids, immunosuppressants, tamoxifen, antipsychotics, and proteases. Inhibitors, etc. Common causes include acromegaly, glycogen accumulation, hypopituitarism, congenital or acquired lipodystrophy, and systemic lupus erythematosus.

Functional lesions (40%):

Many metabolic diseases, certain disease states, hormones, and drugs can cause hypertriglyceridemia, a condition commonly referred to as secondary hypertriglyceridemia.

(1) Diabetes: According to the simplest classification method, it can be divided into insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). The pathogenesis of hypertriglyceridemia varies among different types of diabetes. In uncontrolled IDDM and ketosis patients, severe hypertriglyceridemia is often associated with severe insulin deficiency. This is due to the inhibition of the activity of lipoprotein lipase, which results in the accumulation of CM in plasma. In general, insulin levels in patients with NIDDM are higher than those in IDDM. Hyperinsulinemia in NIDDM patients often causes excessive secretion of endogenous insulin to compensate for the original insulin resistance. This severe hyperinsulinemia is activated by lipoprotein lipase. The effect is significantly weakened and causes an increase in triglyceride levels.

(B), kidney disease: Although kidney disease such as nephrotic syndrome most commonly associated with dyslipidemia is hypercholesterolemia, but hypertriglyceridemia is not uncommon. The mechanism of dyslipidemia in kidney disease is mainly due to increased synthesis of VLDL and LDL, but it is also thought to be related to the slowdown of catabolism of these lipoproteins.

(C), hypothyroidism: this disease often combined with elevated plasma triglyceride concentration. This is mainly due to a decrease in VLDL clearance due to a decrease in hepatic triglyceride enzymes, and may also result in excessive production of intermediate density lipoprotien (IDL).

(4) Obesity: In obese patients, the production of VLDL is significantly increased due to excessive synthesis of apolipoprotein B in the liver. In addition, obesity often coexists with other metabolic diseases. Abdominal obesity is more pronounced than triglyceride in the buttocks.

(5) Fat malnutrition: It is a rare metabolic disease characterized by a decrease in fat in a particular area of the body accompanied by hypertriglyceridemia. The pathogenesis is still unclear. It may be due to a decrease in lipoprotein lipase in the adipose tissue or an increase in the synthesis of VLDL in the liver.

(6) Hyperuricemia: About 80% of patients with gout have hypertriglyceridemia. Conversely, 80% of patients with hypertriglyceridemia have hyperuricemia. This relationship is also affected by environmental factors such as excessive intake of monosaccharides, heavy spills, and the use of thiazides.

(7) Glycogen storage disease (type I): This disease is characterized by a deficiency in glucose-6-phosphatase, which is sensitive to hypoglycemia. When hypoglycemia occurs, adipose tissue is mobilized to replenish energy, and the concentration of free fatty acids and the triglyceride component in VLDL increase.

(8), paraproteinemias: This condition can be seen in patients with systemic lupus erythematosus or multiple bone marrow, due to the inhibition of CM and VLDL in plasma by heterotypic protein, resulting in hypertriglyceridemia.

(9) Effects of sex hormones: The effect of estrogen on blood lipids is twofold. In postmenopausal women, cholesterol in the plasma increases. However, estrogen itself reduces plasma lipase activity (especially liver triglyceride lipase) and thus prevents CM and VLDL clearance in circulating blood.

(10) Nutritional factors: Many nutritional factors can cause elevated levels of plasma glycerides. A large intake of monosaccharides can also cause elevated plasma triglyceride levels, which may be associated with associated insulin resistance; it may also be due to the fact that monosaccharides alter the structure of VLDL and affect its clearance rate.

The structure of the diet also has an effect on elevated plasma triglyceride levels. The diet of our population is characterized by high sugar and low fat. According to some surveys, sugar accounts for 76-79% of total calories, fat only accounts for 8.4-10.6%, and the incidence of hyperlipidemia is 11%, which is endogenous. Triglyceride plasma is most common. Some research results suggest that the proportion of sugar intake is too high, causing blood sugar to rise, stimulating insulin secretion to increase, and hyperinsulinemia. The latter promotes an increase in the synthesis of triglycerides and VLDL in the liver, thus causing an increase in plasma triglyceride concentration. In addition, high-glucose diet can also induce an increase in Apo CIII gene expression, resulting in increased plasma Apo CIII concentration. Apo CIII is known to be an inhibitor of lipoprotein esterase, and an increase in Apo CIII in plasma can result in a decrease in the activity of lipoprotein esterase, which in turn affects the hydrolysis of triglycerides in CM and VLDL, causing hypertriglyceridemia.

Drinking alcohol also has a significant effect on plasma triglyceride levels. In sensitive individuals, even moderate alcohol consumption can cause hypertriglyceridemia. Alcohol increases the rate of lipid synthesis in the body, reduces the proportion of oxidized fatty acids, and increases the proportion of esterified fatty acids. In addition, alcohol can also reduce the activity of lipoprotein lipase, which slows the catabolism of triglycerides.

(11) Effects of drugs: Many drugs can alleviate or aggravate hypertriglyceridemia. The two most common drugs are antihypertensive drugs and steroid hormones. Selective beta blockers (such as metoprolol, atenolol, practolol) have a lower effect on triglycerides than non-selective beta blockers. The other two commonly used antihypertensive drugs are calcium antagonists and angiotensin converting enzyme inhibitors, which have no adverse effects on blood lipids. Another class of drugs that have a significant effect on plasma triglycerides are steroid hormones, the most commonly used of which are estrogens. Whether used for hormone replacement therapy or oral contraceptives, plasma triglyceride levels are elevated, especially in patients with hypertriglyceridemia. Glucocorticoids can also increase plasma triglyceride concentrations.

(12) Lifestyle: People who are accustomed to sitting still have higher plasma triglyceride concentrations than those who insist on physical exercise. Plasma triglyceride levels can be reduced in both long-term and short-term physical exercise. Exercise can increase lipoprotein lipase activity, increase HDL levels, especially HDL2 levels, and reduce hepatic lipase activity. Long-term adherence to exercise can also increase the clearance of exogenous triglycerides from the plasma.

Smoking also increases plasma triglyceride levels. Epidemiological studies have confirmed that smoking increases plasma triglyceride levels by 9.1% compared to normal human mean. However, most people have temporary weight gain after smoking cessation, which may be related to the transient increase of lipoprotein lipase activity in adipose tissue. At this time, attention should be paid to controlling body weight to prevent the increase of triglyceride concentration due to weight gain.

Genetic factors (3%):

(a) Gene abnormalities in CM and VLDL assembly: Human plasma Apo B includes two types, Apo B48 and Apo B100, which are synthesized by a single splicing mechanism of Apo B mRNA. Apo B100 is present in LDL and is secreted by the liver in the form of VLDL. Apo B48 is synthesized in the intestine and secreted in the form of CM. Due to the genetic defect of Apo B during the splicing process, the assembly of CM and VLDL is abnormal, which leads to the abnormal metabolism of these two lipoproteins.

(B), lipoprotein lipase and Apo CII gene abnormalities: the efficient hydrolysis of triglycerides in plasma CM and VLDL requires the involvement of lipoprotein lipase and its complex factor Apo CII. Defects in the lipoprotein lipase and Apo CII genes will cause triglyceride hydrolysis disorders, thus causing severe hypertriglyceridemia. Patients with partial Apo CII deficiency can be confirmed by analyzing lipoprotein lipase activity after heparinization.

(C), Apo E gene abnormalities: Apo E gene mutations, can cause Apo E lipoprotein metabolism disorders, which mainly refers to CM and VLDL. The CM remnant is catabolized by binding of Apo E to LDL receptor-associated proteins, while VLDL is metabolized by binding of Apo E to LDL receptors. The Apo E gene has three common alleles, E2, E3, and E4. Apo E2 is a rare variant in that the binding of E2 to both receptors is poor, resulting in catabolic barriers to CM and VLDL remnants. Therefore, the concentration of CM and VLDL remnants in the plasma of Apo E2 allele carriers is increased, and thus hypertriglyceridemia is often present.

Bloody lesions (30%):

(A), chylomicronemia (type I hyperlipoproteinemia): normal people after fasting for 12 hours, almost no detectable CM in plasma. However, when there is a defect in lipoprotein lipase and/or Apo CII, it will cause glycerol-rich lipoprotein catabolism, and mainly CM metabolic disorders. Causes CM in fasting plasma. Familial lipoprotein lipase deficiency is an autosomal recessive hereditary disease. Heterozygotes showed a 50% reduction in lipoprotein lipase activity, but plasma triglyceride levels were normal or only slightly elevated.

(B), V-type hyperlipoproteinemia: compared with type I hyperlipoproteinemia, V-type hyperlipoproteinemia patients with fasting plasma chylomicrons increased with VLDL concentration. It is difficult to identify type I and type V hyperlipoproteinemia. The biggest difference is that type V hyperlipoproteinemia occurs later in age and is associated with impaired glucose tolerance. The genetic defect of type V hyperlipoproteinemia is unclear.

(C), liver lipase deficiency: This condition is also named high alpha triglyceridemia (hyperalphatriglyceridemia). Triglyceride-rich HDL accumulates in large numbers, and patients present with corneal arcus lesions, rash yellow tumors, palmprint changes, and coronary heart disease. There are two cases of plasma lipoprotein abnormalities in patients with liver triglyceride lipase deficiency: (1) HDL particles are large and mostly composed of triglycerides; (2) VLDL particles accumulate in plasma. The underlying cause of liver lipase deficiency is unclear. Clinically, this disease can be diagnosed by measuring a significant decrease in the activity of the enzyme in plasma after heparinization.

(D), familial abnormal -lipoproteinemia: also known as type III hyperlipoproteinemia, due to genetic variation of Apo E, resulting in Apo E-containing lipoproteins such as CM, VLDL and IDL and receptor binding disorders Thus, these lipoproteins accumulate in the plasma, resulting in a marked increase in plasma triglyceride levels.

(5) Familial hypertriglyceridemia: The disease can be diagnosed if the following criteria are met: (1) The patient has an elevated plasma triglyceride concentration (>2.26 mmol/or >200 mg/dl), and Plasma cholesterol concentration <5.18mmol/L (<200mg/dl); (2) simple hypertriglyceridemia in other members of the family; (3) other members of the family without other types of hyperlipoproteinemia . The disease is autosomal dominant. Primary hypertriglyceridemia is caused by overproduction of VLDL, but the biochemical mechanism by which the liver increases VLDL synthesis is unclear.

(6), familial mixed hyperlipidemia: This is the most common type of hyperlipidemia, mainly characterized by elevated plasma cholesterol and triglyceride concentrations, and often have many different highs in family members. The lipoproteinemia phenotype exists. The main biochemical feature of the disease is an abnormal increase in plasma Apo B levels. Lipoprotein in vivo metabolic kinetics studies suggest that elevated plasma Apo B concentrations are a result of increased synthesis rather than reduced catabolism. The molecular defects of familial mixed hyperlipidemia remain to be further studied.

(VII), HDL deficiency syndrome: This is seen in a group of diseases such as fish-eye disease, Apo AI deficiency or Tangier disease. In most affected patients, plasma triglycerides were only slightly elevated [2.26-4.52 mmol/L (200-400 mg.dl)], while plasma HDL-C concentrations were significantly reduced. Patients have varying degrees of corneal opacity, and other clinical manifestations include xanthoma (Apo AI deficiency), renal insufficiency, fish-eye disease, hepatosplenomegaly, neuropathy or tonsil abnormalities (Tangier's disease).

(8) Familial dyslipidemic hypertension: This is a new comprehensive disease proposed in recent years, mainly characterized by premature familial hypertension with triglyceride-rich lipoprotein metabolism. abnormal. This syndrome occurs in 15% or more of hypertensive patients. Its exact genetic defects are for further study and clarification.

Hypertriglyceridemia prevention

1. Limit high-fat foods.

2. Limit sweets: Sugar can be converted into endogenous triglycerides in the liver.

3, strengthen physical exercise, can enhance the body's metabolism, improve the activity of lipoproteinase, is conducive to the transport and decomposition of triglyceride.

4, abstain from alcohol: alcohol stimulates the liver to synthesize endogenous triglycerides.

5, to avoid excessive tension: emotional stress can also cause increased triglyceride.

6, can take deep sea fish oil and lecithin for a longer period of time.

7, weight exceeds the standard must lose weight.

Hypertriglyceridemia complications Complications, hyperuricemia, diabetes

40% of cases have hyperuricemia and 90% have recessive diabetes.

Hypertriglyceridemia symptoms common symptoms dyslipidemia abdominal pain nausea vomiting hyperlipidemia vascular damage

It is usually found during routine blood lipid testing. Severe HTG can cause pancreatitis, rash xanthomas, and lipemia retinitis. In some cases, very high CM can cause chyluria and manifest as recurrent abdominal pain, nausea, vomiting, and pancreatitis, in which case the TG level is greater than 2000 mg/dl. A rash yellow tumor is a yellow papule with a diameter of 1 to 3 mm above the skin. It can be found in any part of the body but is common in the back, chest and proximal limbs.

Examination of hypertriglyceridemia

Serum turbid or milky, triglyceride, VLDLS and apo-CIII levels increased. When the concentration of triglyceride reaches 40 g/L, the serum is turbid, and when it is higher, the serum is milky.

Triglyceride related indicators

Normal triglyceride levels: <100 mg/dL (1.13 mmol/L) for children and <150 mg/dL (1.7 mmol/L) for adults.

Critical hypertriglyceridemia: 250-500 mg/dL (2.83-5.65 mmol/L).

Clear hypertriglyceridemia: greater than 500 mg/dL (5.65 mmol/L).

Diagnosis and differentiation of hypertriglyceridemia

Diagnosis relies mainly on blood lipid testing.

NCEP recommends checking fasting lipids every 5 years from the age of 20, including total cholesterol, low-density lipoprotein, HDL and TG. Healthy, asymptomatic patients without risk factors can check for non-fasting total cholesterol and HDL cholesterol levels every 5 years.

For patients with coronary heart disease, patients with the same risk of coronary heart disease, familial dyslipidemia, and patients with risk factors for coronary heart disease, blood lipids should be reviewed annually. NCEPATPIII defines TG levels at 150 mg/dl as normal. If the blood TG level of the test results is greater than 150mg/dl, the diagnosis should be confirmed again after 12 to 16 hours of fasting.

If TG is greater than 1000 mg/dl, -quantitative analysis should be performed by ultracentrifugation and electrophoresis techniques to determine the nature of dyslipidemia. The two most common dyslipidemias are familial mixed hyperlipidemia (type IIb) and familial HTG (type IV). In type IIb dyslipidemia, total cholesterol, low density lipoprotein and TG levels increased. In type IV dyslipidemia, total cholesterol and LDL levels are normal, while TG levels are elevated, often between 500 and 1000 mg/dl. Patients with type IV dyslipidemia are very sensitive to dietary adjustment. The discovery of HTG often provides clues for the diagnosis of metabolic syndrome.

In this case, patients should be evaluated for the presence or absence of fasting hyperglycemia, hypertension, abdominal obesity, and decreased HDL levels. At the same time, patients should also be evaluated for thyroid and renal function such as thyroxine, serum urea nitrogen, creatinine and urine routine indicators. The patient's basic liver function should be checked before drug treatment. If pancreatitis is suspected clinically, blood amylase and lipase levels should also be checked. Fasting insulin levels check to help patients find insulin resistance. When the fasting insulin is above 15 ug/ml, it is abnormal. At this point, the ratio of fasting blood glucose to fasting insulin should be calculated, which is a more sensitive and specific indicator for diagnosing insulin resistance. The ratio is normally >4.5, such as <4.5, suggesting the presence of insulin resistance.

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