Hypertriglyceridemia (HTG) is a heterogeneous disorder of triglyceride protein synthesis or degradation. It refers to the highest levels of triglycerides in blood in celiac particles and pre-beta-lipoproteins, and it is strongly associated with the formation of atherosclerosis. Treatment and prevention are also aimed at early prevention and control of the development of cardiovascular disease and its consequences caused by it. Hypertriglyceridemia (HTG) is a heterogeneous disorder of triglyceride protein synthesis or degradation.
It refers to the highest levels of blood triglycerides in celiac particles and pre-beta-lipoproteins, which are strongly associated with the formation of atherosclerosis. The value of elevated serum triglycerides is greater than that of cholesterol, especially in myocardial infarction, where 82% of myocardial infarction patients have hypertriglyceridemia, compared to 47% of those with high cholesterol. Primary hyperlipidemia, obesity, atherosclerosis, obstructive jaundice, diabetes, extreme anemia, nephrotic syndrome, pancreatitis, hypothyroidism, long-term starvation and high-fat diet can increase. Triglycerides can be falsely elevated by alcohol consumption.
All patients with elevated serum triglyceride levels should undergo non-pharmacological treatments such as dietary changes, weight control, smoking cessation, and increased physical activity. When elevated serum triglyceride levels are combined with atherosclerosis-causing lipid disorders such as familial complex hyperlipidemia, pharmacological treatment should be used.
It is usually detected during routine lipid screening. It is important to note that severe HTG can cause pancreatitis, rash yellow tumors, and lipemic retinitis. In some cases, very high CM can cause celiac disease manifested by recurrent abdominal pain, nausea, vomiting and pancreatitis, in which case the TG level is greater than 2000 mg/dl. Rash xanthomas are yellow papules of 1 to 3 mm in diameter that rise above the skin surface and can be seen anywhere on the body, but are common on the back, chest and proximal extremities, which creates the so-called xanthomatosis・.
Requirements for prevention and control
1.Limit high-fat foods.
2, limit sweet food: 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, conducive to the transport and decomposition of triglycerides.
4, abstain from alcohol: alcohol stimulates the liver to synthesize endogenous triglycerides.
5, avoid excessive tension: emotional tension can also cause triglyceride increase.
6, you can take deep-sea fish oil and lecithin for a longer period of time.
7, overweight must lose weight.
In addition to dietary factors (junk food must cause enough attention to do) caused by overweight obesity, lipid metabolism disorders, adults with hypertriglyceridemia diseases are common: common causes are diabetes, hypothyroidism, obesity, alcohol consumption, nephrotic syndrome and taking certain drugs such as beta-blockers, diuretics, estrogen, glucocorticoids, immunosuppressants, triamcinolone acetonide, anti psychotropic drugs and protease inhibitors. Rare causes include acromegaly, glycogen accumulation, hypopituitarism, congenital or acquired lipid metabolism disorders, and systemic lupus erythematosus. Those with a family history of these diseases and conditions must be cautious and take precautions for prevention and early detection on physical examination.
The NCEP recommends fasting lipid screening every 5 years starting at age 20 for total cholesterol, LDL, HDL, and TG. Non-fasting total cholesterol and HDL cholesterol levels can be checked every 5 years in healthy asymptomatic patients without risk factors. The NCEPATP III defines a TG level of 150 mg/dl as normal. If the test result blood TG level is greater than 150mg/dl, it should be rechecked again after 12-16 hours of fasting to clarify the diagnosis on the day.
If TG is greater than 1000mg/dl, β-quantitative analysis by ultracentrifugation and electrophoresis techniques should be performed to clarify the nature of the dyslipidemia. the 2 most common dyslipidemias are familial mixed hyperlipidemia (type IIb) and familial HTG (type IV). In type IIb dyslipidemia, total cholesterol, LDL and TG levels are elevated. 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 modifications. HTG findings often provide clues to the diagnosis of metabolic syndrome. In this case, the patient should be evaluated for conditions such as fasting hyperglycemia, hypertension, abdominal obesity, and reduced HDL levels.
The patient should also be evaluated for thyroid and renal function such as checking indicators of thyroxine, serum urea nitrogen, creatinine and urinary routine. The patient’s basal liver function should be checked before drug treatment. If pancreatitis is clinically suspected, blood amylase and lipase levels should also be checked. Fasting insulin level check helps to find whether the patient has insulin resistance. Fasting insulin is abnormal when it is above 15ug/ml. In this case, the fasting glucose to fasting insulin ratio should be calculated, which is a more sensitive and specific indicator to diagnose insulin resistance. The normal ratio is >4.5, and if it is <4.5, it indicates the presence of insulin resistance.
Methods of clinical treatment
(1) Betablockers: such as benzofibrate, fenofibrate and gemfibrozil, etc.
(2) Niacin: Niacin is a soluble vitamin B, which has beneficial effects on all lipoproteins.
(3) Unsaturated fatty acids: These include 20-carbon-5-enoic acid (EPA) and 22-carbon-6-enoic acid (DHA) extracted from fish oil and linoleic acid extracted from vegetable oil. They inhibit the absorption of lipids in the small intestine and the reabsorption of bile acids.
In terms of diet, intake of fatty acids and cholesterol should be reduced and alcohol consumption should be limited. Daily fat intake should be limited to less than 30% of total calories, with saturated fatty acids limited to less than 7%. In patients with hypertriglyceridemia, small amounts of alcohol can also lead to a significant increase in serum triglyceride levels. Therefore, alcohol consumption must be limited. It should also be noted that a significant increase in carbohydrate content in the diet can also raise serum triglyceride levels and lower HDL-cholesterol levels.
In obesity, the body’s mobilization of free fatty acids decreases and the level of free fatty acids in the blood rises, leading to an increase in serum triglyceride levels, while weight loss can lead to a decrease in serum triglyceride levels in obese patients.
Diabetic patients are often combined with hypertriglyceridemia, and active treatment of diabetes can help reduce serum triglyceride levels.
Exercise and physical activity can result in significant reductions in serum cholesterol, triglycerides, LDL-cholesterol and VLDL-cholesterol levels. Therefore, like patients with hypercholesterolemia, patients with hypertriglyceridemia should engage in long-term, regular physical activity to maintain weight loss.
All patients with elevated serum triglyceride levels should undergo non-pharmacologic treatments such as dietary changes, weight control, smoking cessation, and increased physical activity. When elevated serum triglyceride levels are combined with atherosclerosis-causing lipid disorders such as familial complex hyperlipidemia, pharmacological treatment should be used. In terms of drug selection, niacin or a derivative of niacin, such as Lupin, can be used. In patients with extremely elevated serum triglyceride levels, the use of fibrate derivatives or niacin for the treatment of hypertriglyceridemia can prevent the development of acute pancreatitis.