Metabolic syndrome
Introduction
Introduction to metabolic syndrome Metabolic syndrome refers to the metabolic disorder of proteins, fats, carbohydrates and other substances in the human body. A series of syndromes appear in the clinic, which is called metabolic syndrome. The accumulation of clinical diseases such as obesity, type 2 diabetes, impaired glucose tolerance, hypertension, and hypertriglyceridemia is not accidental. In 1988, the famous American endocrinologist Reaven found insulin resistance, and insulin resistance, hyperinsulinemia, impaired glucose tolerance, hypertriglyceridemia and hypertension were collectively referred to as "X syndrome." Nowadays, the medical profession generally refers to the metabolic syndrome, which refers to Reaven syndrome, which is metabolic syndrome. Since each component of the metabolic syndrome is a risk factor for cardiovascular disease, their combined effect is stronger, so some people call the metabolic syndrome a "death quartet" (central obesity, hyperglycemia, high triglycerides). Hypertension and hypertension), so the metabolic syndrome is a holistic concept of general and economic diagnosis and treatment of a group of highly related diseases that require lifestyle interventions (such as weight loss, increased physical activity and mental coordination), Hypoglycemic, lipid-lowering and antihypertensive treatments are equally important. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious complication:
Cause
Cause of metabolic syndrome
Pathogenesis
The heart of the metabolic syndrome is insulin resistance.
The causes of insulin resistance are hereditary (genetic defects) and acquired (environmental factors). Gene defects can occur in various pathways following insulin receptor and receptor signal transduction. Acquired factors include insulin receptor antibodies, certain glucosamines, amylin, chronic hyperglycemia, hyperlipidemia, lifestyle western And the diet structure is not reasonable.
In the ordinary sense, insulin resistance, or insulin, promotes a decline in glucose utilization. As a result of decreased glucose utilization, elevated blood glucose levels, followed by increased insulin compensatory, manifested as hyperinsulinemia, which is a direct manifestation of insulin resistance.
At present, the methods for measuring the level of insulin resistance are mainly as follows: 1. Insulin clamp test. 2. Sampling intravenous glucose tolerance test (FSIGT). 3, OMA-IR determination, its calculation formula is: IR = insulin (U / mL) × glucose (mmol / L) ÷ 22.5. 4, taking glucose tolerance test.
Among them, the high insulin clamp test is the gold standard for testing insulin resistance, but because of the cumbersome operation, it is difficult to perform clinically, so the most widely used is the HOMA-IR measurement.
Pathophysiology
Insulin resistance causes a series of consequences, damage to vital organs, and the pancreas is also the main organ involved in insulin resistance. In order to compensate for the increased demand for insulin, insulin secretion has also increased accordingly. Under this stress state, the apoptosis rate of individual pancreatic cells in the presence of diabetic genetic susceptibility factors is accelerated, and hyperglycemia is very prone to develop into clinical diabetes. Insulin resistance simultaneously initiates a series of inflammatory responses on islet cells. Both high glucose toxicity and lipotoxicity cause significant damage to beta cells. The deposition of amylin in islets increases, further promoting the apoptosis of cells.
Insulin resistance also has a systemic effect. Insulin resistance initiates a series of inflammatory responses, and inflammatory factor markers such as C-reactive protein (CRP) and cytokine interleukin-6 (IL-6) levels are significantly elevated in individuals with insulin resistance. Insulin resistance also accelerates the progression of atherosclerosis by impairing endothelial function. Endothelial dysfunction in individuals with insulin resistance is characterized by increased adhesion factors, smooth muscle cell proliferation, and decreased vasodilatation. This series of changes is an important factor in promoting the formation of atherosclerosis.
Insulin resistance also causes an imbalance between coagulation and fibrinolysis, and a hypercoagulable state: due to a significant increase in fibrinogen and plasminogen activator inhibitor 1 (PAI-1) levels, patients cannot initiate normally once blood coagulation occurs in the body. The fibrinolysis process is very likely to cause the formation of blood clots.
Fat metabolism and metabolic syndrome
Visceral fat accumulation is an important feature of metabolic syndrome and a major cause of insulin resistance. It is currently believed that the visceral fat content is affected by the genetic background, and the Asian population has the characteristic that fat is easily accumulated in the internal organs. In individuals with visceral fat accumulation, the first organ involved is the liver. Excessive deposition of free fatty acids can lead to fatty liver and can cause elevated levels of liver enzymes and even changes in liver structure. Similarly, fat can cause beta cell dysfunction after accumulation of the pancreas. Fat accumulation in the internal organs can also cause secretion of leptin, adiponectin, resistin, tumor necrosis factor- (TNF-), IL-6, angiotensin, PAI-1 and so on.
Adiponectin is currently considered to play an important role in the development of metabolic syndrome. Adiponectin can increase the sensitivity of insulin by direct or indirect methods, promote the uptake and metabolism of fatty acids in muscles, and reduce the concentration of free fatty acids (FFA) and TG in muscle, liver and circulating blood to relieve insulin caused by hyperlipidemia. resistance. Adiponectin can also inhibit the expression of TNF- gene by inhibiting the proliferation of monocyte precursor cells and the function of mature macrophages, and negatively regulate the inflammatory response, thereby contributing to the recovery of endothelial cells in damaged sites. Indirect protection of the cardiovascular system.
Resistin is resistant to insulin and may bind to receptors on insulin-sensitive tissues and act on one or several sites of the insulin pathway, inhibiting the ability of insulin to stimulate glucose uptake by adipocytes. Resistin may be obese and type 2 One but not the only connection point between DMs. Obese individuals with insulin resistance have increased TNF- mRNA expression in adipose tissue and are positively correlated with fasting insulin (Fins) levels. TNF-a increases FFA levels by promoting lipolysis, inhibits hepatic insulin binding and clearance, and inhibits Synthesis of glucose transporter (GLUT) 4 and tyrosineization of insulin receptor substrate-1 lead to insulin resistance. In addition, plasma PAI-1 activity was significantly increased in patients with metabolic syndrome, and PAI-1 activity was significantly associated with plasma immunoreactive insulin levels. Insulin resistance and hyperinsulinemia insulin and proinsulin increased PAI-1 levels. Fibrinogen and PAI-1 together can lead to hypercoagulable state and promote the occurrence and development of cardiovascular and cerebrovascular diseases.
Prevention
Metabolic syndrome prevention
Prevention can be summarized as "one, two, three, four, five, six, seven, eight", that is, the daily life is regular, do not overwork, work and rest, do not open the night train. Two quits: no smoking, no alcohol. Three combinations: coarse, fine grain mix, vegetarian match, main and non-staple food mix. Thereby achieving three balances: acidity, astringent diet balance, nutritional balance, and heat balance. Fourth, the diet should be close to "four blacks", that is, black rice, black beans, black sesame seeds, and black fungus are often eaten. "Far four white" means less white sugar, white salt, white fat meat, white MSG. Fifth, prevention and treatment should be combined with five major therapies, that is, prevention and treatment of metabolic syndrome should be carried out with recreational therapy, physical therapy, drug therapy, mental (psychological) therapy, new knowledge therapy, and not relying on single preventive therapy. Sixth is to prevent "six kinky", that is, according to the view of Chinese medicine, in life, to prevent sudden climate change, to prevent excessive wind, cold, heat, dampness, dryness, fire and gas damage to the human body. The seventh is to avoid "seven emotions". In life, we should try to avoid the strong mental, irritation, grief, fear, fear, fear, and mental stimulation (psychological trauma). Eight is to adhere to eight inspections, through the "early prevention, early investigation, early treatment", every six months to one year on the basis of comprehensive clinical examination (such as listening to the heart and lungs, touching the liver and spleen, etc.), important tests:
1 blood sugar
2 blood lipids
3 blood uric acid
4 blood urea nitrogen creatinine, urine routine (renal function)
5 blood enzymology examination. Such as alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, transpeptidase and other tests.
6 blood routine. Blood viscosity, blood rheology examination.
7 ECG chest photos.
8 fundus examination. Blood pressure should be measured once every 1-2 weeks. (Note: Tumor markers should also be tested at the same time during physical examination.)
Complication
Metabolic syndrome complications Complication
Patients with multiple risk factors have a greater risk of poor clinical outcome than patients with only one risk factor, and their effects are not simply additive, but synergistically exacerbated. The dangers of metabolic syndrome significantly increase the risk of developing diabetes and coronary heart disease and other cardiovascular diseases. According to the United States Feiminghan Cardiovascular Epidemic Base, 8 years of data analysis of 3,323 Fermin Han children (average 52 years old) were shown;
(1) Metabolic syndrome is a predictor of diabetes. A new case of diabetes in men and women in the Feiminghan cohort is analyzed. It can be seen that the metabolic syndrome of men and women has a high predictive value for the occurrence of diabetes. Nearly half of the population's diabetes-specific risk can be explained by metabolic syndrome.
(2) Metabolic syndrome is a predictor of coronary heart disease - analysis of Fei Minghan data shows that the metabolic syndrome alone predicts a total of about 25% of new coronary heart disease. In the general population without diabetes, the 10-year risk of coronary heart disease is not >20%.
(3) Metabolic syndrome accelerates the development and death of coronary heart disease and other atherosclerotic vascular diseases.
Symptom
Symptoms of metabolic syndrome Common symptoms Abdominal obesity proteinuria hyperuricemia dyslipidemia high blood pressure
1. Abdominal obesity or overweight.
2, atherosclerosis dyslipidemia [high triglyceride (TG) and high density lipoprotein cholesterol (HDL-C)] is low.
3, high blood pressure.
4. Insulin resistance and/or impaired glucose tolerance.
5, some standards also include microalbuminuria, hyperuricemia and pro-inflammatory state (C-reactive protein CRP) increased and prothrombotic state (fibrinogen increase and plasminogen inhibitor-1, PAI-1 ) increase.
The aggregation of these components occurs in the same individual, greatly increasing the risk of cardiovascular disease.
Examine
Examination of metabolic syndrome
1, central obesity (European male waist circumference 94cm, female waist circumference 80cm, different ethnic waist circumference have their own reference values);
2. Combine any two of the following four indicators:
(1) elevated levels of triglyceride (TG): >150 mg/dl (1.7 mmol/l), or have received appropriate treatment;
(2) decreased high-density lipoprotein-cholesterol (HDL-C) levels: male <40mg/dl (0.9mmol/l), female <50mg/dl (1.1mmol/l), or have received appropriate treatment;
(3) elevated blood pressure: systolic blood pressure 130 or diastolic blood pressure 85mm Hg, or have received corresponding treatment or have previously diagnosed hypertension;
(4) Increased fasting blood glucose (FPG): FPG 100 mg / dl (5.6 mmol / l), or has been diagnosed with type 2 diabetes or has received appropriate treatment. Oral glucose tolerance test (OGTT) is strongly recommended if FPG 100 mg/dl (5.6 mmol/l), but OGTT is not necessary in the diagnosis of metabolic syndrome.
Diagnosis
Diagnosis and diagnosis of metabolic syndrome
Diagnosing metabolic syndrome must meet the following criteria:
1, central obesity (European male waist circumference 94cm, female waist circumference 80cm, different ethnic waist circumference have their own reference values);
2. Combine any two of the following four indicators:
(1) elevated levels of triglyceride (TG): 150 mg / dl (1.7 mmol / l), or have received appropriate treatment;
(2) decreased levels of high-density lipoprotein-cholesterol (HDL-C): male <40 mg/dl (1.03 mmol/l), female <50 mg/dl (1.29 mmol/l), or have received appropriate treatment;
(3) elevated blood pressure: systolic blood pressure 130 or diastolic blood pressure 85mm Hg, or have received corresponding treatment or have previously diagnosed hypertension;
(4) Increased fasting blood glucose (FPG): FPG 100 mg / dl (5.6 mmol / l), or has been diagnosed with type 2 diabetes or has received appropriate treatment. Oral glucose tolerance test (OGTT) is strongly recommended if FPG 100 mg/dl (5.6 mmol/l), but OGTT is not necessary in the diagnosis of metabolic syndrome.
Diagnostic criteria for CDS
Have 3 or all of the following 5 components:
1. Overweight and/or obesity BMI 25.0Kg/M2;
2. Hyperglycemia FPG 6.1 mmol / L (110 mg / dl) and / or 2 hPG 7.8 mmol / L (140 mg / dl), and / or have been diagnosed with diabetes and treated;
3. Hypertensive systolic blood pressure 140mmHg and/or diastolic blood pressure 90mmHg, and/or diagnosed hypertension and treated;
4, fasting blood TG 1.7 mmol / L (110 mg / dl)
5. Fasting blood HDL_C<0.9 mmol/L (35 mg/dl) (male), <1.0 mmol/L (39 mg/dl) (female). [1]
IDF Teen Diagnostic Criteria
1, 6 age <10 (years): Obesity: waist circumference 90th percentile, not diagnosed as metabolic syndrome, but abdominal obesity is recommended to lose weight; and the following family history suggests further examination: metabolic syndrome, Type 2 diabetes, dyslipidemia, cardiovascular disease, high blood pressure, and obesity.
2, 10 age <16 (years): obesity: waist circumference 90th percentile; if the adult boundary is lower, take the adult boundary, at least 2:
(1) FPG 5.6 mmol / L (100 mg / dL) (recommended glucose tolerance test) or already type 2 diabetes;
(2) systolic blood pressure 130mmHg (17.3kPa) or diastolic blood pressure 85mmHg (11.3kPa);
(3) HDL-C (mmol/L) <1.03;
(4) TG (mmol/L) 1.70.
3. Age 16 (years old): Obesity: The waist circumference value varies according to race and gender, and at least 2 items at the same time:
(1) FPG 5.6 mmol / L (100 mg / dL) or already type 2 diabetes;
(2) systolic blood pressure 130mmHg (17.3kPa) or diastolic blood pressure 85mmHg (11.3kPa) or have been confirmed as hypertension and treated;
(3) HDL-C (mmol/L) <1.03 (male), <1.29 (female) or lipid-lowering therapy;
(4) TG (mmol / L) 1.70 or have been lipid-regulated.
Differential diagnosis
No need to identify.
