gestational diabetes
Introduction
Introduction to Gestational Diabetes Pregnancy with diabetes includes pregnancy in diabetic patients (ie, diabetes with pregnancy) and gestational diabetes. Gestational diabetes mellitus (GDM) is a high degree of hyperglycemia caused by varying degrees of impaired glucose tolerance and diabetes caused during pregnancy. According to its definition, this type of diabetes includes those that existed before pregnancy but were diagnosed during pregnancy and occurred during pregnancy, and it includes both diabetes and impaired glucose tolerance (IGT) and impaired fasting glucose. (impairedfastingglucose, IFG). Some patients have already diagnosed diabetes or impaired glucose tolerance before pregnancy, persisting or progressively worsening after pregnancy. basic knowledge The proportion of illness: 0.08% Susceptible population: pregnant women Mode of infection: non-infectious Complications: pregnancy-induced hypertension, premature delivery, polyhydramnios
Cause
Etiology of gestational diabetes
(1) Causes of the disease
Gestational diabetes is a general term for impaired glucose tolerance, impaired fasting glucose, and diabetes during pregnancy. Poor control of gestational diabetes can lead to serious maternal and fetal complications and complications, current studies have shown that Age, obesity, race, poor birth history and family history of diabetes are major factors influencing gestational diabetes.
Age factor
Older pregnancy is currently recognized as a major risk factor for gestational diabetes. Vereellini et al found that pregnant women aged 40 years and older were 8.2 times more likely to develop gestational diabetes than pregnant women aged 20 to 30. Other scholars have more similarities. It is found that in addition to affecting the occurrence of diabetes, the older the age, the smaller the gestational age of pregnant women diagnosed with gestational diabetes. Berkovitz et al found that among pregnant women diagnosed with diabetes before 24 weeks of pregnancy, pregnant women aged 30 and over accounted for 63.7%. Only 45.2% (P<0.01) were diagnosed after 24 weeks of gestation.
Obesity
Obesity is an important risk factor for impaired glucose tolerance and diabetes. It is no exception for gestational diabetes. Other environmental factors such as age, economy, cultural level and diet structure are synergistic with obesity.
At present, the body mass index (BMI) is commonly used to measure obesity. As the current obesity is getting more and more attention, waist circumference, hip circumference and waist-hip ratio (WHR) have become important indicators, especially WHR, Jang, etc. The results of the study showed that pregnant women with BMI 20.9 were twice as likely to have gestational diabetes as those with BMI 19.1. Berkovitz et al found that the risk of diabetes in pregnant women with BMI > 32.9 was 2.82 times that of BMI in 27.3 to 32.9. 3.82 times BMI <27.3, a study by Branchtein et al. for pregnant women with no history of diabetes at 28 weeks of pregnancy showed that for each additional standard deviation of WHR and waist circumference, the former was 0.06, the latter was 8 cm, and blood glucose levels were increased. 0.11mmol/L and 0.13mmol/L, Zhang et al. compared the relationship between WHR and gestational diabetes mellitus in pregnant women with WHR 0.6290.705. The relative risk of WHR 0.7060.742 group was 2.74, WHR 0.7431.020 group. At 4.02, the study suggests that WHR may be an extremely important risk factor for gestational diabetes.
3. Race
Similar to adult type 2 diabetes and ethnicity, gestational diabetes has a distinct regional and ethnic relevance, compared with the prevalence of gestational diabetes in white European women, the Indian subcontinent, Asia, Arabia and Black are The former is 11 times, 8 times, 6 times and 6 times. Apart from genetic factors, ethnic factors cannot be excluded from economic culture, eating habits and other factors.
4. Family history of diabetes and history of adverse obstetrics
Family history of diabetes is a risk factor for gestational diabetes. The risk of gestational diabetes in family history of diabetes is 1.55 times higher than that of family history without diabetes, and the family history of diabetes in first-degree relatives is 2.89 times higher.
Among the obstetric factors, factors related to gestational diabetes include high birth times, macrosomia, history of stillbirth, important congenital malformations and history of gestational diabetes. The risk of diabetes in pregnant women with these medical history is 2.0 times, 5.8 times that of normal pregnant women. 8.5 times, 22.5 times and 23.2 times.
In short, the cause of gestational diabetes is complex, and these factors are significantly similar to non-pregnancy type 2 diabetes.
(two) pathogenesis
Gestational diabetes is the sum of impaired glucose tolerance and diabetes diagnosed during pregnancy. The degree of impaired glucose tolerance varies with pregnancy progression. Most pregnant women return to normal glucose tolerance after delivery, and the possibility of diabetes in pregnant women with gestational diabetes. Women who are large and have normal glucose tolerance after birth have a high probability of being diagnosed with type 2 diabetes many years later. Combining the characteristics of gestational diabetes and the etiology of gestational diabetes, gestational diabetes is similar to type 2 diabetes in many ways. Insulin deficiency and insulin resistance are important pathogenesis. In the study of the pathogenesis of gestational diabetes, the special physiological conditions of pregnancy should also be considered. The special endocrine and metabolic changes during pregnancy are the occurrence of gestational diabetes. An important factor.
1. Endocrine and metabolic changes associated with glucose metabolism in pregnant women
(1) Changes in endocrine glands of pregnant women: the islet is enlarged during pregnancy, the number of cells is increased, the plasma insulin level begins to increase in the second trimester, and reaches the peak at the end of pregnancy, while the glucagon secreted by cells also increases, the volume of the pituitary gland and The weight starts from the 7th gestational week, the final volume increases by 20% to 40%, the weight increases by 1 time, the pituitary prolactin secreted by the pituitary, the thyrotropin, the adrenergic and adrenocorticotropic hormones increase, and the thyroid gland during pregnancy Uniformity increases, 65% increase during pregnancy, the total amount of bound T3 and T4 in the blood increases, while the levels of free T3 and T4 remain unchanged or slightly lower. Although the adrenal gland volume during pregnancy does not increase significantly, the adrenal gland secretes sugar. Corticosteroids are significantly elevated, but free hormone levels are not elevated.
(2) Endocrine effect of placenta: In addition to the important organs for the exchange of substances between the fetus and the mother, the placenta is also an important endocrine organ during pregnancy. Placental synthesis and secretion of placental lactogen, estrogen, progesterone and androgen are associated with glucose metabolism. Related to placental lactogen is the most important, placental lactogen can accelerate fat decomposition and oxidation, increase free fatty acids in the blood, accelerate liver use of glycerol and fatty acids to produce glycogen; placental lactogen can inhibit the peripheral action of insulin, so that peripheral tissues use glucose to decline Increase blood sugar to facilitate fetal utilization, and the placenta also synthesizes placental insulinase. Placental insulinase can degrade insulin into amino acids and lose activity.
Among the hormonal changes secreted by the endocrine glands of the mother during pregnancy and the bioactive substances secreted by the placenta, only insulin has a hypoglycemic effect, while placental lactogen, glucagon, placental-secreted steroid hormones, thyroid hormones, adrenocortical hormones In addition, it has the effect of antagonizing insulin. In addition, placental insulinase can accelerate insulin degradation and weaken the ability of hypoglycemic mechanism. Under the combined effect of these factors, the glucose metabolism during pregnancy has the following characteristics:
1 pregnant women are in a relatively low blood sugar state, the cause of hypoglycemia is due to the large demand for glucose in the fetus and the excessive filtration of the kidneys of pregnant women due to the decline of the renal sugar threshold, so pregnant women often have hypoglycemia, especially when starving, hypoglycemia The progress of pregnancy is exacerbated, the blood glucose level during non-pregnancy is higher than that of early pregnancy, and early pregnancy is higher than late pregnancy.
2 pregnant women are in a state of hypoglycemia, hypoglycemia can lead to a decrease in insulin secretion, and due to increased blood volume, hypoalkemia occurs, hypoglycemia causes lipolysis, and free fatty acids and ketone bodies rise, so pregnant women are prone to appear Ketoacidosis or ketoacidosis.
3 The ratio of blood glucose to blood insulin decreases, and blood glucose decline is a cause of a decrease in the blood glucose/insulin ratio, and the main cause of this decrease is the increase in insulin levels and total insulin.
4 After giving glucose load to pregnant women, the peak blood glucose level is higher than that of non-pregnant women and delayed arrival. The time to return to normal level is also longer. The change of blood insulin concentration is similar to the change of blood sugar. According to the glucose tolerance test, the same sugar load, pregnant women The amount of insulin released is significantly more than non-pregnant, so pregnant women are in insulin resistance, but this insulin resistance is the result of a variety of other hormone antagonism, not caused by abnormalities in insulin, insulin receptors and second messenger systems, and should be emphasized This insulin resistance is normal and physiological, and it can ensure the growth and development of the fetus while maintaining the metabolic balance of pregnant women and normal blood sugar.
2. Relative Defects in Insulin Secretion and Insulin Resistance Gestational diabetes mellitus is based on factors such as heredity, age and obesity. The impaired glucose tolerance syndrome is determined by the specific environment or endocrine metabolic state of pregnancy. The important features are as follows:
1 occurs during pregnancy;
2 The level of impaired glucose tolerance during pregnancy is constantly changing;
3 Most of the glucose tolerance decreased after the end of pregnancy;
4 pregnancy again, the incidence of diabetes is very high;
5 gestational diabetes patients have a high incidence of type 2 diabetes after many years;
6 family history of diabetes is an important risk factor for gestational diabetes, so in the study of the pathogenesis of gestational diabetes, not only should consider its relationship with type 2 diabetes, but also consider the special physiological state of pregnancy. At the same time, the study of gestational diabetes can better reveal the secret of type 2 diabetes. The pathogenesis of gestational diabetes is currently considered to be mainly the relative decrease of insulin secretion and the decrease of insulin sensitivity.
(1) Relatively reduced insulin secretion: the fasting plasma insulin level of pregnant women gradually increased to about 2 times of non-pregnancy in late pregnancy, but the increase of insulin secretion in pregnant diabetic patients was relatively reduced. In addition to the increase of fasting insulin level in gestational diabetes patients In addition, the plasma insulin level or the insulin/glucose ratio or the proinsulin index decreases after the glucose load. At present, the reason for the relative decrease in insulin secretion is unclear, which may be related to the genetic heterogeneity of the patient. This genetic heterogeneity In a state of non-pregnancy, it remains quiescent, and under the stimulation of pregnancy, it changes to a dominant state, and there is a relative decrease in insulin secretion. After the pregnancy is terminated, it returns to its original state. In addition to pregnancy, other factors such as age, weight Increased levels can also lead to activation of this genetic heterogeneity.
(2) Insulin resistance: Like insulin resistance in type 2 diabetes, insulin resistance in gestational diabetes also needs to consider multiple processes such as pre-receptor, receptor and post-receptor, and various factors and factors that cause insulin resistance. The mechanism and characteristics should also be analyzed according to insulin resistance in type 2 diabetes. Since most gestational diabetes patients develop type 2 diabetes after many years, many of the causes and mechanisms of the two should be the same or similar; The patient's glucose tolerance returned to normal and did not develop into diabetes later, so the two have differences.
Most gestational diabetes patients have normal glucose tolerance before pregnancy, diabetes during pregnancy, and glucose tolerance returns to normal after pregnancy, so the effect of pregnancy on glucose tolerance is critical. High insulin levels during pregnancy are one of the signs of insulin resistance, ie, decreased insulin sensitivity. Secretion and metabolic changes in gestational diabetes during pregnancy are one of the important causes of this insulin resistance. During pregnancy, a large amount of glucosamine is produced, such as pituitary hormone, glucagon, placental lactogen and steroid hormones, etc. During pregnancy, the concentration of triacylglycerol and free fatty acids in the blood increases, both of which can inhibit the secretion and function of insulin. The placenta secretes insulinase, which can degrade insulin. In pregnant women with normal glucose tolerance, the result of the above interaction is blood sugar. And glucose tolerance is normal, and for gestational diabetes patients, any abnormality in any of the above mechanisms can lead to diabetes.
The etiology and pathogenesis of gestational diabetes are complicated. It is based on certain genetic factors and environmental factors. In the special physiological condition of pregnancy, the syndrome characterized by abnormal glucose metabolism is the main symptom of gestational diabetes. Combined with type 2 diabetes, follow-up studies of gestational diabetes contribute to the study of the etiology, pathogenesis and pathogenesis of type 2 diabetes.
Prevention
Gestational diabetes prevention
Prevention of the disease usually involves the development of targeted preventive measures against the cause and predisposing factors, so as to prevent the disease from occurring and continue to progress in the early stage of the disease or in the early stage of the disease. However, for the patients with gestational diabetes, due to the particularity of the disease, preventive measures Should be targeted to the following two aspects.
1. Impaired glucose tolerance develops into diabetes
According to family history, in the past, the history of adverse production, age, ethnicity, obesity, etc. will be divided into high-risk groups and normal populations of gestational diabetes. Regular glucose tolerance screening tests will be conducted for normal people, and detailed screening and screening for high-risk groups will be made. Closely monitor the program so that early detection of impaired glucose tolerance and diabetes in pregnant women, the early treatment of the above-mentioned pregnant women, including mental, diet, exercise and insulin treatment measures.
(1) To restore normal glucose tolerance to glucose tolerance, avoid developing diabetes, and perform insulin-based treatment on diabetic patients to maintain normal blood sugar levels.
(2) The ultimate goal is to reduce or completely avoid maternal and maternal complications and complications, and to reduce and avoid various abnormalities in the fetus and newborn.
2. Diabetes again and diabetes after many years
After gestational diabetes, the glucose tolerance usually returns to normal, but the chance of recurrence of pregnancy is high. The probability of developing diabetes after many years is high. It should be followed for many years in postpartum diabetes patients.
The implementation of the above preventive measures is quite complicated. It cannot be completely dependent on the obstetrics of a general hospital. It is a social issue that requires the support of national health policies, the formation of specialized institutions, personnel, and the establishment of systems throughout the country. A comprehensive multi-level network system that takes years of effort.
Complication
Gestational complications of gestation Complications, pregnancy, hypertension, premature oligohydramnios
Pregnancy-induced hypertension
Gestational diabetes mellitus (GDM) and pregnancy-induced hypertension (PIH) are diseases that pose a serious threat to pregnant women and perinatal children. There is an interaction between the two in the development of the disease.
Premature birth
Premature birth is a common complication of pregnancy with diabetes, the incidence rate is 9.5% to 25%, significantly higher than non-diabetic patients, premature birth is also the main cause of perinatal morbidity and neonatal death in pregnancy with diabetes.
3. Diabetic giant fetus
Diabetic giants are the most common perinatal complications in pregnant women with diabetes. With the increasing incidence of gestational diabetes, the incidence of diabetic giants and their perinatal and long-term complications has increased accordingly. The treatment of gestational diabetes has been significantly improved, but the incidence of diabetic giants is still high, reaching 25% to 40%.
4. Too much amniotic fluid
The prevalence of polyhydramnios in pregnancy with diabetes is 13% to 36%, which is a common complication of pregnancy with diabetes.
5. Diabetes emergency
Diabetic emergency mainly includes diabetic ketoacidosis (DKA), nonketotic diabetic hyperosmolar coma (NDHSC), diabetic lactic acidosis (DLA), alcoholic ketosis Acidosis and diabetic hypoglycemia, etc., for diabetic patients, the above-mentioned diabetes emergency can also occur for various reasons, but due to the unique age and physiological characteristics of gestational diabetes, gestational diabetes complicated with diabetes It has its own characteristics:
1 The type of diabetes emergency combined with gestational diabetes is mainly diabetic ketoacidosis and hypoglycemia.
2 Diabetic non-ketotic hyperosmolar coma is mainly seen in some elderly people with diabetes, rare in pregnancy; diabetes alcoholic acidosis is also rare.
3 Diabetic lactic acidosis often coincides with various complications, but for ordinary diabetic patients and gestational diabetes patients, there is a lack of sufficient understanding of lactic acidosis, which needs to be paid enough attention and further research.
4 The degree of impaired glucose tolerance in patients with gestational diabetes changes with the progress of pregnancy and the termination of pregnancy, so the cause of the above-mentioned emergencies in diabetic patients has a distinctive feature of pregnancy.
5 gestational diabetes patients need to apply insulin therapy, oral hypoglycemic drugs contraindications.
6 The treatment of gestational diabetes patients should be based on the safety of pregnant women, and the safety of the fetus should be placed in a secondary position.
6. Pregnancy with diabetes and hypoglycemia Diabetic patients have decreased blood glucose due to various reasons. When the venous plasma glucose concentration is lower than 2.5mmol/L (45mg/dl), hypoglycemia is diagnosed. Hypoglycemia is an independent disease. Causes hypoglycemia, which is mainly caused by improper diet, exercise, oral hypoglycemic agents and/or insulin. Diabetic patients can also have hypoglycemia. Hypoglycemia can have serious consequences for pregnant women and fetuses, even death.
7. Infectious diseases In pregnant women with diabetes, due to the existence of endocrine and metabolic disorders and certain acute and chronic complications, the body's defense function is significantly reduced, and the susceptibility to infection is significantly higher than that of pregnant women. Once the infection occurs, the body is in a state of stress. It is inevitable to increase the difficulty of blood sugar control, causing the deterioration of diabetes and endangering the lives of mothers and children. Before the advent of insulin before 1921, pregnancy and diabetes were very serious. Most pregnant women were not controlled, and died of infection, perinatal. The mortality rate is extremely high. With the clinical application of insulin, the research on pregnancy and diabetes has made great progress. The mortality rate of diabetes caused by infection, maternal and perinatal mortality have decreased significantly, but In pregnant women with uncontrolled diabetes, hyperglycemia can still lead to infection and rapid progression. Therefore, infection is still a common and important cause of induced and aggravated diabetes and becomes a metabolic disorder such as ketoacidosis. Common infections related to diabetes: including urinary tract infections, respiratory infections, skin Infection, puerperal infection and other infections.
8. Microvascular disease Insulin therapy restores the fertility of diabetic women. With the development of diabetes treatment and obstetric technology, maternal mortality has decreased significantly. In the early stage of insulin application, the main concern is acute ketosis and ketoacidosis. The occurrence of hypoglycemia, diabetes causes changes in small blood vessels, that is, microvascular complications gradually attract people's attention, pregnant women with diabetes are not well controlled metabolism, further disorder of metabolism during pregnancy, can cause diabetic nephropathy and retinopathy, myocardial Infarction, cerebral thrombosis, high blood pressure, etc. are caused and aggravated. The maternal prognosis is related to diabetes, especially related to vascular complications such as cardiovascular or nephropathy. Therefore, with the progression of diabetes, the prognosis of pregnant women is more Poor, in pregnant women with diabetes, the incidence of retinal, kidney or neurological diseases is not different in the epidemiology or the severity of the damage compared with non-pregnant women with diabetes, pregnant women with diabetes Retinopathy and kidney disease are not contraindications or end-of-pregnancy Grounds of pregnancy, but requires careful pre-pregnancy counseling and treatment programs should be carried out monthly eye examinations during pregnancy.
9. Fundus lesions Diabetic retinopathy is the earliest complication of diabetes. Epidemiological studies have found that diabetic retinopathy is increasing year by year and has become the main cause of blindness. Diabetic damage to the retina is mainly due to increased blood glucose and small vessel wall growth. Thick, increased permeability, making small blood vessels more deformable and leaky, the severity of diabetic retinopathy and the degree of visual decline are related to the control of blood glucose levels and the length of diabetes. Generally, diabetes occurs at least 10 years after diabetes. Retinopathy, non-proliferative diabetic retinopathy of pregnant women on the basis of control of diabetes, can continue to pregnancy, but must be regularly reviewed in high-risk clinics, pay attention to the examination of the fundus; once there is proliferative diabetic retinopathy, simple systemic treatment is difficult to improve the fundus In the case of lesions, local treatment of the eye must be considered.
Symptom
Symptoms of Gestational Diabetes Common Symptoms Polyuria Drinking Pregnancy Glucose High Glucose Ketoacidosis Coma Stretch Marks Stillbirth
The clinical manifestations of type 1 and type 2 diabetes are different, each has its own characteristics. There is no significant difference in the incidence of males and females. The mothers in the family have diabetes, and the incidence of diabetes in the next generation is high.
Type 1.1 diabetes
The incidence of this type of patients accounts for 10% of the incidence of diabetes. The incidence is more common before the age of 40. Most of them require insulin replacement therapy. There are typical polydipsia, polyphagia, polyuria and weight loss, which is "three more and one less". In the case of stress, infection, surgery, discontinuation of hypoglycemic agents, prone to ketoacidosis, very few patients can also develop hyperosmolar non-ketotic diabetic coma, chronic disease, poor glycemic control, kidney disease It occurs early and has serious clinical manifestations. When there is a large amount of proteinuria in the clinic, accompanied by hypertension, renal anemia, and azotemia, the patient may eventually die of uremia.
Type 2.2 diabetes
This type of patient accounts for 90% of the incidence of diabetes. After 40 years of age, the incidence is more common. Most patients do not have "three more than one less" disease, only found in the case of complications or physical examination, the body type is more obese, the body weight after the onset can be It can be reduced in a short time before, and there may be hypoglycemia reaction in the early stage before the meal, and only need to take oral hypoglycemic agents for life to achieve the blood sugar level. Only a few patients who have failed the oral hypoglycemic agents must rely on insulin therapy. After a part of insulin is injected for a period of time, the islet function is restored, and the oral hypoglycemic agent is still effective. Another part of the patient needs insulin treatment for life. When there is infection, stress, surgery and other incentives, ketosis can also occur. Acidosis, the older the older, the previous history of patients without diabetes, the higher the incidence of hyperosmolar nonketotic diabetic coma, the majority of this type of patients died of heart, cerebrovascular complications, but also complicated with diabetic nephropathy, but Type 1 diabetes is rare.
Examine
Examination of gestational diabetes
1. Blood glucose measurement Blood sugar refers to glucose in the blood. After digestion, the carbohydrate in the food is mainly absorbed in the small intestine in the form of glucose. The liver enters the liver through the portal vein. The liver is an important organ regulating sugar metabolism. Under normal circumstances, the body sugar The decomposition and synthesis maintain a dynamic balance, so the concentration of blood glucose is relatively stable.
(1) Fasting blood glucose: Serum glucose provides energy for tissue oxidation. When blood sugar is too high, it can be converted into liver glycogen and fat storage. When needed, fat and protein can also be converted into glucose. Fasting blood glucose concentration reflects insulin secretion from islet cells. ability.
Reference value: non-pregnancy is 3.9 ~ 6.4mmol / L, pregnancy is 3.1 ~ 5.6mmol / L, the cause of pregnancy-induced fasting blood glucose decline is:
1 Pregnant women need to supply the energy needed for fetal growth in addition to their own needs, and the fetus itself does not have the liver enzyme system activity required to promote gluconeogenesis, so it is impossible to use fat and protein as energy, and the energy required must come from the mother. Blood glucose.
2 The renal blood flow and glomerular filtration rate increased during pregnancy, but the reabsorption rate of sugar in the renal tubules could not be increased correspondingly, which led to an increase in the amount of glucose excreted in some pregnant women, causing blood sugar to drop.
When diabetes is combined with pregnancy, fasting blood glucose is elevated during pregnancy; fasting blood glucose may be normal in gestational diabetes patients. Therefore, routine fasting blood glucose examination is often missed. When impaired glucose tolerance is normal, fasting blood glucose is normal. It is recommended that pregnant women with the following high risk factors should do as soon as possible. Blood glucose measurement: Obesity, history of gestational diabetes mellitus (GDM), diabetes, and a clear family history of diabetes.
(2) Sugar screening test: GDM pregnant women often have no obvious symptoms, fasting blood glucose may be normal, routine fasting blood glucose test is often easy to miss diagnosis, it is recommended to do 50g glucose screening for all non-diabetic pregnant women, the method is simple and easy, sensitivity and High specificity, the American Diabetes Association lists age, obesity, first-degree relatives with diabetes, GDM history, huge fetal production history and unexplained stillbirth as GDM risk factors. Those with the above risk factors should be screened for GDM. Key population.
Sugar screening test time: due to placental secretion of placental lactogen, estrogen and progesterone and other antagonistic insulin hormones increased rapidly in the 24th to 28th week of pregnancy, 32 to 34 weeks of pregnancy peak, pregnant women to insulin at this time The need for a significant increase, impaired glucose tolerance, during this period is easy to detect GDM, so the regular blood glucose screening time during pregnancy is set to 24-28 weeks of pregnancy; if the screening is normal but there are high risk factors for diabetes Should be reviewed in the 32 to 34 weeks of pregnancy, for those with symptoms, sugar screening should be carried out in the early pregnancy, in order to diagnose the early diagnosis of diabetes patients before pregnancy.
Sugar screening test method: random oral 50g glucose (50g glucose dissolved in 200ml water, served within 5min), 1h after taking sugar to take blood glucose measurement, blood glucose 7.8mmol / L for sugar screening abnormalities, should be further Oral glucose tolerance test (OGTT). When the blood glucose level is between 7.20 and 7.79 mmol/L, the OGTT should be considered in combination with high risk factors. The sensitivity of the sugar screening test is 59%, and the specificity is 91%. 80% of clinical GDM can be diagnosed by this method.
(3) Oral Glucose Tolerance Test (OGTT): OGTT is a method for checking the blood sugar regulation function of the human body. After a certain amount of glucose is orally administered by a normal person, the blood glucose temporarily increased in a short time can be quickly lowered to the fasting level. The phenomenon is called tolerance. When the glucose metabolism is disordered, the blood sugar rises sharply after a certain amount of glucose is orally administered, and it cannot be restored to the fasting level after a long time; or the blood sugar rise is not obvious, and cannot be reduced to the original level in a short time. It is called OGTT as soon as possible, called abnormal tolerance or impaired glucose tolerance, abnormal sugar screening but blood glucose <11.1mmol / L, or sugar screening blood glucose 11.2mmol / L, but fasting blood glucose is normal.
OGTT 3 days before the normal diet, daily carbohydrates above 150 ~ 200g, to avoid the effect of fasting carbohydrates, fasting 8 ~ 14h after checking fasting blood glucose, and then taking 75g of glucose (75g of glucose dissolved in 400ml of water, Take 5kg of standard flour or take 100g standard flour. Start taking syrup time, take venous blood to measure blood glucose at 1h, 2h, 3h. After taking blood, centrifuge as soon as possible. The measurement should be completed within 2h to avoid glucose decomposition.
Reference value: fasting blood glucose <5.8mmol / L, 1h after eating blood sugar level peak, generally 7.8 ~ 9.0 mmol / L, the peak does not exceed 11.1mmol / L; 2h does not exceed 7.8mmol / L; 3h can return to fasting blood glucose Level, each urine sugar is negative.
Diagnostic criteria: OGTT is a diagnostic method for the diagnosis of diabetes. When oral glucose is 7.8mmol/L 1h or 2h blood glucose 11.1mmol/L, GDM can be diagnosed. If oral glucose is 2h, the blood glucose is 7.8~11.1mmol/L. To diagnose gestational impaired glucose tolerance test (GIGT).
2. Urine examination and measurement
(1) Urine glucose test: urinary glucose qualitative test first, urine glucose is negative in normal people, urine sugar can be positive in diabetes, urine glucose is measured when urine sugar is positive, but GDM pregnant women monitor urine sugar is not beneficial .
(2) Determination of urine ketone body: normal human urine ketone body is negative, urine ketone body determination is extremely important for patients with diabetic ketoacidosis and ketoacidosis. When ketone body production increases, the ketone body discharged from urine also increases accordingly, generally in urine. The amount of ketone body is 5 to 10 times that of blood ketone. When insulin is severely deficient, especially when hormones such as glucagon, adrenaline, glucocorticoid, thyroid hormone, and growth hormone are increased. There may be decreased glucose uptake and utilization by target cells, increased fat decomposition, increased release of free fatty acids, -hydroxybutyric acid, acetoacetic acid, acetone, which are collectively referred to as ketone bodies, and ketone bodies positively found in type 1 diabetes, diabetic ketones. Acidosis, type 2 diabetes is infected, stress, trauma, surgery, etc., ketone body positive also seen in long-term hunger, pregnancy and lactation, high-fat diet, alcoholism, fever and so on.
3. Glycosylated hemoglobin determination Glycosylated hemoglobin (GHb) is used to evaluate the degree of control of diabetes. When diabetes is poorly controlled, glycated hemoglobin can be elevated. GHb is hemoglobin (Hb) synthesized with -chain end. The amino acid reacts with glucose to form HbA1c ketoamine compound. The reaction rate depends mainly on the time of blood glucose concentration and Hb contact. Because the saccharification process is very slow, it is quite wood reversible. Once formed, it is no longer separated and is not affected by blood glucose concentration. The impact of temporary fluctuations, so it has a unique diagnostic significance for patients with high blood sugar, especially blood sugar and urine sugar fluctuations.
Reference value: Calculated as a percentage of GHb to Hb, the electrophoresis method is 5.6% to 7.5%; the microcolumn method is 4.1% to 6.8%; and the colorimetric method is (1.41±0.11) nmol/mg protein.
In diabetes, GHb is 2 to 3 times higher than normal, which can reflect the average level of blood glucose in patients 1 to 2 months before blood draw. The decline of GHb after controlling diabetes is 3 to 4 weeks later than that of blood sugar and urine sugar. Therefore, it is one of the good indicators to understand the degree of diabetes control.
4. Glycosylation serum protein determination In addition to hemoglobin, the amino acid of the N-terminal amino acid of albumin and other proteins in serum can also undergo non-enzymatic glycation reaction with glucose to form a ketoamine structure, called glycated serum protein. Reference value: (1.9± 0.25) mmol/L.
The positive rate of glycated serum protein in diabetic patients can reach 88%-90%, which not only has a high detection rate for diabetes, but also reflects the severity of the disease. Because the half-life of glycated serum protein is short, it can effectively reflect patients. The average blood glucose level in the past 1-2 weeks was not affected by the fluctuation of the temporary blood glucose concentration. The determination of glycated serum protein was of great significance for monitoring GDM. 85% of GDM patients had higher glycated serum protein than normal, during diabetes with pregnancy. Higher values, the level of glycated serum protein in cord blood of newborns born in these patients is also high, and is related to the weight of infants and the thickness of subcutaneous fat, but this test can not differentially diagnose diabetes and impaired glucose tolerance.
5. Determination of serum C-peptide and insulin
(1) Determination of serum C-peptide: Islet cells secrete proinsulin. Under the action of proteolytic enzymes, proinsulin is hydrolyzed into insulin and C-peptide. C-peptide is almost inactive, but for measuring the ability of islet -cell to secrete insulin, C-peptide is more reliable than insulin. Determination of serum C-peptide levels can understand insulin secretion, metabolism and the reserve function of islet -cells, especially in patients with diabetes, when they receive insulin therapy, they can more accurately determine the ability of -cells to secrete insulin.
Reference value: The serum C peptide value of fasting in the morning is 265 to 1324 pmol/L.
When insulin is used excessively, hypoglycemia leads to an increase in serum insulin and a decrease in C-peptide. When insulin antibodies are present in diabetic patients, only the C-peptide is used to detect the function of islet -cells.
(2) Determination of serum insulin: insulin is secreted by islet cells, insulin is regulated by blood glucose concentration, and elevated blood glucose can stimulate islet secretion of insulin. The secretion curves of the two are parallel, and the islet cell function disorder occurs during diabetes. After the blood sugar rises very high, and the secretion of insulin is little or does not respond to blood sugar, the insulin level is still basically in the state of fasting. Therefore, in the OGTT, the blood is measured before and after 30 minutes, 1 hour, 2 hours, 3 hours. Insulin concentration can more accurately reflect the reserve capacity of islet cells.
Reference value: 10-20 mU/L in the morning fasting; insulin (U/ml)/blood glucose (mg/d1) value <0.3.
Fasting insulin concentration was significantly lower in patients with type 1 diabetes; the ratio of insulin to blood glucose was also significantly lower after glucose administration, and the fasting insulin level in patients with type 2 diabetes was normal, slightly lower or slightly higher; delayed release of insulin after glucose injection Response, insulin to blood glucose ratio is also low, insulin secretion decreased or delayed release, is conducive to the early diagnosis of diabetes, it must be noted that in addition to insulin and C peptide in the blood, there is insulin and proinsulin to insulin conversion Intermediates and other substances that share the same structure and a certain degree of immune cross-reactivity with insulin and C-peptide.
6. Islet cell function determination The function changes of islet cells are closely related to the occurrence, development, pathological changes and pathological changes of various types of diabetes. Therefore, cell function test for the diagnosis, differential diagnosis, judgment and treatment of diabetes All of them are important. There are at least four hormones secreted by islet cells: insulin, C-peptide and pro-insulin belong to the same gene expression product, and amylin belongs to another gene. The concentration of these hormones in blood is very low (nmol/ L ~ pmol / L level).
The understanding of the secretory function of -cells is indirectly obtained by the changes in the concentration of hormones secreted by -cells in peripheral venous blood. By analyzing various release (stimulation) or inhibition test results, combined with changes in blood glucose concentration, the function of islet -cells is understood. Commonly used methods are: insulin release test, C-peptide release test, tolbutamide (D860) test, glucose-glucagon-toluene butyrate test.
(1) Insulin release test (IRT): glucose can not only directly stimulate islet cells to release insulin, but also enhance the insulin release of other non-glucose substances. Therefore, glucose-stimulated insulin release test is a study of islets The secretory function of -cells is an important method for barrier-free and resistance. In the glucose release test of diabetic patients, it not only helps to understand the functional status of insulin secretion from islet cells, but also contributes to differential diagnosis.
1 oral glucose tolerance ~ insulin release test: normal people after oral administration of 100g glucose, blood insulin and blood sugar increased in parallel, 30 to 60min reached a peak, and then gradually decreased, blood glucose returned to the basic value after 3h, and blood insulin The recovery takes about 4 hours. The characteristic of diabetes is OGTT, which shows that the initial reaction of insulin is low, and the increase of immunologically active insulin (IRI) in blood (IRIU/ml) and blood glucose increase (ABS) 30 minutes after sugar load Mg/dl), the ratio of the two AIRI / BS (30min) is called the initial response index of proinsulin, which is of great significance in differential diagnosis.
IRI / BS (30min) reference value: 1.49 ± 0.62 (100g OGT-IRT), 0.83 ± 0.47 (50g OGT-IRT), the ratio of diabetes patients is less than 0.5, the ratio of glucose tolerance in non-diabetic patients, the ratio It does not decrease. The IRI of patients with -cell tumors is generally elevated. The IRI and its reactivity in obese patients are increased, which is positively correlated with the degree of obesity. The IRI response in the blood of patients with impaired insulin secretion is generally reduced.
2 intravenous glucose tolerance and insulin release test: this method can eliminate the influence of digestive tract factors, but the IRI response is only 30% to 40% of the oral method, the detection rate of impaired glucose tolerance is not as good as oral method, generally 20% ~50% glucose injection, intravenously according to the sugar content of 10 ~ 30g / kg or 0.5g / kg body weight, completed in 1 ~ 4min, before injection and 1, 3, 5, 10, 20, 30 after injection, Blood was drawn at 40, 50, 60, 90, 120 min. The highest value was reached 1 to 5 minutes after intravenous injection, and then decreased rapidly. The decline curve of 10 to 40 minutes reflected the sugar utilization ability in the tissue.
Normal human plasma insulin reaches a peak 3 to 10 minutes after intravenous glucose injection, and the diabetic patients are reduced, and the secondary diabetes patients can be normal or elevated.
(2) C-peptide release test: The C-peptide release test can determine the function of islet -cells by measuring the secretion of C-peptide after glucose load. In the oral glucose tolerance test, the secretion reaction of C-peptide is the same as IRI, insulin-dependent Patients with diabetes (IDDM) may have reduced or no response, and most insulin autoimmune diseases, the basal value of islet cell tumor patients and the response value after glucose load are increased, and can also be taken 6 minutes after intravenous administration of glucagon 1 mg. The C-peptide value of blood is 0.5-3.0 ng/ml, and the C-peptide value exceeds the basic value by 150%-300% after the stimulation test. If the excitatory test is positive, the islet -cell reserve function is good; otherwise, the negative one Lack of -cell secretion of insulin, insulin therapy in patients with type 1 diabetes, positive insulin test indicates insulin secretion, the condition is relatively stable, while negative patients have no insulin secretion, the condition is often very unstable, can be in hyperglycemia and Hypoglycemia coma, must be repeated insulin injection treatment or insulin pump treatment to stabilize the condition, patients with type 2 diabetes undergo an excitement test, but Islet beta cell function, positive test of excitability indicates that its islet cells can still secrete a certain amount of insulin, suitable for diet exercise therapy or add hypoglycemic agents to control hyperglycemia; if the excitatory test is negative, it means the patient's islet cells Already in a state of exhaustion, insulin therapy is needed sooner or later to control blood glucose levels. There is a close relationship between fasting C-peptide and C-peptide value after stimulation test, but there is also a low fasting C-peptide value and a marked increase after excitement.
(3) Tolbutamide (D860) test: Tolubutamide is combined with islet -cell membrane specific receptor to promote insulin secretion and lower blood sugar. This test can be used to diagnose mild diabetes and can also be used to identify various hypoglycemia. It is one of the important methods for diagnosing islet -cell tumor.
Test method: fasting D860 2g, sodium bicarbonate 4g, blood glucose and insulin before taking the drug and 30, 60, 120, 180min after taking the drug, normal value: 30 ~ 60min blood sugar dropped to 50% ~ 60% of the fasting, 90 ~ 120min blood glucose is close to or returns to normal, or the ratio of insulin to blood glucose <0.3, if 30 to 60min blood glucose drops to 80% to 90% of fasting, suggesting insufficient insulin secretion or insulin resistance.
(4) Glucose-glucagon-tolbutamide test: This test is used to understand the maximum secretory reserve capacity of insulin, mainly used for the diagnosis of diabetes. Method: fasting oral glucose 75g, intravenous glucagon after 30 minutes 1mg and 0.5mg of tolbutamide, blood was collected before injection and 1,5,10,30,60,120min after injection, blood glucose and plasma insulin were measured. Results: The blood sugar of normal people was 4.4mmol/L 30min after taking sugar. It rose to about 7.2mmol/L. After intravenous injection, blood glucose remained at the same level. Plasma insulin rose to 400U/ml 1min after intravenous injection and peaked at 500mU/ml for 5-10min.
7. Normal blood glucose high insulin clamp test In the fasting, the blood glucose concentration is relatively stable. If a certain amount of insulin is infused, causing hyperinsulinemia, blood sugar will decrease, but if glucose is infused at the same time, blood sugar can be supplemented. This test measures the glucose utilization rate in the case of blood insulin and blood glucose homeostasis, expressed as the glucose infusion rate.
Methods: In the morning, fasting, taking two intravenous channels, infusion of insulin and glucose, respectively, after the start of the test, heating by heating pad to maintain the temperature of the hand, in order to take arterial venous blood to determine blood sugar, adjust glucose glucose according to blood sugar level At the rate of injection, the blood glucose was maintained at (5.00 ± 0.28) mmol / L, the test lasted 240 min, blood was taken before the test and 120, 180, 240 min before the test, serum or plasma was separated, and stored at -70 ° C for insulin determination. Calculate the glucose utilization rate every 20 minutes during the clamp test. The formula is: ISI=MCR/logMI, ISI is the insulin sensitivity index, logMI is the certain insulin concentration, and MCR is the glucose clearance rate.
Although this method is currently recognized as the gold standard for sensitivity of peripheral tissues in the world, it is still difficult to be used for pregnant women because of its complicated technology, so it needs further improvement.
8. Blood lactate determination
(1) Lactic acid production: Lactic acid is the final metabolite of anaerobic glycolysis. Free glucose entering the cell is catalyzed by lytic enzymes to produce lactic acid, glycolysis in tissue cells and oxygen consumption. In inverse proportion, under the condition of sufficient oxygen supply, glycolysis is inhibited, glucose consumption and lactic acid production are reduced. In diabetes, oxygen deficiency in the muscle, inhibition of aerobic oxidation of sugar, inhibition of glycolysis, muscle glycogen Increased consumption, increased lactic acid production, and vascular and microcirculatory disorders in diabetes can cause hypoxia, increased glucose utilization and glycolysis, and increased lactic acid production, which can lead to lactic acidosis, metabolic acid Poisoned.
(2) normal value: venous whole blood lactic acid 0.6 ~ 1.8mmol / L, plasma lactic acid is 7% higher than whole blood, arterial blood lactic acid is 1/3 ~ 1/2 of venous blood, postprandial lactic acid level is higher than the fasting base value 20% to 50%.
(3) Clinical significance: severe hypoxia, which can lead to the aerobic oxidation of pyruvate in the Krebs cycle. The enzymatic action of pyruvate to lactic acid is strengthened, the ratio of lactic acid to pyruvate in blood is increased, and lactic acid is increased. Up to 25mmol / L, causing lactic acidosis, severe lactic acidosis is irreversible, in the early and middle stages of hypoxemia with lactic acidosis, appropriate treatment can be reversed, when pregnant women with diabetes with ketoacidosis, dynamic monitoring The level of lactic acid in the blood is especially important.
9. Diabetes microcirculation measurement Diabetes microvascular disease is the most striking of the late complications of diabetes, regardless of retinopathy, kidney disease, diabetic foot disease and diabetic cardiomyopathy are related to microvascular disease, diabetic microangiopathy is diabetes caused by death and disability The main reason, but the current mechanism of microvascular disease in diabetes is not fully understood.
(1) Microcirculation physiology: microcirculation is the blood circulation in the microvessels between the arterioles and venules, which is directly related to the tissue cells, supplies cell nutrition, exchanges metabolites, and maintains the physiological functions of various organs of the body. Microcirculation irrigation The flow rate is reduced, which can not meet the needs of tissue oxidative metabolism, causing insufficiency or failure of tissues and organs, which is the direct cause of many diseases.
(2) Microcirculation measurement: Diabetes microcirculation is mostly measured in the hyperthyroidism site, which is generally determined from the three aspects of microvascular morphology, fluid state and tube circumference.
1 micro-blood flow measurement: At present, multi-spot synchronous scanning method, computer image analysis, space correlation method, time correlation method is used to measure blood flow velocity, the normal reference value is >1000m/s, and the blood flow velocity of diabetic patients is slowed down.
2 Tube diameter and tube length measurement: At present, the cursor reference method is used for measurement. The normal reference value of the tube diameter is: input branch (11±2) m, output branch (14±3) m, dome (15±3) m, Long (200 ± 50) m.
Clinical significance:
1 tube diameter widening: seen in hyperlipidemia, diabetes;
2 increase in length: seen in high blood pressure, high blood fat,
3 Direct visual indicators include the number of fistulas [branch / mm (mm)], malformation, fistula, vascular mobility, nipple morphology, venous plexus, sweat gland duct, fistula bleeding, red blood cell aggregation, white blood cell count and White microthrombotic.
(3) Hypothyroidism microcirculation abnormality classification diagnostic criteria
1 Hyperthyroidism microcirculation severe abnormality: Those with the following changes are severe abnormalities of the hyperthyroidism microcirculation: A. The number of tube defects is reduced to 3 pieces/mm or less, or reduced by more than 80%; B. Red blood cells are heavily aggregated, blood cells and Plasma is separated and most of the blood flow of the tube is granulating, even stopping; C. Most of the white micro-plugs caused by non-local factors appear in the blood flow; D. Tube bleeding is 1 7.
2 Hyperthyroidism microcirculation moderate abnormality: The following two changes are the moderate abnormalities of the hyperthyroidism microcirculation: A. The number of tube defects is reduced by 40% to 60%, and the input branch diameter is reduced by 20% to 60% or 60% widening; or 80% shortening or 50% or more, or 100% or more of the output branch diameter, C. obvious exudation, D. red blood cell moderate aggregation, most tube blood flow is granular Flow, E. tube bleeding up to 3 ~ 6 / 1 nail, F. blood color dark red, G. tube shape changes in a short time, deformity plus cross type up to 40% ~ 100%, H. nipple flat.
3 mild abnormality of the hyperthyroidism microcirculation: the following three changes are mild abnormalities of the hyperthyroidism microcirculation: A. input branch, the diameter of the output branch or dome is widened or narrowed by 20%, and the tube diameter is increased by 20%. %~50% or shortened by 20%, tube fistula deformity plus crossover up to 40%, B. blood flow is granulating, C. mild exudation or bleeding 1~2/1 hyperthyroidism, D. subcannachial vein The plexus is obvious and expands and becomes thicker, E. tube sputum is blurred, F. blood flow has no or increased leukocytes >30/15s, G. sweat gland ducts 3~4/1 hyperthyroidism.
10. Diabetes blood rheology measurement Blood rheology is a branch of biorheology. Clinical hemorheology mainly detects blood fluidity, deformability and coagulability, and can be used as an objective for diagnosis, treatment and observation of diabetes. One of the indicators.
(1) Determination of whole blood viscosity: The high-cut viscosity of whole blood reflects the deformability of human blood cells, and the high-cut viscosity of whole blood is increased, indicating that the blood cell deformability is reduced, the higher the whole blood high-cut viscosity is, the worse the blood cell deformability is. The low-cut viscosity of whole blood reflects the aggregation of blood cells. The higher the low-cut viscosity of whole blood, the heavier the blood cell aggregation.
(2) Determination of plasma and serum viscosity: due to insulin deficiency, increased mobilization of stored fat and decreased lipoprotein lipase activity, diabetic patients have varying degrees of hyperlipidemia, and plasma fibrinogen and other stress proteins in diabetic patients. Significantly increased, so plasma, serum viscosity increased.
(3) Determination of surface charge of red blood cells: There are various charged genes on the surface of red blood cells. The carboxyl group carried by the neuraminic acid on the glycoprotein chain is the main charged group in which red blood cells display a negative charge, and the majority of the negatively charged groups on the surface are dominant. Therefore, under the action of the DC electric field, the cells move to the positive electrode in the medium, and the moving speed is proportional to the negative charge on the cell surface, and the electrophoresis time of the red blood cells in the diabetic patients is prolonged.
(4) Hematocrit determination: The normal reference value is 0.35-0.45. The hematocrit is reduced to 0.31~0.34 due to hemodilution during pregnancy. Hematocrit is one of the decisive factors affecting the viscosity of whole blood.
(5) Determination of red blood cell deformability: abnormal red blood cell deformability is not only an important cause of certain diseases, but also a characteristic of certain diseases. It has an important significance in the occurrence and development of diseases, and the red blood cell deformability of diabetic patients is reduced.
(6) Determination of plasma fibrinogen: reference value, normal human 2 ~ 4g / L, increased plasma fibrinogen in diabetic patients.
(7) Determination of platelet adhesion: The reference value is 29.4%±5.19% in normal women. The platelet adhesion is increased in diabetic patients, which has a tendency to hypercoagulable and is prone to thrombosis.
(8) Determination of platelet aggregation: The platelet aggregation of diabetic patients is increased, and it is related to the condition. Those with a course of more than 5 years have retinal comorbidities, and platelet aggregation is particularly obvious.
11. Determination of blood lipids Lipids, lipoproteins, and apolipoprotein abnormalities are quite common in diabetic patients. The routine examination items include serum cholesterol, triglyceride, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol.
Type 1 diabetes with poor glycemic control, blood cholesterol, triacylglycerol, very low-density lipoprotein can be increased, and high-density lipoprotein cholesterol can be reduced; patients with ketosis can temporarily develop high lactoemia; after insulin treatment, Blood sugar turns to normal, the above dyslipidemia can also return to normal, patients with type 2 diabetes often have dyslipidemia, including elevated triglycerides, high-density lipoprotein cholesterol, total cholesterol and low-density lipoprotein cholesterol can be normal, but Low-density lipoprotein particles are often increased. Diabetic patients not only have abnormal blood lipids, lipoproteins and apolipoproteins, but also lipoprotein components, such as free cholesterol, cholesterol lipids, and apolipoprotein B components in very low-density lipoproteins.;2(triglyceride-rich lipoproteinTRL);GDM0GTT
BX
Diagnosis
diagnosis
1.
GDM
(1)50g(glucose challenge testGCT)50gOsullivan 196450g(50g200ml1)1h50g50gGCTOGTTGCT10.2mmol/L43% OGTTGCT11.1mmol/LGDM20%OGTTGCT13.3mmol /LOGTT(fasting blood glucoseFBG)OGTTFBG5.6mmol/L96%OGTTGDMAgarwalGDMFBGGCT3.7%50g
(2)GDMGDMGDMGDM(ADA)GDMGDMGDM;GDMGDM<25;(BMI25);;()
410%11%10%4%GDMBaliutavicieneADAGCT10.9%GDMGDM
(3)24282428GDMNahtim255141850g(GCT)1h7.5mmol/LGCT100g(OGTT)GDMGCT242856%GDM16Bartha39861GCT1h7.8mmol/L100gOGTT27.7%GDMGDM182424124283234
(4)50g1h7.8mmol/L1h7.8mmol/L75g(OGTT)Coustan7.8mmol/LGDM80%85%7.2mmol/L100%OGTT14%23%125750g7.207.79mmol/LGDMOGTT50g11.1mmol/LGDMOGTTOGTT 50gGDM
2.
50g1225.8 mmol/L;OGTT422h6.79.1mmol/L(gestational impaired glucose tolerance testGIGT)WH0OGTT2;<7.8mmol/L2h7.811.1mmol/LGIGTOGTT4GIGT 632h
Differential diagnosis
1.
C
2.OGTT
3.1h2h
4.()13.9mmol/L(250mg/dl)1213.9mmol/L(250mg/dl)
