What Are Considered Dangerous Blood Sugar Levels?

Hypoglycemia means that the fasting blood glucose concentration of adults is lower than 2.8mmol / L. Hypoglycemia is a group of syndromes caused by multiple causes of venous plasma glucose (glycemic) concentrations, which are clinically characterized by sympathetic nerve excitation and brain cell hypoxia. Symptoms of hypoglycemia are usually hunger, panic, sweating, trembling, pale, etc. In severe cases, there may also be inattention, restlessness, irritability and even coma.

Low blood sugar

Hypoglycemia means that the fasting blood glucose concentration of adults is lower than 2.8mmol / L. Hypoglycemia is a group of syndromes caused by multiple causes of venous plasma glucose (glycemic) concentrations, which are clinically characterized by sympathetic nerve excitation and brain cell hypoxia. Symptoms of hypoglycemia are usually hunger, panic, sweating, trembling, pale, etc. In severe cases, there may also be inattention, restlessness, irritability and even coma.

Chinese name

Low blood sugar

Foreign name

hypoglycemic syndrome

Scientific name

Hypoglycemia syndrome

Hypoglycemic syndrome is a group of syndromes caused by multiple causes.

Low blood sugar

hypoglycaemia

glycopenia; hypoglycemia; hypoglycemia; hypoglycemia; hypoglycemia; hypoglycemia; hypoglycemia

Endocrinology> Hypoglycemia

E16.2

Hypoglycemia (hypoglycemia) is a group of clinical syndromes caused by low blood glucose (glycemic) concentrations caused by multiple causes. Generally, the blood glucose concentration in adults (determined by plasma true sugar, glucose oxidase method) <2.8mmol / L, or whole blood glucose <2.5mmol / L is considered low blood glucose. The diagnostic criteria for hypoglycemia in children is 1.11mmol / L lower than the adult value, but whether there are clinical symptoms or not varies greatly from individual to individual. The incidence of hypoglycemia varies from place to place. The incidence in the U.S.A. and Europe accounts for less than 0.5% of emergency cases, the low incidence of drug-induced blood glucose in Singapore accounts for 0.4% to 0.8% of the number of patients visiting, and the Hong Kong SAR is 1.5%.

Low blood sugar mainly damages the nerves, and the brain and sympathetic nerves are the most important. In 1971, Briely discovered that hypoglycemic brain lesions are similar to ischemic cytopathies. The basic lesions are neuronal degeneration, necrosis and glial cell infiltration. The brain's metabolic energy mainly depends on glucose, and the nerve cell's own glycogen reserve is limited, and it depends on blood glucose to supply. The various parts of the nervous system are inconsistently sensitive to hypoglycemia, with the cerebral cortex, hippocampus, cerebellum, caudate nucleus, and pale bulbs being the most sensitive. The thalamus, hypothalamus, brainstem, and cerebral nucleus are second. Finally, the anterior horn cells and peripheral nerves at the spinal cord level. Histological changes include chromatin agglutination and dissolution of the nucleus of the nerve cell, unclear nuclear membrane, swollen cytoplasm, containing small vacuoles and particles. In 1973, Chang injected mice with 2 units of human insulin. After 15-20 minutes of sleepiness in mice, 30-75 minutes of myoclonus in mice, seizures, and 40-120 minutes of coma. The blood glucose of the drowsy mice decreased from 6.72mmol / L (120mg / dl) to 1.18mmol / L (21mg / dl), and the blood glucose level of the comatose mice was only 1.01mmoL / L (18mg / dl).

Sugar, fat, and amino acids are the sources of energy in neurometabolism. These substances release energy after oxidation and are stored in ATP and creatine phosphate, which are released when needed. When sugar and oxygen are reduced, ATP phosphate creatine creatine and ganglioside-binding glucose synthesis are reduced. As ATP is less, and nucleotide synthesis is also reduced, neurological function is reduced. When the blood glucose is low, the metabolism of high-energy phosphate complexes and neural functions are not only related to blood glucose levels, but also closely related to the partial pressure of oxygen. When the blood glucose is low, because of lower brain oxygen uptake, glucose uptake is also inhibited Relying on sugar alone is not enough to maintain the level of oxidative metabolism, it will necessarily affect the metabolism of fatty acids and amino acids, and the level of cerebral phospholipid molecules can be reduced by 35%. When the blood glucose of the brain tissue is low, the cerebral cortex is inhibited first, then the subcortical center is affected, and it spreads to the midbrain, and finally the brain is damaged and a series of clinical abnormalities occur. When blood sugar decreases, the body has a self-regulating mechanism that can stimulate adrenaline secretion, promote the breakdown of liver glycogen, and bring blood sugar back to normal levels.

The related anti-regulatory mechanism of glucose (also called anti-regulatory hormone) is established to prevent a significant decrease in blood glucose and a protective mechanism that threatens brain function. Glucose against regulatory damage refers to a state in which the plasma grape glucose concentration cannot be maintained at a normal level or cannot prevent further decline in blood glucose.

1. Hypoglycemia has been widely concerned about the secretion of (anti-regulated) hormones. Human experimentally induced weakening of insulin is an important factor in restoring blood glucose levels. Inhibiting the release of liver glycogen, increasing the use of peripheral insulin to induce glucose, leading to hypoglycemic stimulating factors, and reversing the decline of insulin in some plasma islets. Avoiding blood glucose levels that cause hypoglycemia in insulin-treated diabetic patients is key. Anti-regulatory hormone secretion can outweigh the effect of insulin, even when the plasma islet insulin concentration has not decreased. Among the anti-regulating hormones, such as epinephrine, glucocorticoids, glucagon, growth hormone, etc., have obvious anti-insulin effects. These hormones are secreted immediately when the plasma grape glucose drops to a threshold, which rapidly induces gluconeogenesis in the liver. The respective effects of these hormones are similar for liver glucose production. Therefore, the response of any one hormone is insufficient to completely impair glucose anti-regulatory function. Clinically, when people with type 1 diabetes have low blood sugar, the secretion of glucagon is significantly reduced. After adrenalectomy, it is normal for patients to receive appropriate glucocorticoid replacement while receiving alpha and beta adrenergic blockers. Several years after the illness of special type of diabetes, the deficiency of antihormones such as glucagon and epinephrine is caused by some reasons, leading to the tendency of these patients to have severe or prolonged hypoglycemia.

2. Anti-regulatory hormones have an effect not only on the recovery of blood glucose, but also on maintaining the stability of glucose in the later period. However, steroid hormones and growth hormone have a significant role in maintaining the continuous output of liver glucose during hyperglycemia. These hormones and adrenaline can reduce the use of peripheral glucose during the recovery of hypoglycemia. Its effect may be direct or indirect (eg FFA is stimulated to release). In patients with insulin-dependent diabetes and diabetes, due to liver glucose release damage, reduced peripheral glucose uptake is the key to recovery from hypoglycemia. Long-term hypopituitarism, deficiencies in growth hormones, glucocorticoids, and other antihormones are also important causes of severe hypoglycemia.

3. It is common for hormones to impair the regulation of hypoglycemia. Some patients with islet cell tumors have reduced anti-regulatory hormone secretion, but this phenomenon can be reversed after surgery. The clinical glucose anti-regulatory injury is characterized by undetected hypoglycemia, which is the result of the disease's adrenal response injury. Causes severely prolonged hypoglycemia.

4. The normal blood glucose level in maintaining the fasting state mainly depends on the following three factors:

(1) Basal hormone level environment, such as increased secretion of glucagon, growth hormone and steroid hormones and decreased insulin secretion.

(2) Complete glycogen decomposition and gluconeogenesis.

(3) Increased liver glucose production and decreased peripheral glucose use. But severe defense damage will lead to severe prolonged hypoglycemia.

Classification of hypoglycemia

According to the causes are classified as follows:

Islet B cell hyperplasia, adenomas, and cancers, such as islet blastoma, functional B cell secretion defects, latent diabetes, familial multiple endocrine adenomas (including insulinoma, pituitary tumor, and parathyroid adenoma, etc.)

Symptoms caused by stimulation of the adrenal sympathetic nerves include anxiety, tremor, palpitations, and hunger. These symptoms are often a warning sign of low blood sugar. The resulting hemodynamic changes include tachycardia and increased pulse pressure. ECG changes, such as ST-segment shift, T-wave low-level, QT interval prolongation, and arrhythmia, especially heterotopic atrial or ventricular arrhythmias. In severe cases, it can cause angina pectoris attacks or various complications such as myocardial infarction and exacerbation of retinopathy. Or severely stupid patients can show hypothermia, which is particularly noticeable in alcohol-induced hypoglycemia. Like many other signs, peripheral circulation failure can occur, and shock and death can occur.

Other endocrine gland diseases include hypothyroidism, adrenal cortex dysfunction, hypopituitary dysfunction (including growth hormone deficiency, adrenocorticotropic hormone deficiency, thyroid stimulating hormone deficiency), pancreatic islet alpha cell damage and glucagon deficiency.

Liver diseases such as severe hepatitis, cirrhosis, liver cancer, liver necrosis and Reye syndrome (fatty liver, encephalopathy, hypoglycemic syndrome).

Inherited liver enzyme defects such as glycogen accumulation disease, galactosemia, and fructose intolerance.

(5) Digestive diseases

Digestive diseases such as gastrointestinal surgery, peptic ulcer, acute gastroenteritis, chronic gastroenteritis, duodenitis, digestive system tumors, chronic diarrhea and malabsorption and excessive consumption.

Such as insulin, glibenclamide in sulfonylurea drugs, phenformin in biguanide hypoglycemic drugs, etc. others, such as ethanol, sodium salicylate, phentolamine, isoniazid, butazone, anti- Hypoglycemia can occur in histamine preparations, monoamine oxidase inhibitors, propranolol (more than 40 mg per day), and aspirin D860.

Severe malnutrition such as small bowel malabsorption syndrome, Crohn's disease, chronic enteritis, starvation malnutrition, and fasting can all cause hypoglycemia.

Diseases of the central nervous system such as birth trauma, developmental disorders and retardation, nucleus jaundice, traffic hydrocephalus, hypothalamus and brainstem lesions, and brain hypoplasia can cause hypoglycemia.

Transient neonatal preterm infants, infants with diabetic mothers have transient islet hyperfunction, erythroblastosis infants with transient islet hyperfunction, Rh factor immune factors cause a large number of red blood cells to hemolyze, 2 to 3 days after birth Low blood sugar can occur. Under the action of maternal hyperglycemia, B cells proliferate and insulin secretion increases. Transient hypoglycemia can occur after birth is not corrected in time.

Multiple changes in hypoglycemia may complicate the diagnosis: When hypoglycemia occurs, these symptoms can recur, even for minutes to hours. The reason for this relatively short duration is that the endogenous blood glucose counteracts the regulation mechanism and the intake of sugars returns the blood glucose concentration to a normal state. Without these adjustments, blood glucose levels can continue to decrease and can even cause the severity of loss of consciousness, epilepsy, or coma. If the patient complains of chronic fatigue, burnout, or inability to concentrate for hours or days, these reasons are not simply due to hypoglycemia.

Symptoms are relieved when carbohydrates are ingested, not only due to occult hypoglycemia, but symptoms associated with glucose intake are not a specific manifestation of hypoglycemia. Many anxiety-related symptoms can be alleviated by eating, and the presence or absence of hypoglycemia must be confirmed.

It is generally thought that it may be caused by ectopic insulin or due to insulin-like active substances including some insulin-like active factors. It is more common in thoracic and abdominal tumors, such as fibrosarcoma, mesothelioma, abdominal myxoma, bile duct cancer, adrenocortical cancer, renal adenoma, lymphoma, gastrointestinal cancer, lung and liver cancer, and ovarian cancer. , Weighing up to 500-1000 grams, can secrete insulin-like growth factors.

When too much urine sugar is lost, blood glucose levels drop, with a 1% incidence of diabetes, a family inherited disease caused by a low renal glucose threshold.

Phillips report (1989) Malaria can be associated with hypoglycemia.

Sepsis, sepsis, pneumonia, and cellulitis can all be associated with low blood sugar.

Such as low ketogenic blood sugar, low leucine sensitive blood sugar, low familial blood sugar, poisoning factors (mushroom poisoning, lychee fruit poisoning, etc.), long-term fever, lactation and pregnancy, chronic diseases and unknown causes, etc. Can cause hypoglycemia.

Signs and symptoms of low blood sugar

After the occurrence of hypoglycemia, the increase of adrenaline secretion can lead to hypoglycemia syndrome. This is a compensatory response to hypoglycemia. The patient has pale faces, palpitations, cold limbs, cold sweats, hand tremors, soft legs, fatigue, Dizziness, dizziness, hunger, panic, and anxiety are relieved after eating.

Inhibited cerebral cortex, hazy consciousness, decreased orientation, recognition, lethargy, sweating, tremor, impaired memory, headache, apathy, depression, dream-like state, dementia in severe cases, some people may have strange behaviors, etc. These nerves Mental symptoms are often mistaken for insanity.

When hypoglycemia develops to midbrain involvement, muscle tone increases, paroxysmal seizures, epilepsy or seizure-like seizures occur, and most of the seizures are large seizures or persistent epilepsy. When the brain is involved, the patient can enter a coma, go to a state of stiff brain, bradycardia, body temperature does not rise, and various reflections disappear.

When the subcortical center is inhibited, consciousness, restlessness, hyperalgesia, clonic dance movements, dilated pupils, and even tonic convulsions, positive extrapyramidal and pyramidal tract signs, may manifest hemiplegia, paresis , Aphasia and monoplegia. These manifestations are mostly temporary damage, which can be quickly improved after giving glucose. Extrapyramidal damage can involve brain tissue structures such as pale bulbs, caudate nucleus, putamen and cerebellar dentate nucleus, which are mostly manifested as tremor, euphoria and excessive movement, torsion spasm.

Hypoglycemia can damage the cerebellum, manifestations include ataxia, uncoordinated movement, indistinguishable range, low muscle tone, and abnormal gait, etc. Especially in the late stage of hypoglycemia, ataxia and dementia often occur.

Cerebral nerve damage may occur when blood glucose is low, manifested as abnormal vision and visual field, diplopia, dizziness, facial paralysis, difficulty swallowing, and hoarseness.

Peripheral neuropathy and muscle atrophy and paresthesia often occur in the late stage of hypoglycemia, such as limb numbness, muscle weakness or muscle tremor, etc. Clinically, patients with hypoglycemia have developed sock-type dyskinia in the distal limbs. There may also be peripheral irritation and burning changes, which are related to degeneration of the spinal cord anterior horn cells, and some people think that it is related to myositis caused by low blood sugar caused by insulinoma. Hypoglycemic peripheral neuropathy can also cause sagging feet, failure of hand and foot movements, such as being unable to write, eat, walk, or even be bedridden.

The most common is insulinoma low blood glucose, about 70% of which are benign adenomas, 0.5 to 3.0 cm in diameter, mostly located in the tail of the pancreas. The incidence of the pancreatic body and the head of the pancreas is similar, mostly single, followed by hyperplasia. Cancer is rare, such as cancer and more liver and adjacent tissue metastasis. Domestic Hu Lixin has reported a case of multiple insulinomas, a total of 7, pancreatic head 1, pancreatic body 2, pancreatic tail 4, different sizes, diameter 10 ~ 50mm, the smallest reported as 1mm, called micro adenoma, Not easy to detect during surgery.

Insulin tumors with low blood sugar episodes are severe and long-lasting, and often have the following characteristics: hypoglycemia usually occurs on an empty stomach, such as before breakfast; symptoms occur from mild to severe during the onset, from few to many, gradually and frequently; Symptoms are paroxysmal episodes, and patients often cannot recall the symptoms of the episodes; The symptoms of hypoglycemia in different patients are not exactly the same, and the symptoms of the same patient are sometimes not completely the same; Patients with hypoglycemia often cannot Tolerance of hunger often increases food intake to prevent seizures, so patients generally gain weight; fasting blood glucose in patients can be very low, sometimes only 0.56 to 1.68mmol / L (10 to 30mg / dl).

The main manifestations of reactive functional hypoglycemia are: more common in women, milder onset, long history, and more history of emotional stress and trauma; hypoglycemia occurs mostly 2 to 3 hours after meals, and fasting blood glucose is normal or slightly lower ; hypoglycemia episodes are mainly symptoms of increased adrenaline, which lasted 20 to 30 minutes, often without coma, and often self-relieved; patients are often neurotic, obese, negative signs, although the condition does not worsen despite repeated attacks; hypoglycemia Low levels are not as obvious as insulinoma, and fasting blood glucose is mostly 2.24 to 3.36 mmol / L (40 to 60 mg / dl); The patient can tolerate starvation for 72 hours without coma.

Generally, the nerve cells in the brain take glucose from the bloodstream relatively constant, which is not affected by the increase and decrease of blood glucose. Therefore, the symptoms of hypoglycemia can only be shown below 45mg / dl (2.52mmol / L). Hypoglycemia is similar to the hypoxic state of the brain, so when there is a disorder of cerebral circulation (such as arteriosclerosis, cerebral infarction), hypoglycemia may appear early. The degree and speed of blood glucose reduction are roughly parallel to the appearance and severity of clinical symptoms, but there is no absolute quantitative relationship. There is no uniform standard for the threshold of blood glucose for symptoms of hypoglycemia, and there are large individual differences. The same is the blood glucose value of 30 mg / dl (1.68 mmol / L), some coma occurs, and some only have low blood sugar symptoms without coma, but all need to be treated to increase blood sugar levels.

If the hypoglycemia cannot be alleviated, and the blood glucose concentration continues to decrease for more than 6 hours, it can cause irreversible morphological changes in brain cells, such as congestion, multiple point bleeding, and brain tissue damage. If the correct diagnosis and treatment cannot be made in time Cerebral edema, ischemic punctate necrosis, cerebral softening, dementia, coma, shock and even death can occur. Hypoglycemia is not an independent disease. Many causes can cause hypoglycemia, and the cause of hypoglycemia should be checked after diagnosis.

Fasting plasma islet insulin and blood glucose measurement

Non-obese fasting insulin levels above 24 U / ml can be considered hyperinsulinemia. However, sometimes even if the fasting insulin value is normal, the relative blood glucose value has increased. When the fasting blood glucose is lower than 2.8mmol / L, the plasma islet insulin should be reduced to less than 10U / ml. Plasma grape glucose levels are below 2.2 mmol / L, and insulin values will be below 5 U / ml. The ratio of insulin to blood glucose (I: G) is also generally reduced. If the I: G value increases or> 0.3, hyperinsulinemia should be suspected, and I: G> 0.4 indicates that insulinoma is possible.

Oral glucose tolerance test (OGTT)

To determine if there is low fasting blood glucose, OGTT is meaningless. If the glucose tolerance test is extended to 4 to 5 hours, it is of certain value for diagnosing low postprandial blood glucose.

Determination of plasma islet insulin proinsulin and C peptide

Normal plasma contains a small amount of proinsulin, and most patients with insulinoma have elevated levels of proinsulin in the blood circulation. Under normal circumstances, proinsulin generally does not exceed 22% of the total immunoreactive insulin, and more than 85% of patients with insulinoma have a proinsulin percentage of more than 25%.

The plasma islet insulin value measured by the RIA method is called immunoreactive insulin. This is because polyclonal antibodies to insulin cross-react with insulin analogs such as proinsulin, and the normal value of insulin is low, so the results must be interpreted. Very cautious.

C-peptide measurement can be used to distinguish endogenous and exogenous hyperinsulinemia. C-peptide and insulin are secreted with equal molecular weight. Blood C-peptide in exogenous hyperinsulinemia is generally undetectable. High C-peptide levels are indicative of endogenous hyperinsulinemia. Conversely, low C-peptide levels suggest that elevated plasma islet insulin levels are caused by exogenous insulin.

Determination of insulin anti-antibodies and insulin receptor antibodies

The presence of anti-insulin antibodies in the plasma suggests previous insulin or autoimmune insulin syndrome. Insulin autoantibodies can be divided into endogenous and exogenous depending on the source of the antigen. There are excitatory and inhibitory autoantibodies depending on the biological activity and effect of the antibody.

Patients who have been receiving insulin for a long time can produce anti-insulin anti-antibodies, which is related to the structure of the insulin in the preparation being different from that of human insulin and impure preparations, but the use of unimodal human insulin or recombinant human insulin can still produce insulin anti-antibodies. Such antibodies are one of the important reasons for insulin insensitivity.

Some people with diabetes who have never used insulin can produce autoantibodies against insulin. It is characterized by a very low free insulin concentration and a marked increase in total insulin. Patients with this type of insulin resistance syndrome often require large doses of insulin to control hyperglycemia.

Another rare case is that the body's own anti-insulin anti-antibody can excite the insulin receptor and cause severe hypoglycemia, as described below.

Determination of plasma sulfonylurea drugs and their metabolites in urine

The determination of plasma sulfonylurea drugs or their metabolites in urine can help determine the diagnosis of hyperinsulinemia induced by sulfonylurea drugs. Chlorpromide has a high risk of low blood glucose due to its long half-life.

Insulin suppression test

Asymptomatic fasting blood glucose is low or unstable or marginal hyperinsulinemia, and inhibition tests can be used to identify whether it is caused by excessive endocrine insulin secretion.

Exogenous insulin does not completely inhibit the release of C-peptide and proinsulin from insulinomas. However, it has been reported that C-peptide inhibition tests in some patients with insulinoma are normal. Kim et al. Found that normal people's plasma C peptide was inhibited by about 66% after the application of exogenous insulin, but when insulinoma patients have normal blood glucose, plasma islet insulin and C peptide are not inhibited, and when the blood glucose is low, they can Secretion of endogenous insulin and C peptide.

Stimulation test

The susceptibility test for patients with suspected low fasting blood glucose is lower than the I: G ratio, C peptide, and proinsulin assays. Commonly used stimulation tests include tolbutamide, arginine, and glucagon stimulation tests. 80% of patients with insulinoma have abnormal tolbutamide tests, 74% have abnormal arginine tests, and 58% have glucagon. The vegetarian test is abnormal. Calcium injection can stimulate insulin secretion in patients with insulinoma, but it has also been reported that insulin injection in patients with insulinoma does not increase after injection of calcium.

Diagnosis of congenital metabolic disease with hypoglycemia

There are many diagnostic methods, which can be selected according to needs. The diagnosis depends on pathological diagnosis and genetic analysis of enzyme defects.

Glycemic index refers to the relative ability of carbohydrates to raise blood sugar. Compared with carbohydrates with low glycemic index, carbohydrates with higher glycemic index can raise blood sugar to higher levels and more quickly. Depending on the glycemic index, carbohydrates can generally be divided into several types. Amylose reacts slowly and weakly to blood glucose and blood insulin, while amylopectin can significantly increase blood glucose, insulin and glucagon.

After oral administration of fructose at 200 mg / kg, the response of normal people is similar to OGTT, and hereditary fructose intolerance due to fructose-1-phosphate aldolase deficiency causes hypoglycemia, hypophosphatemia, and fructoseuria.

Glucagon acts only on liver phosphorylase and has no effect on muscle phosphorylase. In normal people, after fasting intramuscularly with 1 mg of glucagon, the blood glucose rises, and the peak is seen at about 45 minutes. Patients with insulinoma may have their blood glucose peaks earlier, but they decline rapidly and have a low blood glucose response. Blood insulin secretion is higher than that of normal people. Glycogen storage disease (GSD) type I patients have no peak or small peak of blood glucose after 1 hour, blood lactic acid significantly increased, blood pH and HCO3- decreased. This test can also be used for the differential diagnosis of other hypoglycemia.

GSD type does not exceed 30% in blood glucose after epinephrine injection. Since GSD may also affect the glucose metabolism of neutrophils, there is no significant increase in blood neutrophils after using epinephrine. However, a simple method for the diagnosis of GSDLb is to use phoorbol-myristate-acetate to stimulate the activity of NAPDH oxidase to assist in the diagnosis of GSDLb and neutrophil dysfunction.

Wrap the upper arm with a sphygmomanometer cuff, pressurize it to 200mmHg, let the patient perform a grasping activity for 1 minute, and measure the blood lactate value before and after the test. Normal human blood lactic acid increased more than three times after the test, and those with type III and type V GSD did not increase, but lactic acid production disorders caused by other reasons (such as muscle phosphofructokinase deficiency, etc.) could not be ruled out.

If GSD is suspected, clonidine (0.15 mg / d, or 0.2 mg / M2 body surface area per day) is usually used for several months. GSD (such as type , , and ) can increase height, and its mechanism of action is unknown. Therefore, the drug is also effective for stunted growth and other causes of growth retardation, so it may be related to its role in the center and promote GH secretion.

Analysis of the amino acid composition of blood, urine and cerebrospinal fluid is helpful for the diagnosis of amino acid metabolic diseases. Blood ketones, blood glucose, blood nitrogen, and creatine kinase are the basic detection items for various hypoglycemia. If possible, the enzyme activity of the diseased tissue and abnormal glycogen particles, metabolic substrates, etc. should be measured. Identification of mutations in enzyme genes by molecular biology methods can confirm the types and loci of enzyme defects.

Chromogranin A (CgA)

Chromogranin A (CgA) is one of the markers of neuroendocrine tumors. About 90% of patients with APUD tumors have elevated serum CgA. In patients with carcinoid tumors of midgut origin, blood CgA can increase tens to hundreds of times. After liver metastasis, blood CgA increases more significantly (CgA error measured by RIA method is 30% to 40%).

Other APUD hormone and metabolite assays

Corresponding peptide or amine hormones can be measured according to clinical manifestations, but are generally difficult to popularize due to their high cost. In most cases, 5-hydroxyindoleacetic acid (5-HIAA) in urine and insulin, proinsulin, and C peptide in gastric juice can be measured, and gastrin can be measured if necessary. To determine the growth potential and prognosis of tumors, Ki-67 protein and PCNA (proliferating cell nuclear antigen) can be measured. Tumor tissue can be stained with adhesion molecule CD44 and platelet-derived growth factor alpha (PDGFa) receptors. Somatostatin receptor subtype analysis and PKR measurement also help diagnosis.

EEG

EEG performance is similar to hypoxia, without specific changes, slow wave or other changes, long-term hypoglycemia patients with brain lesions may have abnormal changes.

EMG

Nerve conduction time is normal. The distal muscles showed denervation and the number of motor unit potentials decreased. Diffuse denervation fibers, electrical discharges at the tip and giant motor units, polyphasic potentials. More consistent with changes in peripheral neurons or anterior horn cell types.

X-ray examination

X-ray examination occasionally showed calcified adenomas, with adjacent organs distorted or displaced. Pancreatic arteriography showed increased blood flow. Selective superior mesenteric artery and celiac arteriography are helpful for localization of lesions.

CT and MRI scans

CT and MRI scans can detect space-occupying lesions in the abdominal cavity and pancreas.

B-ultrasound

B-ultrasound can find tumors in the pancreas. Those less than 1 cm are easily missed and not as reliable as CT and MRI.

other

Pancreatic radionuclide scan, ECT scan, and 75Se-methionine examination can find space occupying lesions inside and outside the pancreas.

The main reason for the difficulty of diagnosis is that it is easy to be misdiagnosed and missed due to the rapid onset of disease and the clinical symptoms, signs and biochemical abnormalities. But it mainly depends on the blood sugar level. Healthy people, including women and children, should be diagnosed with hypoglycemia when the fasting intravenous plasma grape glucose value is below 2.8mmol / L (50g / dl), although there are no clinical symptoms and signs. Fasting venous blood glucose higher than 3.9mmol / L (70mg / dl) can rule out hypoglycemia; fasting venous plasma grape glucose 2.8 3.9mmol / L (50 70mg / dl) can indicate that hypoglycemia is possible, but very rare Healthy women with blood glucose as low as 1.4 to 1.7 mmol / L (25 to 30 mg / dl) after 72 hours of fasting, even with intracellular glucose levels close to 0 and newborn blood glucose as low as 1.7 mmol / L (30 mg / dl) Was considered normal. Some experts believe that children and infants should carefully observe when the blood glucose level is below 2.8mmol / L (50mg / dl), and can only be diagnosed and treated when the blood glucose level is below 2.2mmol / L (40mg / dl). Conversely, hypoglycemia often occurs in elderly patients with venous plasma grape glucose values of 3.3 mmol / L (60 mg / dl). Therefore, normal people's blood glucose is maintained at a relatively ideal level, and the fluctuation range rarely exceeds 2.2 to 2.8 mmol / L (40 to 50 mg / dl) within 24 hours. The internal environment of this glucose is regulated by various hormones. Many organs, especially the liver and muscle tissue, are involved in glucose metabolism. Hyperglycemia or hypoglycemia can occur when glucose is used, taken up, and / or generated imbalances. The severity and signs of hypoglycemia are not always consistent with blood glucose levels. Therefore, it is used as a reference value for experimental diagnosis. The following points must be noted.

1. In the same patient at the same time, the arterial blood glucose value is usually slightly higher than the capillary value, while the latter is higher than the venous value. When fasting, the capillary blood glucose value (whole blood is measured) is 5% to 10% higher than the venous blood glucose value.

2. Blood glucose measurement is divided into three methods: serum, whole blood, and plasma. To measure serum blood glucose, the blood must be centrifuged immediately after blood collection, otherwise the time is too long, the sugar is broken down, and the result is low. Whole blood sugar is susceptible to hematocrit and non-sugar. The effect of the substance is also slightly lower by 5% -10% than the plasma blood glucose; therefore, the current clinical measurement of plasma blood glucose is mostly used to judge various causes of hyperglycemia and hypoglycemia.

3. For unknown reasons, low or continuous blood sugar levels, blood insulin, C peptide, proinsulin, and blood and sulfonylurea concentrations should be monitored frequently for identification. Such as hyperinsulinism can be seen in insulinoma, taking sulfonylurea drugs, low autoimmune blood sugar and topical insulin; while elevated blood C peptide is only seen in insulinoma and taking sulfonylurea drugs.

1. For patients with episodic (especially fasting) psycho-neurological disorders, convulsions, behavioral disorders, unconsciousness or coma, especially for diabetic patients treated with insulin or oral hypoglycemic agents, the possibility of hypoglycemia should be considered Check blood sugar in time. It is worth noting that some patients with hypoglycemia have normal blood glucose at the time of consultation, and have no symptoms of hypoglycemia, and often only show the sequelae of chronic hypoglycemia, such as hemiplegia, dementia, epilepsy, mental disorders, and children with significantly lower IQ. As a result, it is often misdiagnosed as mental illness, epilepsy or other organic encephalopathy (such as encephalitis). Therefore, it should be distinguished from other diseases of organic disease of the central nervous system, such as encephalitis, multiple sclerosis, cerebrovascular accidents, epilepsy, diabetic ketoacidosis, ketoacidosis coma, and diabetic nonketotic hyperosmolar coma. , Mental illness, drug poisoning, etc.

2. Hypoglycemia with sympathetic nerve excitement as the main manifestation of fasting, several hours after meals, or physical activity, should be related to diseases with sympathetic nerve excitement, such as hyperthyroidism, pheochromocytoma, and autonomic dysfunction , Diabetic autonomic neuropathy, menopausal syndrome, etc.

3. Hypoglycemia after alcoholism should be distinguished from drunkenness. Ethanol can not only cause hypoglycemia, but also ketosis. Sometimes hypoglycemia and ketosis caused by alcohol can be mistaken for diabetic ketoacid. Acidosis, which should be paid attention to during diagnosis.

Regardless of the acute or chronic hypoglycemia, especially the recurrence of hypoglycemia, it indicates that a certain disease exists, and the etiology is as early as possible, which is the key to treatment. To avoid serious consequences, do the following in advance:

Management of acute hypoglycemia

(1) Glucose application: For patients with acute and severe hypoglycemia with coma, in order to avoid progressive changes in the condition, 50% glucose solution 50 ~ 100ml must be injected intravenously quickly and repeated 1 or 2 times if necessary until the patient is conscious, Following the intravenous drip of 10% glucose solution, the blood glucose was maintained at 8.3 to 11.1 mmol / L (150 to 200 mg / dl) and observed for 12 to 48 hours to facilitate the recovery of brain cells and prevent re-coma. If the above conditions are not met, those with low blood sugar and coma should not drink sugar and cause suffocation. At this time, they can be smeared with honey or jam on the patient's teeth, oral mucosa, or nasal feeding sugar. It is also one of the first aid measures.

(2) Glucagon application: It can be applied at the same time with 50% glucose solution after the onset of the disease. The general dose is 0.5 1.0mg. It can be injected subcutaneously or intramuscularly. It usually recovers in 10 ~ 30min and repeats the application if necessary.

(3) Adrenaline application: When severe hypoglycemia with shock does not meet the above conditions, it can be used in small and medium doses, but it should be used with caution in patients with hypertension and the elderly.

(4) Application of mannitol: After the above treatment, the blood sugar has recovered, but the coma time is longer than 30min. The hypoglycemic coma may be accompanied by cerebral edema. Intravenous infusion of 20% mannitol 40g can be considered. .

(5) Application of adrenal corticosteroids: After high glucose treatment, although the blood sugar has maintained 8.3 to 11.1 mmol / L, but has not been conscious for 15 to 30 minutes, in order to protect the brain, adrenal corticosteroids 100 can be applied. ~ 200mg (or dexamethasone 10mg) once every 4 ~ 8 hours, a total of 2 ~ 3 times.

Management of mild hypoglycemia or chronic hypoglycemia

(1) Symptomatic treatment: when the patient is currently taking oral hypoglycemic or insulin therapy. If you have symptoms or signs of palpitations, sweating, weakness, hunger or dizziness, and you are aware of the symptoms of hypoglycemia, immediately give biscuits, sugar cubes or syrup drinks (containing 10 to 20g of sugar), and monitor blood sugar levels. In general, it can be recovered in about 10-20 minutes to maintain a certain blood glucose level. If the condition is not easy to relieve, 50% glucose solution intravenous injection or 10% glucose solution intravenous drip can also be used.

(2) Diet: high-protein, high-fat, low-carbohydrate diet, and a small number of frequent meals to reduce the role of stimulation on insulin secretion.

Etiology treatment

Hypoglycemia is a disease of various factors. Among them, hypoglycemic drugs only cause some hypoglycemia, and still have diseases such as digestive system, endocrine metabolism, and several types of tumors. Severe hypoglycemia can also occur and should be treated accordingly.

Preventing hypoglycemia is the best treatment for diabetic hypoglycemia. The focus of prevention is to popularize diabetes education, to enable patients and their families to master the basic knowledge of diabetes, fully understand the symptoms of low blood sugar response, learn to self-help and self-made micro-method rapid blood glucose testing, develop good living habits, quit smoking and alcohol. For some reasons, you can adjust the dosage of insulin and other drugs in time when you cannot eat or the amount of exercise increases. When patients go out, they should bring food such as sweets and biscuits to help themselves. Specific methods can be done to remove the incentive and rational use of medicine.

Hypoglycemia is more common clinically, and hypoglycemia can be prevented. Onset of hypoglycemia can cause physical and mental health, especially damage to the central nervous system, and even death. Therefore, active prevention is particularly important. Because of the diversity and complexity of the causes of hypoglycemia, precautions vary widely.

1. Clinically, low blood glucose levels are more common in patients with diabetes treated with insulin and sulfonylurea drugs, especially for patients with liver and renal insufficiency. During the treatment, insulin and sulfonylurea drugs should be gradually increased. Avoid adding too fast. Eat on time after insulin or oral hypoglycemic agents. Should also avoid excessive exercise intensity. Also monitor blood glucose closely, especially during intensive insulin therapy. Diabetics and their families should be familiar with this response, early prevention, early detection and early management. Pay attention to the Somogyi phenomenon to avoid errors in insulin dose adjustment.

2. The dosage of hypoglycemic agents for the elderly should be cautious. Long-acting sulfonylureas, especially glibenclamide, should be used with caution. Early symptoms of hypoglycemia are not obvious. Once the symptoms occur, the symptoms are very serious. Intravenous glucose should be infused immediately, closely observe for at least 72 hours, and blood glucose concentration should be continuously monitored. Adjust treatment in time.

3. When using sulfonylureas for treatment, they may interact with other drugs. Some drugs such as salicylic acid preparations, sulfa drugs, butytaxel, chloramphenicol, guanethidine, and reserpine can be used to reduce Reduce the mechanism of sulfonylurea binding to plasma proteins, reduce drug metabolism in the liver and renal excretion, and enhance the hypoglycemic effect of sulfonylurea drugs. Therefore, care should be taken when using enhanced sulfonylureas to prevent hypoglycemia.

4. For those suspected of B cell tumors, starvation experiments and exercise experiments should be performed as soon as possible to determine the plasma insulin-C peptide concentration of plasma islets, and B-ultrasound, CT and other imaging tests should be performed. For early detection, early diagnosis and early surgical treatment. Can prevent the onset of hypoglycemia.

5. Explain the nature of the disease to patients with idiopathic functional hypoglycemia, and give psychoanalysis and comfort work. Encourage patients to exercise. Proper diet structure

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