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Shanghai Clinical Center for Endocrine and Metabolic Diseases - Healthy LivingHypoglycemia (Hypoglycemia) is a group by a variety of causes low blood glucose levels due to major clinical group of clinical symptoms was stimulated and the central sympathetic
Nervous system affected by a variety of manifestations of hypoglycemia. Low blood sugar can cause temporary brain dysfunction, long-term severe hypoglycemia can cause brain death. So the correct diagnosis andCause of low blood sugar can be divided into two categories according to onset time, fasting hypoglycemia and postprandial hypoglycemia (see Table 16)Drugs
Insulin, sulfonylurea drugs, alcohol, and Pan his meter, quinoline Ning, SASevere liver damage: severe hepatitis, liver cirrhosis with advanced liver cancer, liver congestion (heart failure, etc.), bile duct hepatitis
Abnormal liver enzymes: glycogen storage disease, galactosemia, hereditary fructose intolerance, fructose 16-bisphosphatase deficiency, lack of enzymes in gluconeogenesis, glycogen synthesis enzymes lack
Islet-derived
1. Insulinoma: adenoma, carcinoma
2. Islet cell proliferation1. Mesoderm: fibrosarcoma, leiomyosarcoma, mesothelioma, rhabdomyosarcoma, liposarcoma, neurofibroma, reticular cell sarcoma
2. Cancer: hepatocellular carcinoma, cholangiocarcinoma, stomach, cecum and colon cancer, adrenal cortical cancer, pancreatic cancer, lung cancer, breast cancerAdvanced renal failure (caused by non-dialysisAdrenal insufficiency
H


ypothyroidism
Above polyglandular dysfunctionStrenuous exerciseChronic diarrhea, malabsorption, prolonged feverII. Postprandial hypoglycemia (reactive)
1 nourish hypoglycemia: gastrectomy, gastrointestinal motility dysfunction syndrome
Early type 2 diabetes
Unexplained features of low blood sugarThe clinical symptoms of low blood sugar two groups: autonomic nervous response to low blood sugar and neural hypoglycemia. Low blood sugar signs and symptoms of autonomic nervous system, including sweating, hunger,
Pale, tremor, palpitations, anxiety, heart rate and systolic blood pressure increased. Neural hypoglycemia is the result of a lack of glucose in the central nervous system, can be expressed as vertigo
, Headache, distracted; when the cerebral cortex is affected, there may be hazy consciousness, orientation and discriminating loss, mental disorders, incoherent, drowsiness, tremor
; When the cortex is under the influence by the confusion, irritability, loss of sensation in turn, can dance like and allow both suck, grimace and other childish actions, tachycardia, pupil
Holes scattered large, pyramidal tract sign positive; which brain tired of tension in a timely clonic spasm, paroxysmal convulsions, axial skew, the pathological positive; when the extension of the brain is tired and in a timely manner
Severe coma, decerebrate rigidity, a variety of reflex, miosis, decreased muscle tone, shallow breathing, blood pressure, which lasted for a long time are often not easily reversed. blood glucose using glucose oxidase, normal fasting plasma glucose was 39-61mmol / L (70-110mg/dl0), whole blood glucose for the 36 -
53mmol / L (65-95mg/dl).
oral glucose tolerance test (OGTT) and 6 hours of oral glucose tolerance test
Normal fasting blood glucose 61mmol / L (110mg/dl), blood sugar 30-60 minutes after the serving of sugar reached a peak, but not more than 94mmol / L (160mg/dl), 2
Return to fasting levels or slightly higher, usually 66mmol / L (120mg/dl). Nourished patients with low blood sugar within 60 minutes of 30-that is significantly higher, reflecting the grape
Rapid absorption of sugar. Low blood sugar in patients with mild reactive hypoglycemia within 3-6 hours, 6 hours to go away. Served in patients with islet cell tumors had no significant increase in blood sugar after
, And quickly hypoglycemia, insulin levels were significantly increased.
The determination of low blood sugar and other related hormones
a normal fasting serum insulin measured under 5-25mU / L. Endogenous insulin-induced hypoglycemia increased fasting insulin levels are relatively high.
Hyperinsulinemia is also found in obesity, hypertension, insulin resisters Cushing psychosis, should be identified. Measured by radioimmunoassay of insulin immunoreactivity
Insulin, including proinsulin and its derivatives can not be based solely on clinical diagnosis of insulin results increased endogenous insulin disorder, but should be based on a low blood sugar
While there are insulin, C peptide / or evidence of increased insulin secretion only diagnosis
b Determination of serum C peptide C peptide and insulin determination of the meaning of the same, mainly reflecting the function of islet cells, representing endogenous insulin levels. More in the range
03-06nmol / L.
c proinsulin determination of total serum insulin in normal immune response to insulin 15%, but those of islet cell damage, insulin could have increased significantly, can be accounted for
Immune response to insulin, 25-100%. Contribute to the secretion of proinsulin determination of proinsulin to diagnose insulinoma based
d insulin or C peptide release test methods and the OGTT test, except that in fasting, serving both sugar and blood test after the time-islet 0,180
Prime or C peptide, to direct knowledge of the functional status of pancreatic islet cells. Serum insulin and C peptide peak and the peak blood glucose in line 30-60 minutes after the serving of sugar measured values of insulin
5-10 times for the fasting, C peptide is measured 5-6 times of fasting. Due to endogenous hyperinsulinemia in patients with low blood sugar, glucose tolerance curves are mostly flat, while insulin and
C peptide release curve is relatively high. Some of the insulin resistance of type 2 diabetes or secondary diabetes mellitus (Cushing's disease, broken-hypertrophy) who, insulin and C peptide release
Put curve is higher, but the glucose tolerance curve is also high, easy to distinguish.
e determination of insulin antibodies in patients with insulin autoimmune syndrome, elevated blood insulin antibody.
Provocation test
fasting test and extended test most of fasting hypoglycemia in patients with recurrent non-attack period, or if the fasting blood glucose within the normal range of fasting when the test can be used to help empty
The diagnosis of abdominal low blood sugar. May appear normal during the test ketone urine, pancreatic islet cell tumors by inhibition of ketone bodies due to excessive insulin production, it does not appear ketonuria. In addition,
Longer need to rely on a result of fasting gluconeogenesis to maintain blood glucose, and therefore, liver and pituitary - adrenal disease may also stimulate the hypoglycemia, the clinical need to be identified.
strenuous exercise increased endogenous insulin resistance syndrome in patients who are able to hunger, but once in motion can be induced by low blood sugar, so the sport can be used as insulin-stimulated tumor
Fat test. Test, can be strenuous exercise on the exercise machine for 30 minutes or until the test is unable to continue until every 5-10 minutes to measure blood sugar, insulin and C peptide. Low fasting
Blood glucose after exercise in patients with hypoglycemia, 20 minutes after exercise can not continue.
D860 test before and after oral administration of D860 2 , every 30 minutes to measure blood sugar and insulin total of 3 hours. Such as significantly increased plasma insulin significantly decreased blood glucose over the same time, under
Out standards, should consider the diagnosis of pancreatic islet cell tumors:
Plasma glucose decre 65% of baseline, or reduced to <17mmol / L (30mg/dl).
Blood sugar dropped to 22mmol / L (40mg/dl) below, which lasted 3 hours were not self-recover.
Rise of plasma insulin 60-130u/ml, or peak over 100mu/ml.
Positioning of the
Endogenous hyperinsulinism who should be the line of pancreatic B-, CT, MRI, and ultrasound of gastric
Microscope examination, in order to make diagnosis of tumor localization.
The diagnosis of low blood sugar
The diagnosis of low blood sugar symptoms and attack by the measured blood glucose concentration decreased. Hypoglycemia are nonspecific, although the possibility of providing a history of low blood sugar episodes
Is important, but the signs and symptoms alone can not make a diagnosis. Blood glucose is an important basis for diagnosis of low blood sugar, such as the onset of symptoms in patients with blood glu 39mmol / L may be
Diagnosis of exclusion, such as multiple <28mmol / L, can be confirmed. 60 years old diagnosed with hypoglycemia, blood sugar standards <30mmol/LL. diabetes, low blood sugar hypoglycemia in type 1 diabetes is due to inadequate insulin replacement therapy, causing the relative or absolute hyperinsulinemia due to
, Can occur in the following situations:
Excessive insulin dose, duration, or dosage forms of the selection of inappropriate.
Reduce sugar intake, such as overnight fasting or not eating on time and snacks.
Increase in insulin-dependent glucose utilization, such as the process in sport.
Decreased production of endogenous sugar, such as after drinking.
Increased sensitivity to insulin, such as to intensify the treatment, after exercise, after weight loss.
Decreased insulin clearance, such as renal failure. Low blood sugar may also occur in type 2 diabetes with sulfonylurea drugs or insulin treatment of individuals, and chlorine to glibenclamide
C urea sulfur caused the highest incidence of low blood sugar. Risk factors include increasing age, malnutrition, drug interactions with sulfonylureas, and liver or kidney disease, lead
Induced decrease in drug metabolism or clearance.
According to a history of diabetes patients, treatment and incentives, blood glucose, insulin, or hematuria
Determination of sulfonylurea drug concentration is not difficult to make a diagnosis.
addition to insulin and sulfonylurea drugs most likely to cause low blood sugar, the other drugs cause low blood sugar alcohol, such as quinine, salicylic acid and thiouracil accident
Cause low blood sugar. Alcohol metabolite acetaldehyde and acetic acid consumption of liver gluconeogenesis key factor nicotinamide adenine dinucleotide, so alcohol inhibition of gluconeogenesis
Can be induced by low blood sugar. Salicylic acid in relatively large doses (4-6 g / day) can reduce blood glucose levels, rare in adults, but children in common. Rare cases
Sulfonamides can produce low blood sugar, but the mechanism is unknown. Hypoglycemia is common in severe malaria, quinine induced in some patients is due to the relatively high insulin-induced insulin release
Hyperlipidemia induced factors.
liver disease endogenous glucose production primarily through glycogenolysis and gluconeogenesis of human liver cells in the original 14-80g/100 grams of sugar in liver tissue (
Fasting), the only supply of calories 12552kcal, however, a variety of gluconeogenesis enzymes in the liver is very active, so the liver in the maintenance of fasting blood glucose concentration is very important.
Gluconeogenesis enzymes in infants with congenital defects can cause low blood sugar, but the most common hepatic low blood sugar rapidly and in a large number of damaged liver tissue, such as toxic hepatitis, violence
Recurrent viral hepatitis, cholangitis and cholestasis, primary liver cancer and liver can also be found in extensive destruction of metastatic tumors of the liver tissue. Liver failure liver damage
More than 80% injury to hypoglycemia, gluconeogenesis due to liver damage and reduced insulin clearance, resulting in hyperinsulinemia due to relatively high.
chance of heart disease low blood sugar due to various reasons in patients with heart failure. The pathogenesis of hypoglycemia is unknown; may include liver congestion, gluconeogenesis
Raw material reduced liver hypoxia. History of heart disease, symptoms and signs can help diagnosis.
kidney disease in some patients with renal failure may be hypoglycemia, diabetes, renal failure patients with more hypoglycemia, because the renal clearance of insulin
In addition to lower, with the progress of renal failure, reduced demand for insulin, the insulin-induced hypoglycemia increased risk. Dialysis during or after dialysis can also occur
Low blood sugar. End-stage renal failure may be due to reduced renal gluconeogenesis caused by low blood sugar. History of kidney, kidney failure symptoms and signs of identification can be funded.
anterior pituitary hypofunction endocrine diseases, adrenal cortex, hypothyroidism, hypothyroidism and so easy to hypoglycemia (see the chapter)
islet tumors outside
Fasting hypoglycemia occasionally occurs in islets outside the tumor. According to the tumor origin of approximately three types of tissue.
Interstitial tissue tumors: fibrosarcoma, mesothelioma, rhabdoid tumor, spleen medullary sarcoma, liposarcoma, angiosarcoma, neurofibroma, and lymphosarcoma. C
More than half located in the retroperitoneum, one-third of the abdominal cavity, the other in the chest cavity. Although many tumors are malignant, but usually develops slowly, some of the tumor cut
In addition, the low blood sugar can be long-term relief.
Epithelial tumors, including liver cell tumor, adrenal tumor (usually malignant) and carcinoid tumor. Low blood sugar caused by the adrenal cortex may secrete or not secrete tumor of the skin
Quality of steroid hormones. Carcinoid tumor with low blood sugar can be confined to the ileum, bronchus, and pancreas. Stomach, colon, lung, breast, prostate, kidney, testis and pancreas gland
Cancer and other common cancer accidental bubble hypoglycemia.
Other tumors such as leukemia, lymphoma, multiple myeloma, melanoma, teratoma, or patients with pseudo-myxoma sometimes attacks low blood sugar. Leukemia
, Pseudo-contests of the occurrence of low blood sugar low blood sugar more often (glucose metabolism of in vitro caused by a large number of white blood cells). Low blood sugar false positive white blood cells can also be found in
Polycythemia. Low blood sugar on suspected false, if they were never the clinical symptoms of low blood sugar and blood plasma immediately after separation of the normal blood sugar levels were detected, namely,
Get confirmed. Islets outside the mechanism of tumor hypoglycemia more with increased rates of glucose metabolism. Part of the islets is due to hypoglycemia in patients with cancer outside the tumor produced
A large number of insulin-like growth factor -2 (IGF-2), in particular its precursor big IGF-2. IGF-2 of the RIA can be used for diagnosis of the disease.
endogenous hyperinsulinemia
Endogenous hyperinsulinemia is reduced when blood sugar levels under physiological concentration, the plasma insulin concentration can not be reduced accordingly. When the fasting blood glucose <25mmol / L (
<45mg/dl), whereas plasma insulin le 36pmol / L (6u/ml) or plasma C peptide le 02nmol / L (06ng/ml), can be diagnosed as endogenous
Of hyperinsulinemia.
Insulinoma Insulinoma is caused due to endogenous hyperinsulinemia, the most common cause of low blood sugar. Clinically, the recurrent fasting hypoglycemia
Characterized. Pathology mostly cell adenoma, a small number of cancer or hyperplasia. Sometimes associated with multiple endocrine neoplasia. 99% of insulinoma in the pancreas; different
Bit found in the ectopic pancreas insulinoma, including the duodenal wall, portal, and adjacent parts of the pancreas. More than the diameter of insulinoma in 05-5cm, up to
15cm. Almost all patients with low blood sugar treatment. 5-10% of insulinomas are malignant, and when there is time before the diagnosis of metastasis. In addition to sub-malignant insulinoma
Insulin secretion, but also the secretion of human chorionic gonadotropin, adrenocorticotropic hormone, serotonin, gastrin, glucagon, somatostatin and pancreatic polypeptide. Low blood
Sugar most likely occur in the morning and before breakfast, but can occur at any fasting state, such as, dinner before or during exercise. Low blood sugar, serum insulin levels are relatively
Increase in the diagnosis of insulinoma basic conditions. Of fasting hypoglycemia in patients suspected when there is suspected hypoglycemia, regardless of when, should be measured in time blood
Given glucose, insulin, C peptide and proinsulin, insulin antibodies and to collect blood and urine samples for determination of sulfonylurea screening. Determination if the patient provided blood samples
Show low blood sugar, should be repeated after overnight fasting blood glucose. If the overnight fasting glucose concentration <25mmol / L (<45mg/dl), serum insulin, C peptide, insulin
Relatively higher with the original diagnosis on the basic necessary conditions. Patients with the diagnosis difficult, there are indications line fasting test, fasting for 72 hours if still no episodes of hypoglycemia can be ruled out
Insulinoma.
autoimmune autoimmune hypoglycemia include fasting hypoglycemia, postprandial episodes of hypoglycemia, hyperinsulinemia and high insulin or insulin receptor
Binding antibody syndrome without a history of insulin injections. The patients with multiple and a genetic immune defects, may also suffer from other autoimmune related diseases
Such as hyperthyroidism due to Graves taking methimazole induced hypoglycemia. Disease patients is the presence of insulin antibodies, insulin antibody binding and no biological activity after non-students
Management effect, a large number of islet cells through the release of insulin to maintain normal blood sugar, resulting in antibody binding of insulin in vivo and the accumulation of form similar to the insulin resistance
Anti-hyperinsulinemia. Circulating antibodies play a role in a carrier, so with insulin antibody binding increased significantly, when combined with the antibody dissociation of insulin gradually
Or, in certain factors and antibodies suddenly under a lot of dissociation, the excess of free insulin, causing hypoglycemia. Insulin resistance due to low receptor stimulating antibody
Rare blood sugar, insulin and insulin receptor antibody with competing receptors, antibodies binding to the receptor stimulation of islet cell secretion of insulin induced hypoglycemia
. This class can be measured in serum insulin receptor stimulating antibodies.
Postprandial hypoglycemia
(1) Functional hypoglycemia occurs only after meals, especially within 4 hours after eating there,
Mild clinical manifestations of hypoglycemia, seizure time is short, to relieve itself, blood glucose less than 28mmol / L (50mg/dl). Patients may have nervousness, anxiety
, Irritability and so on. OGTT glucose displayed on the service after the 2-3 hour glucose fell to 28mmol / L ,4-5 hours or so pick-up.
(2) low blood sugar is nourishing the stomach of the patients after surgery postprandial hypoglycemia, is suffering from
Chyme after eating those fast moving into the small intestine (eg, gastrectomy, gastrointestinal resection, pyloroplasty, gastrostomy) to make rapid absorption of nutrients intake, or to promote pancreatic
Insulin secretion caused by the intestinal factor increases postprandial hyperinsulinemia early results, which is characterized by low blood sugar early in the meal, especially in the hours after a meal 15-3
Appears. Dumping syndrome, hypoglycemia must (abdominal account, vomiting, weakness) identification, the disease onset within 1 hour after meal.
(3) Early diabetes, fasting blood sugar normal, due to the delay of insulin secretion caused by low blood sugar, many attacks in the 4 hours after the meal, OGTT can help diagnosis.
Treatment of low blood sugar
1. Insulinoma should be actively positioning later surgery may be cured, low blood sugar before surgery in the attack to relieve the symptoms with high carbohydrates.
2 on the response to hypoglycemia in patients with recommended low-carbohydrate, high protein diet. Eating frequent meals and avoid simple sugar intake. Anticholinergic drugs on idiopathic low blood sugar may
Can be useful, but can cause some side effects. Propranolol to reduce the symptoms of low blood sugar after a meal. Pectin is considered to reduce postprandial hypoglycemia after gastrectomy attack. These
Surgical treatment can be applied in patients with symptoms of distal jejunum reversed intestinal segments.
3 on the endocrine function were low, at a reasonable hormone replacement, you can avoid hypoglycemia.



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