Diabetes in the elderly

Introduction to diabetes in the elderly The concept of age for senile diabetes is still not uniform. Domestically, the 1980-year-old diabetes patients over the age of 60 are called senile diabetes, while in some countries, the 65-year-old is the dividing line. According to the onset time, senile diabetes can be divided into the onset of diabetes in the elderly and the onset of young adults to the elderly. The former are almost all type 2 diabetes; the latter are mostly type 2 diabetes, but also include a very small number of patients with type 1 diabetes. In particular, people and old people are degraded physically and psychologically, and at the same time, it is easy to coexist with many patients. As a result, elderly diabetes is more complicated than the condition of young adult diabetes, and treatment is more difficult. Therefore, it is necessary to understand the many characteristics of senile diabetes in order to prevent it properly. basic knowledge The proportion of illness: 0.005% Susceptible people: the elderly Mode of infection: non-infectious Complications: hyperosmolar nonketotic hyperglycemia coma diabetic ketoacidosis lactic acidosis hypoglycemia myocardial infarction diabetic foot

The cause of diabetes in the elderly

Genetic factors (30%):

The results of various studies in China indicate that the genetic pattern of diabetes in Chinese is mainly multi-gene inheritance. Xiang Kunsan et al. based on the theory of polygenic-multifactorial disease, using large specimens, multiple group associations, and 485 cases in Shanghai and San Francisco, USA Restriction of restriction endonuclease length polymorphism (RFLP) and type 2 DM in 6 genes (or gene regions) in Chinese: insulin receptor gene, apolipoprotein B (Apo-B) Gene and apolipoprotein A1 (Apo-A1) genes are associated with the pathogenesis of type 2 DM in China. It has been widely recognized at home and abroad that insulin receptor gene alteration is the cause of insulin resistance in type 2 diabetes, and the relative deficiency of insulin. Type DM itself can be associated with lipid metabolism disorders, and further studies may reveal more relevant genes for diabetes and its complications in the elderly.

Changes in insulin secretion (10%):

When the human body gradually ages, the changes in the amount of insulin secretion are mixed. There are some reductions, some increase, some delays, and some are normal. Through literature analysis and clinical observation, it can be considered that these different results are different. The course of the disease, the initial diagnosis and short-term insulin levels are often close to normal, the disease is prolonged due to the gradual decline of islet B cell function, insulin levels may be reduced, at this time some patients need to supplement insulin.

Increased proinsulin (10%):

When the human body gradually ages, although the total insulin amount has a certain level, but the proinsulin is relatively increased, the activity of human proinsulin inhibiting hepatic glucose production is only 1/10 of that of insulin. Under the same basic state, the young people's proinsulin The total number of secretions is the same as that of the elderly; however, after glucose load, 22% of the elderly who can detect proinsulin in the blood circulation, while only 15% of young people have more proinsulin, which may be the cause of increased diabetes in the elderly. One.

Decreased basal metabolic rate (10%):

During the aging process, the basal metabolic rate gradually decreases, and the tissues involved in human activities, especially muscle metabolism, decrease, and the body's ability to use glucose decreases.

Increased fat (10%):

During the aging process of the human body, even if it is not overweight, the ratio of muscle tissue to fat is also changed due to the decrease of physical activity. The muscle is reduced from 47% to 36%, and fat is increased from 20% to 36%. Increases will reduce insulin sensitivity, which is one of the reasons for the increase in diabetes in the elderly.

Other factors (25%):

There are many factors that cause the onset of diabetes in elderly people with genetic basis. The important ones are as follows:

(1) Physical activity: Physical activity decreases with age, leading to a decrease in insulin sensitivity, atrophy of muscle disuse, and a decrease in the ability to take glucose.

(2) Diet: Epidemiological and experimental studies have confirmed that the increase in saturated fatty acids in food and the lack of dietary fiber (food too fine) will reduce insulin sensitivity and reduce glucose tolerance.

(3) Concentric obesity, insulin resistance: the centripetal distribution of fat (abdominal obesity, trunk obesity, upper body obesity or visceral obesity) refers to the enlargement of the omentum and mesenteric cells, free fatty acids (FFA) in the portal vein. A series of changes such as increased concentration, increased FFA in the portal vein will lead to increased VLDL, LDL production, increased hepatic glucose output, decreased insulin receptors on the liver cell membrane, decreased tyrosine kinase activity of the receptor, and possibly receptors. Defects, together with the same changes in surrounding tissues, constitute insulin resistance. At this time, the biological effects of insulin are significantly reduced, so there is compensatory hyperinsulinemia. For a long time, there will be hypofunction of islet B cells. On the basis of insulin resistance and compensatory hyperinsulinemia, an insulin resistance syndrome or syndrome X can occur. This syndrome existed before the formation of diabetes, and later diabetes became part of this syndrome. Syndrome includes centripetal obesity, hyperglycemia, hypertriglyceridemia with high LDL, hypertension, microalbuminuria, coronary heart disease and hyperuricemia.

(4) Islet amyloid deposition, islet B cell dysfunction: CecilRI was observed in 1909 when 90 cases of diabetic patients with pancreatic pathological changes, this amyloid deposition was observed, but mistakenly considered to be non-specific changes in the elderly, it The important relationship with type 2 DM is further enhanced by the research of Westermark P, Cooper GTS (1987), Clark A (1988) and later scholars.

90% of type 2 DM patients have this amyloid deposit in islets, which is significantly higher than the same age control group. One of the most important pathological changes of type 2 DM is the deposition of amyloid amyloid, B cells are significantly reduced, and A cells are relatively increased. Severe type 2 DM patients may have 90% of the insulin space occupied by amyloid deposits, which damage and replace B cells, leaving little left to replenish them with exogenous insulin. Isleta myloid peptide (IAPP), also known as amylin, also known as diabetes-related peptide (DAP), has been isolated from islet amyloid deposits. It is an islet B cytokine, which is released together with insulin under the action of glucose and other pro-secretory factors. The concentration of IAPP in the blood of obese people is higher. Animal experiments have confirmed that insulin can be inhibited from B cells when the acrease reaches a certain height in the blood circulation. Internal release, thereby reducing glucose tolerance, IAPP concentration is not increased in patients with type 2 DM who have good metabolic control, because this polypeptide can also reduce the insulin-stimulated glycogen synthesis rate and the glucose treatment rate of skeletal muscle cells. Therefore, it also has a special role in insulin resistance in patients with type 2 DM.

In summary, the pathogenesis and procedures of type 2 DM in the elderly can be summarized as follows: the genetic basis of insulin resistance and/or islet B cell dysfunction, plus age, relative overeating, lack of activity-induced obesity ( In particular, the cumulative effect of acquired environmental factors such as centripetal obesity or relative increase in body fat will cause a slight increase in glucose in the blood, and the toxic effects of chronic persistent hyperglycemia will further trigger and aggravate insulin. Resistance and/or islet B cell dysfunction, causing type 2 DM and various complications. In general, insulin resistance occurs mainly in abdominal obesity (increased insulin and C-peptide secretion after fasting and sugar loading). Can cause islet B cell dysfunction; in non-obese people mainly occurs islet B cell dysfunction, also insulin resistance.

Pathogenesis

The pathogenesis of type 2 diabetes is very complicated and has not yet been fully elucidated. According to the accumulated knowledge in recent decades, it mainly focuses on the defects of islet function, especially the defects of B cell insulin secretion and the deficiency of insulin, namely insulin resistance. In recent years, scholars at home and abroad have begun to notice that in addition to the target organs of the pancreas and insulin, it is likely that the central nervous system plays a role in the pathogenesis of type 2 diabetes.

1. Islet function defect

(1) B cell function defects:

Defects in insulin secretion: Since the establishment of radioimmunoassay in the late 1950s, scholars all over the world have conducted a lot of research on insulin secretion of B cells under physiological and pathological conditions, and have gained more understanding of insulin secretion defects. Summarized as follows:

1 Insufficient insulin secretion: Before the mid-to-late 1980s, it was generally believed that the secretion of type 2 diabetes, especially early insulin, was not lacking but excessive, that is, hyperinsulinemia was present. Until 1989, Temple used net insulin assay. (rather than IRI) patients with type 2 diabetes, regardless of IRI is normal or increased, plasma free insulin levels are reduced, in recent years, more units using pre-insulin and free insulin assays prove Temple's conclusion, the so-called insulin blood in the past The disease is actually hyperpro-insulinemia, especially in the fasting 31,32 before the insulin showed a disproportionate increase, that is, the pre-insulin/insulin ratio (PI/I) increased, but when compared with the NGT pair, the true insulin level is still It is reduced. Some studies have suggested that the PI/I ratio is a sign reflecting pre-insulin processing and insulin secretion defects, and its increase has a predictive effect on the occurrence of type 2 diabetes.

2 abnormal insulin secretion mode is the normal mode of insulin loss of physiological secretion, which includes: selective loss or slow response to glucose stimulation, but retains the response to amino acid stimulation, the first phase of glucose stimulation disappears, the first 2 phase secretion delay; pulse number of insulin secretion, frequency and amplitude changes, rhythm disorder, etc., which leads to insulin level rise and fall and blood glucose levels are not synchronized.

3 Insulin gene mutation synthesis of biologically inactive, structurally abnormal insulin, such as Chicago variant insulin, Tokyo variant insulin, etc., but this situation is rare in type 2 diabetes.

The causes of B cell insulin secretion defects include two aspects: one is hereditary, such as Polnsky et al., which is caused by "B cell gene program control". The most powerful supporting evidence is that pre-diabetes is normal in blood glucose, even in normal blood sugar. Defects in insulin secretion in the first-degree relatives are already present. This deficiency of insulin secretion is called "primary failure" of B cells, and the other factor is acquired. It is caused by hyperglycemia or insulin resistance, that is, hyperglycemia to B. The toxic effect of cells (glucose poisoning), lowering blood sugar can improve B cell function. In recent years, abnormal increase of plasma free fatty acid (FFA) can also inhibit insulin secretion (lipotoxicity). This insulin secretion defect should be insulin resistance. Aggressive decompensation, also known as B cell stress failure.

In the pathogenesis of type 2 diabetes, genetic factors may interact with acquired factors, which together lead to B cell insulin secretion disorders.

The abnormal secretion of amylin has long been known to have a large amount of amyloid deposits in the islets of type 2 diabetes, but its source and mechanism are unknown. It was not until the 1980s that the 37 amino acid polypeptide B cells were synthesized and secreted. It is named as amyloid-like peptide (IAPP) or amylin (amylim), which is secreted together with insulin. Its molecular ratio (IAPP/insulin) in B cells is 0.1-0.05, and B cells are caused by genetic or acquired factors. When the ratio of IAPP/insulin is increased, the fibers of amylin can be deposited on the endoplasmic reticulum or Golgi of B cells to cause apoptosis of B cells, leading to diabetes.

However, in human trials, this hypothesis has not been fully substantiated. Tasaka et al recently reported 44 cases of type 2 diabetes autopsy. They measured serum IRI, C-peptide, blood glucose and serum from 3 years before death to 1 month before death. Amylin levels, death pancreatic tail stained with Congo red and Masson, the patients were divided into IAPP positive and negative groups, compared with IRI, C peptide, blood glucose levels, except 1 case of islet IAPP deposition, high blood IAPP concentration In addition to the decrease in insulin levels, the rest did not find a positive relationship. Therefore, the effect of IAPP on B cell insulin secretion is still controversial.

In addition, IAPP also inhibits the secretion of arginine-stimulated glucagon, but does not inhibit the response of glucagon increased by hypoglycemia. In addition, IAPP also has the effect of inhibiting gastric emptying.

In conclusion, the role of IAPP in the pathogenesis of type 2 diabetes remains unclear and needs further study.

(2) A cells: A cells show increased glucagon secretion in type 2 diabetes, and elevated glucagon promotes the conversion of amino acids and free fatty acids (FFA) to glucose (gluconeogenesis), antagonizing insulin, and increasing sputumFA levels, inhibition of insulin secretion and the role of insulin, as well as ketogenic effects, can lead to or aggravate insulin resistance.

In addition, recent studies have found that pancreatic neuropeptide Y (NPY) secretion is increased during diabetes. Pancreatic NPY is mainly secreted by A cells. It also has an inhibitory effect on insulin secretion. The role of NPY in the pathogenesis of diabetes is still unclear. It plays a role in the onset.

(3) islet dysfunction: In addition to A, B cells secreted by the above hormones, islet secretion is still secreted in the islet (SS, D cells), pancreatic polypeptide (PP, PP cells) and pancreatic peptides, etc., in islets The crosstalking interaction between these hormones forms an imbalance of endocrine regulation in the island, and this imbalance of regulation may have an impact on the onset of diabetes.

2. Insulin resistance

The decrease in insulin action is the decrease in insulin sensitivity (SI) of insulin target cells, also known as insulin resistance. To be precise, the physiological amount of insulin acts on target cells, and its effect is lower than normal; or it is intended to achieve normal physiological effects. Ultra-physiological insulin is required, and insulin resistance mainly occurs in liver, skeletal muscle and fat cells, which are described separately.

(1) Hepatic insulin resistance: Most of insulin enters the portal vein after B cell secretion, more than 50% is liver uptake, and type 2 diabetes patients have reduced hepatic insulin intake, which can not inhibit hepatic sugar production and output, and thus fasting blood glucose is elevated.

(2) Muscle resistance: mainly manifested as postprandial insulin-mediated glucose uptake and utilization, because the amount of insulin required to stimulate glucose uptake and utilization by muscle cells is much greater than that of suppressing glycogen production and output, so muscle Insulin resistance is the first to manifest in the onset of diabetes, which explains the reason why fasting blood glucose is still in the normal range and the postprandial blood glucose has increased in early or early stages of diabetes. Although some cases have not reached the level of diabetes, glucose tolerance has been reduced. This also shows that in the early diabetes screening 2h postprandial blood glucose is more sensitive than fasting blood glucose, so WHO and many diabetes experts in the world recommend the use of two indicators of fasting and postprandial 2h blood glucose in the screening of diabetics, disagree with ADA The use of fasting blood glucose screening alone, because the latter is likely to cause more missed diagnosis, but sometimes the opposite phenomenon of fasting blood glucose and postprandial blood glucose is not high, which may be caused by tissue heterogeneity of insulin resistance.

(3) Fat resistance: The decrease of insulin action in fat cells leads to accelerated lipolysis, increased blood free fatty acid (FFA) levels, and elevated blood FFA levels have the following adverse effects on the human body:

1 inhibits B cell glucose stimulated insulin secretion.

2 inhibit the binding of hepatocytes to insulin, and impair the inhibitory effect of insulin on hepatic gluconeogenesis and output.

3 inhibits the activity of the muscle cell glucose transporter (Glut4), and thus insulin-mediated glucose muscle uptake and utilization (glucose oxidation and muscle glycogen synthesis) are reduced.

4 provides the liver with a raw sugar substrate to promote hepatic gluconeogenesis. Therefore, the role of elevated FFA levels in insulin resistance and the onset of type 2 diabetes is receiving increasing attention.

In addition, tumor necrosis factor (TNF-) and leptin secreted by fat cells are elevated in diabetic patients and animals, and produce insulin resistance, which may also play a role in the pathogenesis of type 2 diabetes.

The link of insulin resistance is thought to occur before the binding of insulin to the receptor, or to the level of the receptor or the receptor. In this complicated process, there are many links, and many links and effects have not been clarified. Insulin antibody formation, insulin molecular structure abnormality and insulin degradation tachycardia (pre-receptor or receptor level), insulin receptor gene mutations cause receptor tyrosine kinase autophosphorylation disorder, receptor synthesis, transformation, binding and degradation Etc. (receptor level) and insulin receptor substrate family (IRS) gene mutations resulted in decreased IRS tyrosine phosphorylation and increased serine phosphorylation, decreased IRS-1 associated PI-3 kinase activity, PKC pathway activation, hexosamine (hexosamine) pathway activation, Glut synthesis and translocation disorders, and decreased intracellular glycogen synthase activity (after receptor).

3. The relationship between insulin secretion defects and insulin resistance in type 2 diabetes

(1) Insulin secretion deficiency and insulin resistance in the pathogenesis of type 2 diabetes: long-term relationship between insulin secretion defects and insulin resistance in the pathogenesis of type 2 diabetes, ie who is the primary who is secondary, or equally important There have been debates on various issues, but from the recent mouse knockont experiments, the above controversial questions can be answered, for example, homozygous mice that knock out the ISSI gene produce hyperinsulinemia and insulin resistance when they are old. Glucose tolerance is normal, and the hybrid mice that knock out the B cell glucokinase (GK) gene have reduced insulin secretion when they are old, and the glucose tolerance is reduced. At the same time, the IRS-1 and GK genes are knocked out to develop dominant diabetes. Therefore, it is currently considered that both must be available in the pathogenesis of diabetes. At the same time, recent studies have concluded that B cell deficiency and insulin resistance are interdependent and inseparable. When insulin sensitivity is reduced, B cell secretion is compensated. Increased sexual (hyperinsulinemia) to overcome fasting hyperglycemia (early); when insulin resistance is further aggravated, B cells increase compensatory capacity Overcoming postprandial hyperglycemia (post-prandial hyperinsulinemia), blood glucose rises more than 78mmol/L 2h after meal, indicating that B cells lose compensatory ability. This relationship is expressed by the mathematical model "disposition index". It is the product of insulin sensitivity × insulin secretion, and it is difficult to assess mild insulin resistance because it masks the increase in glucose response (compensation) by B cells; likewise, when insulin sensitivity decreases, B cell compensation Increased sexual secretion also masks the potential for insulin deficiency, so attention should be paid to clinical considerations of insulin resistance and B cell function.

(2) The causal relationship between B cell function deficiency and insulin resistance and type 2 diabetes: At present, textbooks and many literatures have considered both of them to be the cause of diabetes, but in fact many of the past animal experiments and clinical studies have not been answered. This problem, because these findings are obtained from animal models of diabetes, or from diabetic patients, the only way to solve this problem is to study the natural history of diabetes, that is, type 2 with normal blood sugar or glucose tolerance. Diabetes can be a high-risk group of gestational diabetes, preferably the first-degree relatives of NGT in diabetic patients as observation objects, long-term dynamic observation of their insulin sensitivity and B cell function changes until the development of diabetes.

From the current data, it seems that these high-risk individuals have a phenomenon of decreased insulin secretion or decreased insulin sensitivity during the NGT stage, and the main factor for the conversion from NGT to IGT is B cell function reduction plus insulin resistance, and by IGT The main factor in the conversion of type 2 diabetes is a further increase in B cell function.

Elderly diabetes prevention

Prevention of diabetes can be divided into three levels of prevention:

Primary prevention: Use drugs or publicity education and diet exercise interventions to reduce the risk of developing diabetes in susceptible populations.

Secondary prevention: Various measures are taken to reduce diabetes in people at high risk of diabetes (especially in impaired glucose tolerance, IGT population).

Tertiary prevention: Effectively regulate the diabetes that has occurred, and scientific treatment prevents or delays the occurrence of various complications of diabetes.

The prevention of diabetes in grade 1, 2, and 3 is far less straightforward than the prevention of other diseases. Its particularity lies in the complexity of the cause of diabetes. In the case of type 2 DM, the vast majority of cases belong to the category of insulin resistance syndrome. Hypertension, hyperlipoproteinemia, coronary heart disease, stroke, which can be a diabetic complication can actually occur before clinical diabetes occurs (as a complication of a disease, theoretically it should occur after the disease appears), In this way, the prevention of diabetic complications should be effective before the diagnosis of diabetes. Therefore, the second and third levels of prevention of diabetes are difficult to distinguish in actual work, and secondary prevention also plays the role of tertiary prevention. More important and effective than the latter.

Older diabetes is basically type 2 diabetes. The pathogenesis of type 2 DM is affected by genes, aging and adverse environmental factors. Except for a small part of B cell insulin secretion deficiency, most of the other are insulin resistance with insufficient insulin secretion. Immature, aging can not be reversed, so improving environmental factors is not conducive to the occurrence of insulin resistance in order to reduce the risk of developing diabetes, can be in 1 type 2 DM family history or 2 birth low weight or 3 obesity (BMI 25 Especially central obesity; waist, hip ratio male 0.9, female 0.85) or 4 lifestyle changes from physical activity to more physical activity (such as occupation, position change, retirement, etc.) or 5 existing hypertension, For people with high lipoprotein disease or 6 with a history of gestational diabetes, those with normal glucose tolerance should take the following preventive measures.

1 Reasonable diet (quality and quantity).

2 Encourage appropriate physical activity.

3 maintain the ideal weight, obese people lose weight, birth low weight or for the children should pay attention to not obesity.

4 treatment of hypertension to avoid the use of drugs that reduce the body's insulin sensitivity.

Elderly diabetic complications Complications hyperosmotic non-ketotic hyperglycemia coma diabetic ketoacidosis lactic acidosis hypoglycemia myocardial infarction diabetic foot

Older people with diabetes can also have various acute and chronic complications of diabetes.

Hyperosmolar nonketotic diabetic coma

Mainly seen in the elderly, often without a history of diabetes, even if the condition is mild, a large part of the elderly diabetes is type 2 diabetes, can secrete a certain amount of insulin, can prevent excessive formation of ketone bodies, but in the case of stress, With severe water loss (the elderly thirst central sensitivity is reduced, can not actively drink water), due to cerebrovascular accident use dehydration, diuretics, with diarrhea, vomiting, eating less, mis-compensation of hypertonic glucose can induce this disease, manifested as Severe dehydration, often accompanied by disturbance of consciousness, the main basis for diagnosis is blood glucose >33.3mmol / L (600mg / dl), effective serum osmotic pressure 2 ([Na ] [K ])mmol / L blood glucose (mg / dl) / 18 320mOsm/kg, the main points of treatment are to correct dehydration, correct hyperosmolar state, and supplement small doses of insulin.

2. Diabetic ketoacidosis and lactic acidosis

Although most of the elderly diabetes is type 2 diabetes, ketoacidosis can be induced under stress and other conditions of infection, and the condition is serious and the prognosis is poor. Lactic acidosis often occurs in the elderly. The main reason is that the elderly often have heart. , lung, liver, kidney dysfunction, taking disaccharide hypoglycemic agents (especially hypoglycemic), easily lead to tissue hypoxia, increased production of lactic acid, excretion disorders, poor prognosis.

3. Low blood sugar

Common in the elderly and poorly tolerant to hypoglycemia, many studies have found that the risk of severe or lethal hypoglycemia caused by oral hypoglycemic agents or insulin therapy increases exponentially with age, and older adults and young adults Compared with the most important insulin antagonists, the release of glucagon and epinephrine is reduced. In elderly patients with diabetes, hypoglycemia often lacks symptoms of autonomic stimulation such as palpitation and sweating.

4. Diabetic microangiopathy

Retinopathy and nephropathy are common, and their severity is mainly determined by the course of diabetes and long-term glycemic control.

5. Diabetic macroangiopathy

Including cerebrovascular disease, myocardial infarction and lower extremity vascular disease, cerebrovascular disease is mainly occlusive disease; myocardial infarction symptoms can be atypical, painless more common (heart, cerebrovascular complications have a worse prognosis than younger people), lower limbs Vascular lesions are part of generalized arteriosclerosis in the body, and intermittent claudication occurs in severe cases.

6. Other

Neuropathy is also very common. Lower extremity pain is aggravated at night, affecting sleep. "Diabetes foot" is a combination of lower limb nerves, vascular disease and infection. It is characterized by trauma, ulceration, infection, gangrene, and rapid development of lesions. Bone, therefore, diabetic patients should pay special attention to the protection of the feet, keep clean, shoes and socks soft, avoid any trauma, and timely treatment.

For the prevention and treatment of chronic complications of senile diabetes, the first priority is to actively control the above-mentioned high-risk factors, including:

1 Early detection of diabetes and IGT and active treatment.

2 In order to block the non-enzymatic saccharification process of protein, in recent years, some people advocate the use of antioxidants, such as vitamin C 1.0g / d, vitamin E 300 ~ 500mg / d, or selenium-containing compounds, anti-glycation agents such as amino guanidine tested for chronic complications It has a palliative effect; aspirin has both anticoagulant and anti-glycation effects; traditional Chinese medicines such as baicalin and quercetin also have certain anti-glycation effects.

3 Active control of high blood pressure.

4 For patients with hyperinsulinemia, it is not suitable to use sulfonylureas, and metformin is preferred.

5 lower blood lipids.

6 obese people lose weight.

7 smoking, etc.

Symptoms of diabetes in the elderly Common symptoms Drinking polyuria Diabetes ketoacidosis Diabetes Glucose increased weight loss, fatigue, weakness, impaired glucose tolerance, fatigue

Clinical manifestation

With the aging of the world's population, the absolute number of elderly people and the proportion of the entire population are growing rapidly. It is well known that the prevention and treatment of the latter type of diseases is caused by the gradual reduction of infectious diseases and the increase of chronic non-communicable diseases. More and more prominent, this latter type of diseases include cardiovascular and cerebrovascular diseases, high blood pressure, kidney disease and diabetes. Most of the harmed people are middle-aged and elderly people. Because these diseases are long-term, most of them are in adulthood and gradually accumulate in the middle to old age. The prevalence rate is getting higher and higher. With the improvement of people's living and medical conditions, life expectancy has been significantly prolonged. Coupled with the physiological and metabolic characteristics of middle-aged and old people, the biological aging and dysfunction of various tissues and organs are more likely to suffer. The result of the above-mentioned diseases is naturally that the elderly population has formed a high incidence of chronic non-communicable diseases. These diseases have brought pain to patients, affecting the quality of life and causing enormous economic burden on individuals and society, and have attracted people's attention.

Developed countries generally stipulate that the age of 65 is older, while developing countries (such as China and Asia-Pacific) propose older people over the age of 60, mainly because the average life expectancy of Western countries is longer (70-80 years old). Developing countries are shorter (such as Chinese males 67.32 years old, female 70.63 years old, published in 1987).

Diabetes in the elderly refers to diabetes in the elderly. People over the age of 60 have diabetes. Whenever diabetes occurs, they are elderly diabetics. Most elderly diabetics have diabetes before the age of 60, but new in the old age. Diagnosis or census found that people with early-onset diabetes are not uncommon, and aging itself is one of the high-risk factors for type 2 diabetes.

Studies at home and abroad have shown that with age, fasting blood glucose and postprandial blood glucose have an increasing trend. For the elderly over 50 years old, for every 10 years of age, fasting blood glucose can be increased by 0.056~0.112mmol/L, 1h after meal. Can increase 0.84mmol / L, so a 70 ~ 80-year-old elderly 1h postprandial blood glucose can be as high as 11 ~ 12mmol / L, and 2h is still below 8.9mmol / L, this high blood sugar tendency may be insufficient with islet B cell function It is related to the decrease of systemic metabolic rate. Some studies have shown that in the elderly, B cells secrete insulin with a decrease in the secretion of the first phase and an increase in pre-insulin secretion or an increase in the ratio of pre-insulin/insulin. Phenomenon, so the elderly are easy to gain weight, a little careless, eating too much will be easy to gain weight, especially the abdomen fat, fat will increase insulin resistance, can reduce the use of glucose, glycogen production and output increase, resulting in high blood sugar tendency; Stimulates the increase of B cells, insulin secretion (hyperinsulinemia), and over time, it can cause the compensatory function of B cells to stimulate glucose stimulation, and finally IGTtype 2 diabetes Type 2 diabetes and other age groups is similar, older and more obese people with diabetes have more severe insulin resistance, non-obese subjects with B cell-based functional defects.

(1) No symptoms of diabetes.

(2) Symptoms are not specific and atypical:

1 tired and weak.

2 unclear (mental confusisn).

3 physical activity disorders.

4 mouth rap.

5 weight loss.

(3) Symptoms of other diseases that are present at the same time (especially cardiovascular and cerebrovascular diseases, gangrene and neurological symptoms).

(4) has a typical "three more than one less" symptoms.

(5) Non-ketotic hyperosmolar syndrome.

(6) Diabetic ketoacidosis.

2. Clinical features

The clinical manifestations of elderly diabetic patients are very atypical, often missed diagnosis, misdiagnosis, according to their clinical manifestations can be divided into the following categories:

(1) Insidious onset, more than three symptoms are not obvious, often missed diagnosis and misdiagnosis: many elderly patients with diabetes are not obvious, more than half of the patients were found in the census or accidentally checked blood sugar, due to the elderly The threshold of renal sugar increases with age, hyperosmolar diuresis is not sensitive, and the symptoms of polyuria are not obvious. Sometimes polyuria is mistaken for drinking tea habit or prostatic hypertrophy, and polydipsia is not in the elderly. Obviously, many drinks are not prominent. Diabetic non-ketotic hyperosmolar syndrome is common in elderly diabetic patients. Sometimes it is found as a diabetic after hospitalization due to hyperosmolar coma. The only symptom of some elderly diabetic patients is unexplained wasting. Or unexplained psychological and mental disorders, and often misdiagnosed as "malignant tumors" or "psychiatric diseases", the elderly diagnosed with cataracts by an ophthalmologist, and found diabetic retinopathy, began to refer to internal medicine to make a diagnosis of diabetes.

(2) Complications, comorbidities, rapid progress, high mortality: Most elderly patients with diabetes have different degrees of complications, especially cardiovascular and cerebrovascular, kidney, nervous system and eye diseases, and It is the main cause of disability and death, because:

1 The elderly generally have degeneration of tissues and organs, decreased metabolism and dysfunction, and are prone to chronic non-communicable diseases (such as hypertension, cardiovascular and cerebrovascular atherosclerotic diseases, kidney diseases, cataracts, peripheral neuropathy, etc.), diabetes Aggravation accelerates the development of these lesions.

2 The elderly patients with diabetes have a long course of disease, mostly in 10 to 20 years. The complications of diabetes are known to be related to the course of the disease.

3 According to the "common soil" theory, diabetes, hypertension, cardiovascular and cerebrovascular diseases have a common basis (such as genetic association) and pathogenesis (environmental factors and insulin resistance, hyperlipidemia, etc.), so diabetes in the elderly population The rate is high, and the prevalence of other cardiovascular and cerebrovascular, kidney, and nervous systems is also high. At the same time, there are many people with diabetes and these chronic diseases, more than the general non-elderly group.

4 In the elderly with diabetes, autonomic nervous system damage is quite common, manifested as abnormal heart rhythm changes, orthostatic hypotension, painless myocardial infarction, asymptomatic hypoglycemia and dysuria. These lesions often mask the condition, leading to misdiagnosis and delay of the disease. even death.

5 non-ketotic hyperosmolar syndrome almost all occur in elderly diabetic patients, if not diagnosed and treated, the mortality rate can be as high as 40%.

6 Cerebrovascular accidents, especially cerebral infarction, are more common in elderly diabetic patients than in non-elderly diabetics. Many patients lack self-consciousness (diagnosed by CT or NMB) and can occur repeatedly or even lead to death.

7 elderly people with diabetes have more infectious diseases than non-elderly diabetics, mainly because of the decline of immune function in the elderly, poor control of blood glucose (see below), decreased cellular immune function and multiple vascular complications. As a result, for example, Wang Shuping (1995) reported that the prevalence of concurrent infection in elderly diabetic patients was high (51.4%), significantly higher than non-elderly diabetic group (26.3%, P < 0.001), the most common lung infection, followed by For urinary tract infections, biliary tract infections and tuberculosis, the mortality rate due to infection was significantly higher in the elderly (23.8%) than in the non-elderly group (14.4%, P<0.05). , fungal) and diabetic foot infections are also quite common, and failure to treat them promptly and effectively can lead to serious consequences.

(3) Poor blood glucose control: poor glycemic control affects cognitive dysfunction in elderly diabetic patients, the incidence of depression is high, and emotional changes are unstable. Meneilly et al. (1993) made mental psychology for elderly diabetic patients with poor metabolic control. The trial, after 6 months of improvement in metabolic control, found that patients improved in terms of emotion, concentration, concentration, recent memory, and rational thinking. Gradman et al (1993) found that improved glycemic control made older diabetics Learning ability and memory are improved. Berger believes that fasting blood glucose in elderly diabetic patients is often between 8.1 and 12.3 mmol/L. It is caused by insulin deficiency. Although there are no symptoms of diabetes, some people have psychiatric symptoms such as depression and apathy. Insufficiency, fatigue, insomnia, irritability, etc. are caused by insulin deficiency. It can be treated with small doses of insulin. It can receive obvious effects. The patient's mental state and self-perception are obviously improved. The blood sugar drop allows patients to relax their dietary restrictions and compare them. Pleasant life.

However, due to the influence of many psychosocial factors, it is quite difficult, unstable, and arbitrarily adjusted for some elderly diabetics. Due to poor memory, lack of compliance, timely medication, injection and blood glucose are difficult to guarantee, the insulin is not used. Use, the person who eats 3 times a day often forgets to take a certain medication, and some people have conducted a sample survey to find that elderly people with diabetes really insist on treatment and do their own (family) health care to make blood sugar control meet the requirements of less than 1/4, some The patient's long-term increase in blood glucose was not controlled.

3. Characteristics of senile diabetes

(1) The etiology and morbidity characteristics of DM in the elderly:

1 First, the ageing of the metabolic organs of the elderly, atrophy and weight loss, increased islet transparency in the elderly, the number of B cells in the elderly decreased, A cells increased relatively, D cells accounted for 20% (normal 3%).

2 The common arteriosclerosis in the elderly accounted for 34.6%.

3 The damage of nucleic acid substances increases with age, and the repair function is reduced.

4 lifestyle: high sugar intake, physical activity reduction, abdominal obesity.

5 combined with high blood pressure, high blood lipids.

6 drugs such as thiazides.

(2) Glucose tolerance and aging hyperglycemia in the elderly: Studies at home and abroad have shown that the blood glucose level of the elderly is higher than that of other age groups, and has nothing to do with gender, but it is definitely related to age and begins to appear in the years before and after 60 years old. Among them, the increase of blood glucose increases with age. Except for dominant diabetes, about 10% to 30% of the elderly have abnormal carbohydrate tolerance. The characteristics of aging hyperglycemia are that the fasting blood glucose increases by 0.11mmol every 10 years. /L (2mg/dl), 2h postprandial blood glucose level increased by 0.44~0.11mmol/L (8~20mg/dl) every 10 years, the specific performance is:

1 Fasting blood glucose levels increase less, and the range increases from 0.06 to 0.11 mmol/L (1 to 2 mg/dl) every 10 years after 30 to 40 years old. This small change can only be found when a large population is detected;

The postprandial 2h blood glucose level after 230 to 40 years old increased by 0.44~1.11mmol/L (8-20mg/dl) every 10 years. This change is easy to measure, so a 40-year-old woman has a fasting blood glucose level of 5.0. Mmmol / L (90mg / dl), 2h postprandial blood glucose 7.2mmol / L (130mg / dl), when she is 80 years old, its fasting blood glucose level may reach 5.4mmol / L (98mg / dl), almost no clinical significance However, the blood glucose level after 2 hours of meal can reach 10.6-11.7mmol/L (190-210mg/dl), which is significantly increased.

It is important to clarify whether age-related hyperglycemia is part of the normal aging process, whether it is a benign change, or a pathological phenomenon, and whether treatment is needed. Studies have shown that this hyperglycemia is by no means benign, apparently pathological, which leads to an increase in HbAIC, causing major vascular complications, and the Bedford study and other studies have demonstrated a marked increase in coronary artery disease in elderly hyperglycemia.

Age-related is an independent factor that leads to a decrease in glucose tolerance in the elderly. Other factors associated with this are decreased insulin synthesis and/or secretion, abnormal effects of receptors or receptors or intracellular insulin, and decreased glucose utilization in peripheral tissues. Changes in body composition, changes in dietary structure, decreased physical activity, and significant changes in glucose-stimulated insulin secretion in the elderly, and decreased insulin biosynthesis in islet cells in older animals. In vitro studies have shown that insulin levels in older animals are increased. However, inhibition of insulin secretion indicates that the number of B cells in islets increases, and the insulin content in single islet B cells increases. The dynamic study of insulin secretion shows that the secretion of the aged rats is slow and the release time is slightly delayed; the second phase is secreted. Significantly lower, these results are similar to the results of human mild type 2 diabetes studies. There is no consistent consensus on the role of insulin secretion changes in human aging hyperglycemia. Different studies have found that insulin secretion is increased in the elderly, resulting in results The reason for the difference may be related to the sampling method. Select the group and related subjects standards are not uniform.

Insulin antagonism is the main cause of impaired glucose tolerance in the elderly. Even if the blood glucose is normal, there is insulin antagonism in the elderly. The reason may be double. First, the elderly have slight intracellular or post-receptor defects, which interfere with glucose. Ingestion and metabolism; Secondly, with the increase of age, the composition of the body changes significantly, the muscles and other sugar storage tissues are reduced, and the normal males with thin body shape are 45% of the body weight at the age of 25, and the muscles only account for the body weight at the age of 70. 27%, the reduction of muscle is consistent with the increase of fat, excessive adipose tissue increases the antagonism of insulin, causes high insulin degradation, and the insulin clearance rate also decreases. In addition, the enzyme activity decreases during glucose metabolism in the elderly. It may also be related to aging high blood sugar.

4. Classification

In the past ten years, due to the etiology of diabetes, molecular biology and immunology research has made a lot of breakthroughs. In 1997, the American Diabetes Association (ADA) Committee reported that it has updated the classification and diagnostic criteria for diabetes. Recommended, and approved by the World Health Organization (WHO) Advisory Committee in 1998 and 1999, the latest classification abolished the names of IDDM and NIDDM used in the past and replaced the past type I and type II diabetes with Arabic 1 and 2. The Roman characters I and II canceled the nutritionally-associated diabetes (MRDM) and classified it as a special type of diabetes in the pancreatic exocrine disease.

(1) Type 1 diabetes: Islet B cell destruction usually leads to absolute deficiency of insulin.

1 autoimmune: acute, delayed.

2 idiopathic.

(2)2

(3)

B

(4)(GDM)

OGTT1980WHOWHO19814(1/2h1h1)32(IGT)

1.()

(1)(Somgyi)WHOFolinWu()

(2)3.86.1mmol/L2h4.47.8mmol/L1h()5.68.9mmol/L50101h0.5mmol/L(10mg/dl)801h10mmol/L

IGT(impaired glucore tolerance)IGT432IGT15.3%31.7%IGT53.0%62/3IGT

2.

(1)60min-±++++++++++(14)

-±(<7.80.5mmol/L);2h(<12mmol/L)

12mmol/L

(2)mg/Lg/L;g/24h24h<0.5<25g>25g>40g

(3)OGGT(10mmol/L)()

3.(HbA1HbA1c)

(glycosylated hemoglobinGHb)();GHbGHb

HbA1cHbA1

XCTB

Diagnostic criteria

1994,IGT

19977(IDF)

1.11.1mmol/L

2.7.0mmol/L8h3.OGTT2h11.1mmol/LOGTTWHO

(IGT)(IFG)IGTOGTT2h7.8mmol/L<11.1mmol/L;IFG6.1mmol/L<7.0mmol/L

(GHbHbA1HbA1c)75gOGTT6.7mmol/L(120mg/dl)1h2h13.3mmol/L(240mg/dl)HbA1c

Differential diagnosis

1.12

12

2.

30%()()()()

FPG4590min(60min)120180min;;35h

C2h812/CCC

;-()

3.

()A

4.

(1)();cAMPFPG;BICAGAD-Ab1;212

(2)24.3%27.1%()

(3)(Cushingss syndrome)IGT20%

(4);()80%10%24%

(5)A50%

15%

OGTT[143.5pmol/L(500pg/ml)]CTMRIB(335cm70%50%)

(6)D()()(100)(50%)

5.

OGTT371

6.

(34)()Fanconi

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.