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Diabetes mellitus - Overview of information

 

Diabetes mellitus is a syndrome of chronic hyperglycemia, developing as a result of exposure to genetic and exogenous factors. The disease is caused by a violation of the secretion of insulin and a different degree of peripheral insulin resistance, leading to hyperglycemia. Early symptoms are associated with hyperglycemia and include polydipsia, polyphagia, and polyuria.

Further complications include angiopathy, peripheral neuropathy and a predisposition to infectious processes. Diagnosis is based on determining the level of glucose. Treatment includes diet, exercise and glucose-lowering drugs, which include insulin and oral antihyperglycemic drugs. The prognosis is different and depends on the degree of glucose control.

Epidemiology

The prevalence of the disease is 1-3% among the population of different countries and ethnic groups. The incidence of diabetes in children and adolescents ranges from 0.1 to 0.3%. Taking into account undiagnosed forms, its prevalence in some countries reaches more than 6%.

To date, over 120 million people have diabetes on the globe. Annually, the number of newly diagnosed cases is 6-10% in relation to the total number of patients, which leads to its doubling every 10-15 years. In economically developed countries, diabetes mellitus in this regard has become not only a medical, but also a social problem.

The incidence of the disease depends largely on age. The number of patients on diabetes mellitus up to 15 years is 5% of the total population of diabetics. Patients over 40 years of age account for about 80%, and over 65 years - 40% of the total contingent of patients.

The effect of sex has little effect on the frequency of juvenile diabetes, and with increasing age, there is a predominance of sick women in Europe, the United States, and Africa. In Japan, India, Malaysia, diabetes is more common in men, and in Mexico, in American Indians, it is the same for both sexes. Adult obesity, hyperlipidemia, hyperinsulinemia, arterial hypertension have a significant influence on the prevalence of diabetes in adults. The combination of several risk factors significantly (in 28.9 times) increases the likelihood of developing clinical diabetes.

National and geographical factors also affect the prevalence of the disease. Thus, in some countries of southeast Asia, Oceania, North Africa, among the Eskimos, diabetes is much less common than in Europe and the USA.

Causes of the diabetes mellitus

The first indication of the hereditary nature of diabetes dates back to the 17th century. The first hypothesis about the hereditary nature of the disease was formulated by Wegeli (1896). However, intensive study of the hereditary nature of diabetes began only in the 20-30s of this century, and by the 1960s it was proved that the main etiological factor of this disease is genetic. Evidence of his hereditary conditionality consisted in the predominance of the frequency of family forms over the prevalence of diabetes mellitus in the population and the prevalence of the frequency of concordance among monozygotic twins in comparison with dizygotic.

In 1974, J. Nerup et al., AG Gudworth and J. S. Woodrow, found the association of the B-locus of the histocompatibility leukocyte antigens with type I diabetes-insulin-dependent (IZD) and its absence in patients with type II insulin-dependent diabetes mellitus. The authors' data indicated that the prevalence of H8 B8 antigen was 49% in patients with Type I diabetes, 31% in healthy individuals, and 21% in HLA B15 and 10% in HLA-B15, respectively. Further studies confirmed these findings and made it possible to establish a predominance in patients with type I diabetes and other HLA antigens related to D-, DR- and DQ-loci. Thus, in patients with IZD, H1A antigens - Dw3, DRw3, Dw4, DRw4 - were detected more frequently than in the control group of healthy patients. The presence of H8 or B15 haplotypes in the subjects increased the risk of the incidence of diabetes by 2-3 times, B8 and B15 simultaneously - approximately 10 times. The presence of haplotypes Dw3 / DRw3 increased the relative risk 3.7 times, Dw4 / DRw4 - 4.9, and Dw3 / DRw4 - 9.4 times.

Studies of monozygotic twins, depending on the type of diabetes mellitus, showed that the frequency of concordance in type II diabetes is significantly higher (48 of 55) than among twins with type I (80 of 147). The results of subsequent observations indicate that the concordance of monozygotic twins with type II diabetes reaches 100% (with increasing age), and with type I - 10-50%. The percentage of concordance among twins, patients with IUD, is much higher than among dizygotic or siblings, which confirms the genetic genesis of the disease. However, a rather high percentage of discordance is a strong argument in favor of other factors.

The results of the study made it possible to reveal genetic heterogeneity of diabetes mellitus and a type I diabetes marker. However, the question of the genetic marker (HLA antigens) can not yet be considered completely solved, since it should be detected in 90-100% of patients who are predisposed to diabetes, and absent from healthy ones. Difficulties in the interpretation of "diabetic" HLA phenotypes are that, in addition to the HLA antigens of loci B and D, often found in Type I diabetes, HLA antigens have been found to exert a protective effect that prevents the onset of diabetes. So, HLA B7 among patients with type 1 diabetes was detected only in 13%, and among healthy patients - in 27%. The relative risk of diabetes in HLA B7 carriers was 14.5 times lower than in those with HLA B7 absent. Other HLA antigens, A3, DW2 and DRw2, also have a protective effect. Continuing studies of the association of HLA antigens with diabetes mellitus have shown that HLA A2, B18 and Cw3 are more often found in patients with type I diabetes than in the population.

All of the above creates great difficulties in predicting the relative risk of diabetes in various variants of the HLA phenotype, which includes both diabetic and tentative variants of HLA-antigen loci. Leukocyte antigens of histocompatibility determine the individual immunological response of the body to various antigens and are not directly related to carbohydrate metabolism.

The set of HLA antigens in each person is controlled by a complex of genes localized in the short arm of chromosome 6, as well as the rare type of properdin (BfF-1) found in 23% of patients with type 1 diabetes, compared to 2% in the population. It is suggested that the HLA phenotype in diabetes mellitus is a genetic determinant determining the sensitivity of pancreatic beta cells to viral or other antigens, and reflects the nature of the body's immunological response.

In the process of studying the features of HLA phenotypes in patients with type I diabetes, his genetic heterogeneity was found. Thus, carriers of HLA B8 often had a connection with Dw3, which correlated with concordance in monozygotic twins. It was characterized by "no antibodies to exogenous insulin, an increase in the frequency of microangiopathies, a combination with other autoimmune diseases, the presence of antibodies to pancreatic islet cells and a reduced incidence of B7 antigen. HLA B15 is often combined with Cw3. The presence of antibodies to exogenous insulin, the usual frequency of microangiopathies, the absence of concomitant autoimmune diseases, the normal incidence of HLA B7 and the detection of antigens in both concordant and discordant diabetes-related monozygotic twins are noted.

The main factors provoking the onset of type I diabetes with a genetic predisposition are viral infections.

At the heart of type II diabetes also has a genetic predisposition, which is confirmed by 100% concordance of monozygotic twins. However, the genetic marker of it has not been found to date, although there are data on the localization of genes of type II diabetes in chromosome 11. The main provoking factor in this case is obesity.

The nature of inheritance of type I and II diabetes is not entirely clear. The issue of polygenic inheritance is discussed, where genetic factors (polygenes) and exogenous (exogenous) are interrelated and participate in the manifestation of the disease. Certain environmental factors (disease sellers) should be attached to genetic factors so that polygenically deterministic signs or predisposition to the disease are realized.

More definitive conclusions about the ways of inheritance of type I diabetes can be made after studying the nature of HLA phenotypes in relatives of probands (in a large number of pedigrees). Given the available data obtained from the identification of clinical forms of diabetes, we can conclude that a recessive path of inheritance through generation in the presence of two or more mutant genes with incomplete penetrance.

The results of systematic family surveys are in the best way consistent with the multifactorial conditionality of type II diabetes mellitus. Values that characterize the incidence of the disease among parents of probands and siblings are significantly lower than those expected for recessive or dominant inheritance pathways. Diabetes type II is characterized by the detectability of the disease from generation to generation, which is characteristic of the dominant path of inheritance. However, the frequency of clinical and latent forms of the disease is much lower (even in children of two patients with diabetes of parents) than with the monogenic autosomal dominant path of inheritance. This again confirms the hypothesis of a multifactorial system of inheritance. Genetic heterogeneity of diabetes is found in animals with spontaneous diabetes. Thus, in domestic mice, several types of impaired glucose tolerance are described with different inheritance methods. Goldstein and Motulsky (1975) propose for use a table of actual risk of disease, calculated on the basis of statistical processing on computers of various literature sources containing information on the incidence of diabetes in relatives of diabetic probands.

Absolute risk for the onset of clinical diabetes

Subjects

Diabetic relatives

Absolute risk,%

Parents

Sibs

One

Both

One

More than one

Child

+

-

-

-

5

"

-

+

-

-

10-15

"

+

-

+

-

10

Sibs

-

-

+

-

5

"

"

"

"

"

20

"

-

-

-

+

10

Risk factors

Type 1 diabetes mellitus correlates with various viral diseases, seasonal factors and partly age, since the peak incidence of children falls on 10-12 years.

A common risk factor, especially when inheriting type II diabetes, is the genetic factor.

There is information that the excessive intake of cyanide with food (in the form of cassava), as well as the lack of protein in it, can contribute to the development of a special type of diabetes mellitus in tropical countries.

Pathogenesis

A violation of glucose regulation (impaired glucose tolerance or impaired fasting glucose) is an intermediate, possibly transient, condition between normal glucose metabolism and diabetes, which often develops with age, is a significant risk factor for the development of diabetes mellitus and can be observed many years before the onset of sugar diabetes. It is also associated with an increased risk of developing cardiovascular disease, but typical diabetic microvascular complications usually do not develop.

To date, not only genetic, but also pathophysiological heterogeneity of diabetes mellitus has been fully proved. According to the classification of the disease, proposed by the WHO Expert Committee (1981), two main pathogenetic forms of the disease are distinguished: type I diabetes (insulin-dependent) and type II diabetes (non-insulin-dependent). Pathophysiological, clinical and genetic differences of these types of diabetes are presented in Table. 8.

Characteristics of I and II types of diabetes mellitus

Indicators

Type1

Type II

The age at which the disease occurs Children's, youthful Senior, average

Family forms of the disease

Infrequently

Often

Influence of seasonal factors on disease detection

Autumn-winter period

No

Phenotype Thin Obesity

Haplotype (HLA)

B8, B15, Dw3, Dw4, DRw3, DRw4

No connection found

The onset of the disease Fast Slow
Symptoms of the disease Heavy Weak or missing
Urine Sugar and Acetone Sugar

Ketoacidosis

Are prone

Resistant

Whey insulin (IRI) Low or none Normal or elevated
Antibodies to islet cells Present None

Treatment (basic)

Insulin

Diet

Concordance of monozygotic twins,%

50

100

In addition to other signs, significant differences are also observed in the degree of concordance (reciprocal incidence) of identical twins. Of course, a 50% degree of concordance in monozygotic twins in groups of patients with type 1 diabetes is significantly higher than among dizygotic twins or siblings, which indicates that the genetic factor plays a significant role in the pathogenesis of the disease. The discordance in this group of twins, which is 50%, indicates the greater role of other factors (besides genetic ones), for example, viral diseases. It is suggested that the HLA system is a genetic determinant determining the sensitivity of the pancreatic beta cells to viral antigens, or reflects the degree of antiviral immunity.

Thus, type 1 diabetes is due to the presence of mutant diabetic genes in chromosome 6, related to the HLA system, which determines the individual, genetically conditioned response of the organism to various antigens. Mutant genes, apparently, are associated with the HLAD-segment. In addition to diabetic HLA haplotypes, protective leukocyte antigens, for example, HLA B7 and A3, DR2, that can interfere with the development of diabetes, despite the presence of mutant genes, have also been detected. The risk of developing diabetes is significantly greater in patients with two HLA-B8 and B15 than with one of them.

Despite the fact that type I diabetes is characterized by association with HLA antigens and certain clinical and pathophysiological parameters, it is heterogeneous. Depending on the pathogenetic features, Type I diabetes is divided into two subtypes: 1a and Ib. Subtype 1a is associated with a defect of antiviral immunity, so the pathogenetic factor is a viral infection that causes the destruction of beta cells of pancreatic islets. It is believed that smallpox viruses, Coxsackie B, adenovirus have tropism to the islet tissue of the pancreas. Destruction of islets after a viral infection is confirmed by peculiar changes in the pancreas in the form of "insulites", expressed in infiltration by lymphocytes and plasma cells. When there is a "viral" diabetes in the blood, circulating autoantibodies to islet tissue are found. As a rule, after 1-3 years the antibodies disappear.

Diabetes 1b is 1-2% in relation to all patients with diabetes. This subtype of diabetes is considered as a manifestation of autoimmune disease, which is confirmed by the frequent combination of type 1b diabetes with other autoimmune endocrine and non-endocrine diseases: primary chronic hypocorticism, hypogonadism, autoimmune thyroiditis, toxic goiter, hypoparathyroidism, vitiligo, pernicious anemia, nesting baldness, rheumatoid arthritis. In addition, the circulating autoantibodies in islet tissue are detected before the detection of clinical diabetes and are present in the blood of patients for almost the entire period of the disease. The pathogenesis of 1b subtype of diabetes is associated with a partial genetically determined defect in the immunological surveillance system, i.e., with inferiority of suppressor T-lymphocytes, which normally inhibit the development of forbid clones of T-lymphocytes directed against tissue proteins of the organism.

Differences between the 1a- and 1 b subtype of diabetes confirmed the predominance of HLA B15, DR4 subtype when 1a-and HLA B8, DR3 - at 1b-subtype. Thus, subtype 1a of diabetes is caused by a violation of the body's immune response to certain exogenous antigens (viral), and subtype Ib is an organ-specific autoimmune disease.

Type II diabetes (insulin-dependent) is characterized by a large concentration of family forms of the disease, a significant influence on its manifestation of environmental factors, the main one being obesity. Since this type of diabetes is combined with hyperinsulinemia, lipogenesis processes leading to obesity predominate in patients. Thus, on the one hand, it is a risk factor, and on the other - one of the early manifestations of diabetes. The insulin-independent type of diabetes is also pathogenetically heterogeneous. For example, the clinical syndrome of chronic hyperglycemia, hyperinsulinemia and obesity can be observed with excessive secretion of cortisol ( Isenko-Cushing's disease ), growth hormone (acromegalia), glucagon (gluconoma), excess production of antibodies to endogenous insulin, in certain types of hyperlipidemia, etc. Clinical manifestations of type II diabetes are expressed in chronic hyperglycemia, which can be treated with a diet that helps to reduce body weight. Usually, ketoacidosis and diabetic coma are not observed in patients. Since type II diabetes occurs in people older than 40 years, the general condition of patients and their ability to work often depend on concomitant diseases: hypertension and complications of atherosclerosis, which occur in diabetic patients several times more often than in the general population of the corresponding age group. The proportion of patients with type II diabetes is approximately 80-90%).

One of the most serious manifestations of diabetes, regardless of its type, is diabetic microangiopathy and neuropathy. In their pathogenesis, a significant role is played by metabolic disorders, mainly hyperglycemia, characteristic of diabetes mellitus. Defining processes that develop in patients and underlying the pathogenesis of microangiopathy are glycosylation of body proteins, disruption of cellular function in insulin-independent tissues, changes in the rheological properties of blood and hemodynamics. In the 70s of our century it was found that in patients with decompensated diabetes the content of glucosylated hemoglobin increases in comparison with healthy ones. Glucose by a nonenzymatic process reacts with the N-terminal amino group of the B chain of the hemoglobin A molecule to form a ketoamine. This complex is found in erythrocytes for 2-3 months (the lifetime of the erythrocyte) in the form of small fractions of hemoglobin A 1c or A 1abc. At present, the possibility of glucose addition to the formation of ketoamine and to the A chain of the hemoglobin molecule has been proved. A similar process of increased glucose incorporation in blood serum proteins (with the formation of fructosamine), cell membranes, low-density lipoproteins, peripheral nerve fibers, collagen, elastin and lens was found in most patients with diabetes mellitus and experimental diabetic animals. Changes in the basement membrane proteins, their high content in endothelial cells, aortic collagen and the basement membrane of the renal glomerulus not only can disrupt the cell function, but also promote the formation of antibodies to altered vascular wall proteins (immune complexes) that can participate in the pathogenesis of diabetic microangiopathy.

In the pathogenesis of the disturbance of the cellular function of insulin-independent tissues, the enhanced stimulation (against the background of hyperglycemia) of the enzymatic polyol pathway of glucose metabolism plays a role. Glucose in proportion to its concentration in the blood enters the cells of insulin-independent tissues, where it, without undergoing phosphorylation, turns under the influence of the enzyme aldose reductase in the cyclic alcohol - sorbitol. The latter, with the help of another enzyme, sorbitol dehydrogenase, is converted to fructose, which is utilized without the participation of insulin. The formation of intracellular sorbitol occurs in the cells of the nervous system, pericyte of the retina, pancreas, kidneys, lens, vessels walls containing aldose reductase. The accumulation of excess amount of sorbitol in cells increases osmotic pressure, causing cellular edema, and creates conditions for disrupting the function of the cells of various organs and tissues, contributing to the disturbance of microcirculation.

Hyperglycemia can disrupt metabolism in the nervous tissue in various ways: by lowering the sodium-dependent absorption of myoinositol and (or) increasing the polyol pathway of glucose oxidation (the myo-inositol content in the nervous tissue decreases), or by disturbing the metabolism of phosphoinositide and sodium potassium-ATPase activity. In connection with the expansion of glycosylation of tubulin, the microtubule function of axons and transport of myoinositis, its intracellular binding, may be disrupted. These phenomena contribute to a decrease in nerve conduction, axonal transport, water cellular balance and cause structural changes in nerve tissues. The clinical variability of diabetic neuropathy, independent of the severity and duration of diabetes, allows one to think about the possibility of influencing such pathogenetic factors as genetic and external (nerve compression, alcohol, etc.).

In the pathogenesis of diabetic microangiopathy, in addition to the previously mentioned factors, hemostasis can also play a role. In patients with diabetes mellitus, there is an increase in platelet aggregation with an increase in thromboxane A 2 production , an increase in the metabolism of arachidonic acid in platelets and a decrease in their half-life, disruption of prostacyclin synthesis in endothelial cells, a decrease in fibrinolytic activity and an increase in von Willebrand factor, which may contribute to the formation of microthrombi in the vessels. In addition, the increase in blood viscosity, slowing of blood flow in the retinal capillaries, as well as tissue hypoxia and a decrease in oxygen release from hemoglobin A1, may be involved in the pathogenesis of the disease, as evidenced by a decrease in 2,3-diphosphoglycerate in erythrocytes.

In addition to the aforementioned andogenetic factors in the pathogenesis of diabetic microangiopathy and nephropathy, hemodynamic changes in the form of microcirculatory disturbances can play a role. It is noted that in the initial stage of diabetes, capillary blood flow increases in many organs and tissues (kidney, retina, skin, muscle and fat tissue). This, for example, is accompanied by an increase in glomerular filtration in the kidneys with the growth of the transglomerular pressure gradient. It was suggested that this process can cause the protein to enter through the capillary membrane, accumulate it in the mesangium, followed by the proliferation of mesangium and lead to intercapillary glomerulosclerosis. Clinically, patients develop transitory and then permanent proteinuria. Confirmation of this hypothesis is considered by the authors to be the development of glomerulosclerosis in experimental diabetic animals after partial nephrectomy. TN Hostetter et al. Proposed the following scheme of the sequence of development of kidney damage: hyperglycemia - increased renal blood flow - increased transglomerular hydrostatic pressure (with subsequent deposition of protein in the vessel wall and basal membrane) - protein filtration (albuminuria) - mesangium thickening - glomerulosclerosis - compensatory filtration increase in the remaining glomeruli - renal failure.

Diabetic microangiopathy and histocompatibility antigens (HLA). In 20-40% of patients with a 40-year duration of type I diabetes there is no diabetic retinopathy, which suggests a significant role in the development of microangiopathy, not only metabolic disorders, but also a genetic factor. Controversial data were obtained from the study of the association of HLA antigens and the presence or absence of diabetic proliferative retinopathy or nephropathy. In most studies, there has been no association of neuropathy with the nature of the detected HLA antigens. Given the heterogeneity of type I diabetes, the HLA phenotype DR3-B8 is characterized by the predominance of constantly circulating antibodies to pancreatic islets, increased formation of circulating immune complexes, weak immune response to heterologous insulin, and poorly expressed manifestations of retinopathy. Another form of type I diabetes with the B15-Cw3-DR4 HLA phenotype is not combined with autoimmune diseases or persistent circulating antibodies to islet cells and occurs at an earlier age, often accompanied by proliferative retinopathy. An analysis of published studies that examined the possible association of HLA antigens with diabetic retinopathy in more than 1,000 patients with type I diabetes showed that an increased risk of developing proliferative retinopathy was observed in patients with the HLA B15-DR4 phenotype, while HLA B18- the phenotype plays a protective role in the risk of severe retinopathy. This is explained by the longer secretion of endogenous insulin (C-peptide) in patients with HLA B18 and B7 phenotypes, as well as frequent association with the Bf allele of theperdin, which is localized in the short arm of chromosome 6 and may be related to retinopathy.

Pathanatomy

Changes in the islet apparatus of the pancreas undergo a kind of evolution, depending on the duration of diabetes mellitus. As the duration of the disease increases in patients with type I diabetes, there is a decrease in the number and degeneration of B cells with an unchanged or even increasing content of A and D cells. This process is the result of infiltration of the islets with lymphocytes, ie, a process called insulitis that is related to the primary or secondary (against the background of viral infections) autoimmune pancreatic lesion. Insulin-deficient type of diabetes is also characterized by diffuse fibrosis of the islet system (in about 25% of cases), especially when diabetes is combined with other autoimmune diseases. In most cases, type I diabetes mellitus develops the hyalinosis of the islets and the accumulation of hyaline masses between the cells and around the blood vessels. In the early stages of the disease there are foci of B-cell regeneration completely disappearing with increasing duration of the disease. In a significant number of cases, the residual secretion of insulin, caused by partial preservation of B cells, was noted. Type II diabetes is characterized by a certain decrease in the number of B cells. In the microcirculation vessels, a thickening of the basal membrane is detected due to the accumulation of the SHIC-positive material represented by glycoproteins.

Retinal vessels undergo various changes depending on the stage of retinopathy: from the appearance of microaneurysms, microthrombosis, hemorrhages and occurrence of yellow exudates to the formation of new vessels (neovascularization), fibrosis and retinal detachment after vitreous hemorrhage with the subsequent formation of fibrous tissue.

With diabetic peripheral neuropathy segmental demyelination is observed, degeneration of axons and connective nerves. In sympathetic ganglia, large vacuoles, giant neurons with degeneration phenomena, swelling of dendrites are found. In sympathetic and parasympathetic neurons - thickening, fragmentation, hyperagentophilia.

The most typical for diabetes is diabetic nephropathy - nodular glomerulosclerosis and tubular nephrosis. Other diseases, such as diffuse and exudative glomerulosclerosis, arteriosclerosis, pyelonephritis and necrotic papillitis, are not specific for diabetes mellitus, but are associated with it much more often than with other diseases.

Nodular glomerulosclerosis (intercapillary glomerulosclerosis, Kimmelstyle-Wilson syndrome) is characterized by the accumulation of PAS-positive material in the mesangium in the form of nodules along the periphery of the branches of the glomerular capillary loops and thickening of the basement membrane of the capillaries. This type of glomerulosclerosis is specific for diabetes mellitus and correlates with its duration. Diffuse glomerulosclerosis is characterized by a thickening of the basement membrane of the capillaries of all glomerular sections, a decrease in the lumen of the capillaries and their occlusion. It is believed that diffuse glomerulosclerosis can precede nodular glomerulosclerosis. The study of kidney biopsy specimens in patients with diabetes mellitus, as a rule, makes it possible to detect a combination of changes characteristic of both nodular and diffuse lesions.

Exudative glomerulosclerosis is expressed in the accumulation of a homogeneous eosinophilic material resembling fibrinoid between the endothelium and the basal membrane of the Bowman capsule in the form of lipogialin cups. This material contains triglycerides, cholesterol and PAS-positive polysaccharides.

Typical for tubular nephrosis is the accumulation of vacuoles containing glycogen in epithelial cells of predominantly proximal tubules and deposition in their cytoplasmic membranes of a PAC-positive material. The degree of expression of these changes correlates with hyperglycemia and does not correspond to the nature of the disturbances in tubular function.

Nephrosclerosis is the result of atherosclerotic and arteriolosclerotic lesions of small arteries and arterioles of the kidneys and is found, according to sectional data, in 55-80% of cases against diabetes mellitus. Hyalinosis is observed in the efferent and afferent arterioles of the juxtaglomerular apparatus. The nature of the pathological process does not differ from the corresponding changes in other organs.

Necrotic papillitis is a relatively rare acute form of pyelonephritis, characterized by ischemic necrosis of the renal papillae and vein thrombosis on the background of a violently flowing infection. Patients develop fever, hematuria, renal colic and transient azotemia. In the urine, scraps of the renal papillae are often found due to their destruction. Necrotic papillitis is much more common in patients with diabetes mellitus.

Symptoms of the diabetes mellitus

The most frequent symptoms of diabetes mellitus are: osmotic diuresis caused by glucosuria, leading to frequent urination, polyuria, polydipsia, which can progress to the development of orthostatic hypotension and dehydration. Severe dehydration causes weakness, fatigue, changes in mental state. Diabetes mellitus has symptoms that can appear and disappear when fluctuating glucose levels. Polyphagia may accompany symptoms of diabetes, but is usually not the main complaint of patients. Hyperglycemia can also cause weight loss, nausea, vomiting, poor eyesight, a predisposition to bacterial or fungal infections.

Type 1 diabetes is usually manifested by symptomatic hyperglycemia and sometimes diabetic ketoacidosis). In some patients, after an acute onset of the disease, there is a long, but transient phase of the level of glucose close to the norm ("honeymoon") due to a partial restoration of insulin secretion.

Diabetes mellitus type 2 may manifest symptomatic hyperglycemia, but more often the course of the disease is asymptomatic, the condition is revealed only when the study is planned. In some patients, the initial symptoms are manifested by diabetic complications, which presupposes a prolonged course of the disease until a diagnosis is made. Some patients initially develop hyperosmolar coma, especially during stress or with further impairment of glucose metabolism caused by medication, such as glucocorticoids.

What's bothering you?

Forms

Classification of diabetes mellitus and other categories of impaired glucose tolerance

A. Clinical classes

  1. Diabetes:
    1. insulin-dependent - type I;
    2. non-insulin-dependent - type II: 
      • in individuals with normal body weight;
      • with obesity.
  2. Other types, including diabetes mellitus, associated with certain conditions or syndromes:
    • pancreas diseases;
    • diseases of hormonal etiology;
    • states caused by drugs or chemicals;
    • change in insulin receptors;
    • certain genetic syndromes;
    • mixed states.
  3. Diabetes caused by malnutrition (tropical):
    • pancreatic;
    • pancreatogenic.
  4. Impairment of glucose tolerance (NTG):
    • in individuals with normal body weight;
    • with obesity;
    • violation of glucose tolerance, due to other specific conditions and syndromes.
  5. Diabetes of pregnant women.

B. Reliable risk classes (individuals with normal glucose tolerance, but with a significantly increased risk of developing diabetes)

  1. preceded violations of glucose tolerance;
  2. Potential violations of glucose tolerance.

In turn, this type of diabetes is divided into two subtypes: pancreatic and pancreatic. The pathogenesis of tropical variants of the disease differs significantly from all other species. It is based on malnutrition in childhood.

Pancreatic diabetes in turn is divided into fibrocalculant and protein-deficient. The first is common in India and Indonesia predominantly among men (3: 1) and is characterized by the absence of ketosis in the presence of type I diabetes. Calcinates and diffuse fibrosis of the gland without inflammatory processes are found in the ducts of the pancreas of patients. At this type of disease there is a low secretion of insulin and glucagon and a syndrome of impaired absorption. The course of diabetes is often complicated by severe peripheral somatic polyneuropathy. Compensation of the disease is achieved by the introduction of insulin. The pathogenesis of this form is associated with excessive consumption of products containing cyanides (cassava, sorghum, millet, beans) against the background of a deficit of protein foods. The second variant of pancreatic diabetes is called protein-deficient (Jamaican). It is caused by a low protein and saturated fat diet, occurs at the age of 20-35 years and is characterized by absolute insulin deficiency, insulin resistance (insulin requirement is 2 units / kg) and lack of ketosis.

Pancreatic diabetes is caused by excessive intake of iron in the body and its deposition in the pancreas, for example, in the treatment of thalassemia (frequent blood transfusions), the use of alcohol stored in iron containers (distributed among the Bantu people in South Africa), and other factors that cause secondary hemahromatosis.

Summarizing the above, it should be emphasized once again that diabetes mellitus (by analogy with hypertension ) is a syndrome, genetically, pathophysiologically and clinically heterogeneous. This fact requires a differential approach, not only in the study of pathogenesis, but also in the analysis of clinical manifestations, choice of treatment methods, assessment of the patients' ability to work and prevention of various types of diabetes.

There are 2 main types of diabetes mellitus (DM) - type 1 and type 2, which differ in a number of features. The characteristics of the onset of DM (juvenile or adult diabetes mellitus) and the type of treatment (insulin-dependent or insulin-independent diabetes mellitus) are not adequate, due to the intersection of age groups and treatment methods for both types of disease.

Type 1 diabetes mellitus

Diabetes mellitus type 1 (formerly called juvenile or insulin-dependent) is characterized by the fact that insulin production is absent due to autoimmune destruction of pancreatic cells, probably caused by the action of environmental factors against a background of genetic predisposition. Type 1 diabetes is more likely to develop in childhood or adolescence and until recently was the most common form diagnosed before the age of 30; nevertheless, it can also develop in adults (latent autoimmune diabetes of adults). Diabetes mellitus type 1 is less than 10% of all cases of diabetes.

The pathogenesis of autoimmune destruction of pancreatic cells includes completely unexplored interactions between predisposing genes, autoantigens, and environmental factors. Predisposing genes include genes belonging to the main histocompatibility complex (MHC), especially HLADR3, DQB1 * 0201 and HLADR4, DQB 1 * 0302, which have more than 90% of patients who have type 1 diabetes. Genes of predisposition are more common in some populations than in others, which explains the prevalence of type 1 diabetes in some ethnic groups (Scandinavians, Sardines).

Autoantigens include glutamic acid decarboxylase and other cell proteins. It is believed that these proteins are exposed during normal cell renewal or when they are damaged (for example, by infection) by activating the immune response through mediator cells, which leads to cell destruction (insulin). A-Cells secreting glucagon remain intact. Antibodies to autoantigens, which are detected in the blood, are probably a response to the destruction of cells (rather than its cause).

Some viruses (including Coxsackie, rubella, cytomegalovirus, Epstein-Barr virus, retroviruses) are associated with the onset of type 1 diabetes. Viruses can directly infect and destroy cells, and they can cause indirect cell destruction by exposing autoantigens, activation of autoreactive lymphocytes, mimicry molecular sequences of autoantigens that stimulate the immune response (molecular mimicry), or by other mechanisms.

Diet can also be a similar factor. Feeding infants with dairy products (especially cow's milk and milk protein casein), high levels of nitrates in drinking water and insufficient intake of vitamin D are associated with an increased risk of developing type 1 diabetes. Early (<4 months) or late (> 7 months) contact with The vegetable protein and grains increase the production of antibodies by islet cells. The mechanisms of these processes have not been studied.

Class I type of diabetes mellitus

Criteria

Characteristic

Clinical manifestations

Juvenile type, occurs mainly in children and adolescents; insulin-dependent

Etiological factors

Association with the HLA system, immune response to viruses that have a tropism for beta-cells

Pathogenesis

The destruction of beta cells, a lack of regeneration

Type 1a

Type lb

Cause

Viruses

Violation of organ-specific immunity

Total prevalence of diabetes,%

10

1

Insulin dependence

There is

There is

Floor

Ratio equal to

Women predominate

Age

Up to 30 years

Any

Combination with autoimmune diseases

Not available

Frequent

The frequency of antibodies to islet tissue

At occurrence - 85%, in 1 year - 20%, in process of increase in duration of illness - the tendency to disappearance

At occurrence - it is unknown, in 1 year - 38%, the antibody titer is constant

Antibody Titer

1/250

1/250

The time of the first detection of antibodies to islet tissue

Viral infection

A few years before the onset of diabetes

A clinical form of type II diabetes is described, which is caused by the formation of autoantibodies to the insulin receptors in the body (diabetes combined with acanthosis or lupus erythematosus). However, the pathogenesis of type II essential diabetes is still unclear. The pathology of receptors of insulin-dependent tissues was supposed to explain the decrease in the biological effect of insulin with normal or elevated blood levels. But as a result of a detailed study of this problem in the 1970s, it was revealed that there were no significant quantitative changes in tissue receptors or transformations in the processes of their binding to insulin in patients with diabetes. Currently, it is believed that the insufficient hypoglycemic effect of biologically active endogenous insulin in type II diabetes is apparently due to a genetic defect in the post-receptor apparatus of insulin-dependent tissues.

In 1985, on the recommendation of WHO, in addition to the previously identified types of diabetes, another clinical form was included in the classification. It is caused by malnutrition, mainly in tropical countries in patients 10-50 years old.

Diabetes mellitus type 2

Type 2 diabetes mellitus (formerly called adult diabetes or insulin-independent) is characterized by the fact that insulin secretion does not meet the needs. Often insulin levels are very high, especially at the onset of the disease, however peripheral insulin resistance and increased glucose production by the liver make it insufficient to normalize the glucose level. The disease usually develops in adults, and its frequency increases with age. After eating, higher glucose levels are observed in older people compared with younger ones, especially after taking high-carbohydrate foods, and for a longer time the glucose level returns to normal, in part because of increased accumulation of visceral / abdominal fat and decreased muscle masses.

Diabetes mellitus type 2 is increasingly observed in childhood due to the epidemic growth of childhood obesity: from 40 to 50% of cases of newly diagnosed diabetes mellitus in children are now in type 2. More than 90% of adults in diabetes mellitus have type 2 disease. There are clear genetic determinants, which is confirmed by the wide spread of the disease in ethnic groups (especially American Indians, Spaniards, Asians) and relatives of the patient for diabetes mellitus. There are no genes responsible for the development of the most common forms of type 2 diabetes mellitus.

Pathogenesis is complex and not fully understood. Hyperglycemia develops when insulin secretion can no longer compensate for insulin resistance. Although type 2 insulin resistance is characteristic of insulin resistance, there is also evidence of cell dysfunction, including a violation of the 1st phase of secretion in response to intravenous glucose stimulation, an increase in proinsulin secretion, and accumulation of islet amyloid polypeptide. In the presence of insulin resistance, usually such changes develop over the years.

Obesity and weight gain are important determinants of insulin resistance in type 2 diabetes mellitus. They have some genetic predisposition, but they also reflect diet, exercise and lifestyle. Adipose tissue increases the level of free fatty acids, which can disrupt insulin-stimulated glucose transport and the activity of muscle glycogen synthase. Adipose tissue also acts as an endocrine organ, producing numerous factors (adipocytokines) that are favorable (adiponectin) and unfavorable (tumor necrosis factor a, IL6, leptin, resistin) affect glucose metabolism.

Diagnostics of the diabetes mellitus

Diabetes is indicated by typical symptoms and signs, the diagnosis is confirmed by measuring the glucose level. The most effective measurement after 8-12 hour fasting [fasting glycemia (GH)] or 2 hours after taking a concentrated glucose solution [oral glucose tolerance test (OGTT)]. OPT is more sensitive to the diagnosis of diabetes mellitus and impaired glucose tolerance, but it is also more expensive, less convenient and reproducible compared to GBV. Consequently, it is less commonly used for routine, except diagnosis of gestational diabetes, and for research purposes.

In practice, diabetes mellitus or impaired fasting glucose is often diagnosed by random measurements of glucose or glycosylated hemoglobin (HbA). A random glucose level of more than 200 mg / dl (> 11.1 mmol / L) may be diagnostic, but the values may be influenced by recent eating, thus a reanalysis is required; re-examination may not be necessary in the presence of symptoms of diabetes. The measurement of HbA reflects the glucose levels in the preceding 2-3 months. Values greater than 6.5 mg / dL indicate an abnormally high level of glucose. But the analyzes and the normalized range of values are not standardized, therefore, the values can be false high or low. For these reasons, HbA is not yet considered as reliable as OPT or GH, for diagnosis of diabetes mellitus and should primarily be used to monitor and monitor diabetes mellitus.

Determination of glucose in urine, a previously widely used method, is not currently used for diagnosis or monitoring, since it is neither sensitive nor specific.

If there is a high risk of type 1 diabetes mellitus (for example, relatives and children of patients with type 1 diabetes mellitus), an antibody test for islet cells or antibodies to glutamine decarboxylase that precedes the onset of clinical manifestations of the disease can be performed. Nevertheless, there are no proven preventive measures for a high-risk group, so such analyzes are usually used for scientific research.

Risk factors for type 2 diabetes include age over 45; overweight; passive lifestyle; family history of diabetes mellitus; a disorder of glucose regulation in the anamnesis; gestational diabetes or childbirth more than 4.1 kg; hypertension or dyslipidemia in anamnesis; polycystic ovarian syndrome; ethnic group of blacks, Spaniards or American Indians. The risk of insulin resistance among patients with overweight (body mass index 25 kg / m2 increases with serum triglycerides 130 mg / dl (1.47 mmol / L), high-density triglyceride / high-density lipoprotein ratio 3.0 Such patients should be screened to detect diabetes mellitus with the determination of the level of fasting glycemia at least once every 3 years in the presence of a normal glucose level and at least once a year if there is a violation of fasting glycemia.

All patients who have type 1 diabetes should be screened for diabetic complications 5 years after diagnosis; for patients who suffer from type 2 diabetes mellitus, screening complications begins when a diagnosis is made. Every year, patient's feet should be examined for a violation of feelings of pressure, vibration, pain or temperature, which is characteristic of peripheral neuropathy. The feeling of pressure is best investigated using a monofilamentic estheziometer. The entire foot, and especially the skin under the heads of metatarsal bones, should be examined for cracks and signs of ischemia such as ulceration, gangrene, fungal nail infection, lack of pulse, loss of hair. Ophthalmoscopic examination should be performed by an ophthalmologist; the interval of the studies is contradictory, but varies from annual for patients with established diagnosis of retinopathy to three years for patients without retinopathy at least for one study. A smear or 24-hour urine test is shown annually to detect proteinuria or microalbuminuria, and creatinine should also be measured to assess kidney function. Many consider electrocardiography an important method for the risk of cardiovascular disease. Lipidogram should be performed at least annually and more often when determining changes.

What do need to examine?

Who to contact?

Treatment of the diabetes mellitus

Diabetes mellitus is treated based on glucose control to improve the patient's condition and prevent complications while minimizing hypoglycemic conditions. The goal of the treatment is to maintain the glucose level from 80 to 120 mg / dl (4.4-6.7 mmol / L) during the day and from 100 to 140 mg / dL (5.6-7.8 mmol / L for home monitoring of glycemia) at night and maintenance of HbA1c level of less than 7%. These goals may vary for patients in whom strict glycemic control is impractical: in old age, in patients with short life expectancy, patients experiencing repetitive episodes of hypoglycemia, especially when hypoglycemia is not tolerated, patients who can not report hypoglycemic symptoms (for example, Small children).

The main elements for all patients are training, recommendations on diet and exercise, monitoring glucose levels. All patients who have diabetes type 1 need insulin. Patients who have type 2 diabetes mildly elevated glucose should be given diet therapy and physical activity with the subsequent administration of one oral sugar reduction drug, if lifestyle changes are insufficient, if necessary, an additional second oral drug (combination therapy) and insulin if ineffective 2 or more drugs to achieve the recommended goals. Patients who have type 2 diabetes mellitus with a more significant increase in glucose levels are usually prescribed lifestyle changes and oral sugar reduction drugs at the same time. Patients with impaired glucose regulation should receive advice on the risk of developing diabetes and the importance of lifestyle changes in order to prevent diabetes mellitus. They should be on control for the development of symptoms of diabetes mellitus or increased glucose levels; the optimal study intervals are not defined, but surveys once or twice a year are quite acceptable.

Awareness of patients about the causes of diabetes mellitus; diet therapy; physical activity; medicines, self-checking with a glucometer; symptoms and signs of hypoglycemia, hyperglycemia, diabetic complications is crucial for the optimization of treatment. It is possible to teach the majority of patients who have type 1 diabetes mellitus independently calculate the dose of drugs. Training should be supplemented at each visit of the doctor and each hospitalization. Often very effective are official diabetes education programs, usually conducted by nurses trained in diabetology and nutrition specialists.

Diet, individually adjusted, can help patients to control fluctuations in glucose level, and patients with type 2 diabetes reduce their excess weight. In general, all patients who have diabetes should receive a diet low in saturated fats and cholesterol, a moderate carbohydrate content, preferably from whole grains with high fiber content. Although proteins and fats contribute to the calorie content of food (and thus cause an increase or decrease in body weight), only carbohydrates have a direct effect on glucose levels. A low-carbohydrate diet high in fat improves glucose control in some patients, but the safety of its long-term use is in question. Patients who suffer from type 1 diabetes should use a carbohydrate count or an equivalent product replacement system to select a dose of the drug. The calculation of the amount of carbohydrates in food is used to calculate the dose of insulin before eating. In general, one unit of high-speed insulin is needed for every 15 g of carbohydrates in food. This approach requires detailed training of the patient and is most successful in the control of a dietician who is engaged in diabetes. Some experts recommend the use of the glycemic index to distinguish between slow and fast-assimilating carbohydrates, although others believe that the index has few advantages. Patients who suffer from type 2 diabetes must limit the caloric intake of food, eat regularly, increase fiber intake, limit the intake of refined carbohydrates and saturated fats. Some experts also recommend protein restriction in the diet of less than 0.8 g / (kg-day) to prevent the progression of the initial nephropathy. Consultations of a nutritionist should complement the observation of the therapist; they must be attended by the patient himself and the person who is preparing food for him.

Physical loads should be characterized by a gradual increase in physical activity to the maximum level for a given patient. Some experts believe that aerobic exercise is better than isometric exercises, reduce body weight and impede the development of angiopathy, but resistance training can also improve glucose control, hence all kinds of exercise are helpful. Hypoglycemia during intense exercise may require the intake of carbohydrates during exercise, usually 5 to 15 g of sucrose or other simple sugars. Patients with established or suspected cardio-vascular diseases and diabetes mellitus are advised to perform stress tests before starting the exercise, and for patients with diabetic complications such as neuropathy and retinopathy, it is necessary to reduce exercise levels.

Observation

Diabetes mellitus can be monitored with an assessment of glucose levels, HbA1c fructosamine. The most important role is played by self-monitoring of glucose in whole blood with the use of capillary blood from the finger, test strips, glucometer. Self-control is used to correct the diet, as well as for therapist's recommendations for regulating the doses and timing of medication. There are a large number of different instruments for monitoring. Almost all of them require a test strip and a device for puncturing the skin and obtaining a sample; most are supplied with control solutions, which must be used periodically to confirm the correct calibration. The choice of the device usually depends on the patient's preferences, parameters and characteristics, such as the time to obtain the result (usually from 5 to 30 seconds), the display size (large displays are convenient for patients with poor eyesight), the need for calibration. Also available are glucometers that allow testing in places less painful than fingertips (palm, shoulder, abdomen, thigh). The newest instruments allow to measure glucose transcutaneously, but their use is limited by the appearance of skin irritation, erroneous interpretation; New technologies can soon make the results reliable.

Patients with poor glucose control, as well as patients, when prescribing a new drug or a new dose of the drug, can be recommended self-monitoring from one (usually in the morning on an empty stomach) to 5 or more times a day, depending on the needs and capabilities of the patient, and the complexity of the therapy regimen. For most patients who have type 1 diabetes, testing at least 4 times a day is most effective.

HbA levels reflect glucose control during the previous 2-3 months and allow it to be carried out between visits by a physician. HbA should be evaluated quarterly in patients with type 1 diabetes mellitus and at least annually in patients with type 2 diabetes mellitus who have a stable glucose level (more often with questionable control). Sets for home testing are useful for patients who can strictly follow the instructions. The control suggested by the values of HbA1c sometimes differs from the daily glucose values determined due to falsely elevated or normal values. False ascents can be observed with renal failure (urea interferes with analysis), low rate of red blood cell renewal (iron, folic acid, B12 deficiency anemia), high doses of aspirin, high concentrations of alcohol in the blood. False normal results are observed with an increased update of red blood cells, in particular, hemolytic anemia, hemoglobinopathies (eg, HbS, HbC) or during treatment of scarce anemia.

Fructosamine, which is mainly glycosylated albumin but also represented by other glycosylated proteins, reflects glucose control over the preceding 1-2 weeks. Control of fructosamine can be used in intensive treatment of diabetes mellitus and in patients with hemoglobin abnormalities or high red blood cell renewal (which causes false HbA1c results), but is more often used in scientific studies.

Control of glucosuria is a relative sign of hyperglycemia and can be used only when it is not possible to control blood glucose. Conversely, self-monitoring of ketone bodies in urine is recommended for patients who have type 1 diabetes mellitus who experience symptoms of ketoacidosis, such as nausea or vomiting, abdominal pain, fever, cold or flu symptoms, excessive hyperglycaemia (250 to 300 mg / dl) for self-monitoring of glucose level.

Prevention

There is no treatment to prevent diabetes mellitus and its progression. In some patients, azathioprine, glucocorticoids, cyclosporine may cause a remission of type 1 diabetes, probably by suppressing autoimmune destruction of the cells. However, the toxicity and need for lifelong treatment limits their use. In some patients, short-term treatment with anti-CO3 monoclonal antibodies reduces the need for insulin for at least 1 year at the recent onset of the disease by suppressing the autoimmune response of the T-cells.

Diabetes mellitus type 2 can be prevented by lifestyle changes. Weight loss of 7% of the initial body weight in combination with moderate physical activity (for example, walking 30 minutes a day) can reduce the likelihood of developing diabetes in people at high risk by more than 50%. Metformin also reduces the risk of diabetes in patients with impaired glucose regulation. Moderate alcohol consumption (5-6 servings per week), treatment with ACE inhibitors, angiotensin II receptor blockers, statins, metformin and acarbose can also have a preventive effect, but it needs further study for recommendation to preventive use.

Diabetes mellitus and its risk of complications can be reduced by strict glucose control, namely the level of HbA1c <7.0%, control of hypertension and lipid levels.

Forecast

The expert opinion on the ability to work with diabetics and the correct assessment of their clinical and labor prognosis are based on a combination of medical, social and psychological factors, the combination of which determines the practice of medical and labor expertise. Medical factors include the type of diabetes, severity (the presence and nature of complications) and concomitant diseases; to the social - the main profession of the patient, the nature and working conditions, the possibility of diet, work experience, educational level, living conditions, bad habits; to psychological - the attitude to work, the relationship at work, the attitude to the patient in the family, the possibility of an independent work arrangement in accordance with the state of health, etc.

The formulation of clinical-expert diagnosis should reflect the main clinical manifestations of the disease. An example is the following wording.

  • Diabetes mellitus type I (insulin-dependent), severe form, labile course; retinopathy II stage, nephropathy IV stage, neuropathy (distal polyneuropathy of moderate severity).
  • Diabetes mellitus type II (insulin-independent) of moderate severity; retinopathy of the first stage, neuropathy (a distal polyneuropathy of a light form).

The ability of patients with diabetes mellitus type I and II is affected by the degree of severity of the disease, the type of hypoglycemic therapy, impaired functions of the organ of vision, kidneys, and the nervous system caused by microangiopathies.

Indications for the direction of WTEC

The following readings are considered sufficient for referral to VTEK:

  • a severe form of diabetes mellitus, both insulin-dependent and insulin-independent, characterized by microangiopathy manifestations with significant impairment of vision, kidney, nervous system or labile flow (frequent hypoglycemic conditions and ketoacidosis);
  • the presence of negative factors in the work (significant physical or neuropsychic stress, labor associated with driving, at a height, at the conveyor, contact with vascular poisons, vibration, noise);
  • the impossibility of an employment without qualification reduction or a decrease in the volume of production activity.

Patients are referred to the VTEK after a stationary examination in the therapeutic or specialized departments of hospitals, in the endocrinology offices of the dispensaries, having a detailed extract from the medical history and completed form No. 88.

Criteria for determining the state of work capacity

The first group of disability is diagnosed in patients with severe diabetes mellitus with marked manifestations of microangiopathy with significant impairment of functions: retinopathy of stage III (blindness to both eyes), neuropathy in the form of marked motor disorders (pronounced paresis), ataxia, sensitive, vegetative disorders, as well as diabetic encephalopathy and organic changes in the psyche; Nephropathy of the V stage, with a tendency to hypoglycemic, diabetic coma. Such patients need constant care.

The II group of disability is defined by patients with severe diabetes mellitus, with marked manifestations of microangiopathy and less pronounced functional disorders: retinopathy of stage II, neuropathy in the form of pronounced motor disorders (pronounced paresis), ataxia, sensitive disorders, and persistent organic changes in the psyche, nephropathy IV stages. Such patients do not need constant care. In some cases, the II group is assigned to patients with severe diabetes mellitus with moderate or even initial manifestations of microangiopathy from the side of the organ of vision (retinopathy of 0, I, II stages), nervous system (in the form of moderately expressed motor, sensitive, vegetative disorders), when severe form is caused by a labile course (truly labile or defective treatment - an inadequate dose of insulin) with a chaotic alternation of hypo- and hyperglycemic coma or ketoacidosis, for the period of insulin therapy correction and Leica Geosystems long observation.

The III group of disability is defined by patients with type I diabetes mild with moderate or even initial manifestations of microangiopathy in the organ of vision (retinopathy of the first stage), the nervous system (neuropathy in the form of moderately expressed motor sensitive, vegetative disorders and organic changes in the psyche), kidneys (nephropathy I-III stages), even without clinical manifestations, provided that in the patient's work in the main profession, there are contraindicated factors (work related to driving, with stay at moving mechanisms, with electrical appliances, etc.), and a rational work arrangement entails a reduction in skills or a significant decrease in the volume of productive activity. In this case, young people of the III group of disability is set for the period of retraining, the acquisition of a new profession; Persons who refuse rehabilitation measures (over the age of 46), the third group of disability is established with the recommendation of a rational work arrangement, transfer to another job.

In severe type I diabetes mellitus with a labile course, without inclination to frequent coma, intellectuals (physicians, engineers, accountants) who have a positive attitude toward labor, with initial or even moderate manifestations of microangiopathy in the absence of contraindicated factors in their work in some cases may III group of disability is defined with the recommendation to reduce the amount of work and create conditions for a correct treatment regimen.

Persons with mild to moderate severity of type I and II diabetes are recognized as able-bodied patients in the absence of functional disorders from any organs, systems and contraindicated factors in the work. Some restrictions in the work (exemption from night shifts, business trips, additional workloads) can be provided through the WCC of treatment and prevention institutions. The most frequent reasons for the discrepancy between the expert decisions of VTEK and the consultative expert opinions of CIETIN are inaccurate diagnostics caused by incomplete examination of patients in medical and preventive institutions; underestimation of pathomorphological and functional disorders; a lack of account of the nature of work performed and working conditions. The above diagnostic and expert errors often lead to incorrect professional orientation of patients, to recommendations of contraindicated types and working conditions.

For patients with diabetes young age should be conducted vocational guidance from school. Persons with disabilities in Group III are entitled to mental work occupations associated with moderate neuropsychic stress, as well as occupations of manual labor with mild or moderate stress.

Persons with disabilities of Group I can perform work in specially created conditions (special department, special stages), at enterprises where they worked before disability, taking into account their professional skills or at home.

The work organization of patients with diabetes mellitus according to the medical-physiological classification of work by severity should be carried out taking into account medical, social and psychological factors, as well as the possibility of adherence to dietary regimens and the intake of hypoglycemic drugs.

Modern diagnostics, adequate therapy of diabetes mellitus, dispensary observation, rational employment preserve the ability to work of patients, prevent possible complications and contribute to the prevention of disability and the retention of personnel in the workplace. It should be borne in mind that the range of available works for patients with type II diabetes is much wider than for patients with type I diabetes.

It is important to know!

Insulin is a polypeptide whose monomeric form consists of two chains: A (of 21 amino acids) and B (of 30 amino acids). Insulin is formed as a product of proteolytic cleavage of the insulin precursor, called proinsulin. Read more..

Last reviewed by: Aleksey Portnov , medical expert, on 31.05.2018
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