Diabetes mellitus, symptoms and treatment of diabetes. Central diabetes insipidus. Acute complications of diabetes mellitus

Diabetes Type 1 is an organ-specific autoimmune disease leading to the destruction of insulin-producing beta cells of the pancreatic islets, manifested by absolute insulin deficiency. In some cases, patients with overt type 1 diabetes mellitus lack markers of autoimmune damage to beta cells (idiopathic diabetes mellitus type 1).

Etiology

Type 1 diabetes mellitus is a disease with a hereditary predisposition, but its contribution to the development of the disease is small (it determines its development by approximately 1/3).

The probability of developing type 1 diabetes in a child with a sick mother is 1-2%, father - 3-6%, brother or sister - 6%. One or more humoral markers of autoimmune beta cell damage, which include anti-pancreatic islet antibodies, anti-glutamate decarboxylase antibodies (GAD 65) and anti-tyrosine phosphatase antibodies (IA-2 and IA-2beta), are found in 85-90 % of patients. Nevertheless, the main importance in the destruction of beta cells is given to factors cellular immunity. Type 1 diabetes mellitus is associated with HLA haplotypes DQA and DQB. With increased frequency, type 1 diabetes mellitus is combined with other autoimmune endocrine diseases ( autoimmune thyroiditis, Addison's disease) and non-endocrine diseases such as alopecia, vitiligo, Crohn's disease, rheumatic diseases.

Pathogenesis

Type 1 diabetes manifests itself when 80-90% of beta cells are destroyed by an autoimmune process. The speed and intensity of this process can vary significantly. Most often when typical course diseases in children and young people, this process proceeds quite quickly with subsequent rapid manifestation of the disease, in which from the appearance of the first clinical symptoms It may take only a few weeks for the development of ketoacidosis (up to and including ketoacidotic coma).

In other, much rarer cases, usually in adults over 40 years of age, the disease may be latent. (latent autoimmune diabetes of adults - LADA), Moreover, at the onset of the disease, such patients are often diagnosed with type 2 diabetes mellitus, and for several years, compensation for diabetes mellitus can be achieved by prescribing sulfonylurea drugs. But later, usually after 3 years, signs of absolute insulin deficiency appear (weight loss, ketonuria, severe hyperglycemia, despite taking tableted hypoglycemic drugs).

The pathogenesis of type 1 diabetes mellitus is based on absolute insulin deficiency. The inability of glucose to enter insulin-dependent tissues (fat and muscle) leads to energy deficiency, resulting in intensified lipolysis and proteolysis, which are associated with weight loss. An increase in glycemic levels causes hyperosmolarity, which is accompanied by osmotic diuresis and severe dehydration. Under conditions of insulin deficiency and energy deficiency, the production of contrainsular hormones (glucagon, cortisol, growth hormone) is disinhibited, which, despite increasing glycemia, causes stimulation of gluconeogenesis. Increased lipolysis in adipose tissue leads to a significant increase in the concentration of free fatty acids. With insulin deficiency, the liposynthetic capacity of the liver is suppressed, and free fatty acid begin to engage in ketogenesis. The accumulation of ketone bodies leads to the development of diabetic ketosis, and subsequently ketoacidosis. With a progressive increase in dehydration and acidosis, a coma develops, which, in the absence of insulin therapy and rehydration, inevitably ends in death.

Epidemiology

Type 1 diabetes mellitus accounts for 1.5-2% of all diabetes cases. The lifetime risk of developing type 1 diabetes in a Caucasian person is about 0.4%. The peak age for the manifestation of type 1 diabetes mellitus is approximately 10-13 years. In the vast majority of cases, type 1 diabetes manifests itself before the age of 40.

Clinical manifestations

In typical cases, Especially in children and young people, type 1 diabetes mellitus debuts with a clear clinical picture that develops over several months or even weeks. The manifestation of type 1 diabetes mellitus can be triggered by infectious and other concomitant diseases. Characteristic symptoms common to all types of diabetes, associated with hyperglycemia: polydipsia, polyuria, itchy skin, but in type 1 diabetes they are very pronounced. So, throughout the day, patients can drink and excrete up to 5-10 liters of fluid. Specific For type 1 diabetes, the symptom, which is caused by an absolute deficiency of insulin, is weight loss reaching 10-15 kg over 1-2 months. Characterized by severe general and muscle weakness, decreased performance, and drowsiness. At the beginning of the disease, some patients may experience an increase in appetite, which gives way to anorexia as ketoacidosis develops. The latter is characterized by the appearance of an acetone odor (or fruity odor) from the mouth, nausea, vomiting, often abdominal pain (pseudoperitonitis), severe dehydration and ends with the development comatose state. In some cases, the first manifestation of type 1 diabetes mellitus in children is a progressive impairment of consciousness up to coma due to concomitant diseases usually infectious or acute surgical pathology.

In rare cases of the development of type 1 diabetes in people over 35-40 years of age (latent autoimmune diabetes of adults) the disease may not manifest itself so clearly (moderate polydipsia and polyuria, no loss of body weight) and may even be detected by chance during routine determination of glycemic levels. In these cases, the patient is often first diagnosed with type 2 diabetes mellitus and prescribed tableted hypoglycemic drugs, which for some time provide acceptable compensation for diabetes mellitus. However, over the course of several years (often within a year), the patient develops symptoms caused by an increasing absolute deficiency of insulin: weight loss, inability to maintain normal glycemia on the background of tableted glucose-lowering drugs, ketosis, ketoacidosis.

Diagnostics

Considering that type 1 diabetes mellitus has a clear clinical picture and is also relatively rare disease, screening determination of glycemic levels for the diagnosis of type 1 diabetes mellitus is not indicated. The likelihood of developing the disease in the patients’ immediate relatives is low, which, together with the absence effective methods primary prevention type 1 diabetes mellitus determines the inappropriateness of studying immunogenetic markers of the disease in them. Diagnosis of type 1 diabetes mellitus in the vast majority of cases is based on the identification of significant hyperglycemia in patients with severe clinical manifestations of absolute insulin deficiency. Oral glucose tolerance test for the purpose of diagnosing type 1 diabetes mellitus it is necessary to carry out very rarely.

Differential diagnosis

In doubtful cases (detection of moderate hyperglycemia in the absence of obvious clinical manifestations, manifestation at a relatively advanced age), as well as for the purpose differential diagnosis with other types of diabetes, level determination is used C-peptide(basal and 2 hours after meals). Indirect diagnostic value in doubtful cases may have a definition immunological markers type 1 diabetes mellitus - antibodies to pancreatic islets, glutamate decarboxylase (GAD65) and tyrosine phosphatase (IA-2 and IA-2P).

Treatment any type of diabetes mellitus is based on three main principles: hypoglycemic therapy (for type 1 diabetes mellitus - insulin therapy), diet and patient education. Insulin therapy for type 1 diabetes mellitus is substitutive nature and its goal is to mimic physiological hormone production as much as possible in order to achieve accepted compensation criteria. Intensive insulin therapy is the closest to physiological insulin secretion. The need for insulin corresponding to its basal secretion provided by two insulin injections average duration actions (morning and evening) or one insulin injection long acting(glargine). The total dose of basal insulin should not exceed half of the total daily requirement in the drug.

Food or bolus insulin secretion is replaced by injections of short- or ultra-short-acting insulin before each meal, and its dose is calculated based on the amount of carbohydrates expected to be taken during the upcoming meal and the existing level of glycemia, determined by the patient using a glucometer before each insulin injection.

After the manifestation of type 1 diabetes mellitus and the initiation of insulin therapy for quite a long time, the need for insulin may be small and be less than 0.3-0.4 U/kg. This period is referred to as the remission phase, or "Honeymoon". After a period of hyperglycemia and ketoacidosis, which suppress insulin secretion by the 10-15% remaining beta cells, compensation for hormonal-metabolic disorders by administering insulin restores the function of these cells, which then take over providing the body with insulin at a minimum level. This period can last from several weeks to several years, but eventually, due to autoimmune destruction of the remaining beta cells, the “honeymoon” ends.

Diet for type 1 diabetes mellitus in trained patients who have the skills of self-control and selection of insulin dosage, it can be liberalized, i.e. approaching free. If the patient is not overweight or underweight, the diet should be isocaloric. The main component of food for type 1 diabetes is carbohydrates, which should account for about 65% of daily calories. Preference should be given to foods containing complex, slowly absorbed carbohydrates, as well as foods rich in dietary fiber. Products containing easily digestible carbohydrates (flour, sweets) should be avoided. The proportion of proteins should be reduced to 10-35%, which helps reduce the risk of developing microangiopathy, and the proportion of fats should be reduced to 25-35%, while limiting fats should account for up to 7% of calories, which reduces the risk of developing atherosclerosis. In addition, you should avoid taking alcoholic drinks, especially strong ones.

Forecast

In the absence of insulin therapy, a patient with type 1 diabetes inevitably dies from ketoacidotic coma. With inadequate insulin therapy, against the background of which the criteria for compensation of diabetes mellitus are not achieved and the patient is in a state of chronic hyperglycemia, they begin to develop and progress late complications. In type 1 diabetes mellitus the greatest clinical significance in this regard, there are manifestations of diabetic microangiopathy (nephropathy and retinopathy) and neuropathy (diabetic foot syndrome).

Type 1 diabetes mellitus is an organ-specific autoimmune disease that leads to the destruction of insulin-producing beta cells of the pancreatic islets, manifested by an absolute deficiency of insulin. In some cases, patients with overt type 1 diabetes mellitus lack markers of autoimmune damage to beta cells (idiopathic diabetes mellitus type 1).

Etiology

Type 1 diabetes mellitus is a disease with a hereditary predisposition, but its contribution to the development of the disease is small (it determines its development by approximately 1/3). The probability of developing type 1 diabetes in a child with a sick mother is 1-2%, father - 3-6%, brother or sister - 6%. One or more humoral markers of autoimmune beta cell damage, which include anti-pancreatic islet antibodies, anti-glutamate decarboxylase antibodies (GAD 65) and anti-tyrosine phosphatase antibodies (IA-2 and IA-2beta), are found in 85-90 % of patients. Nevertheless, the main importance in the destruction of beta cells is given to cellular immunity factors. Type 1 diabetes mellitus is associated with HLA haplotypes DQA and DQB. With increased frequency, type 1 diabetes mellitus is combined with other autoimmune endocrine (autoimmune thyroiditis, Addison's disease) and non-endocrine diseases, such as alopecia, vitiligo, Crohn's disease, rheumatic diseases.

Pathogenesis

Type 1 diabetes manifests itself when 80-90% of beta cells are destroyed by an autoimmune process. The speed and intensity of this process can vary significantly. Most often when typical course diseases in children and young people, this process proceeds quite quickly, followed by a rapid manifestation of the disease, in which only a few weeks can pass from the appearance of the first clinical symptoms to the development of ketoacidosis (up to ketoacidotic coma).

The pathogenesis of type 1 diabetes mellitus is based on absolute insulin deficiency. The inability of glucose to enter insulin-dependent tissues (fat and muscle) leads to energy deficiency, resulting in intensified lipolysis and proteolysis, which are associated with weight loss. An increase in glycemic levels causes hyperosmolarity, which is accompanied by osmotic diuresis and severe dehydration. Under conditions of insulin deficiency and energy deficiency, the production of contrainsular hormones (glucagon, cortisol, growth hormone) is disinhibited, which, despite increasing glycemia, causes stimulation of gluconeogenesis. Increased lipolysis in adipose tissue leads to a significant increase in the concentration of free fatty acids. With insulin deficiency, the liposynthetic capacity of the liver is suppressed, and free fatty acids begin to be included in ketogenesis. The accumulation of ketone bodies leads to the development of diabetic ketosis, and subsequently ketoacidosis. With a progressive increase in dehydration and acidosis, a coma develops, which, in the absence of insulin therapy and rehydration, inevitably ends in death.

Epidemiology

Clinical manifestations

In typical cases, Especially in children and young people, type 1 diabetes mellitus debuts with a clear clinical picture that develops over several months or even weeks. The manifestation of type 1 diabetes mellitus can be triggered by infectious and other concomitant diseases. Characteristic symptoms common to all types of diabetes, associated with hyperglycemia: polydipsia, polyuria, itching, but in type 1 diabetes mellitus they are very pronounced. So, throughout the day, patients can drink and excrete up to 5-10 liters of fluid. Specific For type 1 diabetes, the symptom, which is caused by an absolute deficiency of insulin, is weight loss reaching 10-15 kg over 1-2 months. Characterized by severe general and muscle weakness, decreased performance, and drowsiness. At the beginning of the disease, some patients may experience an increase in appetite, which gives way to anorexia as ketoacidosis develops. The latter is characterized by the appearance of an acetone odor (or fruity odor) from the mouth, nausea, vomiting, often abdominal pain (pseudoperitonitis), severe dehydration and ends in the development of a coma. In some cases, the first manifestation of type 1 diabetes mellitus in children is a progressive impairment of consciousness up to coma due to concomitant diseases, usually infectious or acute surgical pathology.

Diagnostics

Considering that type 1 diabetes mellitus has a clear clinical picture and is also a relatively rare disease, screening determination of glycemic levels to diagnose type 1 diabetes mellitus is not indicated. The likelihood of developing the disease in close relatives of patients is low, which, together with the lack of effective methods for primary prevention of type 1 diabetes, determines the inappropriateness of studying immunogenetic markers of the disease in them. Diagnosis of type 1 diabetes mellitus in the vast majority of cases is based on the identification of significant hyperglycemia in patients with severe clinical manifestations of absolute insulin deficiency. Oral glucose tolerance test for the purpose of diagnosing type 1 diabetes mellitus it is necessary to carry out very rarely.

Differential diagnosis

In doubtful cases (detection of moderate hyperglycemia in the absence of obvious clinical manifestations, manifestation at a relatively advanced age), as well as for the purpose of differential diagnosis with other types of diabetes mellitus, level determination is used C-peptide(basal and 2 hours after meals). In indirect diagnostic value in doubtful cases, the definition may have immunological markers type 1 diabetes mellitus - antibodies to pancreatic islets, glutamate decarboxylase (GAD65) and tyrosine phosphatase (IA-2 and IA-2P).

Treatment any type of diabetes mellitus is based on three main principles: hypoglycemic therapy (for type 1 diabetes mellitus - insulin therapy), diet and patient education. Insulin therapy for type 1 diabetes mellitus is substitutive nature and its goal is to mimic physiological hormone production as much as possible in order to achieve accepted compensation criteria. Intensive insulin therapy is the closest to physiological insulin secretion. The need for insulin corresponding to its basal secretion is provided by two injections of intermediate-acting insulin (morning and evening) or one injection of long-acting insulin (glargine). The total dose of basal insulin should not exceed half of the total daily requirement for the drug.

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia that results from defects in insulin secretion, insulin action, or both. Chronic hyperglycemia in diabetes mellitus is associated with damage, dysfunction and failure various organs, especially the eyes, kidneys, nerves, heart and blood vessels.

Type 1 diabetes mellitus is caused by destruction of the beta cells of the pancreas, usually leading to an absolute deficiency of insulin. There are two main subtypes:

Autoimmune diabetes mellitus.

This form was previously called insulin-dependent diabetes. It is the result of autoimmune destruction of pancreatic beta cells. Markers of immune destruction of beta cells include autoantibodies to islet cells(ICAs), insulin autoantibodies (lAAs), decarboxylase autoantibodies glutamic acid(GAD65) and a number of other autoantibodies. There is no doubt about the presence of genetic predisposing factors, in particular the connection of the disease with the HLA system. In autoimmune diabetes mellitus, beta cell destruction can occur at varying rates, typically being rapid in children and slower in adults. In any case, insulin secretion sharply decreases or stops completely, which manifests itself low level C-peptide in the blood.

Idiopathic diabetes mellitus.

The etiology of some forms of type 1 diabetes is unknown. Many of these patients constantly experience insulin deficiency and a tendency toward ketoacidosis, but signs autoimmune process are missing. Most patients with idiopathic diabetes mellitus are of African or Asian origin. This form of diabetes mellitus has a pronounced familial pattern; no connection with HLA has been identified. The absolute need for insulin replacement therapy in patients may appear and disappear.

Clinical picture of type 1 diabetes mellitus

The onset of the disease is acute. Clinical picture at the time of detection of the disease is a consequence of absolute insulin deficiency, which leads to severe hyperglycemia and glycosuria, which in turn causes characteristic symptoms diabetes mellitus These include:

polyuria (including at night) is a consequence of osmotic diuresis;
thirst; dry mouth;
weight loss despite increased appetite and polyphagia;
skin manifestations, including skin itching (itching of the mucous membranes is possible - in women in the vulva area), a tendency to bacterial and fungal infections of the skin and mucous membranes (furunculosis, candidiasis);
glucose and ketone bodies in the urine.

Also characteristic nonspecific symptoms: weakness, fatigue.
If treatment is not started in time, patients develop diabetic ketoacidosis with progressive impairment of consciousness up to diabetic coma.
In patients receiving glucose-lowering therapy, Clinical signs may be erased even with persistent hyperglycemia. During development chronic complications diabetes mellitus ( diabetic retinopathy, diabetic nephropathy, diabetic polyneuropathy) the corresponding clinical picture will be observed.